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Organisers


J S S University (Established under section 3 of the UGC Act 1956) Sri Shivarathreeshwara Nagara, Mysore – 570 015, Karnataka, India

Dr B.Suresh, M.Pharm, PhD, D.Sc Vice Chancellor

June 29, 2012

MESSAGE It is indeed a matter of pleasure that the Department of Anaesthesiology, JSS Medical College, Mysore, is organising a Continuing Medical Education Programme, PG Excel-2012, on 21st and 22nd July. To enhance health care delivery, this CME provides educational activities which serve to maintain, develop, or increase the knowledge, skills, performance and relationships that a physician uses to provide service for patients and the profession. Physicians need to participate in educational activities for nurturing a balanced personality. I am sure the CME activities will throw light on developing and enhancing the knowledge and skills of the postgraduates which help in delivering a better service for patients, the public and the profession. On this occasion, I convey my best wishes and greetings and wish the CME a success. With Best Wishes,

President, Pharmacy Council of India, New Delhi __________________________________________________________________________________________________ Phone: +91 – 821 – 2548391; Fax: +91 – 821 – 2548394 e-mail: sureshbhojraj@hotmail.com, vc@jssuni.edu.in; web: www.jssuni.edu.in


MESSAGE It gives me immense pleasure to note that the Department of Anaesthesiology, JSS Medical College, Mysore, is organizing PG Excel – 2012 on 21st and 22nd July 2012. Your intention to cover the new diagnostic tools, complex therapeutic modalities and anaesthetic management of variety of clinical cases will certainly be useful. All the P.G. students and the young faculty in the Dept of Anaesthesia will certainly be benefitted with this programme. Realizing the importance of continuing medical education and professional development the faculty is well versed with the modern concepts of participatory learning. Medical education does not and should not be confined to acquiring the knowledge of Medicine, Surgery and other medical subjects. It ought to be a holistic concept, encompassing human qualities expected of the medical profession. We feel this education should provide opportunities for the students to acquire modern knowledge and necessary skills while developing moral and ethical values characteristic of a humane society. The objective is to have medical graduates of unmatched quality who are highly skilled, caring and cultured professionals. I believe that this event will bring out the best in terms of academic excellence and social extravaganza. I hope that this programme will be very useful for exchanging the knowledge. Once again I take this opportunity to thank and congratulate the organizing committee of PG Excel – 2012 and wish the programme a grand success.


MESSAGE With the blessings of His Holiness Sri Sri Sri Shivarathri Deshikendra Maha Swamiji, Suttur Sri Kshethra, the Department of Anaesthesiology, J.S.S. Medical College Mysore is conducting the PG EXCEL 2012 for the second time. First time the PG EXCEL was conducted in 2005 by the Department of Anaesthesiology, J.S.S. Medical College, Mysore.

The Organising Committee has taken all the efforts to make PG EXCEL 2012 a memorable one for the faculty as well as for the post graduates. For the last several months the ground work has been done by all the committees to make it an event to remember. We have invited well known senior faculty from Karnataka and other states for the benefit of the post graduate students so as to face the academic examination and their future career in Anaesthesiology. My association with Dr G.S.Venkatesh, Director of Medical Education, Government of Karnataka dates back to days of his post graduation as my student. I am very proud indeed to have him here to grace this occasion. On behalf of the organising committee of the PG EXCEL 2012, I thank Dr.B.Suresh Vice Chancellor of J.S.S. University and Dr. H.Basavanagowdappa the Principal J.S.S. Medical College for all the help extended to conduct this programme. I appreciate the enthusiasm of all the guest faculty and post graduates who have gathered here and helped us in making this program a wonderful academic experience. I thank all the pharmaceutical companies who helped directly and indirectly to conduct PG EXCEL 2012. Dr. P.N. VISWANATHAN Professor and HOD Dept of Anaesthesiology, JSS Medical College, Mysore.


From the desk of Organizing Secretary, Dear Friends, It is a privilege for any institution to conduct a Continuing Medical Education like PG Excel which introduces the pattern of examination to the post graduate students. The Department of Anaesthesiology, JSS Medical College along with Indian Society of Anaesthesiologists takes immense pride and pleasure in presenting PG Excel 2012. We promise you a feast of scientific deliberations encompassing all the probable examination oriented discussions presented in six courses. It would be a great occasion to interact with the experienced faculty each an authority in their field in a novel approach to break the monotony. However, let not your minds be overtly preoccupied with the business, fasten your seatbelts to enjoy the cultural extravaganza that we have to offer at PG Excel 2012. I am spellbound with the overwhelming response from the faculty who are taking part in this event with great enthusiasm. My sincere thanks to all of them. No work of real merit can be undertaken and finished successfully without the cooperation of all the committee members. My heartfelt thanks to all my colleagues for working towards the goal.

It would be a pleasure to have you all with us in this beautiful ‘Royal City’ to enjoy the mix of scientific, social and cultural bonanza.

Welcome to PG Excel 2012. Affectionately, Dr Akkamahadevi P. Organising Secretary


From the editor’s desk…, The year 2005 marked the birth of the CME under the banner of PG EXCEL KARNATAKA – 2005 for the very first time, at JSSMC under the able guidance of the then Professor and HOD, Dr.N.V.Nagalakshmi. The euphoria of its success still lingers on as we gear up for another academic extravaganza, PG EXCEL-2012 with an ambition to leap beyond excellence. Way back in 2004, when we gathered at KLE, Belgaum, for the PG Exam oriented CME, organized by Prof. Kotur, little did we realize that it would be the beginning of an annual landmark event. It was decided then that such a programme would be conducted every year, in rotation, in various medical colleges of Karnataka and the baton was passed on to JSSMC, Mysore to conduct the next event in 2005. Gathering the very best of faculty under one roof would not have been possible, but for the enthusiasm shown by eminent teachers from various colleges and institutes. July 21st and 22nd 2012 will see jam-packed brain storming sessions where the PGs will interact with renowned teachers and tough examiners. Laborious efforts have gone into the planning of an exhaustive scientific programme consisting of Interactive Case discussions, Focus sessions, Expert opines, Video sessions, PG debates and Quiz. We hope the postgraduates will enjoy these precious pearls as much as we enjoyed compiling and threading them together.

Notwithstanding our great expectations from our contributing authors, it is indeed commendable that they not only met them but far exceeded them as well (mercifully, they put up with our constant cajoling and threats, to meet deadlines, with equanimity!). The result is a CME book with highly commendable write-ups. We sincerely appreciate their enthusiastic efforts in helping us bring out the highly informative and knowledge-packed book which promises to be a great “carry home” gift. It is said that the human brain is a super computer which came without an instruction manual. As teachers, experience tells us, that youngsters can be moulded to develop into highly successful, dependable and competent professionals – at times they just need the right push. We have included an article on “How a PG excels” to provide that little push. Event of such magnitude is invariably the product of compounded efforts of many individuals. Team Anaesthesia JSS works as a family every time we organize an event, with each member contributing their might. We appreciate the support and help extended to us by our whole department who pitched in directly or indirectly (by taking care of the immense clinical work-load) in making this academic experience an iconic event.

Dr Nalini Kotekar,

Dr Uma.G,

Scientific Committee – PG Excel 2012

Dr Pratibha.R.Matche


ON HOW A POST GRADUATE STUDENT EXCELS Dr. Nalini Kotekar, Professor, JSSMC, Mysore.

A simple statement, and yet one that was packed with lessons for all of us was made a few weeks ago by Novak Djokovic as part of his post match speech after his final round loss to Spaniard Rafael Nadal. Despite having lost his crucial chance to make history by winning the last of all the Grand Slams, he remarked, “The better player won today”. For five time winner Djokovic, the reigning Wimbledon, US Open and Australian Open Champion, it was the end of his dreams. Medical Post Graduate exams are no less than Grand Slams of our professional careers, throwing us the challenge of becoming better players in the journey of life. THE WINNING EDGE “It might have been”. “I should have”. “I could have”. “I wish I had”. “If only I had given a little extra” Sounds familiar, doesn’t it? When a PG says, “I will do it one of these days”, you can be sure it means none of these days. On the other hand, I am sure all winners wanted to be procrastinators but never got around to it! In order to get the Winning Edge, we need to strive for excellence. All that is needed is a little edge. The winning horse may only be faster by a fraction, but the rewards are five or ten times greater. Is it fair? That does not matter. Those are the rules of the game. That is the way the game is played. The same is true in our lives. Successful people are not ten times smarter than people who fail. They may be fractionally better, but the rewards are ten times bigger. We do not


need to improve 1000% in any one area, but to improve 1% in 1000 different areas, which is a lot easier, and gives the winning edge. Life is like a cafeteria. You take your tray, select your food and pay at the other end. You can get anything as long as you are willing to make choices and pay the price. If you wait for people to serve you, you will wait forever. Life is like that too. You make choices and pay the price to succeed. Just the right mix of the following ingredients: Desire, Enthusiasm, Commitment, Responsibility, Hard work, Character, Positive belief in oneself, Perseverance and Performance goes into making a successful student. To get through an examination creditably, vigorous training is necessary. Even a good student has to have a special preparedness and bring all his resources to the spear-head for the final thrust at the exam hall. He has to bring to a focus -his concentration, writing power, memory, reproduction and so on, besides having his subject matter at his finger tips. On the basis of his actions now, his future rewards will follow. The power of the training imparted by facing stiff examinations helps in inculcating patience, tolerance, judgment, calmness, self confidence and builds up the character of young medical professionals to face future eventualities. TRAINING AS AN EXAMINEE HAVING A GOAL People confuse goals with dreams and wishes. Dreams and wishes are nothing more than desires. Desires become goals when they are supported by 5 Ds - Direction, Dedication, Determination, Discipline and Deadlines. Identify the specific goal, take measurable steps to start, add deadlines and stick to it. TIME MANAGEMENT Your prime time is yours ‌ Spend it wisely! To a large degree, the key to making the very most out of your day lies in knowing when you get your best work done and then acting on that knowledge. Develop your sense for your peak time and this is the time when you are likely to be


most effective, most enthusiastic and most detail oriented. We all have good times when we can get the most done and the quality of work tends to be the best, thanks to body chemistry, mindset and accumulated habits. During this time we ought to be careful about deviating our energy towards non-productive activities (like surfing the net). You are doing yourself and your grades a disservice if you spend this time on non study activities. Many a poor grade can be traced back to poor personal scheduling. . It is important for you to manage your hospital related work, seminars or class related commitments in a way that allows you to take advantage of whatever portion of peak time you can claim during the course of the day. If your “prime time” slot is not available to you, deciding not to study is not an option! Resolve to make the most of the time available to you. Tackle the tough stuff first. You know that important bit of your study work which you are really not looking forward to doing? Put it at the top of the list and don’t move on to the next item until you have accomplished it. Now, isn’t that a goal reached?! On any given day, apart from long OT lists and exhaustive PAEs, you would be required to read up for 1. Specific cases on your list the next day. 2. Seminar topics. 3. Literature search for your dissertation. 4. Brushing up on a technique you would be given a chance to do. Etc….So now that you know that you just have to do it, isn’t it a good idea to prepare a power list and practice the sequence till it becomes a habit?

DISCUSSION

In most teaching hospitals, group discussions in the form of interactive seminars with active participation of the teachers are a routine practice. Topics covered in the course period, if religiously attended, with preparation, could help the student cover over 85 to 95 % of his exam portions. One should never shy away from such discussions as they may point out specific deficiencies in the students and will point out to them, in advance, their loop holes which they still have the time to check and correct. The fear of hard work can deter an average student from discussing the subject with others. On the other hand, the intelligent ones take the opportunity to discuss what they have learnt, in order to find out if somebody may know something better; or


whether their own preparation is in any way sub – standard, in which event they can improve their knowledge when there is still time. (This is a shrewd game played often by the toppers!). Individual thought process can get clogged at times, but in a group discussion on a subject, the different members in the group will add to the different points and views and the conclusions arrived at, will be just about perfect. ATTITUDE OF AN EXAMINEE Having gone through the vigorous training during his tenure, the student has to acquire mental and physical calm, a serenity, a detached personality before the exams which would prove that he has been able to master his senses and has come to this state where he is unruffled by the agitations about and around him. He requires to practice restraint from diversions that take his mind off his ultimate goal before his exams. Physical well being is very important for him to stand the strain of exams and also his mental peace and strength to carry him through any out – of – the way occurrences. Examinations are mainly held to assess and award the educational qualifications of a student, But the primary objective of the examination is to subject the student to some rigid discipline and regulation, so that, his mental and physical prowess are harnessed to serve him in various contingencies in his future. Examinations, therefore are great personality builders making the youngsters to unconsciously prepare and accumulate stamina in the face of any crisis. At this point it wouldn’t be inappropriate to mention that post graduation is an excellent time to learn the skills of building better interpersonal relationships. Conscious efforts need to be made to keep out negativity with regard to fellow students, teachers and day to day occurrences. Petty mindedness, back biting and prejudices are for the ordinary. Shun mediocrity! You are made for bigger things. Learn to nurture a spirit of co-operation, sincerity and mutual help, all of which will increase your productivity and stand by you now and forever. Remember – difficult situations and people are going to be a part of your life. There is no point fretting or fuming about things you can’t change. Faster you adapt to your world, better are your chances at thriving in it.


WHAT THE EXAMINERS WANT Apart from the student’s depth of knowledge, the answer paper conveys a lot about the student even in the first few lines. The student’s hand writing, his way of expression, correct numbering and general neatness are few of the things that the examiner unconsciously registers in his mind. Short-hand lingo ( the kinds used for SMSing), haphazard or disjoint answers and lousy spellings disgusts any examiner. Imagine if yours is the last paper in a bundle of two dozen papers and your examiner is exhausted (paper corrections are energy draining procedures) do you really expect him to play God and have the patience to go through your messy paper with cuts and scratches and flood you with marks? On the other hand, if he has a paper, with precise answers, a good handwriting, with neat presentation and a strong command of the language – no matter how tired he is, marks and blessings are sure to flow! Also, remember the examiner sets the question with some objective and then expects a definite answer from the student. Voluminous pages lacking in precision will surely not get good grades. ON BEING A TOPPER In order to keep your head and shoulder above the average, you must adopt a more positive attitude of defeating others. Your compatriots are your competitors. Unless there is the constant will to contest and better yourself, you cannot hope to be placed among the chosen few. Remember Knowledge is Power

The constant effort in assimilation, percolation and

reproduction can make all the difference. Prior learning by writing the answers and acquiring the style of inserting more substance in less length should be the motto of a good writer. You also have the advantage of not having the superfluous sense of knowing something which you really do not know. It pays to routinely renew, recollect and retain! The examination hall is not the place for practicing the art of brevity and shaping answers. THE GRAND FINALE Remember prior hard work make exams a pleasure and well preparedness is the best antidote for anxiety. Get adequate sleep the day before. Staying awake the whole night to revise is a serious mistake indeed. Your mind may chalk out a plan or performance for last-minute


preparation, but your body may fail to keep up with this, refusing to serve you. Result – poor performance due to extreme fatigue inspite of good preparedness. Avoid heavy meals, alcohol, excess diuretics, E.g. Caffeine. Do avoid the company of nervous students. It could be contagious! Do not be restless, irritable or jittery. A good start at your seat with a calm disposition could give you a better lead in answering your questions. Don’t try learning new things before an exam. Use all the positivity you can channelize. Visualize yourself doing well. Arrive early. Keep the first five minutes for reading up questions and letting your pulse rate slow down. Deep breathing helps! Budget your time wisely and according to marks. Getting stuck on tough ones wastes time, builds frustration and blocks free flow of recall. Be aware of pattern of question and be prepared for changes as well. If the questions are tough, don’t panic, let the thought process flow from a clear mind. Examiners are sympathetic if questions are tough. Classifications, headings, sub-headings, summary, labeled diagrams and legibility carry good impression. You need to handle essays by furnishing the following combinations: Definition, description,

comparison,

signifying

the

differences,

outline,

justification,

aetiology,

pathophysiology, clinical features, investigations, treatment modality, PAE, pre-op preparation, premedication, anaesthetic management, post-op pain, ventilatory support, Etc. Do not assume, that one answer’s 60% will compensate for another answer’s 40%. Do attempt all the questions. Put in whatever you can remember. Each mark counts. Do number your answers correctly. If you are running out of time, at least jot down the points, let the examiner know what you planned to write. Keep out gimmicks to occupy space. Enlarged answers are easily recognized – no extra marks for that! THE FINAL ENCOUNTER


Viva voce is an essential part of post graduate exams which calls for training in the vocal art of communication. If you have been regular with discussions as a PG you are at an advantage. Along with correctness of the answers, the mannerisms and general dispositions matter. Keep your mental faculty open and understand the question straight away, without asking for repetitions and proceed to answer. Using the time allotted sensibly, mentally prepare for all possible questions you may have to answer pertaining to your major and short cases. Be prepared for interruption and tangential questions. Don’t be surprised if discussion moves to other topics, if the examiners so wish. Keep your cool, it helps clear thought process. Remember, no examiner intends to harm. The second portion of your practical exam assesses your accumulated knowledge on drugs, equipment, instruments ,x-rays, Ecgs, capnograms etc.. Answer confidently whatever you know on what is asked. If not sure, do not waste the examiner’s and your time. Tell them you are sorry that you are not sure so that they could proceed to the next. Whatever may have gone into the past 2 or 3 precious years of post graduation, there is one ultimate event the student faces, THE JUDGEMENT DAY. Be it theory or viva voce, it is now that the fate of the postgraduates will be settled differently. The brilliant will shine and utilize these hours to go ahead in life, while the others can only wish, “if only I had”. After all this, one has to have at the back of his mind that exams don’t constitute life and life is not only about exams – as unambitious a thought as this might be, this thought serves to reduce the expectant stress, thereby contributing to a better more clear headed approach – something that will assure a better outcome. So buck up and let it be said of you, “THE BETTER PLAYER WON!” GOOD LUCK!


Scientific Programme on 21st July, Saturday Time

Topic

Speaker

Chairperson

8:30 a.m. -8:50 a.m.

Focus Session: Applications of Gas Laws in Anaesthesiology Case Discussion – A Patient with Bronchiectasis posted for left lower lobe lobectomy

Viswanathan P N Mysore

Padmanabha S Mangalore

8:50 a.m. -9:50 a.m.

10:00 a.m.-10:30 a.m. 10:30 a.m. -11:15a.m.

11.15 a.m. -12.15p.m.

12:15 p.m. -1:00 p.m. 1:00 p.m. –1:45 p.m. 1:45 p.m. –2:30 p.m.

Gurudatt C L Mysore Mahantesh Sharma Davangere

Inauguration Focus Session – The Electrical activity of the heart-ECG Case Discussion – A Diabetic patient for below knee amputation Focus Session – Vaporizers

Muralidhar K Bangalore

Shenbagavalli S Bangalore

Madhusudhan U Mangalore Ravikumar C Davangere Aruna Parameswari Chennai

Nagalakshmi N V Mysore

LUNCH Expert OpinesAnaesthetic Management of a patient with Bronchial Asthma Case Discussion – A Patient with End Stage Renal Disease for Renal Transplantation Expert opines- A Neonate for Herniotomy

Harsoor S S Bangalore

Gayathri Bhat Mangalore

Sunita U Bangalore Sanikop S Belgaum Aruna Parameswari Chennai

Mahabala S Mangalore

4:00 p. m. -4:30 p. m.

Focus Session: Examination of the CVS

Lakshmi Kumar Cochin

Devanand B Bellary

4:30 p. m. -5:30 p. m.

Case DiscussionPrimigravida with pregnancy induced hypertension PG Debate Proseal LMA in Laparoscopic surgery Expert opines-An Obese patient for Bariatric Surgery PG Debate Third space:The History and Mystery of it

Kodandaram N S Bangalore Rangalakshmi S Bangalore Nidhi Pooja Shah

Kotur P F Belgaum

Radhika Dhanpal Bangalore

Radha M K Bellur

Bhagirath S N Subramanian V V

Uma G Mysore

2:30 p.m. –3:30 p.m.

3:30 p. m. -4:00 p. m.

5:30 p. m. -6:00 p. m.

6:00 p. m. -6:30 P. m.

6:30 p. m. -7:00 p. m.

7:00 p. m. onwards 7:30 p. m.

PG QUIZ (written) Entertainment and Dinner


Scientific Programme on 22nd July, Sunday Time 8:00 a.m. -8:30 a.m.

8:30 a.m. -9:30 a.m.

9:30 a.m. -10:15 a.m.

10:15 a.m. -11:15 a.m.

11:15 a.m. -12:00 p.m. 12:00 p.m. -12:30 p.m.

12:30 p.m. -1:00 p.m.

Topic Expert opinesAnaesthesia for Cleft Lip and Cleft Palate repair Case Discussion- A Patient with Obstructive Jaundice for laparoscopic cholecystectomy Focus sessionAnaesthesia Workstation Case Discussion- A Patient with IHD and Hypertension for hemicolectomy Focus Session- Acid Base Physiology Video Session- Lower extremity Peripheral nerve blocks Expert opinesAnticoagulant therapy and Regional Anaesthesia

1:00 p.m. -1:45 p.m. 1:45 p.m. -2:45 p.m. 2:45 p.m. -3:15 p.m.

3:15 p.m. -4:15 p.m.

4:15 p.m. -4:45 p.m.

4:45 p.m. -5:15 p.m.

5:15p.m.-5:45 p.m

Speaker Balabhaskar S Bellary

Chairperson Somashekaram Potli Kolar

Brig(retd) Mohan C V R Bangalore Chidananda Swamy Bangalore Ramkumar Venkateswaran Manipal

Mallikarjun D Davangere

Murali R. Chakravarthy Bangalore Gangadhar S B Tumkur Lakshmi Kumar Cochin Balavenkatasubramanian J Coimbatore

Srikantamurthy T N Bangalore Kodandaram N S Bangalore

Balavenkatasubramanian J Coimbatore

Vasudev Upadhya Bangalore

LUNCH PG Quiz conducted by Sripad Mehandale & Anand Bangera, Mangalore Video Session – An Approach to Difficult Airway Case Discussion – Patient with Graves disease posted for Thyroidectomy Focus Session – X rays and Anaesthesiology PG Debate Can Regional Anaesthesia be given in a patient with difficult airway Expert Opines – Intensive Care Management of Severe Traumatic Brain Injured Patients.

Raveendra U S Mangalore

Malathi C N Mysore

Safia Shaikh Hubli Ragavendra Rao Dharwad Saraswathi Devi Bangalore Usha N K Amita Mahesh

Radha M K Mysore Raveendra U S Mangalore

Venkatesh H K Bangalore

Pai A V Hoskote


Contents FOCUS SESSIONS 1

Application of gas laws in Anaesthesiology Viswanathan P N

2

The Electrical Activity of the Heart – ECG Muralidhar K

3

Vaporizers Aruna Parameswari

4

Examination of the CVS Lakshmi Kumar

5

Anaesthesia Workstation Ramkumar Venkateswaran

6

Acid-Base Physiology Lakshmi Kumar

7

X-rays and Anaesthesiology Saraswathi Devi

EXPERT OPINES 1

Anaesthetic Management of a patient with Bronchial Asthma Harsoor S S

2

A Neonate for Herniotomy Aruna Parameswari

3

An Obese Patient for Bariatric Surgery Radhika Dhanpal

4

Anaesthesia for Cleft Lip and Cleft Palate repair Bala Bhaskar S

5

Anticoagulant therapy and Regional Anaesthesia Balavenkatasubramanian J

6

Intensive Care Management of Severe Traumatic Brain Injured Patient Venkatesh H K

7

Is there a role for dopamine or diuretics in acute renal failure Akkamahadevi P


VIDEO SESSIONS 1

Lower extremity Peripheral nerve blocks Balavenkatasubramanian J

2

An Approach to Difficult Airway Raveendra U S

PG DEBATE 1

ProSeal LMA in Laparoscopic surgeries Kotur P F, Nidhi, Pooja Shah

2

Third Space: The History and Mystery of it Uma G, Subramanian V V, Bhagirath.S.N

3

Can Regional Anaesthesia be given in a patient with difficult airway Radha M K, Raveendra U S, Usha N K, Amita Mahesh

CLINICAL CASE DISCUSSIONS 1

A Patient with Bronchiectasis posted for left lower lobe lobectomy Gurudatt C L, Mahantesh Sharma

2

A Diabetic patient for below knee amputation Madhusudhan U, Ravikumar C

3

A Patient with End Stage Renal Disease for Renal Transplantation Sunita U, Sanikop S

4

Primigravida with pregnancy induced hypertension Kodandaram N S, Rangalakshmi S

5

A Patient with Obstructive Jaundice for Laparoscopic Cholecystectomy Brig. (retd.) Mohan C V R, Chidananda Swamy

6

A Patient with IHD and Hypertension for right hemicolectomy Murali R. Chakravarthy, Gangadhar S B

7

Patient with Graves disease posted for Thyroidectomy Safia Shaikh, Ragavendra Rao


Disclaimer The information and opinions presented in the lecture write-ups reflect the views of the authors and not of editorial committee or organizers of PG Excel 2012, Mysore. Inclusion in the CME book does not constitute endorsement by the organizers. Neither the scientific committee nor anyone else involved in creating this volume assumes any liability or responsibility for the accuracy, completeness or usefulness of any information provided in the CME book. Readers are encouraged to confirm the information contained herein with other sources.

Scientific Committee PG Excel 2012 Mysore


FOCUS SESSIONS


1

APPLICATION OF GAS LAWS IN ANAESTHESIOLOGY Dr P. N. Viswanathan Professor and HOD, JSSMC, Mysore

Introduction All matters exist in one of the three states- solid, liquid or gas. The origin of the gas laws came out of experimental work conducted during the seventeenth and eighteenth centuries by several people. When describing the behavior of gases the properties of temperature, pressure and volume are related in a consistent manner, which makes it possible to formulate three “gas laws”. The knowledge of these gas laws will help us to understand the behavior of gases in changing conditions. Pressure- Pressure is the force applied or distributed over a surface and is expressed as force per unit area. Temperature- Temperature is the thermal state of a substance which determines whether it will give heat to another substance or receive heat from it. Volume- Space occupied by a substance measured in three dimensions. Compressed gas- A nonliquified compressed gas is a gas that does not liquefy at ordinary ambient temperatures regardless of the pressure applied. k constant- The Boltzmann constant is the physical constant relating energy at the individual particle level with temperature. 1. BOYLE’S LAW- Postulated by Robert Boyle in 1662 states that at constant temperature, the volume of a fixed mass of gas is inversely proportional to its pressure. 1. Vα1/P

or

PV = k is a constant.

Figure 1 Illustration of Boyle's Law


2

Applications1. The content of any gaseous cylinder depending on its physical capacity and its pressure showing on the bourdan gauge can be calculated. Consider an oxygen cylinder with capacity of 5 litres and a pressure of 13800k Pa. Calculate the volume of oxygen available at one atmospheric pressure. As per Boyle’s law P1V1 = P2V2 V1 - Volume of cylinder V2 - Volume of gas at one atmosphere P1 - The cylinder pressure P2 - Atmospheric pressure 13800k Pa × 5L = 100k Pa × V2L V2 = 13800 × 5/100 = 690L 2. Same principle has been used in whole body plethysmography to determine the lung volume change depending on the pressure changes. 3. The action of the diaphragm of our body. When we inhale the diaphragm moves downward allowing the lungs an increased volume. This decreases the pressure inside the lungs so that the pressure is less than the outer pressure. This results in forcing air into the lungs. When we exhale the diaphragm moves upward and decreases the volume of lungs. This increases the pressure inside the lungs above the pressure on the outside of the lungs so that gases are forced out of the lung. 4. Drawing fluid into a syringe, we increase the volume inside the syringe; this correspondingly decreases the pressure inside. The pressure outside the syringe is greater and forces fluid into the syringe. 5. Intrapleural pressure becomes negative because as the inspiratory muscles act to increase the thoracic volume, the intrapleural space increases in volume thereby decreasing the pressure. 6. Negative pressure in epidural space due to indentation of duramater by Huber point needle 7. Decompression sickness- As a diver descends; the water pressure around him increases, causing air in his scuba equipment and body to occupy a smaller volume (compress). As he ascends, water pressure decreases, so Boyle's Law states that the air in his gear and body expand to occupy a greater volume. 2. CHARLES LAW- described by Jacques Charles in 1787 states that, at a constant pressure the volume of a fixed mass of gas is proportional to its absolute temperature.


3

VαT V/T = k (constant) V1/T1 = V2/T2

or V1/V2 = T2/T1 or V1T2 = V2T1

Figure 2 Illustration of Charle's Law Applications1. Determination of amount of vapour of a volatile anaesthetic agent at room temperature. If we know that the amount of halothane vapour at 273K (0°C) is 270ml, how much is present at 293K (20°C). V1T2 = V2T1 V2 = V1T2/T1 V2 = 207 × 293/273 = 222ml 2. One way of heat loss from the body is that air next to the body surface gets warmer and moves up and thus patient loses heat this way. 3. Respiratory gas measurements of tidal volume and vital capacity are done at ambient temperature while these exchanges actually take place in the body at 37°C. Volume measured by spirometer are at ambient temperature, pressure and saturated conditions, it gives a lower volume and therefore must be adjusted for the temperature difference between the spirometer and the patient’s body temperature. 3. GAY – LUSSAC’s LAW- Postulated by Joseph Louis Gay-Lussac in 1808 states that, at a constant volume the pressure of a fixed mass of a gas is proportional to its absolute temperature. PαT

or P/T = k (constant)

P1/T1 = P2/T2 or P1T2 = P2T1


4

Figure 3 Illustration of Guy Lussac's Law Applications1. Medical gases are stored in the cylinders have constant volume and high pressures. If these are stored at high temperature, pressure will rise causing explosions. 2. Molybdenum steel can withstand pressure till 210 bars. Weakening of metal in damaged cylinders is at a greater risk of explosion due to rise in temperature. 3. Hydrogen thermometer- Used as a standard for scientific temperature measurement. When a constant volume of hydrogen is heated increase in the pressure may be accurately recorded and it gives a measure of the absolute temperature rise.

4. COMBINED GAS LAW AND UNIVERSAL GAS CONSTANT The combined gas law combines Boyle’s law, Charles law, and Gay-Lussac’s law. P = 1/V Boyle’s law VαT

Charles law

PαT

Gay-Lussac’s law

Product of volume and pressure over temperature is a constant for any given gas. P1V1/T1 = P2V2/T2 = k Universal gas constant- The concept of gas laws can be combined with that of Avogadro’s hypothesis and the mole as follows


5

PV/T = k PV/T is constant for a given quantity of any gas. For one mole of any gas PV/T is a constant known as Universal gas constant. For an ideal gas PV = n RT, where n is the number of moles of the gas and R is the Universal gas constant. The Universal gas constant is expressed in units of energy per Kelvin per mole. R = 8.314JK-1mol-1 Applications1. In operating room for a gas like oxygen, the volume of the cylinder and the temperature remains constant so the pressure directly reflects the number of moles present in the cylinder. Thus, the oxygen pressure gauge acts as a content gauge. This does not apply to nitrous oxide because nitrous oxide is in liquid form. 5. AVOGADRO’S LAW: - Described by Amedeo Avogadro in 1811 States that, equal volumes of ideal or perfect gases, at the same temperature and pressure, contain the same number of particles or molecules. V/n = k V = Volume of the gas n = number of moles in the gas k = proportionality constant Applications: 1. Calculation of amount of nitrous oxide present in the cylinder is by weighing the cylinder. Molecular weight of nitrous oxide is 44. As per Avogadro’s law 44gm of nitrous oxide occupies 22.4L at STP. If a full cylinder contains 3200g (3.2Kg) of nitrous oxide (full cylinder wt- empty cylinder wt) The amount of nitrous oxide at STP = (3200 x 22.4)/44 = 1629L 2. To calculate the amount of volatile liquid used while administering a known concentration of a volatile agent. E.g. If we administer 1.5% of isoflurane with 5L/ min of fresh gas flow for one hour then the amount of isoflurane vapour used is, Total fresh gas used = 5 X 60 = 300L


6

If isoflurane concentration is 1.5% then the amount of vapour administered = (300 X 1.5) /100 = 4.5L The molecular weight of isoflurane is 184.5 and the specific gravity 1.496. As per Avogadro’s law 184.5gm of isoflurane occupies 22.4L at STP 4.5L weighs = 184.5 × 4.5 / 22.4 = 37g As the specific gravity is1.496, 37gm of isoflurane = 37/1.496 = 24.7ml The isoflurane used is 24.7ml. CRITICAL TEMPERATURE AND CRITICAL PRESSURE: Critical temperature is a point above which a gas cannot be liquefied, no matter how much pressure is applied to it. The pressure needed to maintain the liquid and gas phase of a substance at critical temperature is known as the critical point.The critical temperature and critical pressure together is known as critical point. Applications: 1. Nitrous oxide with a critical temperature of 360C and a boiling point -88°C exists as gas at room temperature, but it can be compressed to liquid as its critical temperature is 36°C. So, in nitrous oxide cylinder most of it is made to liquid form by comprising it. 2. Oxygen with a critical temperature of 118.30C cannot be liquefied at room temperature, so it exists as gas in the cylinder in spite of having pressure higher than nitrous oxide. The liquid oxygen is stored in large container with temperature – 1600 C. The vapour pressure at this temperature is 7bars. Liquid oxygen is heated to get oxygen vapour. 3. Pointing effect- Entonox, a 50% oxygen and 50% nitrous oxide gas mixture has a critical temperature of -5.50C. Below this temperature, the mixture dissociates and the nitrous oxide liquefies while the oxygen remains as a gas. If one were to breathe this in, one would inspire virtual 100% oxygen, until this is used up, and then 100% nitrous oxide. This outcome would be disastrous.

4. DALTONS LAW OF PARTIAL PRESSURE: Described by John Dalton in 1801 and is related to the ideal gas laws states that the total pressure exerted by a gaseous mixture is equal to the sum of the partial pressure of each individual component in a gas mixture. P = P1+P2+P3+…. P is the total pressure of the gas mixture


7

P1, P2, P3 are the pressure exerted by individual components of the gas mixture. Applications1. To calculate alveolar gas constituents. Alveolar gas mixture contains oxygen 13%, nitrogen 76%, CO25% and water vapour 6%. Applying the Dalton’s law of partial pressure total pressure at one atmosphere (760mm of Hg) can be divided as PO2 = 13/100 X 760 = 98.8 mm of Hg. PN2 = 76/100 X 760 = 577.6mm of Hg. PCO2 = 5/100 X 760 = 38.0 mm of Hg. Water vapor = 6 /100X 760 = 45.6mm of Hg Total = 760mm of Hg.

2. To calculate partial pressure of oxygen in air.

6. GRAHAMS LAW: - Postulated by Thomas Graham states that the rate of diffusion of a gas is inversely proportional to the square root of its molecular weight. V1/V2 = √m2/√m1 Applications1. Flow meters: - each gas with its own physical property (density/ molecular weight) must pass through its own calibrated flow meter. 2. Rate of diffusion is slow in liquids and thus local anesthetics, if not injected in close proximity to the nerve fibers will not be effective. 3. Helium, a lighter gas is used in airway obstruction to improve diffusion of oxygen and gas exchange. 7. HENRY’S LAW: - Postulated by William Henry States that, at constant temperature, the amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid. V=α×P V is the volume of gas dissolved α is the solubility constant of that gas in the given liquid


8

P is the partial pressure of the gas above the liquid ApplicationsThe solubility coefficient of oxygen in plasma is 0.003 ml dL-1. At normal oxygen tension of 100mm of Hg, 100ml of blood carries 0.3ml of oxygen in dissolved form. By increasing the oxygen tension to 500mm of Hg during pre-oxygenation we can improve dissolved oxygen content to 1.5ml in 100ml of blood. In a similar way this can be applied to hyperbaric oxygen therapy. 1. Deep sea diving: - Compressed air illness or Caisson’s disease is a sequel of deep sea diving. Here air is breathed up to 10 bar pressure. When breathing air at very high pressure, nitrogen is in solution in the tissues and in the blood. Its tension is in equilibrium with the partial pressure of N2 in the alveoli. As the diver rises to the surface, his tissues are subjected to less pressure when the ambient pressure falls below the sum of partial pressure of the gases dissolved in the tissues, minute gas bubbles are formed. If the rate of ascend is too rapid gas bubbles coalesce and expand resulting in decompression sickness.

2. According to Henry’s law the partial pressure of anesthetic agent dissolved in the blood is proportional to the partial pressure exerted by the anesthetic vapour in the alveoli.

8. HAGEN POISEUILLE’S LAWLaminar flow through tubes is directly proportional to the pressure gradient and fourth power of radius and inversely proportional to viscosity and length. Q=

π(

)

P1 - P2 = pressure difference across the tube. r4 = radius to the power of four n = viscosity l = length π and 8 are constants


9

Applications: 1. Intravenous infusions – when the cannula is large and short and pressure head is higher, doubling the size of the cannula effectively increases the flow 16 times. 2. Using a under size ETT and increased length of endotracheal tube may cause a transition from laminar to turbulent flow of gas causing increased resistance to flow through the tubes. 3. Every piece of anesthetic instrument, because of diameter and shape of connectors, number and arrangement will affect FGF. Wide bore and curved rather than sharp angles should be preferred. 4. In respiratory tract obstruction, oxygen – helium mixtures are given to reduce density and improve the flow of oxygen. 5. If laminar flow during quite breathing is changed to turbulent during speaking and coughing leading to dyspnea. 6. In the flow meter at low flows, Hagen poiseuille’s law applies because the flow is laminar, while at higher flows, the law applicable to turbulent flow is applicable. 7. Numerical value for critical gas flow in liters per minute for the anesthetic gas mixture of O2 + N2O is the name as the internal diameter in millimeters. At these flow rates the flow changes to turbulent from laminar. 8. Blood versus crystalloid fluid infusion

BERNOULLI’S PRINCIPLE Postulated by the Dutch – Swiss mathematician Daniel Bernoulli states that for an in viscid flow, an increase in speed of the fluid occurs simultaneously with a decrease in pressure or a decrease in the fluid’s potential energy. This implies that when the velocity of fluid flow increases as in the case of flow across a constriction, the lateral pressure exerted by the fluid decreases.

Figure 4 Illustration of Bernoulli's Principle Applications-


10

1. Air injectors- pressurized gas, usually oxygen passes through a nozzle or jet, the negative lateral pressure generated entrains air into the primary flow, thereby increases the total flow. The amount of air entrained depends on the forward velocity of primary flow and the entrainment port. 2. Same principle is used in jet ventilation, humidifiers and small volume nebulizers.

VENTURI PRINCIPLE- named after Giovanni Battista Venturi. A constriction with an entry and exit in which the diameter changes gradually and which maintains laminar flow is known as a venturi.

Figure 5 Illustration of Venturi Principle Applications1. Venturi masks- These are tubes with jet orifice and entrainment port. The air entrainment ratio is adjusted such a way that adequate total flow with fixed FiO2 can be delivered. 2. Used in suction apparatus and nebulizers. 3. Ventilators working on injecter principle. 4. Pethick’s test for Bain’s circuit.

COANDA EFFECT If constriction occurs at bifurcation because of increase in velocity and reduction in the pressure, fluid tends to stick to one side of the branch causing misdistribution.

Figure 6 Illustration of Coanda Effect


11

Applications 1. Mucus plug at the branching tracheobronchial tree may cause misdistribution of respiratory gases. 2. Unequal flow may result because of atherosclerotic plaques in the vascular tree. 3. Fluid logic used in the ventilators employs this principle to replace valves or mobile parts. 4. Infusion sets – intravenous fluids tends to accumulate along the walls of infusion set if not properly designed. For the safe & efficient use of anaesthetic apparatus, the anesthetist must have a clear concept of the physical aspects of the equipment in use. Understanding of basic concepts may avert unnecessary accidents & near misses. References 1. G.D.Parbrook, P.D.Davis, E.D.Parbrook. Gas Laws. Basic physics and measurement in anaesthesia. 5th ed. p20-23 2. Matthew Cross, Emma Plunkett. The Gas laws. Physics, Pharmacology and Physiology for Anaesthetists.p24-26


THE ELECTRICAL ACTIVITY OF THE HEART-ECG Dr. Muralidhar K, Consultant & Professor of Anaesthesiology, Narayana Hrudayalaya Hospitals, Bangalore The electrocardiogram (ECG) is a record of the electrical activity of the heart. Monitoring of ECG is an essential mandatory component of any anaesthetic procedure. The following text describes the basic fundamentals of ECG. The Cardiac Action Potential: Resting cells have a potassium concentration (about 140 mmol/litre) which is high in comparison with that in the extracellular tissues (about 4 mmol/litre), whereas extracellular sodium concentration is much greater than intracellular. This ionic disequilibrium between the cell and its environment is maintained by a sodium-potassium exchange pump which simultaneously transports potassium ions the cell and sodium ions out of the cell.

A)

Transmembrane potential.

Phase

O corresponds with

depolarization, and phase 1,2 and 3 with repolarization. Phase 4 is the period pf diastolic rest. When the cell is electrically stimulated, the transmembrane potential is reduced to the threshold potential, after which the process of depolarization is self-perpetuating. (B) Transmembrane potential in a pacemaking cell. In these cells,


phase 4 is a period of slow depolarization. When the threshould potential is reached the cell rapidly becomes depolarized. During diastole there is relative negative potential within the cell of the order of 90 mV; this is the transmembrane resting potential. This is primarily due to two factors, the high concentration of potassium ions intracellularly and the high permeability of the cell membrane to potassium ions. As a result, potassium ions tend to diffuse out of the cell down their concentration gradient, creating a negative charge in the interior of the cell, which offsets and almost balances the concentration gradient for potassium. The cardiac action potential arises due to a sequence of changes in permeability to sodium, calcium and potassium ions. At rest, the cell membrane is relatively impermeable to sodium ions. The rapid upstroke of the action potential is due to a sudden increase in sodium permeability, causing a rapid influx of sodium ions. This sodium current is short-lived, because the ion channels which open to cause the increase the increase in sodium permeability rapidly close once again. The first inward sodium current is succeeded by a slower inward current, comprised predominantly of calcium ions and to lesser extent sodium ions. This slow inward current is responsible for the plateau phase of the cardiac action potential, preventing the cell from repolarizing rapidly like a nerve. During the plateau of the action potential permeability to potassium ions is reduced. Repolarization to the resting potential is achieved by a gradual increase in potassium permeability once again, accompanied by a gradual decrease slow inward current. The pathways of conduction and the ECG: The sinus node is situated in the right atrium close to the entrance of the superior vena cava. The AV node lies in the right atrial wall immediately above the tricuspid valve. The fibres of the AV bundle (of His) arise from the AV node and run along the posterior border of the septum between the ventricles. On reaching the muscular part of the septum, they spilt into right and left bundle braches and then spread out in the subendocardium of the ventricles as the Purkinje system. The right bundle is slender, compact structure. The left bundle soon splits into two or more division


or fascicles, one of which proceeds anteriorly, sharing the same blood supply as the right bundle, and another is directed posteriorly. In the usual sequence of events, the electrical impulse arises in the sinus node and spreads across the atria to reach the AV node. It can then only reach the ventricles by passing into the rapidly conducting AV bundle and its branches. The first part of the ventricles to be activated is the septum, followed by the endocardium. Finally, the impulse spreads outwards to the epicardium. The spread of the cardiac impulse gives rise to the main deflections of the ECG: P, QRS and T waves:

(A) Normal ECG complexes (B) PR, QRS and QT segments 

the P wave is the first deflection of the cardiac cycle and represents atrial depolarization:

the PR interval represents the time taken for the cardiac impulse to spread over the atrium and through the AV node and His-Purkinje system

the QRS complex represents the spread of depolarization through The ventricles

the T wave represents ventricular repolarization.

The Normal electrocardiogram Normally, ECG are recorded at a rate of 25 mm /s and the ECG paper is printed with thin vertical lines 1 mm apart and thick vertical lines 5 mm apart .The interval between the thin lines represents 0.04 s and that between two thick lines 0.20 s. If the heart rhythm is regular, the rate can be counted by dividing the number of small squares between two consecutive R waves into 1500 or large squares into 300. If the rhythm is irregular, one can multiply the number of complexes in 6 s (i.e. 15 cm) by 10.


Normal 12-lead electrocardiogram. Note the progression in the upright deflection from ‘r’ over the right ventricle (VI) to an ‘R’ over the left ventricle (V6). There are also thin horizontal lines at 1-mm intervals and thick horizontal lines at 5-mm intervals. An ECG recording is standardized so that 1 mV gives a deflection of 10 mm on the paper. The height of a deflection therefore indicates its voltage. The P Wave

P wave (Normal) The normal P wave results from the spread of electrical activity across the atria (the activity of the sinus node itself cannot be detected in the ECG). Because the impulse spreads from right to left, the P wave is upright in leads I, II and aVF, is inverted in aVR and may be upright, biphasic or inverted in lead III, aVL and V1. It should not be higher than 3 mm in the bipolar leads or 2.5 mm in the unipolar leads or greater than 0.10s in duration.


When abnormal, the P wave may become: 

inverted (i.e negative in the leads in which it is usually positive).

This indicates depolarization of the atria in an unusual direction, and that the pacemaker is not in the sinus node, but is situated either elsewhere in the atrium, in the AV node or below this; or there is dextrocardia; 

Broadened and notched, due to delayed depolarization of the left atrium when this chamber is enlarged (P mitrale). In preceding a deep and broad negative one;

tall and peaked, exceeding 3 mm, as a result of right atrial enlargement (P pulmonale);

absent or invisible due to the presence of junctional rhythm or sino-atrial block;

Replaced by flutter or fibrillation waves.

PR interval This is measured form the beginning of the P wave to the beginning of the QRS complex (i.e. to the onset of the Q wave if there is one, and to the onset of the R wave if there is not). This interval corresponds to the time taken for the impulse to travel from the sinus node to the ventricular muscle. There is an iso-electric segment between the end of the P wave and the beginning of the QRS, whilst the impulse is passing through the AV node and the specialized conducting tissue, as an insufficient amount of tissue is being electrically stimulated to produce a deflection detectable on the body surface. The PR interval varies with age and with heart rate. The upper limit in children is 0.16, in adolescents 0.18 and in adults 0.20s, although it may be even longer in a few normal individuals. The faster the heart rate the shorter is the PR interval. It is regarded as abnormally short if it is less than 0.10s. A shortened PR interval is seen when the impulse originates in the junctional tissue and in the Wolff-Parkinson-White syndrome. The PR interval is prolonged in some forms of heart block.


The QRS complex

Variations in the QR complex The QRS complex represents depolarization of the ventricular muscle. The components of the QRS complex are defined as follows 

the R wave is any positive (upward) deflection of the QRS. If there is more than one R wave, the second is denoted R’; an R wave of small voltage may be denoted r;

a negative (downward) deflection preceding an R wave is termed Q;

a negative deflection following an R wave is termed S;

if the ventricular complex is entirely negative (i.e. there is no R wave), the complex is termed QS.

The whole complex is often referred to as the QRS complex irrespective of whether one or two of its components are absent.

Genesis of the QRS complex. Note that the first phase, directed form left to right across the septum, produces a Q wave in V6 and an R wave in VI. The second phase, due mainly to depolarization of the left ventricle form endocardium to epicardium, results in a tall R wave in V6 and a deep S wave in VI. Finally, depolarization


of the basal part of the ventricle may produce a terminal S wave in V6 and a terminal R wave in VI. Ventricular depolarization starts in the middle of the left side of the septum and spreads across to the right (phase 1 of ventricular depolarization). Subsequently, the main free walls of the ventricles are activated, the impulse spreading from within outwards and from below upwards. Because of the dominating bulk of the left ventricle, the direction of the vector of phase 2 is to the left and posteriorly. Finally, the base of both ventricular walls and the inter-ventricular septum are depolarized. The appearances of the QRS in different leads can be largely explained by the major vectors of these phases. In leads facing the left ventricular surface, there is a small Q wave due to septal depolarization and a large R wave due to left ventricular depolarization. On the right side of the heart, as seen from V1, there is usually an r wave due to septal depolarization and a large S wave due to left ventricular forces directed away fro the electrode. Pathological Q waves: Small, narrow Q waves are normally to be found in leads facing the left ventricle (e.g. lead I, aVL, aVF, V5 and V6). These Q waves do not normally exceed 2 mm in depth, or 0.03 s in width. It should be noted that QS waves are normal in aVR, and are common in V1. Abnormally broad and deep Q waves are often a feature of myocardial infarction). Q waves in lead III are difficult to evaluated but can be ignored if there are no Q waves either in lead II or in aVF, or if they do not exceed 0.03 s. Usually, a ‘normal’ Q wave in lead III diminishes or disappears on deep inspiration because of an alteration in the position of the heart, whilst the ‘pathological’ Q wave of infarction persists. The QRS complex should not exceed 0.10s in duration, and usually is in the range 0.06-0.08s. Broad QRS complexes occur in bundle branch block, ventricular hypertrophy and ventricular ectopic beats. The T wave The T wave is due to repolarization of the ventricles. If repolarization (the T wave) occurred in the same direction as depolarization (the QRS complex) the T wave would be directed in an opposite way to that of the QRS. In fact, depolarization takes place from endocardium to epicardium, whereas repolarization takes place from epicardium to endocardium. Because of


this, the T wave usually points in the same direction as the major component of the QRS complex. Thus, the T wave is normally upright in leads I and II as well as in V3 to V6, is inverted in aVR, and upright or inverted in lead III, aVL, aVF and V1 and V2. The T waves are usually not taller than 5 mm in standard leads and 10 mm in precordial leads. Unusually tall and peaked T waves may be seen in hyperkalaemia and in early myocardial infarction. Flattened T waves are seen when the voltage of all complexes is low, as in myxoedema, as well as in hypokalaemia and in a large number of other conditions in which it may be regarded as a non-specific abnormality. Slight T wave inversion is also often nonspecific, and may be due to such influences as hyperventilation, posture and smoking. The most important causes of T wave inversion are: 

myocardial ischaemia and infarction;

ventricular hypertrophy;

bundle branch block.

The QT interval The QT interval represents the total time form the onset of ventricular depolarization to the completion of repolarization. It is measured from the beginning of the Q wave (or the R wave if there is no Q wave) to the end of the T wave. Its duration varies with heart rate, becoming shorter as the heart rate increase. In general, the QT interval at heart rates between 60 and 90 per minute does not exceed in duration half the preceding RR interval. The measurement of the QT interval is often difficult as the end of the T wave cannot always be clearly identified, and the relationship between heart rate and duration of the QT is a complex one. In practice, the main importance of a prolonged QT interval is that it is associated with a risk of ventricular tachycardias (particularly torsades de pointes) and sudden death. A long QT is sometimes an inherited abnormality but may result form such drugs as quinidine, procainamide, disopyramide, amiodarone and tricyclic antidepressants. The ST segment The ST segment is that part of the electrocardiogram between the end of the QRS complex and the beginning of the T wave. The point of junction between the S wave and the ST segment it known as the J point. The ST segment occurs during a period of unchanging polarity in the


ventricles, corresponding with phase 2 of the action potential. The normal ST segment is situated on the isoelectric line but curves upwards.

Normal and abnormal ST segment and T waves. (A) Normal ST segment with J point, (B) Horizontal ST depression in myocardial ischaemia. (C) ST segment sloping upwards in sinus tachycardia. (D) ST sagging in digitalis therapy. (E) Asymmetrical T wave inversion associated with ventricular hypertrophy. (F) Similar pattern sometimes seen with out voltage changes in hypertrophy – ‘strain’. (G) ST sagging and prominent U waves of hypokalaemia. (H) Symmetrically inverted T wave of myocardial ischaemia or infraction. (1) ST elevation in acute myocardial infarction. (J) ST elevation in acute pericarditis.

(K)

Peaked T

wave in

hyperkalaemia Displacement of the ST segment and variation in its shape are of great importance in electrocardigraphic diagnosis. Depression of more than 0.5 mm is abnormal. When ST elevation occurs in normal individuals, it is often preceded by a slight notch on the down stroke of the R wave: 

acute myocardial infarction. The ST segment is elevated with a curve which is convex upwards in the leads facing the infarct. At wave inversion develops.


pericarditis. This also causes ST elevation, but the ST segment are concave upwards and the changes are widespread rather than localized as in myocardial infarction;

digitalis therapy depresses the ST segment, particularly in leads II and III, so that there is a gentle sagging, but the T wave remains upright or flattened;

ventricular hypertrophy. ST segment depression may occur in leads facing the relevant ventricle and be accompanied by asymmetrical T wave inversion. This contrasts with the symmetrical T wave inversion seen in myocardial infarction and ischaemia;

acute myocardial ischaemia. The ST segment is horizontally depressed or slightly downward sloping from the point onwards;

sinus tachycardia. There may be ST depression which slopes upwards from the J point;

hypothermia. There is a prominent J wave (the junction of the S wave and the ST segment).

The U wave The U wave is a broad, low-voltage wave present in most normal ECGs. Its cause is unknown; it may become unusually prominent in hypokalaemia and with digitalis therapy.

ECG interpretation ECG interpretation is largely a matter of experience and pattern interpretation. However, while building experience, it is useful to develop a method of ‘systematic’ ECG analysis. This is most easily performed by asking one self a number of questions in a logical sequence about P, QRS and T waves in turn as follows:

Rate and rhythm What is the rate? Is it regular or irregular? P wave Are P waves present? Is the P wave axis normal?


Is there evidence of left or right atrial enlargement? PR interval (normal range 0.12-0.20s) Is the PR interval normal? Is each QRS complex preceded by a P wave? Is there evidence of a slurred QRS upstroke (delta wave) ? QRS Complex Is the QRS duration within normal limits (0.08-0.11s)? Is there evidence of bundle branch block? Is

the

QRS

axis

normal?

Are pathological Q waves present? Is there a normal R wave progression across the chest leads? ST segment and T wave Is there abnormal ST elevation or depression? Are the T waves upright (except aVR and VI)? QT Interval Is the QT interval normal (in general less than 0.44 s)? Intraoperative ECG monitoring is necessary in the following: •

diagnosis of cardiac arrhythmia

diagnosis of myocardial ischaemia

diagnosis of conduction defects

diagnosis of electrolyte disturbances

DISTURBANCES OF RATE AND RHYTHM Sinus node abnormalities Scenario 1: A 35-year female is undergoing thyroid surgery develops a heart rate of 140/min. The ECG shows the following:

Sinus tachycardia


Sinus tachycardia Sinus tachycardia is sinus rhythm at a rate faster than is normal. In adults, this is commonly defined as a heart rate greater than 100/min. Factors associated with sinus tachycardia are: 

anaemia;

pain, anxiety, and light level of anaesthesia

hyperthyroidism

fever;

blood loss and hypovolaemia;

heart failure;

drugs such as adrenaline, isoprenaline, ephedrine, atropine and thyroxine.

The diagnosis of sinus tachycardia is usually obvious when there is a regular pulse at a rate of more than 100/min.

Carotid sinus pressure causes little slowing in contrast to its usually

dramatic effect in atria tachycardia or atrial flutter. The ECG shows P waves having a normal relationship to QRS complexes. The J point may be depressed; the ST then slopes upward. Sinus tachycardia does not of itself require treatment although the underlying cause of tachycardia should be sought be sought and, where necessary, treated. Scenario 2: A 74-year male undergoing prostratectomy under spinal anaesthesia develops a hear rate of 40/min.

Sinus bradycardia. A marked sinus bradycardia of 40 bets per minute is followed by a 2.7 second pause before the next sinus beat Sinus bradycardia Sinus bradycardia describes a slow heart in sinus rhythm , this term is commonly applied to heart rates of less than 60/min, although such rates are frequently see in healthy elderly people; in the


highly trained athlete the heart rate may be less than 40/min. Amongst factors causing sinus bradycardia are: 

increased vagal tone (e.g. during carotid sinus massage);

myxoedema;

hypothermia;

raised intracranial pressure;

drugs including digitalis and the beta-adrenergic blocking agents such as propranolol.

AHA ALGORITHM FOR ADULT BRADYCARDIA

Supraventricular arrhythmias A variety of rhythm disturbances can arise in the atria and AV junctional area (that is, the AV node and adjacent specialized tissues). These may result from either increased automaticity or reentry.


Scenario 3: A 65-year male undergoing herniorrhaphy under general anaesthesia develops an irregular pulse.

Atrial ectopic beat. A premature P wave (arrowed) is followed by a QRS complex of normal appearance. Atrial ectopic beats (atrial extrasystoles, atrial premature beats) Atrial ectopic beats are common in normal individuals, but seldom give rise to symptoms, apart from an awareness of hart irregularity from time to time. They cause an occasional irregularity in an otherwise normal pulse, and are usually abolished by exercise. The diagnosis is readily confirmed from the ECG which shows a premature beat occurring earlier than the next anticipated sinus beat. The P wave differs in configuration from that of a sinus beat, because depolarization of the atria takes place in an abnormal direction. The accompanying QRST complex is usually similar to that of previous beats of sinus origin because the pathway of ventricular depolarization is normal. Occasionally, the QRST complex is abnormally broad (‘aberrant’) because the impulse passes down only one of the bundle branches, the other still being refractory from the preceding beat. It then simulates the appearance of a ventricular ectopic beat but is usually preceded by a P wave. Atrial ectopic beats may presage the appearance of other atrial arrhythmias but they require no treatment. Junctional (nodal) ectopic beats Ectopic beats deriving from the junctional tissue are quite common and, like atrial ectopic beats, usually benign. They are responsible for an occasional irregularity in an otherwise regular pulse and cannot be diagnosed without an electrocardiogram, which shows the same features as with atrial ectopic beats except that the P wave inverted in lead II and is either buried in the QRS complex, or precedes of follows it by a very short interval. No treatment is necessary.


Scenario 4: A 10-year child under halothane anaesthesia for undescended testis develops a bradycardia of 50/min and has a blood pressure of 70/50mmHg.

Junctional rhythm. In this example retrograde conduction into the atria is relatively slow and a P wave can be distinguished after the QRS complex, interrupting the ST segment.

Junctional (nodal) rhythm In this condition the junctional tissues is acting as the pacemaker of the heart and the ECG appearance is that of a succession of junctional ectopic beats. It is usually a transient condition resulting from a depression of sinus node activity. It occurs in some normal individuals and may be provoked by digitalis or ischaemic heart disease. The heart rate is usually in the region of 5060/min and no treatment us required. If the heart rate is undesirably slow, it can be accelerated by the use of atropine. In patients with acute myocardial infarction treated with thrombolytic therapy, the occurrence of junctional rhythm is an indicator of successful reperfusion.

Paroxysmal supraventricular tachycardia


Supraventricular tachycardia. Regular narrow QRS tachycardia at a rate of 220 beats/ min In its broadest sense, the term paroxysmal supraventricular tachycardia might refer to any recurrent supraventricular arrhythmias. However, arrhythmias originating within the atrium (atrial tachycardia, atrial flutter and atrial fibrillation) are generally excluded. The term encompasses a number of different arrhythmias, which share certain characteristics- starting abruptly, usually being regular at a rate of 140-220/min, and being associated with narrow QRS complexes, closely resembling those seen in sinus rhythm. Aberrant conduction with broadening of the QRS may, however, occur as may rates above and below those quoted. Atrial flutter

Atrial flutter. Flutter waves are most readily apparent in the right-sided chest leads VI and V2. They are also seen in inferior leads, III and aVF. A high degree of AV block is apparent with five to six flutter waves for every one QRS complex. Rhythm strip lead is V1


In this arrhythmia, the atria beat regularly at a rate of 250-350/ min usually close to 300/min. In most cases the arrhythmia arises due to a re-entry circuit within the right atrium, due to an area of slow conduction in an isthmus of myocardium between the inferior vena cave, tricuspid valve and coronary sinus. Some degree of AV block is almost is almost invariable. In most instances the ventricles beat regularly because of a 2:1, 3:1 or 4:1 responses to the regular atrial activity, but it is irregular if the degree of block varies from cycle to cycle. The commonest variety is that of 2:1 block which characteristically has a ventricular rate of 140-160. In cases with 2:1 block flutter waves are not always obvious. Any regular, narrow QRS complex arrhythmia in this rate band should be closely scrutinized for the presence of flutter waves. Atrial flutter is commonly a complication of underlying organic heart disease, although it occasionally occurs as a primary condition in patients with no definable cardiac abnormality. Common associations include: 

rheumatic heart disease;

ischaemic heart disease;

myocarditis;

hyperthyroidism.

It may be persistent or occur in paroxysms which are usually self-limited to hours or days, but it may progress to atrial fibrillation. The symptoms resemble those of atrial tachycardia, with palpitation, dizziness or syncope. The arrhythmia often provokes cardiac failure. The heart rate is usually regular at a rate of 140-160/min. It may be possible to see venous ‘flutter’ waves in neck. Carotid sinus massage leads to a transient increase in the atrio-ventricular block, with a slowing of the ventricular rate only as long as the pressure is maintained. The electrocardiogram is diagnostic with ‘flutter’ waves of a sawtooth appearance, best seen in leads VI and III occurring at approximately 300/min. The sawtooth nature of the complexes may be obscured by the QRS complexes when there is 2:1 block, but it be readily revealed when carotid sinus massage is applied.


Scenario 5: A 35 year female patient for mitral valvotomy is found to have an irregularly irregular pulse on preoperative examination.

Atrial fibrillation. The rhythm strip shows narrow QRS complexes which are irregular

Atrial fibrillation In atrial fibrillation, irregular atrial impulses occur at rates over 300/min. It may be due to multiple foci of ectopic activity or to wavelets of excitation following variable courses through the atrial myocardium depending upon the location of patches of excitable and refractory muscle. Some degree of AV block is invariable; the ventricular rhythm is slower then the atrial but it is also irregular. The presence of atrial fibrillation suggest that there has been either a pathological process involving the atria, as in rheumatic heart disease, or that there has been a rise in pressure with atrial dilatation secondary to mitral valve or left ventricular disease. Common causes of atrial fibrillation include: 

rheumatic mitral valve disease;

ischaemic heart disease, particularly acute myocardial infarction;

Alcohol

thyrotoxicosis;

hypertension;

acute infections, particularly when these affect the lungs

cardiopulmonary surgery.


Atrial fibrillation may be paroxysmal, with attacks lasting for a few minutes or hours. This is particularly likely in acute myocardial infarction, in chest infections, and in the early stages of thyrotoxicosis and mitral valve disease. In rheumatic cases, the arrhythmia usually becomes established eventually and persists for the rest of the patient’s life. Atrial fibrillation leads to untoward effects for three major reasons: 

the ventricular response may be so fast there is inadequate time for diastolic filling and the cardiac output falls;

the atrial contribution to ventricular filling is lost;

stasis in the ineffectively contracting atrium encourages thrombosis. As a consequence, embolism is common, particularly in patients with mitral valve disease. Emboli from the right atrium produce pulmonary artery obstruction; those from the left atrium may lodge in cerebral, renal or other peripheral vessels.

There are four aspects to the treatment of atrial fibrillation: 

the control of ventricular rate;

the restoration of sinus rhythm

the maintenance of sinus rhythm

prevention of embolism.


AHA ALGORITHM FOR ADULT TACHYCARDIA

Ventricular arrhythmias Scenario 6: A 70-year- male patient undergoing laparoscopic cholecystectomy develops irregular heart rate after CO2 insufflation of the abdomen.

Ventricular ectopic bets. Each sinus beat is followed by a broad complex ventricular ectopic beat. The constant coupling in this example is termed ventricular bigeminy.


Ventricular ectopic beats (extrasystoles, premature beats) An ectopic focus in the ventricles may arise because of ventricular escape, enhanced automatic activity, or re-entry. Ventricular ectopic beats are not uncommon in normal individuals but are encountered frequently in organic heart disease, especially in myocardial infarction. If they occur every second beat (bigeminy or ‘coupling’) they are frequently due to digitalis therapy. The diagnosis may be suspected from an irregularity of the pulse interrupting an otherwise regular rhythm, but cannot be made without an ECG, in which there are bizarre and broadened QRS complexes followed by T waves pointing in the direction opposite to the of the main QRS component. The QRS complexes are not preceded by a P wave and are usually succeeded by a long period (the compensatory pause) before the next sinusScenario 7: a 72-year-male ,a known case of coronary artery disease with poor LV function , undergoing resection of hemicolon under GA develops a tachycardia of 200/min with a BP of 60/35mmHg.

Ventricular tachycardia. Regular wide QRS tachycardia at a rate of 170/min

Ventricular tachycardia In this condition a tachycardia arises in the ventricles at a rate of 120-220/min; the atria usually remain under the control of the sinus node. It may be a consequence of either re-entry or enhances automaticity of ventricular pacemaker cells. Ventricular tachycardia is a frequent complication in patient with severe heart failure. The ECG shows rapidly occurring broad QRS complexes resembling those of bundle branch block. P waves may be identified at a rate different from that of the ventricles. The RR intervals are usually equal, but may vary by up to 0.03 s from one another. The lack of response to carotid pressure assists in the differentiation from atrial tachycardia with bundle branch block


Scenario-8: a 72-year-male, a known case of coronary artery disease with poor LV function, undergoing resection of hemicolon under GA develops pulseless situation with no recordable blood pressure.

Ventricular fibrillation In this condition there is a chaotic electrical disturbance of the ventricles, with impulses occurring irregularly at a rate of 300-500/min. Ventricular contraction is uncoordinated and ventricular filling and emptying cease. The cardiac output falls precipitously to zero. Ventricular fibrillation is the commonest cause of sudden death. It may occur as a primary arrhythmia or as a complication of acute myocardial infarction. It may also result from drowning, electrocution and over dosage of drugs including digitalis, adrenaline and isoprenaline. Because of its catastrophic effects, ventricular fibrillation gives rise to the clinical features of cardiac arrest, with sudden disappearances of arterial pulses, cessation of respiration, loss of consciousness and dilatation of the pupils. On the electrocardiogram, there is a chaotic rhythm with ventricular complexes of varying amplitude and rate. Eventually asystole ensues. Ventricular fibrillation is almost invariably fatal, and immediate treatment is necessary if death is to be prevented. As with other forms of cardiac arrest, an effective circulation and ventilation must be obtained with 4 min if irreversible brain damage is not to occur, Sinus rhythm can usually only be restored by electric shock, which should be administered as soon as possible. If an electrical defibrillator is not immediately available, the standard treatment of cardiac arrest should be started with closed chest cardiac compression and artificial ventilation.


AHA ALGORITHM FOR ADULT CARDIAC ARREST

Summary: Electrical activity is a basic characteristic of the heart and is the stimulus for cardiac contraction. Disturbances of electrical function are common in heart disease and are one of the most common cardiovascular abnormalities under anaesthesia and post-operative period. Electrocardiogram (ECG) plays an essential role in the diagnosis and management of myocardial ischaemia/infarction, rhythm/conduction abnormalities can contribute to the detection of electrolyte disorders and drug intoxication.


VAPORIZERS Dr. Aruna Parameswari Professor of Anaesthesiology, Sri Ramachandra Medical College, Chennai.

OUTLINE Introduction Physics and laws of vaporization Factors affecting vaporization of a liquid Classification of vaporizers Hazards of vaporizers Safety features in vaporizers Specific vaporizers Conclusion

Introduction Volatile inhalational agents have been in use from the dawn of anesthesia; from the Schimmelbusch masks to modern electronically controlled vaporizers. Vaporizers are an integral part of modern-day anesthesia, allowing the delivery of safe concentrations of volatile anesthetic agent. Most of the inhalational anesthetic agents in use today are liquids under normal conditions and must be converted into vapors before they can be used.

A vaporizer is an instrument designed to: a) Facilitate the conversion of a liquid anesthetic into its vapor form and b) Add a controlled amount of this vapor to the fresh gas flow.


The purpose of the vaporizer is thus to deliver reliably an accurate, adjustable concentration of anesthetic vapor. Physics For safe administration of inhalational agents using vaporizers, it is essential to understand the physics behind vaporization: vapors and gases, saturated vapor pressure, boiling point, heat of vaporization, specific heat and thermal conductivity. Vapor and gases Every substance has its unique critical temperature above which it exists only as a gas, irrespective of how much pressure is applied to it. At or below this critical temperature, it can exist in both its liquid and gaseous forms; the latter is called a vapor. Thus, a vapor is the gaseous phase of a substance which is a liquid at room temperature and atmospheric pressure. Vapor pressure When a volatile liquid is kept inside a container closed to atmosphere, molecules of liquid break away from the surface (due to their kinetic energy) and enter the space above, forming a vapor. The vapor exerts a pressure on its surroundings, which is known as vapor pressure. Some of the molecules that have escaped while moving freely in the gaseous state will collide with the surface of the liquid and re-enter it. Eventually, there will occur an equilibrium in which the number of molecules re-entering the liquid equals the number leaving it. At this stage, the vapor pressure is at a maximum for the temperature of the liquid and so is called the saturated vapor pressure (SVP).

Fig.1. SVP increases non-linearly with temperature If heat is supplied to the container, the equilibrium will be shifted so that more molecules enter the vapor phase and the vapor pressure will rise. If heat is taken away from the system, more molecules will enter the liquid state and the vapor pressure will be lowered. It is meaningless, therefore, to talk about vapor pressure


of a liquid without specifying the temperature. However, the relationship between SVP and temperature is non-linear (Fig.1). Vapor pressures of the commonly used anesthetic agents at 20°C are shown in Table.1. The concentration of anesthetic vapor in a gas is given by the equation: Gas concentration = Vapor pressure / Ambient pressure For example, at 20⁰C, the concentration of gas in a sevoflurane-vaporizing chamber (assuming it is saturated) will be: Sevoflurane concentration = 160/760 = 21% In order to give clinically useful concentrations of the agent, we dilute this with fresh gas. Vapor pressure depends only on the liquid and the temperature The most important factor governing vaporizer design is the saturated vapor pressure (SVP) of the anesthetic. SVP is a measure of the volatility of the liquid anesthetic in the carrier gas: after equilibration between the carrier gas and the liquid anesthetic, the concentration of highly volatile anesthetics (e.g. isoflurane) in the gas will be higher than that of poorly volatile anesthetics (e.g. methoxyflurane). Anesthetics with a high SVP will require a smaller proportion of the total gas flowing through the vaporizer to pass through the vaporizing chamber to produce a given concentration than will anesthetics with a low SVP. It follows that it can be extremely dangerous to deliver anesthetics from vaporizers for which they were not designed. Boiling point At a certain temperature, the boiling point, liquid molecules can enter their vapor phase within the liquid, creating bubbles of saturated vapor that rise to the surface and break free. Below this temperature, any formation of a bubble would be instantly crushed by the greater atmospheric pressure. Thus, boiling point of a liquid is the temperature at which the saturated vapor pressure is equal to the atmospheric pressure. The lower the atmospheric pressure, the lower the boiling point. The boiling points of some commonly used anesthetic agents at sea level are shown in Table.1. Agent

Boiling point

SVP (torr, (°C, 20°C)

760 mmHg) Halothane

50.2

243

Enflurane

56.5

175


Isoflurane

48.5

238

Desflurane

23.5

664

Sevoflurane

58.5

160

Table.1 Boiling point and saturated vapor pressure of some common agents CONCENTRATION OF GASES Two methods are used commonly to express the concentration of a gas or vapor: partial pressure and volumes percent.

Partial pressure A mixture of gases in a closed container will exert a pressure on the walls of the container. The part of the pressure exerted by any one gas in the mixture is called the partial pressure of that gas. The total pressure of the mixture is the sum of the partial pressures of the constituent gases. Volume percent It is the number of units of volume of a gas in relationship to a total of 100 units of volume for the total gas mixture. Volumes percent expresses the relative ratio of gas molecules in a mixture, whereas partial pressure expresses an absolute value. Partial pressure/total pressure = Volumes percent / 100 Although gas and vapor concentrations are most commonly expressed in volumes percent, patient uptake and the level of anesthesia are directly related to partial pressure but only indirectly to volumes percent. Heat of vaporization Latent heat of vaporization is the number of calories needed to convert 1 g of liquid to vapor, without temperature change in the remaining liquid. Thus, the temperature of the remaining liquid will drop as vaporization proceeds, lowering vapor pressure, unless this is prevented. Specific heat is the number of calories needed to increase the temperature of 1 g of a substance by 1 degree C. Manufacturers select materials for vaporizer construction with high specific heats to minimize temperature changes associated with vaporization. Thermal conductivity - a measure of how fast a substance transmits heat. High thermal conductivity is desirable in vaporizer construction.


Factors affecting vaporizer output 

Flow

through

the

vaporizing

chamber

varying the proportion of gas passing through the vaporizing chamber and bypass is the method by which vaporizer output is controlled. 

Efficiency of vaporization/ surface area of the liquid gas interface The greater the surface area of the liquid anesthetic agent exposed to the fresh gas, more is the vaporization of the liquid agent. Vaporizers may incorporate a system of wicks and channels in the vaporizing chamber to improve efficiency of vaporization and increase the output concentration of anesthetic.

Temperature The SVP of an agent decreases with decreasing temperature. Changes in agent temperature can occur for two reasons – fluctuations in ambient temperature and the loss of the latent heat of vaporization (the latter being exacerbated at high gas flow rates). As temperature decreases, the output of the vaporizer will decrease. These problems can be overcome by Temperature stabilization and temperature compensation. Temperature stabilization: Construction of the vaporizer using materials with high

specific

heat capacity and thermal conductivity provides a heat sink, allowing heat to move rapidly between the vaporizing chamber and the atmosphere. Plenum vaporizers are made of dense metals, while the Oxford Miniature vaporizer (a draw-over vaporizer) uses glycol as a heat sink. Temperature compensation: This is dealt with separately under vaporizer classification 

Time Vaporization causes the liquid anesthetic to cool since heat is lost because of the latent heat of vaporization of the anesthetic. Therefore, the output concentration will tend to fall over time.

Gas

flow

rate

Changes in carrier gas flow rate may affect vaporizer output by: -

Altering the proportion of the total gas flow that passes through the vaporizing chamber.

-

Altering the efficiency of vaporization. For example, at high flow rates, the gas leaving the vaporizing chamber will tend to be less saturated (since the gas spends less time in the chamber), so the output of the vaporizer will tend to fall.


Carrier gas composition The composition of the carrier gas may affect vaporizer output by: -

Changes in the viscosity and density of the gas mixture affecting the proportion of the total flow that passes through the vaporizing chamber. The viscosities of air and nitrous oxide are lower than those of oxygen. In the variable bypass vaporizers, the characteristic of the flow splitting valve results in decreased gas flow through the vaporizing chamber, and hence reduced output, when using air and especially nitrous oxide compared with 100% oxygen. This effect is however, not clinically significant.



Ambient..pressure Saturated vapor pressure is solely a function of temperature. Therefore, if ambient pressure is reduced, the (constant) SVP becomes a greater proportion of the total (reduced) pressure, and the output concentration (in volumes %) rises. The change in the agent concentration in the delivered gas flow can be calculated by: Pcal

Agent %1 = Agent %cal x P1

Where agent %1 is the agent concentration at the present ambient pressure, P1 is the present ambient pressure, Pcal is the atmospheric pressure at which vaporizer was calibrated and agent %cal is the agent % delivered at the calibrated atmospheric pressure. But the partial pressure of the agent will not change with change in ambient pressure and since it is the partial pressure that determines level of anesthesia, the clinical effect of change in ambient pressure is insignificant and the vaporizer can be used in the same way at high altitude, sea level or under hyperbaric conditions. This, however, does not apply to the desflurane Tec 6 vaporizer. The Tec 6 vaporizer is pressurized to 2 atm; there is no compensation for ambient pressure and thus the concentration delivered in the fresh gas flow is stable, regardless of ambient pressure. Thus, the dial setting must be increased to maintain partial pressure of the

agent

at

high

altitudes.


Classification of vaporizers Vaporizers are classified based on various methods. Some of the most commonly used methods are: A). Based on regulating the output concentration - Variable bypass - Measured flow - Electronic vaporizers B). Based on the method of vaporization - Flow over - Bubble through - Injection C). Based on the method of temperature compensation - Mechanical thermo compensation - Supplied heat - Computerized thermo compensation D). Based on the location of the vaporizer - Plenum - low Resistance E). Based on the agent specificity - Agent specific - Multiple agent Method of regulating output concentration The vapor pressures of most anesthetic agents at room temperature are much greater than the partial pressure required to produce anesthesia. To produce clinically useful concentrations, a vaporizer dilutes saturated vapor in one of several ways. Depending

Conc. Halotha

Enflura

Isoflura

Sevoflur

/

ne

ne

ne

ane

1%

46:1

29:1

44:1

25:1

2%

22:1

14:1

21:1

12:1

3%

14:1

9:1

14:1

7:1

Agen t


on this, vaporizers can be classified as: A) Variable bypass vaporizer The gas that flows through the vaporizer is split so that some of the gas flows through the vaporizing chamber (the part of the vaporizer that contains the liquid anesthetic agent) and the remainder goes through a bypass (without passing through the vaporizing chamber) to the Vaporizer outlet. Both gas flows (flow through the vaporizing chamber and the bypass) join downstream of the vaporizing chamber where gas exits the vaporizer at the desired concentration. The ratio of the bypass gas to the vaporizing chamber is called the splitting ratio. Splitting ratio = Gas going through the bypass/ Gas going through the vaporizing chamber

The splitting ratio depends on the ratio of resistance in the two pathways. The resistance in turn depends on the size of the variable (adjustable) orifice which is present at the inlet of old vaporizers and at the outlet of modern vaporizers. The splitting ratio may also depend on the total flow to the vaporizer.

Table 2: Gas flow splitting ratios for different agents B) Measured flow vaporizers

In these vaporizers, the vaporizer heats the anesthetic agent to a temperature above its boiling point (so it behaves as a gas) and this is then metered into the fresh gas flow. A measured flow is sent by a separate oxygen flow meter to pass to the vaporizer with the output being at saturated vapor pressure for the anesthetic agent. In order to dilute this otherwise lethal concentration, output from that flow meter is combined with gas passing from the main flow meter. Some of the older Measured-flow vaporizers include Copper kettle, Verni-trol and Metomatic vaporizers. The modern example of a measured flow vaporizer is the desflurane Tec 6 vaporizer. C) Electronic vaporizers In these vaporizers, a computer calculates the carrier gas flow that needs to pass through the vaporizing chamber in order to produce the desired anesthetic gas/vapor concentration. Another type of electronic vaporizers withdraws a calculated amount of liquid agent from the agent bottle and injects that liquid into the breathing system or fresh gas flow. The amount of liquid that is injected is adjusted to achieve the desired anesthetic concentration.


Vaporization methods 1. Flow over A stream of carrier gas passes over the surface of the liquid i.e. it “FLOWS OVER� the surface of the liquid. Increasing the area of the gas liquid interface enhances the efficiency of the vaporization. This can be done by using baffles or spiral tracks to lengthen the gas pathways over the liquid. Another method is to employ wicks that have their bases in the liquid anesthetic agent. The liquid moves up the wick by capillary action. (Fig. 2 a and b)

Fig. 2a: Flow over Vaporizer Fig. 2b: Flow over Vaporizer with wicks and baffles

2. Bubble through The carrier gas is bubbled through the liquid anesthetic agent. A known amount of the liquid anesthetic agent is then injected into the fresh gas flow. (Fig.3)


Fig. 3: Bubble through vaporizer

3. Temperature compensation Energy in the form of heat is lost as liquid is vaporized and the liquid temperature falls. This results in fall in saturated vapor pressure which decreases the vaporizer output. Methods have been employed to maintain constant vapor output with fluctuation in liquid anesthetic temperature. a) Mechanical compensation This is done by altering the splitting ratio as temperature changes so that the percentage of carrier gas that is directed through the vaporizing chamber is increased or decreased. With fall in temperature, the thermal element restricts the bypass flow causing more carrier gas to pass through the vaporizing chamber and the opposite occurs as the temperature increases. Two types of mechanical compensation are normally used: The first consists of two dissimilar metals or alloys placed back to back (i.e a bimetallic strip). As the two metals have different rates of expansion and contraction with temperature, the device has the ability to ‘bend’. It can therefore be used to vary the degree of occlusion in the aperture of the gas channel (usually the bypass) and thus alter the flow of carrier gases through it. (Fig.4a and b) In the second arrangement, the bimetallic device consists of a central rod made of Invar, a metal alloy with a low coefficient of expansion, sitting inside a brass jacket, the top part of which is attached to the roof of the vaporizing chamber. The rod is attached only at the base of the brass jacket, which has a higher coefficient of expansion. The outer surface of the jacket is immersed in liquid anesthetic agent in the vaporizing chamber. As the aforementioned liquid cools, the brass jacket contracts more than the Invar, which is pushed upwards into the bypass, restricting the flow of gas. (Fig. 4c and d)


Fig. 4: Two different types of mechanical thermocompensation b) Supplied heat An electric heater can be used to supply heat to a vaporizer and maintain it at a desired constant temperature. c) Computerized thermocompensation Temperature compensation is achieved by computer control.

4. Based on resistance Plenum Vaporizers have high resistance and therefore require a pressurized source to provide a flow of gas. They are usually placed outside the breathing circuit (VOC or “vaporizer out of circuit” configuration), on the back bar of the anesthetic machine, downstream of the flow meters. Most of the modern vaporizers are plenum vaporizers. Draw-over vaporizers require a sub-atmospheric pressure distal to the vaporizer, to ‘draw’ the fresh gas flow through. This is typically the patient’s own respiratory effort, so they require a low internal resistance. This type of vaporizer is most useful when pressurized gas sources are not available. They are not as accurate as plenum vaporizers owing to such variable flow rates, but can be used within the breathing circuit (VIC or


“vaporizer in circuit� configuration). Examples include the ether vaporizer EMO and the OMV (Oxford Miniature vaporizer). Effect of altered barometric pressure Most vaporizers are calibrated at sea level. Since they can be used in hyperbaric chamber or at high altitudes where atmospheric pressure is low, it is important to know how they will perform when barometric pressure is changed. The ASTM (American Society of Testing and Materials) requires that the effect of changes in ambient pressure on Vaporizer performance be stated in the accompanying documents. Effect of rebreathing Rebreathing causes a difference between vaporizer setting and inspired concentration. With significant rebreathing, only an agent analyzer can provide an accurate value of the inspired agent concentration. Effect of intermittent back pressure Pumping effect It is due to the effect of intermittent back pressure transmitted from the breathing circuit due to positive pressure ventilation or use of the oxygen flush valve. It can increase vaporizer output. The surge in back pressure forces gas in the back bar (which is not saturated with vapor) back into the vaporizing chamber, and the gas in the vaporizing chamber (which is saturated with vapor), retrogradely into the bypass channel. When the pressure subsequently falls, the forward flow increases the concentration of the delivered vapor. The effect is maximal with large pressure swings, low flows and a low dial setting. Modern vaporizers are relatively immune (older vaporizers are certainly not immune) due to check valves between the vaporizer outlet and the common gas outlet, smaller vaporizing chambers, or tortuous inlet chambers. Any of these design features prevent gas which has left the vaporizers from re-entering it. (Fig.5)

Fig.5: Elongation of the inflow channel prevents saturated vapor from reaching the bypass


Pressurizing effect This is a decrease in concentration of the vaporizer output when the overall pressure (that is, both in the bypass and the vaporizing chamber) in the vaporizer is raised. The mechanism is that the partial pressure of vapor generated is dependent solely on temperature, and therefore at a high internal pressure, the vapor forms less of the fractional composition of the number of molecules. Consequently, when the gas expands to atmospheric pressure at the common gas outlet, the delivered concentration of the vapor will be less than that intended. The effect is maximal with large vaporizing chambers at high flows and high pressures. Hazards and safety features of contemporary vaporizers Hazards 

Incorrect agent

Tipping

Simultaneous inhaled agent administration

Reliance on breath by breath gas analysis rather than preventive maintenance

Overfilling

Leaks

Electronic failure

Safety features Important safety features include: 

Keyed fillers

Low filling port

Secured vaporizers (less ability to move them about minimizes tipping)

Interlocks

Concentration dial increases output in all when rotated counterclockwise (as seen from above)

Filling systems There are a number of filling systems available. Many are designed to allow a vaporizer to be refilled only with a specific agent. Some systems are specific to one vaporizer manufacturer only. The ASTM (American Society of Testing and Materials) machine standard recommends that a vaporizer designed for a single agent to be fitted with a permanently attached agent specific device to prevent accidental filling with a wrong agent.


In addition to preventing a vaporizer from being filled with a wrong agent, these systems may reduce the air pollution associated with filling or draining a vaporizer. Types (Fig.6)

Funnel fill system Keyed fill system Quick fill system Easy fill system Desflurane specific filling system

KEYED FILL SYSTEM

SCREWED FILL SYSTEM


QUICK FILL SYSTEM Fig 6: Different types of filling systems

Fig.7. Bottle adaptors that are colour coded

Vaporizer mounting systems

Permanent mounting Permanent mounting means that tools are required to remove or install a vaporizer on the anesthesia machine. Advantages include less chances of physical damage and leaks. Disadvantages include not having enough mounting locations to accommodate all vaporizers and difficulties in removing a malfunctioning vaporizer.

Detachable mounting These are standard on most of the modern anesthesia machines. They allow the Vaporizer to be mounted and removed without the use of tools. Select – a – tec system (Fig.8 a and b) and a similar system from Drager Medical are widely used and Vaporizers cannot be interchanged between these two systems.


Fig 8a. Select-a-tec mounting system.

Fig 8b. Select-a-tec mounting system

Interlock devices Interlock (vaporizer exclusion) systems prevent more than one vaporizer from being turned ON at a time.(Fig. 9 AND 10)

Fig.9a. Select-a-tec in Datex Ohmeda


Fig.9b.Datex Ohmeda Interlock

Fig.10. North American Drager interlock system Tec 6 desflurane vaporizer Desflurane has two physical properties, making it unsuitable for use with a conventional vaporizer. First, it has a very high SVP (664 mm Hg at 20â °C). A conventional vaporizer would require high fresh gas flows to dilute it to within clinically useful concentrations, making it uneconomical. Secondly, it has a low boiling point (23.5â °C). At room temperature, it will intermittently boil resulting in large fluctuations in agent delivery. When boiling, there will be excessive agent delivery; however, it will


then cool due to a large loss of latent heat of vaporization, resulting in an exponential decrease in SVP and under delivery of agent. The Ohmeda Tec 6 overcomes these problems by using an electrical filament that heats the desflurane to 39â °C, raising its SVP to 1460 mm Hg, that is nearly 2 atm. In addition to providing a stable SVP, this high pressure removes the need for a pressurized carrier gas- instead, the fresh or diluents gas is entirely separate from the vaporizing chamber.

Fig.11. Schematic diagram of the TEC 6 vaporizer

Newer vaporizers The GE Aladin cassette vaporizer The vaporizer system used in the GE Anesthesia Delivery Unit (ADU), is unique in that the single electronically controlled vaporizer is designed to deliver five different inhaled anesthetics including halothane, isoflurane, enflurane, sevoflurane, and desflurane. The Vaporizer system consists of a permanent internal control unit housed within the ADU and an interchangeable Aladin agent cassette which contains anesthetic liquid. The Aladin cassettes are color keyed to their respective anesthetic agent, and are also magnetically coded so that the Aladin system can identify which anesthetic cassette has been inserted. Though very different in external appearance, the functional anatomy of the Aladin cassette vaporizer (Fig. 12) is very similar to that of the Dräger vapor 19.n, 20.n and the GE/Datex-Ohmeda Tec 4, Tec 5, and Tec 7 vaporizers.


Fig. 12: Aladin cassette and a cutaway cassette showing the lamellae The Aladin system is functionally similar to these conventional Vaporizers because like them, it consists of a bypass chamber and Vaporizing chamber. The heart of the Aladin system is the electronically regulated flow control valve located in the Vaporizing chamber outlet. This valve is controlled by a central processing unit (CPU). The CPU receives input from multiple sources including the concentration control dial, a pressure sensor located inside the Vaporizing chamber, a temperature sensor located inside the Vaporizing chamber, a flow measurement unit located in the bypass chamber, and a flow measurement unit located in the outlet of the Vaporizing chamber. The CPU also receives input from the flow meters regarding the composition of the carrier gas. Using data from these multiple sources, the CPU is able to precisely regulate the flow control valve to attain the desired Vapor concentration output. Appropriate electronic control of the flow control valve is essential to the proper function of this Vaporizer.

Fig. 13: Diagram of an Aladin cassette, 1 = lamellae, 2 = metal plate, 3 = inflow back valve, 4 =outflow back valve, 5 = temperature sensor, 6 = handle, 7 = filling system, 8 = ball valve, 9 = air channel, 10 = cassette ID magnets, 11 = liquid level window

A fixed restrictor is located in the bypass chamber, and it causes flow from the Vaporizer inlet to split into two flow streams (Fig. 13). One stream passes through the bypass chamber, and the other portion enters the


inlet of the vaporizing chamber and passes through a one-way check valve. The presence of this check-valve is unique to the Aladin system. This one-way valve prevents retrograde flow of the anesthetic vapor back into the bypass chamber. Its presence is crucial when delivering desflurane if the cassette temperature is at or above the boiling point for desflurane (22.8°C). A precise amount of vapor-saturated carrier gas passes past the flow control valve, which is electronically regulated by the CPU. This flow then rejoins the bypass flow and is directed to the outlet of the vaporizer. During operating conditions in which high fresh gas flow rates and/or high dial settings are used, large quantities of anesthetic liquid are rapidly vaporized. As a result of vaporative cooling, the temperature of the remaining liquid anesthetic and the vaporizer cassette decrease. To offset this cooling effect, the Aladin system is equipped with a fan which forces warmed air from an “agent heating resistor� across the cassette (the sump for the vaporizer) to raise its temperature when necessary. The fan is activated during two common clinical scenarios: (1) when rapidly increasing the desflurane concentration, and (2) during inductions using high sevoflurane concentrations.

Fig.14. Working principle of the ADU

Drager DIVA Vaporizer

The Drager DIVA (Direct injection of vapor anesthetic) vaporizer (Fig.15.a) is a measured-flow type of vaporizer requiring a separate air supply. Integrated into the Zeus anesthetic machine, it can form part of a closed anesthetic system. It utilizes closed-loop feedback control to determine the amount of volatile agent allowed through a closing valve into a heated vaporization chamber; (Fig. 15.b.) this then passes either directly into the breathing system or through a mixing chamber into the fresh gas flow. The control unit monitors the pressure of volatile agent in the vaporizing chamber, the fresh gas flow, and the target-expired volatile concentration, to ascertain the amount of volatile agent required to be released to maintain the desired concentration at the patient end. Thus, quantitative closed-system anesthesia can be realized.


Fig.15a. DIVA (Direct injection of vapor anesthetic) vaporizer

Fig. 15.b. Schematic drawing of the DIVA metering system Conclusion Knowledge of the principles of operation of vaporizers is essential to the proper understanding of their functions. Modern plenum vaporizers, if used as intended by the manufacturers are (apart from recommended service schedules) maintenance free devices that provide accurate concentrations of vapor over the range of conditions encountered in everyday clinical practice. Future developments may occur in conjunction with the discovery of novel volatile anesthetic agents and there is the possibility of closed systems, where vaporizer control may be linked directly to patient parameters via feedback mechanisms. Recommended reading 1. Jerry A Dorsch, Susan E Dorsch. Understanding anesthesia equipment. Fifth edition. Lippincott Williams and Wilkins: 121 – 189. 2. Andrew J Davey, Ali Diba. Ward’s Anaesthetic Equipment. Fifth edition. Elsevier Saunders: 65 – 89. 3. Young J, Kapoor V. Principles of anaesthetic Vaporizers. Anesth Int Care Med 2010;11:140-143. 4. Boumphrey S, Marshall N. Understanding Vaporizers. CEACCP 2011; 11(6):199-203. 5. Schober P, Loer SA. Closed system anaesthesia – historical aspects and recent developments. Eur J Anaesthesiol 2006; 23:914-920. 6. Hendrickx et al. The ADU Vaporizing Unit: A New Vaporizer. Anesth Analg 2001;93:391-5.


7. Baum JA. New and alternative delivery concepts and techniques. Best Pract Res Clin Anaesthesiol 2005;19(3):415-428.


EXAMINATION OF THE CVS Dr.Lakshmi Kumar Professor of Anaesthesiology, Amrita Institute of Medical Sciences, Kochi.

History:

A thorough history should be elicited from the patient including symptoms,and the

duration, factors that precipitate and factors that worsen the symptoms. Any history of fever with joint pain, dyspnea, orthopnea should be asked for. In a patient with ischemic heart disease, a history of angina should be elicited, characteristic features of the pain, its provocative and relieving factors. Is it associated with symptoms of sweating and nausea? Previous episodes? history of syncope, dizziness and hemoptysis should also be elicited. Effort Tolerance: What levels of exertion does the patient usually tolerate? Estimated Energy Expenditure for various activities. MET 1 MET =oxygen consumption of 3.5 ml/kg/min 1 MET: Takes care of oneself. Eats, dresses onself and uses the toilet without help Walks indoors around the house Walks on level ground at 2-3 mph(3.2 – 4.8 km/hr) for 1 or 2 blocks Does light housework like dusting and washing dishes

4 METS: Climbs a flight of stairs or walks uphill Heavy work in the house like scrubbing floors Walking on level groungd at 4 mph (6.4 km per hour) Participates in doubles tennis or dancing

> 10 METS: strenuous sport like swimming, singles tennis & skiing The patient who has a moderate effort tolerance can undergo surgery that is elective without significant increase in morbidity. A person who may have an effort tolerance of 4 METS and less can undergo low risk surgery or an emergent surgery.


History of hospitalizations or interventions performed. Ask for history of valvular heart disease, if present any history of hopitalisation or surgery ( emergency valvotomy during the second trimester of pregnancy or other surgical repairs). History of 3 or 4 weekly penicillin injections, beta blockers, diuretics or anticoagulants for atrial fibrillation or for prosthetic mechanical valve should be taken. A patient with IHD may bring forth past history of angina or LV failure needing hospitalizations. A history of a ‘heart attack� should be followed with history of hospitalization related to the MI, thrombolysis or interventions and antipltelet therapy. If the patient has had an angioplasty only, then an elective surgery needs to delayed by only 2 weeks and the patient can be taken for surgery on aspirin only. A bare metal stent would thrombose if the dual antiplatelets are not continued for 4-6 weeks after the procedure which is the time needed for endothelialisation of the stent. It is important to schedule elective surgery and semi elective surgery after4- 6 weeks (depending upon the clinical condition) and continue one of the antiplatelet therapies throughout the perioperative period.A drug eleuting stent carries a much higher risk of in-stent thrombosis and the recommendations are to continue dual antiplatelet therapy for 6 -1 2 months after the intervention. For a patient with IHD a clear history of effort tolerance as outlined above should be elicited and medications assessed. The medications commonly used are beta blockers/calcium channel blockers, ACE inhibitors, statins, AR blockers and nitrates. The guidelines require ACE inhibitors and AR blockers to be discontinued the day prior to surgery because of the possibility of uncontrolled hypotension with the induction of anaesthesia. The mechanism for this is the obtundation of the renin angiotensin mediated response to hypovolemia during surgery. A history of anticoagulation or DVT prophylaxis should be elicited. Anticoagulation is usually indicated in mechanical prosthetic valves, in LV clot or with atrial fibrillation. Their action will persist for 3 -5 days after discontinuation and they can be reversed with administration of vitamin K or the transfusion of FFP. In a patient for elective surgery, the advice is to discontinue the drug 5 days before the surgery and start the patient on heparin (Unfractionated or low molecular weight) and to target an INR of around 1.5 for the surgery. The heparin is discontinued six hours prior to the anticipated time of surgery and started 6 hours after and


LMWH discontinued 12 hours prior to surgery and restarted 4 – 12 hours later based upon the surgery and the risk for bleeding. Examination of the Cardiovascular System General Examination: 1) Posture - Semi recumbent or sitting posture and flaring or use of accessory muscles may suggest LVF. 2) Pallor – suggests anemia and also a poor circulatory state. 3) Elevated JVP – suggests right heart failure, with tricuspid regurgitation. 4) Pedal edema – suggests congestive cardiac failure or hypo-proteinemic states. Auscultation for the Anaesthesiologist: Auscultation of the heart provides perhaps the most useful diagnostic information.

It is

necessary to listen to the precordium in the four cardinal areas and the back with both bell and diaphragm, the former better suited for detecting low-frequency events, while the diaphragm selectively picks up high frequency events. It is important to be systematic in auscultation and note the following aspects: 1. Heart rate and regularity: Extremely fast or slow rates or irregularity in the rhythm should be evaluated by an ECG and a long rhythm strip. 2. Heart sounds: Intensity and quality of the heart sounds, especially the second heart sound (S2) should be evaluated. Abnormalities of first, third and presence of gallop rhythm or the fourth sound (S4) should be noted. 3. Heart murmurs: Heart murmurs should be evaluated in terms of intensity, timing (systolic, diastolic or continuous), location, transmission and quality.

First Heart Sound (S1) This represents closure of the mitral and tricuspid valves and occurs as the ventricular pressure exceeds the atrial pressure at the onset of systole. Splitting of the first sound is normal (but barely discernible) as mitral valve closes earlier than tricuspid, although patients with complete


right bundle branch block exhibit wide splitting. The first heart sound is soft if atrioventricular conduction is prolonged or if myocardial diseases are present and is accentuated with increased blood flow across atrio ventricular valve as in left to right shunt or in high cardiac output. Second Heart Sound (S2) The second heart sound has two components that represent the asynchronous closure of the aortic and pulmonary valves and signal the end of ventricular ejection. Aortic closure normally precedes the closure of pulmonary valve. The presence on auscultation of two components, aortic (A2) and pulmonic (P2), is called splitting of the second heart sound. The time interval between the components varies with respiration i.e. with inspiration the degree of splitting increases and with expiration it shortens. For all practical purposes, the most useful aspect of S2 from the point of view of the anesthesiologist is the P2. A loud P2 is fairly specific and moderately sensitive for pulmonary hypertension. A palpable P2 is always abnormal and strongly suggests severe pulmonary arterial hypertension. Third Heart Sound (S3): This is normally heard in many children and is accentuated in pathological states. This sound occurs early in diastole and represents the transition from rapid to slow filling phases. Conditions with increased blood flow across either the mitral valve as in VSD or mitral insufficiency or the tricuspid valve as in atrial septal defect may accentuate the S3. A gallop rhythm found in congestive cardiac failure often represents exaggeration of the third heart sound in the presence of tachycardia. A pathologic S3 consistently accompanies conditions associated with significant ventricular dysfunction. Left ventricular enlargement and dysfunction that accompanies cardiomyopathy, anomalous coronary artery from pulmonary artery (ALCAPA) are characteristically associated with a prominent S3 that is accompanied by a soft S1. Fourth Heart Sound (S4): An S4 is almost always abnormal and found in conditions in which the atrium forcefully contracts when ventricle has decreased compliance as seen in fibrosis or marked hypertrophy and when flow from atrium to ventricle is increased. HEART MURMURS Each heart murmur must be analyzed in terms of intensity (grade 1 to 6), timing (systolic or diastolic), location, transmission and quality. Intensity: Murmurs are graded as follows:


Grade 1

Heard only with intense concentration after a period of “tuning in�

Grade 2

Faint but heard immediately

Grade 3

Easily heard, of intermediate intensity

Grade 4

Easily heard and loud (may be associated with a thrill)

Grade 5

Very loud, thrill present and audible with the edge of the stethoscope on the chest

Grade 6

Audible with the stethoscope off the chest

The difference between 2 and 3 or grades 5 and 6 may be somewhat subjective. Timing: Based on the timing of the heart murmur to the S1 and S2, the heart murmur may be classified as systolic, diastolic or continuous. Location: On the chest wall with regard to area where the sound is loudest and other areas where the sound is audible (extent of radiation) Duration:

The time of the murmur from beginning to end.

Pitch:

The frequency range of the murmur.

Quality:

The presence of harmonics and overtones.

1. Systolic Murmurs i) Holo-systolic or pansystolic murmurs : These murmurs begin with S1. They often continue at the same intensity to S2. Pansystolic murmurs occur when a regurgitant atrio-ventricular valve is present (tricuspid or mitral) or in association with most VSDs. In physiologic terms pansystolic murmurs occupy the isovolumetric contraction phase of the cardiac cycle. ii) Ejection systolic murmurs:: They arise from the outflow tracts after the isovolumetric contraction phase. There is therefore a small gap after the first heard sound after which ejection systolic murmurs are audible. In practice however, it may be difficult to identify this gap after the first heart sound. Additional features include a crescendo - decrescendo character.


Innocent murmurs are ejection systolic murmurs commonly heard in children. They have a vibratory character to them and occupy mid-systole. They are seldom loud (unless the child is febrile or anemic). They are best heard in the left second or third intercostal space. The second heart sound is always normally split with normal intensity. iii) Early systolic murmurs;They start abruptly with S1 but taper and disappear before the S2 and are usually seen with small muscular VSDs iv) Mid or late systolic murmurs: These begin midway through systole and are often heard in association with the mid systolic clicks in insufficiency of mitral valve prolapse.

2. Diastolic murmurs (i) Early diastolic murmurs (EDM): These murmurs result from semi-lunar valve leaks.(aortic and pulmonary ) The murmur of aortic regurgitation is typically high pitched with a rapid decline in intensity (decrescendo). They are there for heard best with the diaphragm of a stethoscope pressed firmly against the chest wall (to selectively transmit the high frequencies) The intensity of the murmur correlates poorly with the severity of AR. Peripheral signs (bounding pulses, wide pulse pressure with reduced diastolic pressure) are better indicators of AR severity. Infants may have significant AR with faint or sometimes even inaudible EDM. The character of murmur of pulmonary regurgitation (PR) is critically dependent of whether or not there is associated pulmonary artery hypertension (PAH). In absence of PAH (normotensive PR) the murmur is low pitched and typically starts a little after the second heart sound (reflecting a relatively prolonged hang-out interval). In presence of PAH the murmur is often harsh (hypertensive PR). It commences with a loud P2 and occupies a significant duration of diastole and sometimes all of diastole (pan-diastolic). The loudness and duration correlates poorly with severity of PR. Very loud murmurs may result from a jet of PR striking the anterior wall of the right ventricular outflow tract (just beneath a stethoscope in the second intercostal space).


(ii) Mid-diastolic murmurs (MDM): They result from flow disturbance at the level of the atrioventricular valves. This may be the result of stenosis of the orifice or excessive flow across the orifice. Flow murmurs from shunt lesions correlate well with hemodynamics. The mid diastolic murmur of mitral stenosis has certain specific characteristics. A pre-systolic accentuation is typical and reflects flow acceleration resulting from atrial contraction. The MDM of rheumatic mitral stenosis commences with an opening snap and is accompanied by a loud first heart sound. Continuous Murmurs: Continuous murmurs result from flow disturbance that occurs both in systole and diastole without any interruption. The murmur results from pressure difference across a communication during the entire cardiac cycle and the direction of blood flow does not change during the cardiac cycle. While PDA is the most well-known cause, the anesthesiologist may encounter a child who has been previously operated for a BT shunt. This results in a continuous murmur in the chest wall adjacent to the BT shunt. Pericardial Rub: Pericardial rubs have a rather specific character. They are superficial and scratchy heart, best over the precordium. Three components are identifiable. They include a systolic, an early diastolic and a late diastolic component. Respiratory and postural variations are common.

They often tend to be transient and disappear as fluid accumulates in the

pericardium. Child with congenital cardiac disease for Non cardiac surgery Although a bewildering number of anatomic possibilities exist with congenital heart disease (CHD), the physiological consequences are relatively limited. Therefore it is not necessary to get intimidated by the extraordinary variety of congenital heart lesions when a patient is being considered for non-cardiac surgery. It is important, however, to understand the physiology of the defect in order to anticipate the consequences of surgical stress and anesthesia.

While a

consultation with a pediatric cardiologist should be sought to understand the patient’s specific lesions and their physiological consequences, the following background information can help plan non-cardiac surgery better.


A practical checklist for the anesthesiologist while evaluating patients with congenital heart disease Table 1: Item in Checklist Comprehensive assessment of

Purpose patient

records

1. What

is

the

comprehensive

clinical diagnosis? 2. Has the CHD been corrected / uncorrected /palliated? 3. What are the specifics of the operation or catheter intervention performed?

Consultation with Pediatric Cardiologist

4. What is the current physiology?

followed, if needed, by:

5. What hemodynamic consequences

ECG

Chest X-ray

Oxygen saturation’

ABG

Echocardiography

Exercise testing

can be anticipated from the stress of surgery and anesthesia? 6. Is there a risk of worsening of hypoxia? 7. Is there a need for endocarditis prophylaxis? 8. Is there a potential risk for rhythm disturbance? 9. Is there a risk for paradoxical embolization because

of R-L

shunt? 10. Are there specific concerns during postoperative recovery?


Assessment of Valvular Heart Disease: The following scheme is useful in the clinical evaluation of valvular heart disease. Clinical Classification of Severity of Heart Valve Lesions Valve Lesion

Mild

Moderate

Mitral stenosis

Normal S2,

S2

wide A2-OS interval, relatively

soft

late-onset

and mid

diastolic murmur

split

Severe may

be Evidence

normal but P2 loud, A2-OS

significant pulmonary

interval

identifiable,

hypertension,

short

mid interval,

diastolic murmur

close

splitting of S2, loud P2,

prominent

of

A2-OS prominent

mid

diastolic

murmur* Mitral regurgitation

Normal apex, Normal Hyperdynamic

apex, Cardiac enlargement,

S2, no S3, apical pan widely split S2, S3 downward systolic murmur, no may flow murmurs

be

and

present, outward

prominent pansystolic apex, murmur

displaced hyperdynamic

precordium,

widely

split S2, P2 may be loud, frequently

S3

and a

mid-

diastolic flow murmur Aortic stenosis#

Normal

carotid Some delay in carotid Delayed

pulsations, no clinical upstroke evidence

of

left appreciable,

may

carotid

be upstroke,

clinical evidence

clinical of

LVH,

ventricular

evidence of LVH in long ejection systolic

hypertrophy,

the

relatively ejection

form

of

a murmur with delayed

short sustained heave in the peaking systolic apical

impulse.


murmur that peaks in Prominent early systole

ejection

systolic

murmur,

relatively

longer

duration peaking in mid-systole Aortic regurgitation

No peripheral signs, Wide pulse pressure Wide pulse pressure Early

diastolic (>

murmur

50

diastolic

mm

Hg), (>80

mm

Hg),

pressure diastolic pressure < 50

usually > 50 mm Hg, mm Hg, often as low hyperdynamic apical as 0 mm Hg (freee impulse

AR),

signs

of

increased aortic runoff

are

easily

demonstrable, cardiac enlargement, hyperdynamic apical impulse Tricuspid

Pansystolic

murmur Prominent

TR Liver enlarged with

regurgitation

of TR audible in the murmur

systolic

pulsation,

left lower parasternal

elevated

jugular

region.

venous

pulsations

(JVP) with prominent ‘v’ waves. Tricuspid (TS)

stenosis Mild and moderate TS are usually clinically Elevated silent

JVP

with

prominent ‘a’ waves, prominent pre-systolic pulsations; the mid diastolic murmur of TS may also be heard


in

the

left

lower

sternal area * Rarely severe mitral stenosis may not be associated with a identifiable mid diastolic murmur (silent MS); usually this is accompanied by severe pulmonary hypertension and gross right ventricular enlargement # Aortic stenosis (AS) is rarely seen in children with rheumatic heart disease. Isolated AS is exceptional. Some aortic regurgitation invariably accompanies AS and typically, signs of AR are masked by AS. Conclusions: The CVS examination is very vast and it is difficult to include all the clinical situations that one encounters . A good elicitation of history followed by a clinical examination and understanding of the pathophysiology of the disease will help in providing optimum care during anesthesia and uneventful recovery.


ANAESTHESIA WORKSTATION Dr Ramkumar Venkateswaran Professor of Anaesthesiology, Kasturba Medical College, Manipal

Over the past two decades, anaesthesia machines have evolved from simple gas mixing devices into complex equipment termed anaesthesia workstations that not only generate and deliver specific concentrations of anaesthetic gases and vapours but also serve several other functions. Modern anaesthesia workstations also include vaporisers, breathing circuits, anaesthetic ventilators, patient monitors and gas scavenging systems. An in-depth discussion of all these components that constitute the anaesthesia workstation is well beyond the purview of this lecture. This lecture will therefore concentrate on the components that constitute the anaesthesia machine in its simpler connotation.

Anaesthesia workstations integrate recent technological developments with the twin objective of convenience and safety. Presence of a well-informed anaesthesiologist who understands how the machine works is probably equally if not more important than the advanced capability and versatility of the anaesthesia machine per se. Only an anaesthesiologist who understands his anaesthesia machine well will be able to use it to the optimum.

It is convenient to divide the anaesthesia machine into three zones - the high pressure zone, intermediate pressure zone and low pressure zone - based on the absolute pressures that exist in these three zones of the anaesthesia machine. The high pressure zone begins from the point where the gas source (such as cylinder or medical gas pipeline) is connected to the machine up to the pressure regulator where pressure reduction (regulation) occurs. The components of the anaesthesia machine between the pressure regulator and the flowmeter control knob constitute the intermediate pressure zone. The low pressure zone includes all the components of the anaesthesia machine from the flowmeter control knob to the common gas outlet of the anaesthesia machine where the breathing circuit is connected.

ď&#x201A;ˇ

Hanger yoke assembly (including pin index safety system)

ď&#x201A;ˇ

Pressure gauge

ď&#x201A;ˇ

Pressure regulators


Oxygen pressure failure safety/warning devices

Flowmeters

Oxygen ratio control devices

Oxygen analyser

Individual components will be discussed briefly below to give a comprehensive review of the whole machine.

Hanger yoke assembly The hanger yoke assembly supports the cylinder and connects it to the machine. It has a body that is the framework and main supporting structure. A swinging gate with a retaining screw helps to securely fix the cylinder to the yoke. The outlet port of the cylinder sits over the nipple meant to conduct gases into the anaesthesia machine. A gas seal or washer made of rubber or neoprene (with a metal rim) called the Bodok seal is placed over the nipple to ensure a gas-tight fitting onto the yoke. Pins that constitute the pin index safety system (vide infra) prevent connection of a wrong cylinder to the cylinder yoke. A filter located beyond the yoke assembly prevents dirt and other suspended particles from entering and damaging the more delicate components of the anaesthesia machine. A simple ball-and-spring loaded check valve assembly ensures unidirectional flow of gas from the cylinder (or medical gas pipeline connection) towards the pressure regulator. The check valve assembly prevents transfilling of an empty or near-empty cylinder from a full cylinder.

Piped gas supply can be connected to the machine either through the hanger yoke assembly (using a yoke block that resembles a flush-type cylinder valve) or through a diameter indexed safety system.

Pin index safety system The pin index safety system is used with small cylinders with flush-type cylinder valves that fit directly on to the machine. The pin index consists of two pins projecting from the inner surface of the yoke that fit into two corresponding holes drilled onto the cylinder valve. There are seven pin positions located along the circumference of a circle of 9/16 inch whose radius is centered on the nipple. The pins are 4 mm in diameter and 6 mm long. Two pins are assigned for each gas, one on either side of the midline. This prevents fixing a wrong gas


cylinder onto the yoke assembly. The pin index number for oxygen is 2,5 and that for nitrous oxide is 3,5. Pin position number 7 (that is located in the midline between position 3 and 4) is assigned for entonox.

Pressure gauge All machines have a pressure gauge on the cylinder side of the regulator to measure the cylinder pressure. These gauges are usually of the Bourdon type. They consist of a hollow metal tube that is closed at one end and bent into the shape of a question mark. The vertical lower end of the question mark is connected to the high pressure line beyond the hanger yoke. Application of pressure to the inside of the tube causes the tube to straighten out in a manner similar to the loose end of a garden hose that straightens out when the flow of water is started (â&#x20AC;&#x153;garden-hose effectâ&#x20AC;?). This movement is transmitted to the indicator needle which moves over a gauge that is marked in units of pressure. Pressure gauges are used for the measurement of high pressure. Machines are provided with pressure gauges for both cylinder pressures as well as pipeline pressures.

Pressure regulator Pressure regulators convert the high, variable pressure in the cylinder into a constant working pressure suitable for use in anaesthesia machines. Because of the use of pressure regulators, frequent adjustments are not necessary to maintain a constant gas flow and fine adjustment of low flows is possible. Pressure regulators work on the principle that a high pressure acting over a small surface area can be balanced by a low pressure acting over a larger surface area. Though pressure can be reduced if only this principle is used, it is not possible to keep it constant as the outlet pressure will fall along with the fall in cylinder pressure (pressure decay with reduction of cylinder contents). To keep the outlet pressure constant, a large force that is much more than the cylinder pressure is added over the balancing diaphragm by means of a spring and the area of the larger diaphragm is further increased. This minimises the decay in outlet pressure. Modern regulators are factory preset by the manufacturer and enclosed in a closed system such that it cannot be tampered with by unauthorised individuals.

Oxygen pressure fail-safe system This device is designed to prevent delivery of an anaesthetic gas without oxygen when the oxygen supply fails. It is incorporated at the level of the pressure regulators. The oxygen


pressure regulator works as the primary (or master) regulator. The output from this regulator controls the secondary regulators or the slave regulators such as the nitrous oxide regulator. In such systems, if the pressure from the oxygen regulator falls below a critical level, the slave regulator of nitrous oxide will automatically close and will not allow flow of nitrous oxide. There are two types of oxygen fail-safe devices. In the first type, the nitrous oxide regulator will be totally cut off when the oxygen pressure falls below a critical level. In the other type, the nitrous oxide outlet pressure will drop proportionate to the fall in oxygen pressure. The proportioning device will ensure that the desired proportion is maintained but the total gas flow will fall and finally stop.

Oxygen pressure failure warning devices It is mandatory that in addition to cutting off the flow of nitrous oxide, an alarm should sound that will alert the anaesthesiologist to failing oxygen supply. Devices have been developed which activate an alarm when the oxygen pressure fails. The alarm may be visual, audible or both. With the activation of the alarm, the device either cuts off the flow of nitrous oxide or directs it into the atmosphere. The earlier series of Boyleâ&#x20AC;&#x2122;s machine made by Indian Oxygen Limited (also referred to as the Boyle Basic, Boyle Tec and Boyle Ultima) incorporate a device with a small oxygen tank which gets pressurised during normal use when the oxygen pressure in the intermediate pressure zone is above the statutory value of 25 to 30 psig. When the oxygen pressure at the source falls, stored oxygen from this small cylinder flows through a whistle incorporated on line, giving rise to an audible alarm for a period of seven to ten seconds. Cessation of the alarm does not mean that the alarm condition has been rectified and measures must be taken to correct it.

The oxygen pressure fail-safe systems and warning devices control the gas in its associated gas line in response to the pressure in the oxygen line. Its safety potential is limited. It will permit administration of hypoxic gas mixtures when the gas flow is erroneously composed with low oxygen flow, the oxygen flow control valve is accidentally adjusted downward or the oxygen pipeline system carries a gas other than oxygen.

Flowmeters All flowmeters have a flow control valve, a graduated flow tube to measure the flow, and an outlet. The flow control valve is a needle valve or pin valve used to adjust the amount of gas


entering the flowmeter. It consists of a body, a stem that screws into the body and ends in a pin, and a seat.

The control knob attached to the stem will control the relative position of the pin within the seating and hence the orifice for the gas flow. The gland of the flow control valve is filled with packing material to maintain a grip on the stem. If the packing is not tight, the flow control knob may move easily, resulting in accidental flow alterations even with the slightest touch.

A flowmeter measures the flow-rate of the gas passing through it. The one used in modern anaesthetic machines is of the variable orifice type. It consists of a transparent tapered tube with a double taper known as a Thorpe tube. The double taper implies that the tube has a smaller bore at the bottom than at the top. The flowmeter tube contains a float which has oblique notches cut into the rim at the top. These notches or flutes cause the float to rotate freely in the middle of the gas stream without touching the walls of the tube. Flowmeter tubes are thus also known as rotameters. The taper of the rotameter tube increases slowly at the bottom of the scale in order to obtain finer control at the lower end of the scale. In contrast, the gradations at the top of the scale are closer together as the tube tapers more abruptly at the top. The gas flow pathway between the float and the tube varies from the bottom to the top. At the bottom of the rotameter, it is tubular and the flow rate is more dependent on the viscosity of the gas. As the tube widens above, it becomes an orificial flow and flow rate is dependent on the density of the gas.

Flowmeter tubes are individually calibrated with their matched floats for a particular gas at a specific temperature and pressure. A flowmeter calibrated for one gas cannot be used for another with the same calibration as the viscosity and density of the gases differ. Flowmeters will be inaccurate if the float sticks to the tube. Sticking may be caused if the tube is not mounted vertically, if static electricity collects on the tube or if dirt gets stuck in between the tube and the float.

Oxygen ratio control devices Most modern anaesthesia machines utilise proportioning systems at the level of the flowmeter in an attempt to prevent delivery of a hypoxic mixture. Oxygen and nitrous oxide


flowmeters are interfaced either mechanically or pneumatically so that the minimum oxygen concentration at the common gas outlet is 25 percent.

Oxygen ratio monitor Recognising the limitations of the oxygen pressure fail-safe system, the manufacturers of the Drager machine developed a device called oxygen ratio monitor (ORM) which is incorporated at the level of the flowmeter. The ORM consists of a set of linear resistors inserted between the oxygen and nitrous oxide flow control valves and their respective flowmeters. Pressure drop across the resistors is monitored and transmitted via pilot lines to an arrangement of opposing diaphragms. These opposing diaphragms are linked together with the capacity of closing a leaf-spring contact and actuating an alarm in the event of oxygen percentage in the mixture of oxygen and nitrous oxide dropping below a certain predetermined value. The ORM generates an alarm but does not actively control the gas flow. It will not sound an alarm if a hypoxic mixture is administered because the oxygen piping system contains a gas other than oxygen.

Oxygen ratio monitor controller (ORMC) This device not only monitors the ratio of oxygen flow and gives an alarm when it falls below 30% but also reduces the flow of nitrous correspondingly to maintain the ratio. The basic design is similar to the ORM with the exception that the slave regulator (delivering nitrous oxide) is additionally controlled by a ball-valve mechanism which controls the nitrous oxide flow by controlling the delivery pressure to the nitrous oxide control valve. The advantage of ORMC is its capability to automatically respond to reduction in oxygen pressure or operator error. The disadvantage is that the operator cannot override the function when desired.

Link-25 control system Ohmeda anaesthesia machines (including the Boyle Ultima machine introduced in India) use this Link-25 proportion limiting control device. The heart of the system is the mechanical integration of the nitrous oxide and oxygen flow control valves using a gear-and-chain arrangement. This mechanism allows independent adjustment of either valve, but automatically intercedes to maintain a minimum oxygen concentration of 25%. In this system, the nitrous oxide flow control spindle has a gear with 14 teeth attached to it. Oxygen has a gear with 29 teeth which is mounted on the oxygen spindle with threads so that it can


float over the spindle. For every 2.07 rotations of the nitrous oxide spindle, the oxygen gear will rotate once.

The thread mounting of the oxygen gear allows independent rotation of the oxygen flow control valve. The link arrangement is set such that opening of nitrous oxide will always rotate the oxygen gear, but the gear itself will engage the oxygen control valve spindle only when the proportion of nitrous oxide in the mixture exceeds 75%. The flows in the flowmeters are precisely linked to the rotation by regulating the supply pressure of these gases with secondary regulators situated just before the flowmeter. Nitrous oxide is supplied at 26 psig and oxygen at 14 psig. This combination of pneumatic and mechanical control maintains the minimum oxygen percentage at 25% whenever a mixture of oxygen and nitrous oxide are used. The oxygen percentage can be independently varied between 25% and 100%.

The disadvantage of this system is in the mechanical linkage. If the spindle and gear are not properly aligned or if the threads in the spindle undergo wear and tear, the link system is likely to malfunction. Secondly, the proportioning devices link only oxygen and nitrous oxide. If a third gas such as air is included in the flowmeter block, then it no longer assures a 25% oxygen delivery in the mixture. Most modern machines provide an air flowmeter in the flowmeter block. Some of them provide a flip switch that helps the user to select the use of either nitrous oxide or air, thereby avoiding the concomitant use of both nitrous oxide and air.

Other proportioning devices Proportioning devices such as the Quantiflex and the Ohmeda proportioning system allow only two gases to be administered, namely oxygen and nitrous oxide, through a pneumatic and mechanical control system. Basically there are two control knobs, one for percentage control and the other for flow control. The flow control knob controls the total flow and the percentage control knob maintains the set percentage. The flow of each gas cannot be individually adjusted. Oxygen analyzer The use of an oxygen analyser with an anaesthesia system is the only foolproof method to prevent delivery of a hypoxic mixture. This is possible as an oxygen analyser does not depend on pneumatic or mechanical links. Instead, it actually measures the oxygen percentage in the gas mixture either by the paramagnetic principle or by using a fuel cell. One still has to make sure that the analyser is working properly and the alarms are set accordingly.


The fuel cell should undergo a 2-point calibration every day at both ends of the range that it is expected to monitor, namely 21% and 100%. It is logical that an oxygen analyser will be most accurate within the range that it is calibrated for.

DAILY CHECK OUT PROCEDURE OF THE ANAESTHESIA MACHINE Just as one would ensure that one’s car is functioning well before driving to work every morning, it is mandatory that the anaesthesiologist conducts a systematic check of the anaesthesia machine in the morning prior to the start of an anaesthetic. This check is divided into the following segments to ensure that all important areas are covered.

Check the cylinders beginning with the colour code and label of the oxygen and nitrous oxide cylinders. Open the oxygen cylinder and ensure that the cylinder pressure gauge registers at least a half-filled oxygen cylinder (1000 psig). Open the oxygen flow control knob and note whether a flow of 4 to 5 litres per minute can be consistently delivered. Also ensure that opening the nitrous oxide flow control knob at this point will not register any nitrous oxide flow. Close the oxygen cylinder valve and note whether oxygen flow drops to zero and the oxygen failure alarm gets triggered.

Open the nitrous oxide cylinder and note that the cylinder pressure gauge registers 750 psig. Turning the nitrous oxide flow control knob should not produce a flow of nitrous oxide as the oxygen line (that controls the flow of nitrous oxide through the master-slave mechanism) is not pressurised. Opening the oxygen cylinder at this point should result in the ability to deliver both oxygen and nitrous oxide. Closing the oxygen cylinder should result in cutting off of both gas flows with a triggering of the oxygen pressure failure alarm. Now close the nitrous oxide cylinder as well and return both flowmeter control knobs to zero.

Attention is now diverted to the piped gas supply. As a part of the “single hose test”, the oxygen pipeline is connected and the “tug test” is performed to ensure that the Schrader valve (quick coupler) is properly secured. It should be possible to obtain a free flow of gas with opening of the oxygen flow control knob. This test ensures that the gas coming through the oxygen pipeline is flowing through the oxygen flowmeter and there is no cross connection of the flexible pipeline. However, it still does not ensure that the gas flowing through this flowmeter is indeed oxygen. This assurance can be obtained only with the help of an oxygen analyser (vide infra). The nitrous oxide flowmeter is now opened and note is made that the


flowmeter bobbin will register a flow initially and then drop to zero (this flow is from the intermediate pressure zone wherein nitrous oxide gas is trapped after the nitrous oxide cylinder was closed as the last step just prior to testing of the piped gas supply. Connect the nitrous oxide pipeline to the central supply outlet and note that the nitrous oxide flowmeter registers a flow. Disconnect the oxygen pipeline and note that both flowmeter bobbins fall to zero. Reconnect the oxygen pipeline and check whether the pipeline pressure gauges of both gases are registering pressures in the range of 55 to 60 psig. Close the flow control knobs and turn the vaporisers off. Check the level of liquid anaesthetic in the vaporisers and close the filler caps firmly. Perform a leak check of the low pressure zone of the anaesthesia machine from the flowmeter control knobs to the common gas outlet. Close the flow control knobs and keep both vaporisers in the closed position. Attach the suction bulb to the common gas outlet and squeeze the bulb repeatedly till the bulb is fully collapsed. Allow the system to stand and check whether the bulb remains deflated for at least 10 seconds. Repeat the test with each vaporiser open, one at a time. Remove the suction bulb and connect the fresh gas hose/breathing circuit to the common gas outlet. Attempt delivering gas flows on both flowmeters throughout the range available, noting whether the bobbins are moving freely. If the machine has a proportioning device (such as a Link 25 system, ORM or ORMC), test that the flows are changing as expected.

Turn on the main switch of the machine and all electrical monitoring equipment. Connect the breathing circuit and the oxygen analyser to the common gas outlet. Perform a 2-point calibration of the oxygen analyser using room air (21%) and a flow of 100% oxygen. Check the individual breathing circuits as per specific recommendations for proper functioning including a leak test at 30 cmH2O. Check the anaesthetic ventilator as per the manufacturerâ&#x20AC;&#x2122;s recommendations. Ensure all airway equipment (including laryngoscopes and other adjunctive equipment) is available in proper working condition. A properly functioning self-inflating bag should be available as it will serve as the backup device in the event of total gas supply failure.

Check, calibrate and set alarms for all parameters that are planned for the anaesthetic (including electrocardiogram, noninvasive blood pressure, pulse oximeter, capnograph, airway pressure and anaesthetic gas monitors).


Leave the anaesthetic machine in the final working position with vaporisers off, all flowmeters in zero position, adjustable pressure limiting valve in fully open position, reservoir bag attached to the breathing circuit, selector switch turned to the circuit that one plans to use, airway equipment in readiness for use and working suction that is generating adequate suction.

The above steps of machine check should be performed at the start of the day. An abbreviated check should be performed in between 2 patients.


ACID- BASE PHYSIOLOGY Dr Lakshmi Kumar, Professor of Anaesthesiology, Amrita Institute of Medical Sciences, Kochi.

The body maintains a homeostasis between the acid produced and excreted to maintain a pH between 7.36-7.44. A number of regulatory mechanisms exist that keep the balance. The pH of the body is kept in control by 3 systems. 1. The chemical acid- base buffering system that combines with the body fluids and will immediately keep the pH under control. 2. The respiratory center that regulates the removal of volatile carbon-dioxide as a gas in the expired air from the plasma and regulates bicarbonate from the body fluids through the pulmonary circulation. This response occurs within minutes. 3. The kidneys that adjust the acidity and alkalinity of the urine and thereby regulate the pH of the blood. This response can take as long as several hours or days but is a more powerful regulatory system. The metabolic balance in the body is a balance between acids and bases. The acids are classified as volatile acids (carbon- dioxide as bicarbonic acid) and fixed acids. Carbon dioxide is the endproduct of complete oxidation of carbohydrates and fatty acids. It is called a volatile acid meaning in this context it can be excreted via the lungs. The fixed acids are usually referred to by their anion(lactate, phosphate, sulphate, acetoacetate or b-hydroxybutyrate). Fixed acids are produced due to incomplete metabolism of carbohydrates ( lactate), fats ( ketones) and protein ( sulphate, phosphate).Net production of fixed acids is about 1 to 1.5 mmoles of H+ per kilogram per day: about 70 to 100 mmoles of H+ per day in an adult. This non-volatile acid load is excreted by the kidney. The above total for net fixed acid production excludes the lactate produced by the body each day as the majority of the lactate produced is metabolized and is not excreted so there is no net lactate requiring excretion from the body .For acid-base balance, the amount of acid excreted per day must equal the amount produced per day. The routes of excretion are the lungs (for CO2) and the kidneys (for the fixed acids). Each molecule of CO2 excreted via the lungs results from the reaction of one molecule of bicarbonate with one molecule of H+. The H+ remains in the body as H2O.


Buffer systems in the body: A buffer is a solution containing substances that has the ability to minimize changes in pH when an acid or base is added to it. The major buffer system in the ECF is the CO2-bicarbonate buffer system. This is responsible for about 80% of extracellular buffering. It is the most important ECF buffer for metabolic acids but it cannot buffer respiratory acid-base disorders. The components are easily measured and are related to each other by the HendersonHasselbach equation. pH = pKa + log10 ( [HCO3] / 0.03 x pCO2) The pKa value is dependent on the temperature, [H+] and the ionic concentration of the solution. It has a value of 6.099 at a temperature of 37C and a plasma pH of 7.4. At a temperature of 30C and pH of 7.0, it has a value of 6.148. For practical purposes, a value of 6.1 is generally assumed and corrections for temperature, pH of plasma and ionic strength are not used except in precise experimental work. pH = 6.1 + log ( [HCO3] / 0.03 pCO2 ). The bicarbonate buffer system is an effective buffer system despite having a low pKa because the body also controls pCO2 Site

Buffer System

Comment

ISF

Bicarbonate

For metabolic acids

Phosphate

Not important

Protein

Not Important

Bicarbonate

For metabolic acids

Haemoglobin

Important for carbon Dioxide

Protein

Minor Buffer

Phosphate

Concentration low

Proteins

Important buffer

Phosphate

Important Buffer

Phosphate

For titratable acidity

Ammonia

For ammonium ion

Blood

ICF

Urine


Bone

Calcium carbonate

Metabolic Acidosis

The other buffer systems in the blood are the protein and phosphate buffer systems. These are the only blood buffer systems capable of buffering respiratory acid-base disturbances as the bicarbonate system is ineffective in buffering changes in H+ produced by itself. The phosphate buffer system is not an important blood buffer as its concentration is too low The concentration of phosphate in the blood is so low that it is quantitatively unimportant. Phosphates are important buffers intracellularly and in urine where their concentration is higher. Haemoglobin is an important blood buffer particularly for buffering CO2. Protein

buffers in

blood include haemoglobin (150g/l) and plasma proteins (70g/l). Buffering is by the imidazole group of the histidine residues which has a pKa of about 6.8. This is suitable for effective buffering at physiological pH. Haemoglobin is quantitatively about 6 times more important then the plasma proteins as it is present in about twice the concentration and contains about three times the number of histidine residues per molecule. Deoxyhaemoglobin is a more effective buffer than oxyhaemoglobin and this change in buffer capacity contributes about 30% of the Haldane effect. The major factor accounting for the Haldane effect in CO2 transport is the much greater ability of deoxyhaemoglobin to form carbamino compounds.

The buffer systems which participate in defence of acid-base changes are in equilibrium with each other. There is after all only one value for [H+] at any moment. This is known as the isohydric Principle. Conventionally, the components of the bicarbonate system ( [HCO3] and pCO2) alone are measured. They are accessible and easy to determine. Blood gas machines measure pH and pCO2directly and the [HCO3] is then calculated using the Henderson-Hasselbalch equation. Bone also acts as a buffer as the carbonate and phosphate salts present in the bone particularly in prolonged metabolic acidosis. Bone matrix contains hydroxyapatite crystals that account for nearly 65% of the bone volume. Bone contains carbon dioxide as bicarbonate and this can be substituted for phosphate and hydroxyl in the apatite crystals. The mechanism by which bone acts as a buffer is by ionic exchange or by dissolution of bone crystal.


Respiratory Regulation: The respiratory regulation refers to the alterations in the pH secondary to the changes in ventilation. Carbon-Dioxide is lipid soluble and crosses the cell

membranes rapidly and

changes in ventilation will very rapidly effect changes in pH. The two key equations that establish this relationship are 1.

Alveolar Ventilation â&#x20AC;&#x201C; Arterial pCO2 Relationship.

Changes in alveolar ventilation are inversely related to the changes in arterial carbon dioxide. PaCo2 â&#x2C6;&#x17E; VCO2/ VA Alternatively, PaCO2 = 0.863 x (V co2/VA) 2.Henderson-Hasselbalch Equation pH = pKa + log { [HCO3] / (0.03 x pCO2) } or The Henderson equation: [H+] = 24 x ( pCO2 / [HCO3] ) The lungs are responsible for the excretion of carbon dioxide and nearly 12,000 to 13,000 mmol/day is excreted. Kidney Regulation The kidneys in contrast are responsible for the excretion of fixed acid which although account for a smaller amount of 70 -100 mmol/l is still crucial as there are no alternative. The other major role by the kidneys is the reabsorption of the filtered bicarbonate of about 4000-5000 mmol/day.


The functions

of the proximal tubule is in bicarbonate reabsorption and ammonium ion

production. Daily filtered bicarbonate equals the product of the daily glomerular filtration rate (180 l/day) and the plasma bicarbonate concentration (24 mmol/l). This is 180 x 24 = 4320 mmols/day (4000 to 5000 mmols/day). About 85 to 90% of the filtered bicarbonate is reabsorbed in the proximal tubule and the rest is reabsorbed by the intercalated cells of the distal tubule and collecting ducts. The reactions that occur are outlined in the diagram. Effectively, H+ and HCO3- are formed from CO2 and H2O in a reaction catalysed by carbonic anhydrase. The H+ leaves the proximal tubule cell and enters the PCT lumen by 2 mechanisms, Na-H antiporter(major route) and also by H-ATPase (proton pump) filtered HCO3- cannot cross the apical membrane of the PCT cell. Instead it combines with the secreted H+ to produce CO2 and H2O. The CO2 is lipid soluble and easily crosses into the cytoplasm of the PCT cell. In the cell, it combines with OH- to produce bicarbonate. The HCO3-crosses the basolateral membrane via a Na+-HCO3- symporter. This symporter is electrogenic as it transfers three HCO3- for every one Na+. In comparison, the Na+-H+ antiporter in the apical membrane is not electrogenic because an equal amount of charge is transferred in both directions .

The basolateral membrane also has an active Na+-K+ ATPase (sodium pump) which transports 3 Na+ out per 2 K+ in. This pump is electrogenic in a direction opposite to that of the Na+HCO3- symporter. Also the sodium pump keeps intracellular Na+ low which sets up the


Na+ concentration gradient required for the H+-Na+ antiport at the apical membrane.The H+Na+ antiport is an example of secondary active transport. The net effect is the reabsorption of one molecule of HCO3 and one molecule of Na+ from the tubular lumen into the blood stream for each molecule of H+ secreted. This mechanism does not lead to the net excretion of any H+ from the body as the H+ is consumed in the reaction with the filtered bicarbonate in the tubular lumen. The 4 major factors which control bicarbonate reabsorption are luminal bicarbonate concentration, luminal flow rate, arterial pCO2 and angitensin II. An increase in any of these four factors causes an increase in bicarbonate reabsorption. Parathyroid hormone also has an effect: an increase in hormone level increases cAMP and decreases bicarbonate reabsorption. Ammonium (NH4) is produced predominantly within the proximal tubular cells. The major source is from glutamine which enters the cell from the peritubular capillaries (80%) and the filtrate (20%). Ammonium is produced from glutamine by the action of the enzyme glutaminase. Further ammonium is produced when the glutamate is metabolised to produce alpha-ketoglutarate. This molecule contains 2 negatively-charged carboxylate groups so further metabolism

of

it

in

the

cell

results

in

the

production

of

2

HCO3- anions.

The pKa for ammonium is so high (about 9.2) that both at extracellular and at intracellular pH, it is present entirely in the acid form NH4+. . Most of the ammonium is involved in cycling


within the medulla. About 75% of the proximally produced ammonium is removed from the tubular fluid in the medulla so that the amount of ammonium entering the distal tubule is small. The thick ascending limb of the loop of Henle is the important segment for removing ammonium. The ammonium level in the DCT fluid is low because of removal in the loop of Henle and the ammonium levels in the medullary interstitium are high (and are kept high by the recycling process via the thick ascending limb and the late PCT). Distal Tubular Mechanism This is a low capacity, high gradient system which accounts for the excretion of the daily fixed acid load of 70 mmols/day. The processes involved are:1.

Formation of titratable acidity (TA)

2.

Addition of ammonium (NH4+) to luminal fluid

3.

Reabsorption of Remaining Bicarbonate

Regulation of renal H+ Excretion The major factors which regulate renal bicarbonate reabsorption and acid excretion are: 1. Extracellular volume Volume depletion is associated with Na+ retention and this also enhances HCO3 reabsorption. Conversely, ECF volume expansion results in renal Na+ excretion and secondary decrease in HCO3 reabsorption. 2. Arterial pCO2 An increase in arterial pCO2 results in increased renal H+ secretion and increased bicarbonate reabsorption. The converse also applies. Hypercapnia results in an intracellular acidosis and this results in enhanced H+ secretion. This renal bicarbonate retention is the renal compensation for a chronic respiratory acidosis. 3. Potassium & Chloride Deficiency Potassium has a role in bicarbonate reabsorption. Low intracellular K+ levels result in increased HCO3 reabsorption in the kidney. Chloride deficiency is extremely important in the maintenance of a metabolic alkalosis because it prevents excretion of the excess HCO3 ( the bicarbonate instead of chloride is reabsorbed with Na+ to maintain electroneutrality).


4. Aldosterone & cortisol (hydrocortisone) Aldosterone at normal levels has no role in renal regulation of acid-base balance. Aldosterone delpetion or excess does have indirect effects. High aldosterone levels result in increased Na+ reabsorption and increased urinary excretion of H+ and K+ resulting in a metabolic alkalosis. 5. Phosphate Excretion Phosphate is the major component of titratable acidity. The amount of phosphate present in the distal tubule does not vary greatly. Consequently, changes in phosphate excretion do not have a significant regulatory role in response to an acid load. 6. Reduction in GFR It has recently been established that a reduction in GFR is a very important mechanism responsible for the maintenance of a metabolic alkalosis. The filtered load of bicarbonate is reduced proportionately with a reduction in GFR. 7. Ammonium The kidney responds to an acid load by increasing tubular production and urinary excretion of NH4+. The mechanism involves an acidosis-stimulated enhancement of glutamine utilization by the kidney resulting in increased production of NH4+ and HCO3- by the tubule cells. This is very important in increasing renal acid excretion during a chronic metabolic acidosis. Role of the Liver in Acid Base Metabolism 1.

Carbon dioxide production from complete oxidation of substrates.

2.

Metabolism of organic acid anions (such as lactate, ketones and amino acids)

3.

Metabolism of ammonium.

4.

Production of plasma proteins (mainly albumin).

Complete oxidation of carbohydrates and fat which occurs in the liver produces carbon dioxide but no fixed acids. The CO2 diffuses out of the liver and reactions in red cells result in production of H+ and HCO3-. The metabolism of various organic anions in the liver results in consumption of H+ and regeneration of the extracellular bicarbonate buffer. These anions may be:


1.

Exogenous (citrate in blood transfusion, acetate and gluconate from Plasmalyte 148 solution, lactate from Hartmannâ&#x20AC;&#x2122;s solution)

2.

Endogenous ( lactate from active glycolysis or anaerobic metabolism, keto-acids produced in the liver)

If the endogenous production of these anions is followed by later consumption in the liver then there is no net production of acid or base because the H+ produced (from the dissociation of the acid) is consumed when the anion is subsequently metabolised by the liver. When these organic anions are exogenously administered (eg in intravenous fluids), administration of the anion (the conjugate base) without any H+ occurs because the cation involved is Na+. Any subsequent metabolism of these anions in the liver will consume H+ and result in excess bicarbonate production. As an example, a metabolic alkalosis can result after a massive blood transfusion when the citrate anticoagulant is metabolised to bicarbonate. The important point to note is how some of these anions (eg lactate, acetate) are used in IV crystalloid solutions as a bicarbonate source (though this is indirect of course as the bicarbonate is only produced when they are metabolised in the body). The key point to remember is that lactic acid is an acid but lactate is a base. The administration of lactate in Hartmannâ&#x20AC;&#x2122;s solution can never result in a lactic acidosis because it is a base and not an acid. The solution contains sodium lactate and not lactic acid. The lactate anion is the conjugate base of lactic acid and represents potential bicarbonate and not potential H+. Endogenous Lactate Some excess lactate is normally produced in certain tissues and 'spills over' into the circulation. This lactate can be taken up and metabolised in various tissues ( myocardium) to provide energy. Only in the liver and the kidney can the lactate can be converted back to glucose (gluconeogenesis) as an alternative to metabolism to carbon dioxide. The glucose may re-enter the blood and be taken up by cells (muscle cells). This glucose-lactate-glucose cycling between the tissues is known as the Cori cycle. Typically there is no net lactate production which is excreted from the body. The renal threshold for lactate is relatively high and normally all the filtered lactate is reabsorbed in the tubules. The total amount of lactate involved is large (1,500 mmols/day) in comparison to the net fixed acid production (1 to 1.5 mmols/kg/day). The metabolism of lactate in the liver indirectly


eliminates the H+ produced subsequent to the tissue production of lactate. Lactic acidosis will result if this hepatic metabolism is not adequate. . Metabolism of lactate sourced from IV Hartmannâ&#x20AC;&#x2122;s solution also results in a net consumption of H+, but as this lactate was associated with Na+, the overall result is a net bicarbonate production. Effectively, metabolism of this lactate results in generation of an equivalent amount of bicarbonate. The situation is similar with metabolism of citrate and gluconate in other IV fluids. Ketones Keto-acids such as acetoacetate are produced in hepatic mitochondria due to incomplete oxidation of fatty acids. The ketones are released into the blood stream and metabolized in the tissues muscle). Hepatic production of ketoacids produces H+ and the oxidation of the ketoanion in the tissues consumes H+ and thereby regenerates the HCO3 which had buffered it in the blood stream. The liver is the major producer of plasma proteins as nearly all except the immunoglobulins are produced here. Albumin synthesis accounts for 50% of all hepatic protein synthesis and has the following functions. 1. it is the major unmeasured anion in the plasma which contributes to the normal value of the anion gap 2. extracellular buffer for CO2 and fixed acids 3. abnormal levels can cause a metabolic acid-base disorder. The above described mechanisms are the bodyâ&#x20AC;&#x2122;s responses to maintain equilibrium in acid base balances. The changes occur with

disorders of the respiratory and the metabolic state and

compensations occur to keep the pH within the normal range. References: 1. Ohâ&#x20AC;&#x2122;s Intensive Care Manual. Fifth Edition. Butterworth Heinemann pg 873-884 2. Acid base Book. www.anaesthesiamcq.com


X RAYS & ANAESTHESIA Dr Saraswathi Devi Professor &HoD Department of Anaesthesia & Pain relief Kidwai institute of oncology, Bangalore.

READING CHEST X RAY First label Projection â&#x20AC;&#x201C; PA or AP view, lateral view

Normal PA view

Standard view Scapula away from lung fields. Medial end of clavicle lower than lateral end. Posterior part of vertebrae well defined. Fundus gas shadow well defined.


Normal AP view

Scapula over hangs on lung field Body of vertebrae well defined Cardiac size appears enlarged Clavicle horizontal No well defined fundus gas shadow

Rotation of film

Well centered film shows medial ends of clavicle equidistant from spinous process of T4-T5


Exposure / penetration Upper 4 thoracic vertebral bodies and disc spaces should be visible Vertebral bodies should be visible through the lower part of cardiac shadow

DEGREE OF INSPIRATION

At midpoint of right diaphragmShould be able to count 5-7 ribs anteriorly & 8-10 ribs posteriorly

INSPIRATORY

EXPIRATORY


Periphery to center Soft tissues Bones & thoracic cage Trachea Mediastinum & Heart size Diaphragm Costo/ cardiophrenic angles Hilum Lungs & Fissures

Soft tissues : Look for any enlargement Bones & Thoracic Cage Evaluate ribs, scapulae and vertebrae Follow edge of bones ( look for fracture) Compare with other side Trachea Should be central/ may be slightly deviated to right near aortic knuckle Mediastinum Edge of mediastinum should be clear . Some fuzziness acceptable at cardiophrenic angle, apices & right hilum


Heart size and border Diaphragm Right diaphragm is higher than left Difference should be less than 3 cm Costo/ cardiophrenic angles Should be well defined acute angles Hilum Left hilum higher than right.Compare shape &density

Lung fields Upper zone: Lies above anterior border of 2 nd rib Mid zone: Between anterior border of 2nd and 4th rib Lower zone: Between 4 th rib and the diaphragm


Pleural Effusion

No air bronchogram Blunting of costo/ cardiophrenic angle Shift of mediastinum Opacity of hemithorax Upper border of white shadow is S shaped( Ellis curve)


Pneumothorax

Plueral line No parenchyma behind the line Displacement of diaphragm

Consolidation Homogenous opacity of invoved lobes(without displacement of diaphragm) Opacified areas limited by fissures Air bonchogram Silhoutte sign


Air Bronchogram

Silhouette Sign Silhouette - outline or shape Difference in density between air & heart creates a border When air in lungs is replaced with soft tissue the silhouette is lost

Collapse

Shift of fissure Mediastinal shift Air bronchograms


Lung Abscess

C/C Bronchitis


Emphysema

Pulmonary edema( cardiogenic)

Air bronchograms Perihilar hazzines Kerley b lines Cephalization of pulm vessels Peribronchial cuffing


Cephalization of flow

Kerley B Lines


Peribronchial cuffing

ARDS

Non cardiogenic pulmonary edema B/l patchy ill defined densities Densities peripheral in distribution Upperlobe blood vessels normal in size


Pulmonary embolism

Triangular density- wedge shaped Peripheral- blunting of CP angle

Emphysematous bullae

Diaphragm flattened Shape of heart â&#x20AC;&#x201C; elongated narrow heart Bullae â&#x20AC;&#x201C;densely black areas surrounded by hairline shadows


Superior Mediastinal Mass

Anterior Mediastinal Mass


Pericardial effusion

Heart shadow globular Vascular markings in lung fields normal


Mitral stenosis Straigtening of left heart border Right heart border appears more right than normal Angle of carina more than 90%

TOF

Abdomen & Diaphragm Diaphragm Right higher than Left Look for hernia eventeration Gastric shadow Gas under the diaphragm


EXPERT OPINES


ANAESTHETIC MANAGEMENT OF PATIENTS WITH BRONCHIAL ASTHMA Dr. S. S. Harsoor, Professor of Anaesthesiology, BMC & RI., Bangalore

“ The anxiety felt by Anaesthesiologist, when one of his patient develops acute severe bronchospasm has only to be experienced ”. Though mild wheeze & elevated peak inspiratory pressures are common, life threatening bronchospastic attacks under anaesthesia are relatively uncommon. Asthma & atopy are regarded as diseases of civilisation. Asthma is a disease of airway smooth muscle ‘such that, it contracted excessively’ on minimal stimulation.(1950). Current definition of Bronchial asthma is “Chronic inflammatory disorder of airways with reversible airflow obstruction, owing to variable narrowing of airways in response to various stimuli & airway hyperreactivity ”. The incidence of Asthma is 5% in 5-34 years age group. But in patients older than 40 years, cigarette smoking with prior diagnosis of chronic bronchitis or emphysema (COPD) forms the major cause sometimes referred to as ‘Asthmatic Bronchitis’. Bronchial asthma in itself is regarded as reversible COPD Classification: Types of Asthma I a. Extrinsic Asthma ( Allergic, IgE mediated response) b. Intrinsic Asthma ( non allergic & infection) c. Mixed Asthma – Combined intrinsic / Extrinsic II. Drug induced Asthma -

Aspirin, NSAID

III. Exercise induced Asthma IV. Occupational Asthma – Toluene, Diisocyanate, PVC, metallic salts ( Platinum, Nickel) Classification based on severity Night Sx Mild Intermittent

Sx < 2 times per week

< 2 per month

Normal PEFR between attacks

RFT FEV1 or PEFR >80% PEFR Variability < 20%

Brief exacerbations.

Mild Persistent

Sx > 2 times per week But < once a day Exacerbations affecting activity

> 2 per month

FEV1 / PEFR > 80% PEFR variability 20-30%


Moderate persistent

Daily

> one per week

FEV1/ PEFR 60-80% of predicted

Rx inhaled short acting β-agonists

PEFR variability > 30%

Affect activity Exacerbation >2 per week Severe Persistent

Limited physical activity

Frequent

Frequent exacerbations

FEV1/PEFR <equal to 60% PEFR variability > 30%

Genetics of Asthma The Specific areas of genome harbour genes that contribute to asthma and atopy. The β adrenergic receptor gene (BAdR) is believed to be associated with several characteristics of asthma including bronchial hyper-responsiveness, bronchial reversibility and some measures of asthma severity. The serum IgE concentration is closely linked to IL-4 gene. The gene for CD14 receptor is known to mediate cellular response to endotoxins. Such type of research helps to identify and develop therapies against ‘Rogue genes’ and ultimately manipulate pathogenesis and pharmacological responses of disease. Pathophysiology:The

possible explanations for clinical features of asthma include chronic airway

inflammation, reversible airflow obstruction and bronchial hyper-reactivity. The eosinophils of the asthmatic bronchial wall are believed to be responsible for the prediction of asthmatic symptoms. The repeated exposure leads to synthesis and secretion of specific IgE antibodies, which in the presence of antigens can lead on to explosive release of bronchoactive and vasoactive mediators like interleukins, leukotrines, prostaglandins etc from mast cells. 1. Abnormal ANS regulation of airway function. -

The presence of an imbalance

between excitatory bronchoconstrictor and inhibitory bronchodilator neural input is presumed to be responsible for expiratory airflow obstruction and other features of asthma. The chemical mediator released from mast cells interact with ANS, causing directly reflex bronchoconstriction or sensitizing the bronchial smooth muscles to the effect of other drugs. This forms the basis of either short term or long term β-agonist drug treatment of asthma 2. Airway remodelling - In asthmatics, the airway walls thicken due to increases in quantity of submucosal tissues, basement membrane and smooth muscles by hypertrophy and hyperplasia. There is enhanced subepithelial fibrosis by collagen deposition due to increased


myofibroblast activity. This phenomenon is also seen in patients with COPD, eosinophilic bronchitis. This process is responsible for greater rate of decline of predicted FEV1 per year, in asthmatic patients compared to non-asthmatics. Adequate treatment to reduce inflammation will limit airway remodelling and thus prevent development of irreversible damage. Clinical manifestations & Diagnosis â&#x20AC;&#x201C;. There are no definite diagnostic criteria available for asthma. But more than 15 % increase in airflow after bronchodilator drug inhalation suggests asthma. The classical manifestations include wheezing, cough, and dyspnoea. The wheeze is the expiratory sound produced by turbulent gas flowing through narrowed airway. Though the quantity of sputum varies considerably, it is mucoid and often tenacious. The presence of eosinophils causes yellow discolouration even when there is no infection. The dyspnoea varies depending on severity of airflow obstruction. The air hunger or tightness of chest frequently accompanies dyspnoea. Spirometry:- Forced expiratory volume in 1 sec (FEV1) and maximum mid expiratory flow rate (FEF

25-75)

provide the objective data to asses the severity of asthma and also to monitor the

effectiveness of treatment. Typically FEV1 is less than 35% of normal and maximum mid expiratory flow rate is 30% of normal or lower in an asthmatic patient. The flow volume loop shows downward scooping of expiratory limb of the loop. In contrast, the flow volume loop in patients with upper airflow obstruction show flat inhaled and exhaled portion (foreign body, tracheal stenosis etc)

FEV1%

FEF 25-75

PaO2

PaCO2

of predicted

of predicted

mm/HG

Mild

65- 80

60-75

>60

<40

Moderate

50-65

45-60

>60

<45

Marked Severe

35-50 <35

30-45 <30

mm/HG

<60 <60

>50 >50

In severe asthma, the FRC may increase as much as 1-2L, though total lung capacity (TLC) remains normal. The tachypnoea and hyperventilation observed during acute asthmatic attack is mainly due to neural reflexes in the lungs, because the PaO2 and PaCO2 both are normal. These patients may even show hypocarbia and respiratory alkalosis. But with FEV1 less than 25-30% of the predicted, the PaCO2 may increase. When the FEV1 returns to above 50% of normal, the patients usually have either minimal or no symptoms. Chest radiograph may show hyperinflated lung fields and ECG may reveal acute right heart failure.


All that wheezes is not asthma – Upper airway diseases (Allergic Rhinitis, sinusitis), upper airway obstruction due to foreign body, small airway obstruction due to viral bronchiolitis and even psychogenic factors can cause wheezing.

Aims of management of asthma include 1. To achieve near normal life style. 2. To minimise or have no chronic symptoms. 3.

Avoid nocturnal symptoms and awakening &

4. Prevent further exacerbation of the disease. Hence advice patients not to smoke, avoid allergens if specifically sensitive and if overweight, reduction of weight can be helpful. The pharmacological agents used for asthma can be relievers- which produce rapid relief from symptoms and controllers used for long term prevention of symptoms probably by anti inflammatory actions. Regular administration of anti inflammatory drugs preferably inhaled corticosteroids is recommended as the first line of therapy for treatment of clinically significant asthma (Barnes.P.J.,NEJM,1995). Bronchodilator β2 agonist drugs are recommended for symptomatic relief of acute exacerbations when anti inflammatory drugs are insufficient. The algorithm recommended by British thoracic society (1997) Step 1. Short acting β agonist as required Step 2. 1 + inhaled corticosteroids 200-800 µgms per day. Step 3. 2 + long acting β agonist or Leukotrine receptor antagonist Step 4. 3 + increase inhaled steroid to 2000 µgm per day + Long acting β agonist + Leukotrine receptor antagonist + Theophylline as and when necessary. Step 5. 4 + daily oral steroids. Once the symptomatic control is achieved a step down can be considered over 3-6 months. However the airway hyperreactivity can continue to improve during and up to next 2 years of treatment. Drugs

A.

Anti-inflammatory drugs – Corticosteroids Mast cell sabilisers (Cromolyn) Leukotrine Inhibitors B. Bronchodilators-

β agonists

Anticholinergic drugs


Xanthine alkaloids (Theophylline)

C.

Other Drugs- Magnesium sulphate Helium Ketamine Anti IgE therapy A. Anti inflammatory drugs 1.Inhaled corticosteroids are recommended as first line therapy for patients with persistent asthma since early 1990. Inhaled corticosteroids have anti inflammatory effects on bronchial mucosa and also reduce airway hyperresponsiveness. The lung functions and symptom scores improve, and inflammatory cell recruitment is attenuated. Only 10-20% of inhaled corticosteroids enter respiratory tract and being highly lipophilic, it rapidly enters the airway cells. The most important effect is increase in synthesis of lipocortin-1, a protein that has inhibitory effect on production of anti inflammatory lipid mediators. Corticosteroids also inhibit the activity of NF–κB which plays a pivotal role in inflammation through increased transcription of inhibitory protein IκB. There is reduction in eosinophil number and the number of activated CD4+ cells and accordingly reduction of asthma symptoms. The side effects include dysphonia (due to myopathy of laryngeal muscles), glossitis, pharyngitis & candidial infection etc. The ihhaled corticosteroids in dose of 1500 µg per day or 400 µg per day in children have little effect on pituitary adrenal axis. There are no evidences to show altered bone metabolism, impaired growth or metabolic effects. The drugs include beclomethasone, triamcinolone, fluticasone and budesonide. 2. Mast cell stabilisers- Cromoglycate and nedocromil act by inhibiting the release of chemical mediators from mast cells, by membrane stabilising effect. Cromolyn is not effective once the bronchospasm is present. It is administered by inhalation through MDI about 7 days before expected exposure to allergen. They are largely superseded by low dose inhaled corticosteroids. 3. Leukotrine receptor antagonists(LRA) are effective in patients with mild to moderate asthma. They play significant role in asthma induced by exercise, allergens or aspirin. The cysteinyl leukotrines and other products of 5-lipo-oxygenase (5-LO) pathway can induce pathophysiological changes similar to those associated with asthma such as, smooth muscle contraction, chemotaxis and increased vascular permeability. LRA drugs antagonise cys-LT1 receptor and have generic suffix lukast. They include zafirlukast and monelukast sodium which are given orally and they improve lung functions in 1-3 hours and also reduce the need for rescue β-agonist drugs. Presently they have lesser clinical effects and have less evidence behind them for aggressive clinical use. Leukotrine synthesis inhibitors and leukotrine receptor antagonists are probably useful for long term maintenance therapy.


B. Bronchodilator drugs:1. β-agonists stimulate β2 receptors on tracheobronchial tree smooth muscles with consequent activation of adenylate cyclase and increases in intracellular cyclic AMP concentration. The Short acting β-agonists are effective in prevention of exercise induced asthma and also relieve acute attacks (salbutamol, Terbutaline). But when used regularly, they may not provide the desired effect. The long acting β-agonists are recommended in patients suffering from persistently symptomatic asthma. Salmetrol and formoterol are highly selective β-agonists, with bronchodilator effects, lasting more than 12 hours after inhalation. Other drugs include albuterol, terbutaline. fenoterol(Barrett), and pirbuterol. Current evidences demonstrate that long acting β-agonists produce better disease control when added on to inhaled corticosteroids (ICS) in persistently symptomatic patients than the addition of Theophylline or Leukotrine receptor antagonists. But the Use of therapeutic does of inhaled β-agonists is associated with mild decreases of serum potassium (0.5 meq/ltr or less). It is observed that additional long acting β-agonists allow the dose of inhaled corticosteroids (ICS) to be reduced. The presently available combinations include salmeterol 50µg + fluticasone propionate 125-250 µg and (symbicart) formoterol 4.5 µg + budesonide 80-160 µg. Etc. 2. Anticholinergic drugs block muscarinic receptors in airway smooth muscles, leading to decreases in vagal tone. The Ipratropium and oxitropium are administered by metered dose inhaler, but they are less effective than β-agonists. The bronchodilatation is seen within 15-20 min and effect lasts for 4-6 hours. The quaternary structure of Ipratropium limits its systemic absorption and production of anticholinergic side effects. The Primary indication for ipratropium is treatment of bronchoconstriction in patients with COPD 3. Xanthine Derivatives- Theophylline increases the cardiac output, diaphragmatic contraction and even possess anti inflammatory effects. Its primary role appears to be in the prophylaxis of acute attacks in chronic patients and in the prevention of night time episodes of bronchospasm. Theophylline has a very low toxic / therapeutic index and the toxic effects are seen at levels below maximal therapeutic effects. The toxic effects include nausea, vomiting, headache, restlessness, life threatening dysrhythmias and convulsions. The incidence of arrhythmias is increased during halothane induction, when theophylline is used in a loading dose of 3mg/kg, followed by infusion of 0.5mg/kg/hr. The drug interaction is seen with a number of drugs such as cemitidine, erythromycin, ciprofloxacin etc.

C. Other Drugs


1.Magnesium sulphate is believed to act as an antagonist of voltage gated calcium channels. In airway smooth muscles, increased cytosolic calcium leads to the activation of contractile system. Increases in cytosolic calcium are believed to be dependent on release from intracellular compartments and on calcium influx through voltage dependent channels. Evidences show that asthmatic patients had better improvements in peak expiratory flow rate and even hospital admission rates declined following treatment with magnesium sulphate. Combined with Nebulised salbutamol, MgSO4 produces significantly better PEFR improvements after 10 min. Currently MgSO4 appears to be safe and beneficial in the treatment of acute asthma but is not needed in most patients who respond to conventional therapy. 2. Helium- Heliox is a mixture of helium and oxygen, which reduces inspired gas density, turbulence and airway resistance and hence decreases the work of breathing. Also it helps in increasing the distribution of nebulised bronchodilator drug within the lung. Presently its role is limited to serve as an adjunct to conventional treatment in deteriorating patients, so that invasive ventilation can be avoided. 3. Ketamine is beneficial in the maintenance of GA during mechanical ventilation of severe asthmatic patients. This is to be used in conjunction with other bronchodilator drugs. Additional sedative benzodiazepines are needed to prevent its side effects such as visual and auditory hallucinations. 4. Anti IgE therapy: Recombinant humanised monoclonal antibody against IgE (rhuMAbâ&#x20AC;&#x201C; E 25) is tested in moderate to severe asthma and atopic rhinitis and the drug is in its experimental stage. The IgE antibody is prevented from finding the IgE receptor on mast cells and basophils, thus preventing activation of these cells. Intravenous rhuMAb â&#x20AC;&#x201C; E 25 given once every 2 weeks, improves the symptom scores & reduces inhaled steroids and it is well tolerated by patients. Presently this drug can be considered as steroid sparing agent. 5. Vaccination against asthma to manipulate Th-1 / Th -2 balance of the CD 4+ lymphocyte is the dream of many scientists and clinicians.

ANAESTHETIC CONSIDERATIONS Though mild wheeze and elevated peak inspiratory pressures are often seen in clinical practice, the life threatening bronchospastic attacks under anaesthesia are relatively uncommon. However symptomatic asthmatic patients are at increased risk of morbidity. A. The goal of preoperative evaluation is to formulate an anaesthesia plan that prevents or blunts obstruction to expiratory airflow. While an exaggerated bronchoconstrictor response to a trigger is characteristic of asthma, an increased reaction to a trigger consists of a complex response, including airway oedema, increased secretions and smooth muscle contractions. Airways


inflammation is present even in mild asthmatic patients and steroids are definitely beneficial. Peter Banes (1989), a prominent asthma researcher even suggested that we redefine asthma clinically as “airway obstruction, that improves with steroids” (NEJM 1989). Preoperative evaluation begins with a clinical history to elicit severity and characteristics of patient’s asthma, infection and role of medications. In addition, recent infection alters airway reactivity even in normal individuals. Exacerbations of asthma are linked to recent viral infections. Cessation of smoking, with chest physiotherapy and adequate hydration are beneficial. Other co-morbid conditions such as obesity and CVS problems may have a bearing on anaesthetic management.

B. Medications –β-agonists were traditionally the mainstay in the management of both chronic and acute asthmatic attacks especially following use of MDI. These drugs have LD-50 level much greater than therapeutic drug level and hence are safe. But of late, inhaled corticosteroids (ICS) are used as first line of therapy, with β-agonists often kept in reserve. Theophylline is primarily used as a prophylactic drug but it has a very low toxic / therapeutic index. The incidence of arrhythmias is high under halothane anaesthesia in patients receiving theophylline. The onset of benefit from steroids is within few hours, makes steroids useful as preoperative medicants in patients with moderate to severe asthma. There are no evidences to prove that steroids delay wound healing or increase incidence of infection.

C. The clinical examination should always include match blowing test, which reliably indicates forced expiratory flow. Any active accessory muscles of respiration and pursed-lip breathing indicate obstructed airflow. The examination of Nasal passages may sometimes reveal polyps, infection or nasal discharge. Any rise in CVP indicates RVF or cor pulmonale and they should be excluded. Spirometry – FEV1 & FVC are reliable tests for airway obstruction and are useful to assess baseline function, as well as to determine if preoperative bronchodilator therapy has maximised lung function. National Asthma Education and Prevention Programme (NAEPP) 1991 suggests that a reversibility of more than 30% FEV1, following bronchodilator inhalation indicates that, disease is not optimally controlled. Further, NIH expert panel (1991) recommends that asthmatic with FEV1 < 80% of normal should receive a preoperative course of oral steroids. D. Premedication: - There are no recommended premedication drugs. The argument that opioid premedication can produce bronchoconstriction or release of vasoactive substances from mast cells is not substantiated with evidences but respiratory depressant effects should be kept in mind.


Anticholinergic drugs can increase viscosity of airway secretions. Evidences show that Histamine induced bronchoconstriction occurs through H1 receptors and bronchodilatation is mediated through H2 receptors. Hence H2 blockers may unmask H1 receptor induced bronchoconstriction (Theoretical consideration). It is suggested to continue all bronchodilator drugs to the time of anaesthesia induction. If Hypothalamic-pituitary-adrenal axis suppression is suspected, then supplemental exogenous corticosteroids can be administered. But it is unlikely that ICS can induce hypothalamic pituitary Adrenal suppression. Several adult asthmatic patients may react adversely to aspirin or NSAIDs and they have to be avoided. E. Choice of Anaesthesia â&#x20AC;&#x201C; Regional V/s General - Airway instrumentation is a major trigger for wheezing and should be avoided. Choose regional anaesthesia wherever possible. A high neuraxial blockade can affect the strength of accessory muscles of respiration and even up to 48% reduction in ERV can be seen, which means decreased cough efforts. Sensory deprivation with high levels of blockade required for upper abdominal surgeries may produce anxiety in the asthmatic patient and thereby induce an attack of bronchospasm. The theory of high sympathetic blockade per se resulting in bronchospasm has no evidence to support. Among the local anaesthetics, the ester group of drugs and the preservatives used in Amide group are associated with histamine release and allergic reactions. It is necessary to avoid lighter planes of anaesthesia in the event of the failed regional anaesthesia. Insertion of LMA produces lesser degree of airway resistance compared to ET tube insertion. Induction drugs: - The incidence of wheezing is higher in asthmatic patients receiving Thiopentone compared to Propofol. Though IV thiopentone 5mg / kg rarely causes bronchospasm, but at the same time, it is unlikely to suppress upper airway reflexes and thus, airway instrumentation may trigger bronchospasm. The airway resistance following Inj. Propofol 2.5 mg/kg induction is comparatively low. The mechanism of Propofol causing bronchodilatation effect is not definite, but they appear to be neurally mediated. Ketamine produces smooth muscle relaxation both via neural mechanism and via release of catecholamines. Inhaled albuterol administered 1-2 hrs in advance is shown to blunt airway response to tracheal intubation (Maslow AD, Anaesthesiology 2000). IV lignocaine also prevents bronchoconstriction and has no toxicity at 1.5mg/kg given 1-3 min prior to intubation. But direct intra-tracheal lignocaine spray has the possibility of triggering airway reaction, unless there is adequate depth of anaesthesia. The bronchospasm following tracheal intubation can be prevented by volatile anaesthetics. Though all volatile anaesthetics produce same degree of bronchodilatation, Halothane is found to be more effective. Also lesser pungency of halothane and Sevoflurane make the coughing less likely, compared to desflurane and Isoflurane. However sensitisation of myocardium to dysrhythmias by


Halothane especially when patient is on theophyline, should be kept in mind when compared to Isoflurane and Sevoflurane. Succinylcholine, atracurium and mivacurium are known to release histamine, especially if large doses are administered rapidly and are therefore best avoided. But the incidence of bronchospasm is no different compared to other muscle relaxants. Vecuronium may be used satisfactorily, without major problems. Analgesia is maintained with moderate doses of opioids, keeping in mind the well known inhibition of respiratory responses to hypoxia and hypercarbia. Fentanyl and Sufentanil may be used in a balanced anaesthesia technique. Combined Epidural analgesia and general anaesthesia will allow low doses of opioids to be used. Intraoperatively a desirable level of PaO2 and ventilation are to be provided. The ideal ventilator setting should, reduce dynamic hyperinflation (DHI), slow inspiratory rate to allow distribution of gas, combined with sufficient time for passive expiration to occur so that air trapping is prevented. A low but adequate tidal volume should provide tolerable level of gas exchange and permissible hypercapnia. Avoid intrinsic PEEP, which can occur due to obstruction from bronchospasm. It can worsen DHI barotraumas and air leak risks. Humidification and warming of inspired gases is logical, especially in exercise induced asthma. But particulate humidification as produced by ultrasonic nebulizers and pneumatic aerosols can trigger bronchospasm. Maintaining adequate hydration makes secretions less viscous and thus easy expulsion from airways. Extubation should be attempted while anaesthesia is still sufficiently deep enough to suppress hyperreactive airway reflexes. Even continuous IV infusion of lignocaine 1-3 mg/kg/hr can be used. Theoretically anticholinesterase drugs can precipitate bronchospasm secondary to stimulation of postganglionic cholinergic receptors in airway smooth muscles. This may be due to protective effects provided by anticholinergic drugs.

Introperative Bronchospasm (BRONCHOSPASTIC CRISIS)ď &#x152; A. ANALYSIS 1. Why peak airway pressures rise - Constriction of airways, increases the resistance to airflow. In addition to patient coughing and bucking, airway secretions and mucosal engorgement also contribute to the problem. Chest becomes hyperinflated and less compliant due to air trapping and auto PEEP. 2. What is auto PEEP - A short expiratory time combined with airway compression results in incomplete exhalation. Due to obstruction between alveoli and airway system, a pressure in the


airway may appear zero, though substantial positive pressure exists in chest. This high intrathoracic pressure may decrease the venous return to heart and cause hypotension. 3. Desaturation - Hypoxia is generally not a problem in bronchospastic states, although spasm and secretions result in airway closure and underventilation of lungs. But the actual problem may be poor peripheral perfusion resulting in low reading on pulse oximeter especially when Hypotension is obvious. Application of PEEP can worsen the situation. 4. Why PCO2 goes up – though EtCO2 is low - Uneven distribution of ventilation results in a few overdistended and a few other underventilated alveoli, leading on to Ventilation Perfusion mismatch. When there is associated hypotension, the overdistended alveoli may not be perfused at all, and this results in increased dead space and low ETCO2 reading. 5. Ventilator: Due to increased airway pressure, the minute ventilation may actually come down. The causes for this can be, compressible gas volume in. Anaesthetic breathing ciraint (710ml / cm H2O of wasted ventilation). Thus at about 60 cm H2O pressure, nearly 500ml out of each set breath may not be delivered to the patient. Also the anaesthesia ventilator may not be able to deliver such high pressure. B. RESPONDING TO CRISIS In acute asthma, bronchospasm is dominant and lasts for only the first 30 to 60 min and a second episode of airway obstruction occurs 3 – 8 Hrs later, caused by inflammation and oedema in the wall of smaller airways. Thus bronchodilators are effective in early stages of acute asthma, and anti–inflammatory properties of corticosteroids are beneficial in relieving the airway obstruction that occurs later in the episode. 1.Deepen plane of Anaesthesia - Halothane or Sevoflurane is better than Isoflurane to deepen the plane of Anaesthesia as it can lower intrathoracic pressure and even improve venous return. Use of muscle relaxants also reduces the respiratory impedance. If ventilation improves with paralysis produced by muscle relaxants, then the cause of the ventilatory disturbance is not likely to be bronchoconstriction. 2. Depth of anaesthesia can be achieved with the Propofol or IV Ketamine also. It can overcome the problem of drug delivery via inhalational route, even while maintaining the Blood pressure. 3. Pharmacological Support: a. Use of β-agonists – Even during bronchospastic state, inhalational drug route is as effective as parenteral therapy, along with the advantage of fewer side effects. Terbutaline is an useful drug both by inhalation or by subcutaneous route. β-agonist salmeterol is a long acting drug and takes more than 20 min to show the onset of action. About 10 - 15 puffs of Albuterol via


metered dose inhaler, given through a T – Piece (only 10% of metered dose actually reaches the airway through ETT) produces maximum effects even in patients on mechanical ventilator. b. I.V Lignocaine (2 mg/kg) and atropine (1-2 mg) may be help, to some extent in reversing bronchoconstriction. c. The use of Aminophylline in anaesthetised patient, in acute asthmatic crisis is controversial. d. Corticosteroids can be used for prophylaxis because of delayed action. 4.Oxygen: Decreased airway calibre due to bronchiolar spasm and pulmonary vasodilating effects of many bronchodilating drugs can lead onto arterial hypoxemia. Thus increase in inspired concentration of O2 is necessary for maintaining oxygen saturation. 5. ICU ventilator – Anaesthesia ventilators are not designed for adequate

ventilation in

the face of high impedance. An ICU ventilator which can withstand airway pressures as high as 120 cm H2O, are feasible, with minimal compression of gases and wasted ventilation. High flows - short inspiratory time - adequate time for expiration helps to lower auto PEEP. During experimental bronchospasm, a simple ICU ventilator Siemens 900C can deliver better minute ventilation at low PEEP, compared to Anaesthesia ventilator. The major disadvantage of ICU ventilator is the need for IV anaesthetics, as inhalational anaesthesia can not be delivered. 6. The approach to the Bronchospasm not due to Asthma – Deepen plane of anaesthesia & Skeletal muscle relaxants. β-agonist therapy with Albuterol through MDI – 90µg / each actuation of MDI, may help. If Bronchospasm persists – Inhaled corticosteroids to be added but the actual clinical benefits will be seen only after 3-4 Hrs.

EMEREGENCY SURGERY – During acute Asthmatic attack regional anaesthesia preferable wherever possible. Otherwise the conflict of triggering bronchospasm V/s protection of airway from aspiration is to be balanced. If time permits, bronchodilators to be used.

BRONCHIAL ASTHMA IN CHILDREN Laryngospasm and bronchospasm can be precipitated by viral or bacterial infections, if a wheezing child is subjected to anaesthesia. Their trachea is very sensitive to stimuli and react to the presence of any foreign body (e.g. ETT) by increasing bronchomotor tone. Elective procedures are best postponed, if the child has wheeze or has just wheezed (after apparently well controlled asthma) during pre-anaesthestic evaluation. Inhalational induction is preferred but if an I.V. induction is chosen, Ketamine with its sympathomimetic actions is useful. Cardiovascular depression of deep inhalational anaesthesia should be kept in mind. If child wheezes during surgery, mechanical causes of airway obstruction and congenital problems should be quickly checked: if no problem is revealed,


increasing the depth of anaesthesia and administering bronchodilators directly through ETT may be helpful. As a general rule, wheezing during and after induction of anaesthesia usually indicates a light level of anaesthesia.

PREGRENCY AND ASTHMA Asthma occurs in approximately 1% of pregnant women. In one study it was seen that in about 50% of them, asthamatic status remained unchanged, worsened in ¼th and improved in the rest. Increases in plasma cortisol, progesterone, cAMP and maternal histaminase may alleviate asthmatic symptoms during pregnancy. A decrease in T– cell lymphocyte function may decrease maternal response to antigen challenge. At the same time, this may make the mother susceptible to URI’s, which may precipitate asthmatic attacks. Bronchonconstricting prostaglandins, congestion of upper airway and increased antigen exposure from developing foetus may contribute to worsening of symptoms. Maternal pain and hyperventilation may lead to anxiety and apprehension, which also can precipitate an attack. Incidence of preclampsia is found to be more in patients with severe asthma. The incidence of Preterm deliveries, LBW babies, perinatal deaths are increased. Inhaled corticosteroids are beneficial in mild to moderate asthma as first line therapy (inhaled beclomethasone appears to be safe and effective ). β2 agonists are best given by inhalational route, to avoid systemic effects. Aminophylline therapy is generally safe during pregnancy, but high serum levels in first trimester may cause foetal caffeine toxicity. Large dose steroid therapy has been associated with IUGR. Aminophylline, β sympathomimetics and epinephrine have all been shown to slow the progress of labour. Pitocin but not the Prostaglandins should be used to augment labour. Epidural analgesia is the ideal method of labour pain relief. Low dose of LA’s with 1:200000 epinephrine (aids bronchodilation) and Fentanyl is said to offer the best recommended regime. Prostaglandin-f2 and ergonovine should be avoided as therapy for PPH, as both have shown to aggravate asthma in this setting.


A NEONATE FOR HERNIOTOMY Dr.ArunaParameswari Professor of Anaesthesiology Sri Ramachandra University, Chennai.

INTRODUCTION The neonate is not just a small adult. There are several anatomical, physiological, functional and pharmacological issues associated with the provision of anesthesia care to a neonate. A thorough knowledge and understanding of these is an important step towards providing safe anesthesia to this delicate group of patients. DEFINITIONS Infant: Child less than 1 year of age Full term neonate: Born between 37-40 weeks of gestation and age less than 1 month Moderately premature neonate: Gestational age 31 – 36 weeks Severely premature neonate: Gestational age 24 – 30 weeks Low birth weight: Birth weight < 2500 g Very low birth weight: Birth weight < 1500 g Extremely low birth weight: Birth weight < 1000 g Postconceptional age: Gestational age + Postnatal age NEONATAL PHYSIOLOGY IN RELATION TO ANESTHESIA CARDIOPULMONARY: The neonate has a high metabolic rate and the oxygen consumption is 5 – 8 mg/kg/min, in comparison to the adult oxygen consumption of 3 mg/kg/min. The entire cardiopulmonary system is driven towards delivery of this excess oxygen demand. The minute ventilation in a neonate is 210 ml/kg/min compared to adult values of 90 ml/kg/min and the alveolar ventilation is 130 ml/kg/min as against an adult value of 60 ml/kg/min. This increase in alveolar ventilation is brought about by an increase in respiratory rate of 40 – 60 breaths/min as against an adult value of 12 – 14 breaths/min. The tidal volume is the same at 6 ml/kg in


both the neonate and the adult. The FRC of a new born (30ml/kg) is only slightly less than the mean adult value (34 ml/kg), but the FRC/VA ratios differ greatly (new born 0.23, adult 0.56). This indicates a much lesser reserve volume of gas in the lung of the new born in relation to alveolar ventilation and oxygen consumption. Parameter

Newborn

Adult

Oxygen consumption (ml/kg/min)

5-8

2-3

Carbon di oxide production (ml/kg/min)

6

3

Exhaled minute volume (ml/kg/min)

210

90

Alveolar ventilation (VA)(ml/kg/min)

130

60

Respiratory rate (breaths/min)

40 - 60

12 - 14

Tidal volume (ml/kg)

6

6

Vital capacity (ml/kg)

35

70

Functional residual capacity (FRC) (ml/kg)

30

34

FRC/VAratio

0.23

0.57

Total lung capacity (ml/kg)

53

85

Anatomical dead space (ml/kg)

2.5

2

Physiological dead space/tidal volume ratio

0.3

0.3

Tracheal diameter (mm)

4

16

Tracheal length (mm)

57

120

Table 1: Differences in pulmonary function between newborn and adult Airway: The tongue is large; the occiput prominent so that the head tips forward and the airway is easily obstructed. The prominent occiput also renders a natural sniffing position, so that an intubation pillow is not needed. Airway patency is maintained best by chin lift, taking care to avoid compression of the soft tissues of the neck and floor of the mouth. The epiglottis is long and straight and tends to flop back over the laryngeal inlet. The larynx is also more cephalad. Intubation is thus best achieved using a straight blade laryngoscope. The larynx is conical in shape and the narrowest portion is at the level of the cricoid cartilage, necessitating use of uncuffed tubes to avoid airway edema. The trachea is short and endobronchial intubation is common and should be avoided.


Respiratory mechanics: Work of breathing is composed of compliance and resistive components. Resistive work is 6 times greater in the neonate.Lung compliance is high and the chest wall compliance is higher compared to adults due to the soft and elastic ribs. Due to this, the distending pressures on the lung are low and the newborn is prone to lung collapse. The circular configuration of the rib cage (versus ellipsoid in adults) and the horizontal angle of insertion of the diaphragm (versus oblique in adults) cause inefficient diaphragmatic contraction. Also, the diaphragm contains only 25% of Type I (fatigue resistant, slow twitching, highly oxidative) fibres in term neonates as against 55% of Type I fibres in adults. In a preterm neonate, this is further reduced to only 10% of Type I fibres. This results in a further mechanical disadvantage to the neonate and easy fatigability when allowed to breathe spontaneously under anesthesia. The relatively large abdomen in a neonate also displaces the diaphragm cephalad, placing the lungsâ&#x20AC;&#x2122; closing capacity within the expiratory reserve volume.

Control of breathing: Chemoreceptor responses are blunted in neonates, especially premies. The normal biphasic response to hypoxemia (hyperventilation followed by hypoventilation or apnea) is replaced by apnea only. Apnea of central origin is due to poor organization and integration of afferent input from proprioceptive receptors, which are located in the diaphragm and intercostal muscles, and from medullary and peripheral chemoreceptors. The incidence of apnea varies from 25% in the low birth weight premature to 84% in the extremely low birth weight group. Apnea in the neonate decreases gas exchange in the lungs and is associated with hypoxemia and bradycardia. Apnea is pathological when > 20 seconds alone, or < 20 seconds with bradycardia (30 beats/min decline from resting heart rate), or with cyanosis, pallor or hypotonia. Susceptibility to central apnea is exacerbated by anemia, sepsis, hypoglycaemia, hypothermia and hypocalcaemia and also by opioids. Central apnea due to immaturity of the respiratory centre is often treated with xanthine derivatives, caffeine and theophylline. Infants up to 60 weeks post conceptional age are at risk of developing postoperative apnea.


Cardiovascular system The newborn has the highest cardiac output per weight than any other age group (200 ml/kg/min). The major differences in myocardial function between the neonate and the adult heart translate into important clinical applications. The high content of collagen and high ratio of Type I to type III collagen may account for the relative non compliance of the neonatal heart and consequently, its limited capacity to handle a volume load. The Frank Starling response is limited and the heart rate is the critical factor in maintaining cardiac output in the newborn. The normal range of heart rate in a neonate is 120 â&#x20AC;&#x201C; 180 beats/min. Neonate

Adult

Cardiac output

Rate dependent

Stroke volume and rate

Contractility

Reduced

Normal

Starling response

Limited

Normal

Catecholamine response

Reduced

Normal

Compliance

Reduced

Normal

Table 2: Cardiovascular differences between a newborn and an adult Parasympathetic control of heart rate matures earlier in gestation and to a greater extent than beta adrenergic control. For this reason, neonates may not respond to hypovolemia or an inadequate depth of anesthesia with tachycardia. Additionally, the vagotonic response caused by laryngoscopy and succinylcholine and synthetic opioids may lead to bradycardia. These reflexes can be offset by the vagolytic effects of atropine. The newborn also requires a higher extracellular calcium concentration to achieve maximal contractility. Extracellular, rather than intracellular calcium has a primary role in control of contractility of the neonatal myocardium. Neonates are more sensitive to the negative inotropic effects of anesthetic agents than older children. Any factor which increases the pulmonary vascular resistance in a neonate (hypoxia, hypercarbia, acidosis) may result in a return to the fetal-type circulatory pattern with shunting of deoxygneated blood from the right to left side of the heart through the PFO and the PDA.


This right to left shunting explains in part why some infants remain hypoxemic despite ventilation with 100% oxygen after severe desaturation. HEMATOLOGY The full term neonate has a haemoglobin concentration of 18 – 20 g/dl; a preterm neonate has a lower haemoglobin concentration, between 13 – 15 g/dl. Approximately 70 – 80% of the haemoglobin at birth is fetal haemoglobin (HbF) and it decreases to physiologically insignificant levels by 3 – 6 months of age. HbF has a high affinity for oxygen, that shifts the haemoglobin-oxygen dissociation curve to the left, so that the P50 of HbF is 18 – 20 mm Hg (compared to adult P50 of 27 mm Hg). The high affinity of Hb for Oxygen decreases the amount of oxygen released at the tissue level. In the normal newborn, the higher haemoglobin levels, the greater blood volume, the increased cardiac output per unit weight can adequately compensate for HbF. Blood loss exceeding 10% of the blood volume in the neonate has to be replaced with blood. The synthesis of prothrombin and factors II, VII and X in the liver is immature in the newborn. Also, perinatal asphyxia and septicaemia affect the function and the concentration of both clotting factors and platelets, resulting in coagulopathies.

Blood

volume Weight (kg)

(ml/kg)

Total

blood 25

volume (ml)

ml

Blood

loss percentage total

blood

volume (%) Micropremie

110

1

110

23

Premie

100

1.75

175

14

Full-term

90

3

270

9

Infant

80

10

800

3

Child

70

20

1400

2

neonate

Table 3. Circulating blood volume in micropremature infants, premature infants, full-term neonates, infants and children


TEMPERATURE REGULATION The neonate is prone to hypothermia due to several reasons: 

Large body surface area to body weight ratio

Large surface area of the head relative to the body increases heat dissipation

Shivering as a mechanism of heat production is not developed in the neonate

They rely on non-shivering thermogenesis by brown fat metabolism to maintain body heat and that is suppressed by anesthesia.

Increased evaporative heat loss in premie due to decreased keratin in skin

Increased conductive and convective heat loss in premie due to lack of insulation by subcutaneous fat.

Hypothermia is detrimental as it leads to acidosis, apnea, transitional circulation, hypoxia, coagulopathy, cerebral and myocardial depression and delayed recovery from anesthesia. RENAL AND METABOLIC FUNCTION At birth, the glomerular filtration rate is only 15 – 30% of adult levels. It reaches adult levels at approximately 1 year of age. The kidney’s tubular function and hence sodium retaining ability does not develop till 32nd week of gestation. The immaturity of the kidney affects the metabolism of many drugs in the neonate. The total body water of neonates is greater than infants, children and adults. In the term infant, 70% of the body weight is water. This along with changes in serum protein concentrations can affect the volume of distribution of drugs in the neonate. GLUCOSE HOMEOSTASIS The neonate has limited glycogen stores and gluconeogenetic pathways. Full term infants who have been excessively fasted, small for gestational age infants and neonates of diabetic mothers are particularly prone to develop hypoglycaemia. In infants less than 24 hours old, a plasma glucose of less than 40 mg/dl is a cause for concern and should be treated. After 24 hours of life, plasma glucose values less than 45 mg/dl should be considered abnormally low. Preterm neonates require glucose infusion rates of 8 – 10 mg/kg/min and full term neonates require an infusion rate of 5 – 8 mg/kg/min. As administration of hypertonic solutions


increases the incidence of intraventricular haemorrhage in preterm neonates, it is prudent to avoid bolus administration of hypertonic glucose to treat hypoglycaemia. A bolus of 3 – 4 ml/kg of 10% dextrose (0.1 – 0.2g/kg of glucose) can be administered followed by an infusion. GASTROINTESTINAL AND HEPATIC FUNCTION Gastric emptying in neonates is prolonged and lower esophageal sphincters are incompetent and reflux of stomach contents is common. Hepatic metabolism is immature in neonates, particularly the preterm. Drug metabolism may be prolonged and careful titration of drugs is required. Phase I processes are significantly reduced at birth whilst phase II processes (conjugation) may be well developed (sulfation) or limited (glucuronidation). Paracetamol is useful in neonates as it is excreted by sulfation rather than glucuronidation as in adults. Plasma protein binding is reduced in neonates (low levels of alpha 1 – acid glycoprotein) and drugs that are plasma protein bound (such as local anesthetics) may demonstrate increased toxicity. A 30% decrease in local anesthetic dose is required in neonates. CENTRAL NERVOUS SYSTEM, NOCICEPTION AND STRESS RESPONSE The central nervous system is incompletely developed at birth. However, early in gestation, the pain pathways are integrated with the somatic, neuroendocrine and autonomic systems. The hormonal responses to pain and stress may be exaggerated in neonates. The potential lack of autoregulation of cerebral blood flow and an infant’s fragile cerebral blood vessels may be important factors in the development of intraventricular haemorrhage. An association has also been noted between fluctuations in blood pressure (as during awake laryngoscopy) and intraventricular haemorrhage. PHARMACOLOGY IN NEONATES The response of newborns to narcotics and potent inhalation agents is variable, and meticulous titration is critical for neonates undergoing surgery to avoid cardiovascular collapse and to maintain acid-base balance but to eliminate awareness and pain. Drug pharmacokinetics and pharmacodynamics are affected by anatomic factors relating to body composition and distribution of water as well as physiologic factors (metabolism [i.e., hepatic biotransformation], protein binding), and pathologic factors (disease, anesthesia, and surgery).


The binding of drugs to serum proteins depends on several factors, such as the concentration of protein, the number of binding sites on these proteins, and the affinity of the binding sites. The concentration of total serum protein, albumin, and Îą1-acid glycoprotein is lower in early infancy and reaches adult levels by approximately 1 year. The concentration of these two proteins and their binding affinities are deficient in the newborn Inhaled anesthetic agents Infants have a higher incidence of cardiovascular instability and cardiac arrest during induction of inhalation anesthesia than do older persons This untoward effect of potent inhalation agents can be attributed to several factors, including faster equilibration, rapid myocardial uptake in infants, increased anesthetic requirement, and sensitivity of the neonatal myocardium. Moreover, the neonatal myocardium has decreased contractile mass, and the magnitude and velocity of fiber shortening are less than in the adult myocardium. These factors and the increased anesthetic requirement, which is inversely related to age, all produce a higher incidence of adverse cardiovascular effects in infants. Minimal alveolar concentration (MAC) is an estimate of anesthetic requirement. The MAC of Sevoflurane in neonates is 3.2 as against an adult MAC of sevoflurane of 2.05. The MAC of halothane is 0.87 (as against an adult value of 0.75) and that of isoflurane is 1.6 (as against adult values of 1.2) Intravenous anesthetics and analgesics The elimination half-life of thiopental in neonates is greater than that in adults and children because of the reduced clearance in neonates.The dose of thiopentone in neonates is 3 -4 mg/kg. Clearance of propofol in neonates is 66% less than that in children and adults. A myriad of causes of bradycardia associated with propofol administration have been proposed and caution should be exercised in using propofol in neonates. The elimination half-life of fentanyl is prolonged in preterm neonates but is same as in adults in term neonates. The elimination half life of morphine is prolonged even in full term neonates.


Muscle relaxants Higher doses of succinylcholine (2 mg/kg) are required to produce adequate relaxation in the neonate. Since neonates do not fasciculate or get elevations in intragastric pressure from succinylcholine, precurarization is not required. Neonates, however, do frequently become bradycardic following succinylcholine and atropine premedication is recommended. Neonates demonstrate reduced neuromuscular function when compared with older children. No change in dose of non-depolarizingmusclerelaxants is needed in neonates because the greater sensitivity of the immature myoneural junction of the neonate to non depolarizing relaxants is offset by their larger volume of distribution. The duration of action of vecuronium is longer because of diminished renal clearance. It is better to choose atracurium as the relaxant for short procedures like hernia repair.

The new concerns is neonatal anesthesia are about neurotoxicity of inhalational anesthetics, ketamine and midazolam and about the toxic effects of hyperoxia. It has been shown that prolonged exposure to isoflurane, ketamine or midazolam precipitates apoptosis in many regions of the brain in immature rats. The potential for neurotoxicity from inhaled anesthetics,midazolam, and ketamine may be greater in preterminfants than full-term infants, although there is no evidence thatsimilar neurotoxicity occurs in humans at any age exposed to any anesthetics. Till such evidence exists and alternate drugs are available, it is neither possible nor necessary to remove these drugs from the anesthesia armamentarium. The potential risks of unnecessary exposure to high inspired oxygen are described. Although it is essential to continue to zealously avoid hypoxemia and tissue hypoxia, we must avoid causing hyperoxemia, oxidant damage and reperfusion injury. The lowest inspired oxygen concentration necessary to maintain adequate oxygen saturation on the pulse oximeter should be chosen and no more. PREOPERATIVE ASSESSMENT This should include a detailed history taking and physical examination for skin colour, capillary filling time, trends in the blood pressure, heart rate, and intensity of the peripheral pulses. Ventilatory frequency, presence of intercostal retractions and upper airway appearance should be assessed. The anatomy of the neck and the upper airway may provide


crucial warnings about likely difficult intubation. Chest auscultation should be performed for heart sounds, breath sounds and murmurs. Hemoglobin, haematocrit, platelets and coagulation profile should be within acceptable limits before surgery. Neonates undergoing elective surgery can be fed breast milk until 4 hours before anesthesia and then given clear fluids until 2 hours before surgery. Formula is in the same category as solid food. PREMEDICATION Premedication is not required routinely. However, atropine (10 – 20 mcg/kg) should be considered to pre-empt transient bradycardia. Preparation of the Operating Room: THERMAL PROTECTION Measures must be taken to protect against heat loss during surgery. These include 

Transporting the baby in a warmer

Warming the operating room to at least 27°C

Using a warming mattress

Heat and humidify gases to 36°C

Use a radiant heat warmer with a servo control mechanism

Wrap non involved areas with plastic

Warm intravenous fluids and blood

Warm scrubbing and irrigation solutions

MONITORING General observation: Color (cyanosis, pallor), chest mobility (bilateral expansion, respiratory pattern) and palpation (warmth, pulses, peripheral perfusion) are often difficult to assess because of the patient’s position and draping, but must be done.


Monitors: A precordial stethoscope is a simple and effective means to assess the quality of heart sounds, rate and rhythm. A change in the intensity of heart sounds indicates a decrease in blood pressure and possibly cardiac output. The other routine monitors include pulse oximeter, ECG using neonatal electrodes, non invasive blood pressure using an appropriate sized cuff, capnography and temperature monitoring. BREATHING CIRCUIT Non-rebreathing (open) circuits like the JRMATP have a low resistance and are simple and effective for delivering anesthetic agents to infants weighing less than 10 kg. Alternately, the circle system can also be used, with paediatric breathing tubes. ANAESTHESIA FOR HERNIA REPAIR During the seventh month of gestation, the testicle descends from the abdomen through the inguinal wall into the scrotum. The processusvaginalis, a peritoneal covering, encloses the testicles during their descent. In term infants, the processusvaginalis is usually closed at birth, but it remains patent in 15% to 37% of people. In premature infants, the incidence is much higher depending on the gestational age at the time of birth. The continued patency of the processusvaginalis is the principal factor in the development of congenital hernias and hydroceles. Inguinal hernia repair is the most frequent general surgical procedure performed by pediatric surgeons. Males are more frequently affected than females, and the incidence of inguinal hernia is highest in the first year of life. Right-sided hernias (60%) occur more frequently than left-sided (30%) and bilateral (10%) hernias. The following medical and postsurgical conditions have been associated with the development of congenital inguinal hernias: undescended testis, birth prematurity, ascites, and a ventriculo-peritoneal shunt, to name a few.


Clinical presentations Most inguinal hernias are asymptomatic. Once the bowel and other viscerabecome incarcerated, however, typically at the level of the internal ring,infants will present with a myriad of signs and symptoms. Early in thecourse, the neonate will be irritable.As the disease progresses to strangulation, abdominal distention, vomitingand obstipation will occur. Physical examination will reveal a massin the inguinal area with or without a scrotal mass.If the incarcerated inguinal hernia is left unreduced, they progressrapidly to strangulation. Ischemia to the testes and ovaries also is described. Patients who have strangulated bowel present extremelyirritable. The abdominal distention and vomiting can be pronounced. Onexamination, a tender, tense, nonfluctuant mass is found in the inguinalarea. Late signs of strangulation are shock, blood per rectum, and peritonitis. An abdominal radiograph will show a partial or complete bowelobstruction. If the bowel extends into the scrotum, airâ&#x20AC;&#x201C;fluid levelsmay be seen in the scrotum.

Preoperative management of such a patient should focus on aggressive fluid resuscitation, initiation of broad-spectrum antibiotics, and attention to airway, breathing, and circulation. Hernitomies are commonly performed as elective procedures; however, in children with incarceration and signs of bowel obstruction, it can be an emergency procedure necessitating a rapid-sequence induction. Elective repair of a non incarcerated hernia can be carried out under general anesthesia or regional anesthesia. GENERAL ANESTHESIA Anesthesia can be induced with inhalational agents or intravenous agents. Airway can be maintained using a 1 size Laryngeal mask airway or an endotracheal tube for an elective hernia repair. A rapid sequence induction of anesthesia with cricoid pressure and endotracheal intubation is recommended in neonates posted for emergency hernia repair due to bowel obstruction.

The Miller-0 straight laryngoscope blade is probably the most commonly recommended device for visualizing the airway of a tiny neonate (preterm or of low birth weight), and the Miller-1 is used in the full-term neonate.


The tube size depends on the age and birth weight. A preterm neonate weighing < 1000g would require a 2.5 mm ID ETT, a premie weighing between 1000 and 2500 g would require a 3.0 mm ID ETT, while a term neonate weighing between 2.5 â&#x20AC;&#x201C; 3.5 kg would require a 3.5 mm ID ETT. To ensure that the endotracheal tube is not too large, inspired gas should leak around the endotracheal tube while delivering a manual positive breath (20 to 25 cm H2O pressure). A tightly fitting tube can damage the subglottic mucosa, causing edema and postoperative stridor or possibly subglottic stenosis. The length at which the endotracheal tube should be fixed at the angle of the mouth is decided by the 123-789 rule meaning neonates weighing 1, 2 and 3 kg respectively need the tube to be fixed at 7, 8 or 9 cm at the angle of the mouth. This is only a rough guideline and actual confirmation of bilateral air entry by auscultation should aid exact placement.

Maintenance of anesthesia can be with inhalational agents,short acting muscle relaxants like atracurium and short acting opioids like fentanyl (1 mcg/kg). The use of opioids is associated with an increased incidence of postoperative apnea. Analgesia can also be provided with caudal administration of local anesthetics or an iliohypogastric and ilioinguinal block. This will decrease intraoperative anesthetic requirements and provide postoperative analgesia. Ilioinguinal/iliohypogastric nerve blocks consist of injecting 0.25% bupivacaine with epinephrine (1: 200,000) (1 mg/kg/side) around the nerve by direct vision through the surgical incision, which provides 6 to 8 hours of analgesia. Caudal analgesia can be provided with 1 ml/kg of 0.25% bupivacaine. A caudal catheter can be inserted and continuous caudal epidural infusions can be used for post- operative analgesia. Orallyadministered acetaminophen (10-15 mg/kg) can also be used for providingpostoperative analgesia.

The patient must be well anesthetized when the spermatic cord is being manipulated. Inadequate depth at this stage can result in laryngospasm and bradycardia.

Neonates are at increased risk for potential local anesthetictoxicity because of decreased protein binding (resulting inincreased unbound drug) and possibly immature drug metabolism.Hence, a conservative maximum infusion dose for bupivacaineof 0.2 mg/kg/hr for no longer than 48 hours in neonates isstrongly recommended, when epidural infusions are used.


SPINAL ANESTHESIA Spinal anesthesia is used as an alternative to general anesthesia, especially in preterm neonates, to decrease the incidence of postoperative apnea. In neonates, the spinal cord extends to a lower segment of the spine than in older children and adults. The conus medullaris (the terminus of the spinal cord) in neonates and infants is located at the L3 vertebral level, which is more caudal than in adults. Thus, lumbar puncture for subarachnoid block in neonates and infants should be performed at the L4-L5 or L5-S1 interspace to avoid needle injury to the spinal cord. The vertebral laminae are poorly calcified at this age, so a midline approach is preferable to a paramedian one in which the needle is walked off the laminae. The distance from the skin to the subarachnoid space is very small in neonates (approximately 1.4 cm). The volume of CSF and the spinal surface area are proportionally larger in neonates, whereas the amount of myelination is less than in older children and adults. These factors may account in part for the increased amount of local anesthetics (mg/kg) required for a successful spinal anesthetic in a neonate. The CSF turnover rate is also considerably greater in infants, accounting in part for the much briefer duration of subarachnoid block with any given agent compared with adults. These anatomic differences necessitate meticulous attention to detail to achieve successful and uncomplicated spinal anesthesia in a neonate. Technique After routine monitors are affixed, the child is placed in a sitting or lateral decubitus position. Care must be taken to avoid excessive flexion of the neck as it may obstruct the airway. The sitting position may aid in recognizing successful dural puncture because of the increased CSF hydrostatic pressure and hence increased flow through the spinal needle. The skin is infiltrated with a minute quantity (0.25 ml) of 1% lignocaine. Spinal anesthesia may be administered through a 1½-inch, 22-gauge spinal needle. Once CSF is obtained, 0.5 â&#x20AC;&#x201C; 1 mg/kg of 0.5% hyperbaric bupivacaine is injected. Once the block is placed, the infant should be maintained in a supine position. Leg lifting, especially during placement of the electro cautery grounding pad, should be avoided because


it has been associated with a high spinal blockade. Apnea or sudden cessation of crying may be the presenting sign of a high spinal blockade in a neonate. In contrast to older children and adults, subarachnoid block in neonates and infants is associated with hemodynamic stability.

FLUID MANAGEMENT Intraoperative fluid therapy has the same four components described for any clinical setting where intravenous treatment is considered: (1) maintenance fluid, (2) replacement of fluid deficit, (3) replacement of third-space loss, and (4) replacement of other losses. For inguinal hernia repair, intravenous fluids consist of Ringerâ&#x20AC;&#x2122;s lactate solution (4 mL/kg/hr) with dextrose (5 mg/kg/min administered by infusion pump) to maintain normoglycemia.

RECOVERY Following elective inguinal hernia repair, the neonate can be extubated, once extubation criteria are met (spontaneous eye opening present, muscle power adequate, respiratory rate and depth adequate). It is necessary to monitor the neonate for postoperative apnea. So, it is not recommended to do the procedure on a day care basis till 60 weeks post conceptional age. Neonates with bowel obstruction/gangrene may need postoperative mechanical ventilation. CONCLUSION Inguinal hernia repair in a neonate is one of the commonly performed surgical procedures. Provision of anesthesia care should take into account the gestational age, the presence of comorbid conditions and the presence of bowel obstruction to plan appropriate care. RECOMMENDED READING 1. Cote CJ, Lerman J and Todres ID. Practice of Anesthesia in Infants and Children. 4th edition. Elsevier Saunders 2. Motoyama. EK and Davis PJ. Smithâ&#x20AC;&#x2122;s Anesthesia for Infants and Children. 7th edition. Mosby Elsevier.


3. Peiris K and Fell D. The prematurely born infant and anaesthesia. CEACCP 2009; 9(3):73-77. 4. Sola A. Oxygen in neonatal anesthesia: friend or foe? Curr Opin Anaesthesiol 2008; 21:332-339.


AN OBESE PATIENT FOR BARIATRIC SURGERY Dr. Radhika Dhanpal, Professor of Anaesthesiology, St. John’s Medical College Hospital, Bangalore.

The prevalence of obesity is rising both in the developed and developing countries and is associated with an increased incidence of a wide spectrum of medical and surgical pathologies. These patients can present to the anaesthesiologist for an elective, emergency or bariatric procedure; for obstetric analgesia and anaesthesia or in the intensive care unit. Simply treating these patients as being “ larger than usual” is inappropriate. Definition : Obesity is a condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health leading to reduced life expectancy . It is derived from the latin word “obesus”, meaning fattened by eating. Classification a) WHO: Class I

BMI 30-34.99

Class II

BMI 35-39.99

Class III

BMI ≥ 40

b) Quetelet’s index: 

Obese

BMI >35 kg/m2

Morbid obesity

BMI >30 kg/m2 with no co-morbidity BMI >40 kg/m2 with no co-morbidity

Super – morbid obesity : BMI >50 kg/m2

The duration of obesity ( fat years ) and the distribution of adipose tissue rather than the absolute weight or BMI is an important predictor of disease. Centrally distributed adipose tissue ( android obesity ) is associated with an increased incidence of metabolic complications than those with an peripheral distribution of fat ie.apples vs pears.


Indications for bariatric surgery i)Supervised non – surgical measures for weight loss have failed to achieve or maintain clinically beneficial weight loss for at least 6 months. This guidance refers to adults with a BMI of ≥ 40 kg/m2 or ≥ 35 kg /m2 with obesity related disease likely to improve with weight loss. ii) Super – morbid obesity Types of bariatric surgery

Malabsorptive

Restrictive

(Rare ) i)

Jejuno – ileal bypass

i) Vertical banded gastroplasty

ii)

Bilio – pancreatic bypass

ii) Adjustable gastric banding iii) Roux –en-Y gastric bypass(the GOLD STANDARD) iv) Gastroplasty

Contra- indications i) Mental and cognitive impairment ii) Advanced liver disease with portal hypertension iii) Malignancy with poor 5- year prognosis iv) Unstable coronary artery disease v) Uncontrolled, severe OSA with pulmonary hypertension vi) Ongoing substance abuse

Obstructive sleep apnea ( OSA) – is defined as apnoeic episodes secondary to pharyngeal collapse that occur during sleep. It may be obstructive, central or mixed. Its incidence increases with obesity and age.


The characteristic features are i) Frequent episodes of apnoea or hypopnoea during sleep, 5 or more /hr or > 30/night are considered clinically significant. An apnocic episode is defined as 10 second or more of total cessation of airflow despite continuous respiratory effort against a closed airway. Hypopnoea is a 50% reduction in air flow or enough to drop the arterial oxygen saturation by 4%, ii) Snoring

iii) Day time somnolence associated with impaired concentration and morning headaches

iv) Pathophysiological changes : hypoxaemia ( leading to secondary polycythemia ) , hypercapnia

systemic vasoconstriction or pulmonary vaso constriction leading to

ventricular failure.

There is increased adipose tissue in the pharyngeal wall, particularly between the medial and lateral pterygoids. This results in increased pharyngeal wall compliance with a tendency to airway collapse when exposed to negative pressure. There is also a change in airway geometry, so the axis at the open part of the airway is predominantly antero – posterior rather than lateral consequently the increase in genioglossus tone seen during inspiration is far less effective at maintaining airway patency. In the long term , OSA affects control of breathing by desensitization of the respiratory centres, increasing reliance on hypoxic drive and eventually causing type 2 respiratory failure. After confirmation by nocturnal polysomnography, patients are commenced on nocturnal CPAP or BIPAP for 6-12 weeks prior to surgery. Polysomnography PSG also known as a “ sleep study” , is a multi- parametric test used in the study of sleep. It is a comprehensive recording of the biophysiological changes that occur during sleep. It monitors the brain ( EEG) ,eye movement ( EOG), skeletal muscle activity (EMG) and heart rhythm ( ECG) during sleep Respiratory airflow thermistor and pulse oximetry.


It is used to diagnose sleep disorders, narcolepsy, periodic limb movement, REM behaviour disorder , parasomnias and sleep apnea.

After the test is completed, a “ scorer” analyses the data by reviewing the study in 30 sec “ epochs” and determines the Apnoea /hypopnoea index.

Metabolic syndrome (Syndrome) : According to AHA and NHLBI, metabolic syndrome is present if you have 3 or more of the following signs

BP ≥ 130/85 min Hg

FBS ≥ 100 mgs %

Waist Measurement Male 40” or > Female 35” or >

HDL Male < 40 mg % Female < 50mg %

Triglycerides≥ 150 mg %

Pre-operative assessment : the objective is to optimize patient outcomes. It ensures that patients are appropriately selected, informed, motivated and optimized medically. A multi- disciplinary team approach by nurses, dieticians, psychologists, endocrinologists, respiratory physicians, anesthetists and bariatric surgeons sees the patient 6-12weeks in advance. A comprehensive history, thorough physical examination with particular attention being paid to the airway, respiratory and cardiovascular system is performed.


History : The following additional information should be elicited i) Limited mobility therefore they may have asymptomatic cardio- respiratory dysfunction. ii) OSA, snoring iii) Cardiac failure iv) Inability to tolerate supine position. v) Intake of Amphetamine based appetite suppresants as they contribute to increased peri-operative cardiac risk vi) Bleeding tendency and paraesthesia.

Airway : Obese patients have traditionally been considered to be at increased risk of difficult tracheal intubation. However, studies have shown that absolute weight and BMI per se are poor predictors of difficult tracheal intubation. A H/ O of OSA, a large neck circumference >40 cms (


collar size 17.5), Mallampatti >3, thyromental distance < 6cms, limited cervical and temporo mandibular joint mobility are more specific indicators of potential difficulty. Respiratory system: Baseline respiratory function should be established from the patient history and physical examination. Cessation of smoking for >8 weeks pre – operatively is associated with improved cardiovascular parameters and decreased post-operative pulmonary complications . Cardiovascular system: Obesity , particularly the android variety, is an independent risk factor for coronary artery disease. As mobility is limited and clinical examination unreliable , functional capacity may be better assessed by the patient’s ability to undertake activities of daily living. Based on this and the revised Cardiac Risk Index , a framework for proceeding or not to provocative cardiac testing has been developed.

Endocrine : Glycemic control is desirable to reduce the incidence of adverse events. Others : Patients at increased risk for thromboembolism ( BMI> 60, a history of OSA /OHS or previous thrombo – embolism ) should be considered for IVC filter insertion pre – operatively. Scoring systems : It stratifies peri-operative mortality risk , standardization and comparison of outcomes, prognostication and development strategies. The OS-MRS (Obesity Surgery Mortality


Risk Score) is a recently validated scoring system specific to obese patients undergoing bariatric surgery. It allocates a point to each of 5 pre-operative variables BMI â&#x2030;Ľ 50kg/m2 Male gender Systemic hypertension Risk factors for pulmonary embolism Age â&#x2030;Ľ 45 years

Score

Risk

Class

Mortality

0-1

Low

A

0.31%

2-3

Intermediate

B

1.9%

C

7.56%

4-5

High

De Maria EJetal Investigations : Routine : Blood tests CBC, Serum electrolytes , renal , liver, thyroid function tests. ECG, CXR, PFT, ABG Special : Polysomnography when indicated. SPECT, PET, Pharmacological Stress Test , Cardiac catheterization Cardiopulmonary exercise testing (CPEX)

Anesthetic management : Obesity pack i) Informed consent


ii) Staff training – A designated lead consultant , anaesthesiologist and staff nurse who are responsible for ensuring that appropriate systems are in place , that suitable equipment is readily available and protocols are laid down . iii) Risk reduction Appropriate risk reduction strategies could take the form of a guideline or checklist of key points to be considered at each stage of the patient journey ; outpatient , pre-anaesthetic assessment, admission, PACU

Special equipment – Ambulance, Transfer trolley, operating table with secure attachments , critical care bed should be appropriate .Pressure areas must be protected and skin should not be in contact with metal . BP cuffs, TED stockings , tourniquets should be larger. Anesthetic management Monitoring : 

ECG

Blood Pressure – if an appropriately sized BP cuff produces inaccurate readings, invasive BP monitoring should be used. It is also advisable to monitor BP invasively if the patient is high risk or the operation is prolonged. Ultrasonographically assisted central venous access is obtained only if good peripheral access can not be obtained.

Depth of anaesthesia monitoring – BIS, Entropy

Induction : When General Anaesthesia is chosen, drug dosing regimens should keep the following in mind TBW (Total Body weight ) LBW / LBM (Lean body weight / mass). Males = 1.1 (weight) kgs – 128 ( weight / height , cms) 2 Female = 1.07 (weight) kgs - 148 ( weight / height, cms )2 IBW (Ideal body weight) kgs = Height ( cms)- X Where X = 100 in males and 105 for females.


Airway management

AAGBI -2007

• Previous anaesthetic charts should be checked for evidence of airway problems. • A history of obstructive sleep apnoea is an important predictor for airway problems after induction. • Evidence of gastro-oesophageal reflux should be sought at the preoperative visit, with a low threshold for prescribing antacid prophylaxis. • Adequate manpower is essential, such that turning the patient in an emergency should be possible and accomplished without too much delay.


• More assistance than normal for the anaesthetist may be necessary. • The anaesthetic assistant should be familiar with and prepare difficult airway equipment prior to induction. • Pre-oxygenation should be performed in a reversed Trendelenberg position as this prolongs the time to desaturation during apnoea [4,5]. • Consideration should be give to modifying the traditional “sniffing the morning air” intubation position to the “ramped” position [6]. • Surgical access to the airway is technically more difficult and is associated with an increased risk of peri-operative complications in the obese patients. • Some patients may require awake intubation; appropriate skills and equipment must be immediately available.

Presence of OSA, a previous history of difficult intubations, Mallampatti score ≥ 3, neck circumference > 40 cms, thyromental distance <6 cms and limited cervical or temporo – mandibular joint mobility have been cited as predictors of difficult intubation . Awake fibre optic intubation may be considered or else all gadgets for difficult airway must be available.

Pre – oxygenation in the 25° head –up and the application of pre – intubation PEEP 10 cms for 5 mins have been shown to prolong the duration of non – hypoxic apnoea in these patients.

The HELP and PS( Head Elevated Laryngoscopy position ; Pinna Sternum in line ). positions with the help of rolled blankets, pillows or inflatables should be adopted for intubation.

Propofol dosed on lean body weight and non – depolarizing neuro-muscular blocker based on ideal body weight , a rapid sequence induction with suxamethonium

may be

chosen. 

A Guedel airway always helps in preventing insufflation of the stomach.

Patients who have had previous bariatric surgery are at increased risk of pulmonary aspiration and should undero rapid sequence induction with cricoid pressure always.


A large bore naso or oro – gastric tube should be in place and care taken to see that it is not transfixed surgically .

Desflurane is undoubtedly the agent of choice for maintenance of anaesthesia as it facilitates early recovery. Fentanyl does not need any dose modification in the obese

However , a

combination of remifentanil TCI and BIS guided desflurane anaesthesia is highly recommended.

The 50% reduction in FRC, 10-25% increase in intrapulmonary shunt and an increase in alveolar – arterial oxygen gradient have to be kept in mind. tidal volumes of 10 ml/kg , moderate amounts of PEEP and permissive hypercapnia should be used.Rrespiratory acidosis should be avoided as tachycardia, dysrhythmias,

↑ SVR and PVR may result. The reverse Tredelenburg

position significantly improves respiratory dynamics. Creation of a pneumoperitoneum causes inferior vena caval compression, an increase in Systemic Vascular Resistance and a reduction in cardiac output and GFR . the reverse Trendelenburg position, IPPV and PEEP further exacerbate the cardiovascular effects.

Aggressive multimodal thromboprophylaxis including LMWH, pneumatic , calf compression devises and graduated compression stocking is mandatory.

The ideal fluid regimen is not known. Figures of 4-10 ml/kg/hr have been recommended. Central venous pressure recommended monitoring should be used to guide fluid administration in patients with IHD or cardiac failure.

Hypothermia, pressure sores, neuropathies and rhabdomyolysis are other peri- operative complications which should be avoided by proper patient positioning , cushioning and changing position during prolonged surgery Extubation should be in the Semi – upright position in a fully awake patient with no residual neuro – muscular blockade .

Regional anaesthesia : An experienced anaesthesiologist is needed for performance of regional blocks in the obese. Ultrasound guidance is invaluable and doses for sub – arachnoid and


epidural blocks must be scaled down . For analgesia local anaesthetic infiltration of trocar sites ,opioids, NASID’s , paracetamol , TENS, TAP block , PCA are all recommended . Vit K deficiency ( bleeding tendencies) Folate, B12 deficiency ( Sub-acute combined degeneration of the cord) must be kept in mind epically in those who have had bariatric surgery .

Bleeding tendencies, Sub – acute combined degeneration must be kept in mind especially in those show have had bariatric nurgery.

Post – operative management : Patients should be managed in the PACU with attention being paid to airway, pain and thrombo – embolism. O2 should be administered till they can maintain baseline saturation on room air alone. Individuals requiring CPAP or NIV should be reestablished on them , especially during sleep. Continuous pulse oximetry until room air saturation remains greater than 90% is recommended, also chest physiotheraphy and incentive spirometry.

Bibliography 1 Adams JP etal “ obesity in anaesthesia and intensive care “ Br. J anaesth 2000; 85 (1) : 91108) 2 Babatunde etal “ Anaesthetic condierations for bariatric surgery. Anesth Analg 2002: 95:1793-1805. 3 Brodsky JB etal “ anesthetic consideration for bariatric surgery : proper positioning is important for laryngoscopy” anaesth Analg 2002; 95:4793 4 Luc EC DE Baendemaker etal “ Pharmacokinitics in obese patients “ crit Care and pain J 2004; 4(5) : 152-155 5 Collins JS etal “ Laryngoscophy and morbid obesity : A comparison of the “ Shiff “ and “ ramped” positions . Obes Surg 2004;14:1171-5 6 Chand B.etal “ Perioperative management of the buriatric surgery patient: Focus on cardiac and anesthesia considerations” Cleverl and Clinic Journal of Medicine 2006;75 (1): 551-556


7 Malhotra N “ Morbid obesity and its anaesthetic implications “ conference prodedings , ISACON 2006, India 8 Gayes MJ et al “ An inflatable device supporting the obese patients in the Head- Elevated Laryngoscopy Position ( HELP)” Anaesthesiology 2007;107: A953 9 “ Peri – operative management of the morbidly obese patient “ AAGBI June 2007. WWW. aagbi.org 10Lotia S etal “ Anaesthesia and morbid obesity Br.J Anesth 2008; 8(5): 151- 156. 11 O. Nill T etal “ Anesthetic consideration and management of the obese patient presenting for bariatric surgery “ Curr anaesth andCrit Care 2009. Pub – Elsevier Ltd, UK 12 Ingrande J et al. “ Dose adjustment of anaesthetics in the morbidly obese” Br. J Anaesth 2010; 105 ( SI) 116-123

AAGBI 2007

KEY RECOMMENDATIONS All trained anaesthetists should be competent in the management of morbidly obese patients and familiar with the equipment and protocols in the hospitals in which they work. All patients should have their height and weight recorded. Where possible this should be measured rather than relying on the patient’s estimate. The Body Mass Index (BMI) should be calculated and recorded. Although BMI is not an ideal measure of risk, it is the most useful of the currently available markers and is a simple measure to apply.


Every hospital should have a named consultant anaesthetist and a named theatre team member who will ensure that appropriate equipment and processes are in place for the peri-operative management of morbidly obese patients. Protocols including details of the availability of equipment should be readily to hand in all locations where morbidly obese patients may be treated. Mandatory manual handling courses should include the management of the morbidly obese. Pre-operative assessment is a key component in the assessment and management of risk. Early communication between those who will be caring for the patient is essential and scheduling of surgery should include provision for sufficient additional time, resources and personnel. The absolute level of the Body Mass Index should not be used as the sole indicator of suitability for surgery or its location.


ANAESTHESIA FOR CLEFT LIP AND CLEFT PALATE REPAIR Dr.S.Bala Bhaskar Professor of Anaesthesiology Vijayanagar Institute of Medical Sciences, Bellary

INTRODUCTION Cleft lip and cleft palate are congenital anomalies with defects in the upper lip and palate. Cleft lip

and

cleft

palate

may

occur

together

or

separately.

(Fig.1

and

2)

CLEFT LIP with or without cleft palate occurs in 1:1,000 births. Cleft lip is associated with cleft palate in 75% of cases. Cleft lip may be unilateral (in 80%) or bilateral (in 20%). Cleft lip (with or

without

cleft

palate)

is

more

common

in

BOYS.

CLEFT PALATE alone occurs in approximately 1:2,500 births. The most common cleft of the palate is a left complete cleft of the pre-palatal and palatal structures. The second most common is a midline cleft of all the soft palate and part of the hard palate without a cleft in the pre-palatal area.

Cleft

palate

is

more

common

in

GIRLS.

The highest incidence of cleft lip and cleft palate occurs among Asians (1.61:1,000 births) and is least in Africans (0.3:1,000). EMBRYOLOGY/ANATOMY OF CLEFTING The defect in cleft lip/palate is multifactorial. Multiple genetic / chromosomal abnormalities are found and there could be a familial predisposition, especially for subsequent pregnancies after an affected child. Incidence of cleft lip is more with increased maternal age but not cleft palate. Maternal intake of diazepam, cortisone, teratogens (including phenytoin, sodium valproate and methotrexate), excessive maternal vitamin A intake, folic acid deficiency, maternal tobacco or alcohol abuse (fetal alcohol syndrome) and maternal diabetes mellitus have also been implicated. Maternal age (younger than 20 years or older than 39 years of age) and increased paternal age have all been associated with orofacial clefting. (1)


Major facial structures develop in the first 4 to 7 weeks of gestation from the frontonasal prominence and the paired maxillary and mandibular processes.

The normal epithelial fusion and mesenchymal migration may be disturbed causing facial clefting. Failure to fuse causes pre-palatal clefts; failure of palatal ridges to migrate medially, contact, and fuse cause palatal clefts.(Fig.3)

Failure of fusion of the maxillary and the medial and the lateral nasal processes leads to cleft (upper) lip. Anatomically, it may vary from notch in the upper lip to a cleft through the lip and the floor of the nose involving the alveolar ridge, or they may be complete cleft of the lip and the palate.

The cleft palate can be pre-palatal, post-palatal (incisive foramen marks the boundary between the two) or of sub-mucosal variety. Pre-palatal cleft involves anterior palate, alveolus, lip, nostril floor, and ala nasi. Post-palatal clefts may extend anywhere from soft and hard palate to the incisive foramen. The sub-mucosal cleft involves a bone defect without a mucosal defect.

ASSOCIATED CONDITIONS / ANOMALIES / SYNDROMES Approximately one in six newborns with a cleft may have other congenital defects (especially affecting heart or kidney). Associated anomalies occur 30 times more frequently in the patient with isolated cleft palate than in the noncleft population. They may occur alone (Non syndromic) or as part of a syndrome (>300 syndromes are associated with facial clefting), or as a component of a sequence, for example, Pierre Robin sequence (2). (Table 1).The common nonsyndromic associations are umbilical hernias, clubfoot, limb and ear deformities. The common syndromes associated with cleft lip and cleft palate are Pierre Robin syndrome, Klippel-Feil Syndrome, fetal alcohol syndrome, Goldenhar's syndrome, Treacher Collins syndrome, Down syndrome, etc. Pierre Robin Syndrome In Pierre Robin sequence, the tongue is displaced superiorly and posteriorly as a result of mandibular hypoplasia and interferes with palatal fusion resulting in cleft palate. Pierre Robin syndrome is characterized by retrognathia or micrognathia, glossoptosis, and airway obstruction.


The main triad in Pierre Robin syndrome is retrognathia, severe respiratory and/or digestive disorders in early infancy and cleft palate. Treacher Collins Syndrome

Treacher Collin’s syndrome is associated with hypoplastic cheeks, zygomatic arches and mandible, microtia with possible hearing loss, high arched or cleft palate, macrostomia (abnormally large mouth), antimongoloid slant to the eyes, colobomas (notching of the outer portion of the lower eyelid), increased anterior facial height, malocclusion (anterior open bite), small oral cavity and airway with normal-sized tongue and pointed nasal prominence.

CONSEQUENCES OF CLEFT LIP / PALATE: THE EFFECTS OF CLEFTING (1, 2, 3)

Face has important role in functions of breathing, eating, swallowing, speech, hearing (through the eustachian tube) and communicating. Cleft palate affects the normal communication of pharynx with the nasal fossae and the oral cavity, resulting in disorders of most of the above functions. In a neonate, cleft lip and palate result in feeding difficulties; negative pressure needed for sucking action is inadequate or totally lost. This can interfere with breast-feeding and bottlefeeding. Failure to thrive is common with recurrent infections. Middle ear disease is common as abnormal nasopharynx adversely affects eustachian tube function. Chronic infections here can produce varying degree of conductive hearing loss. Food and air streams mix up with absent bony separation between mouth and nose; chronic rhinorrhea may be observed, without infection. Airway patency is well maintained in a child with cleft lip; in infants with cleft palate or cleft lip/palate, the tongue may fall into the cleft and obstruct the airway (nose breathing). Secondary defects of tooth development, growth of the ala nasi, and velopharyngeal function (contact between the soft palate and the posterior pharynx for speech and swallowing) can also occur. The speech of these children is typically nasal with an inability to produce ‘plosives’ (p/k/d/t) and ‘fricatives’ (s/f). Presence of abnormal facial structures may precipitate psychological problems as the child approaches school age and peer association. Hence, repair of cleft lip (cheiloplasty)


is needed for a normal facial appearance and function and normal psychological well-being. Repair of cleft palate (palatoplasty) allows for normal speech, hearing and normal mastication of food (maxillofacial growth) - ‘the functional goals’ of surgery. MANAGEMENT OF CLEFT LIP AND CLEFT PALATE Surgical repair is the definitive approach. Supportive medical management is aimed at improving nutrition, treating ear, upper and lower respiratory infections and providing psychological support in grown up children. Associated non syndromic or syndromic features must also be managed pari passu. Surgical Repair of cleft lip and palate consists of approximating the tissue on either side of the defect and rotating and advancing flaps for anatomic correction of the defect. Some of the common procedures are Furlow procedure (most common), von Langenbeck technique, Schweckendiek technique, two-flap technique and three flap/V-Y technique. A team approach is needed for good patient outcome ; pediatrician to maintain overall health, surgeon and anesthesiologist for perioperative period, a speech therapist to overcome the speech deficiencies and orthodontist to develop and maintain relatively normal bite and dentition. Geneticist, psychologist, medical social worker and public health workers have special roles to play.

THE TIMING OF SURGERY FOR CLEFT LIP AND PALATE Overall, the timing and sequencing of repair is based on surgeon preference. Primary repairs are performed as early as possible in the newborn period. If soft palate is repaired at the time of lip repair, an additional anesthetic is avoided. Staged / sequential repairs ‘allow’ for growth of muscle and alignment of alveolar segments to obtain the best functional repair (dentomaxillary appliance insertion, alveolar-lip adhesion release, cleft lip repair, and finally cleft palate repair). Pharyngeal flap and oronasal fistula repair may be needed subsequently for velopharyngeal insufficiency.Cleft

lip

alone

is

usually

repaired

at

6

to

10

weeks

of

age.

For cleft palate alone, the repair is carried out at 6 to 12 months of age. The exact age of repair will depend on the size and health of the child and the surgeon's preference. Early repair cleft palate (before 24 months of age) may improve speech and hearing. Closure of the soft palate at 3 to 6 months, with secondary closure of the residual hard palate at 15 to 18


months of age helps take advantage of the early physiology and growth that occurs in the soft palate,

which

is

vital

in

the

development

of

speech.

Delayed closure (after 4 years) may be associated with less retardation of midfacial growth, avoids the potential pitfalls of the growth disturbance related to early periosteal undermining of palatal and vomerine tissue and also provides total palatal closure before speech evolves. ANAESTHESIA

CONSIDERATIONS

FOR

CLEFT

LIP/PALATE

SURGERIES

(‘AASTMMAA’) 

Age-appropriate anaesthetic considerations apply, such as airway, fluid, temperature, anaesthetic circuits,etc. (neonatal or pediatric)

Considerations related to Cleft lip / palate surgery :

Airway Considerations and use of Special Tubes (oral RAE, polar tubes, reinforced endotracheal tubes) for a low facial profile, unhindered surgical field and secure protection.

Minimal bleeding

Minimal narcotics at the end of the procedure in order to have the patient breathing spontaneously and adequately assess depth of anesthesia.

Awake child at extubation

Post-operative Analgesia

PREANAESTHETIC EVALUATION (2, 3, 4) a. Some children have poor general health including malnourishment due to poor feeding, anaemia, vitamin deficiencies. Correct weight of the child should be noted pre-operatively. Conductive deafness is common because of chronic middle ear infection. b. Presence of upper/lower respiratory infections: With cleft palate, crusting and low-grade infection of the nasopharynx may be present due to food and fluid regurgitation through the cleft. It is persistent despite antibiotics; unless an acute inflammation process is present, this does not lead to complications. c. Airway management may be influenced by history of apnoea, breathing, or feeding problems; various options for airway management including ET tubes and gags can be identified.


Examination of the mouth may indicate potential intubation problems. Upper airway anomalies such as retrognathia, micrognathia, fused cervical spine, etc. are noted during evaluation as conventional airway assessment is not applicable in this age group. d. Because of high incidence of associated syndromes and cardiac abnormalities, high index of suspicion must be maintained for cardiac murmurs. Antibiotic prophylaxis may be needed for some cardiac abnormalities. e. In a sequential approach, children come for surgeries at intervals and a history and review of the previous anaesthetic management would be useful for current management.

Pre-Operative Investigations:

Should include haemoglobin level estimation (anaemia is common and there could be need for blood transfusion in cleft palate procedures, not cleft lip), blood grouping and Rh typing (for cleft palate repairs),blood counts and ESR for identifying presence of infections. Chest X ray is obtained for assessing lower respiratory tract infections and head and neck X rays for possible syndromic facial and cervical spine anomalies (Klippel Feil Syndrome with cervical spine fusion). In presence of Treacher Collins or Pierre Robin syndrome, an x-ray of the mandible is useful. If maxilloâ&#x20AC;&#x201C;pharyngeal angle on lateral X-ray is less than 900 (normally greater than 100°), it implies that the larynx will not be visible at direct laryngoscopy (5). Electrocardiogram and echocardiography would help in diagnosing associated congenital heart diseases. The diagnosis of clefting is made after birth; in utero diagnosis with ultrasonography is however possible as early as at the beginning of the second trimester of pregnancy. Clinically, while cleft lip and cleft lip/palate should easily be detectable, an isolated cleft palate may be more discrete, sometimes requiring meticulous inspection, and palpation of the hard and soft palate.(1) PREOPERATIVE

PREPARATION:

Psychological,

physical

and

pharmacological

preparations are needed before surgery. Elderly children may have psychological issues, especially with a previous anaesthetic exposure. Child and parental counseling and parental cooperation are essential for proper pre-operative preparation and postoperative care. Anaesthesiologist can attempt bonding with the child with repeated visits in pre-operative period. Improvement in general well-being with suitable nutrients and feeding techniques, correction of


anaemia with iron supplements, supplements for deficiencies of vitamins and calcium is advised. This will promote weight gain and improved milestones and growth. Before surgery, use of special nipples allows feeding of the child in upright position; with Haberman nipple the child does not have to generate suction to get the fluid from the nipple. Rarely, feeding may need to be provided through a nasogastric tube. (2) Antibiotics may be administered as needed as also antipyretics and antihistamines for a dry nose. A running nose is however common with nasal crusts in the absence of infection in the presence of cleft lip and cleft palate. Antibiotics are also indicated for ear infections and lower respiratory tract infections. Children younger than 8 months may not require sedative premedication. Mild sedation is all that may be permitted and tolerated; sedation should be avoided if there is significant risk of difficult airway and respiratory depression. Syrups of Trichlofos (70-100 mg/kg) or Promethazine (0.5 mg/kg)1/2 hr before surgery can be given orally. Promethazine has additional benefits of antiemetic, anticholinergic, antihistaminic effects and can allow reduced doses of opioids because of potentiation of opioid analgesia. A list of some of the sedative premedicants is given in the table 2. Intravenous access, if not already secured, may be facilitated by using Eutectic Mixture of Local Anaesthetics (EMLA, 0.25% each of Lignocaine and Prilocaine) before the surgery or after inhalational induction is started; iso-osmolar solutions (such as Ringer Lactate, dextrose in saline or pediatric maintenance solutions) are started based on age of the child and based on Holliday-Segar recommendations. Antiemetics such as metoclopramide (0.15 mg/kg) or ondansetron (0.16 mg/kg) are helpful. Blood loss is not significant in cleft lip repair and rarely exceeds 10% of circulating blood volume in cleft palate repair. Cross-matched and typed blood should

be

available

and

used

only

if

absolutely

necessary.

The RULE OF 10 includes broad guidelines for an adequately prepared child: Weight:

Approximately

10

lb

HaemoglobinI:10g/dl White

blood

cell

for

Cleft

lip

or count:

and

10

kg

more Less

than

10,000

for

palate

for per

repair both

ÂľL

for

both

Age for surgery: Approximately 10 weeks for cleft lip repair and 10 months for cleft palate repair. THE PRE-OPERATIVE FASTING GUIDELINES


The standard guidelines for preoperative fasting allow patient comfort with less potential for intra-operative hypoglycemia. (Table 3) CHOICE OF ANAESTHESIA TECHNIQUE FOR CLEFT LIP AND PALATE REPAIR (2, 3, 4, 6) General anaesthesia with intubation aided by inhalational or intravenous (IV) induction and relaxants is the standard technique. Pre Induction : Allowing the parent to accompany the child and be present during induction helps in a calm and co-operative child especially for inhalational induction. Usual pre induction check-list is performed and basal monitors are connected (discussed later). Anticholenergics are advisable to reduce secretions. The risk of bradycardia during laryngoscopy and intubation in neonates, in the presence of suxamethonium or halothane are also reduced with anticholenergics (Inj.Atropine 20 µg/kg or Inj.Glycopyrrolate 10 µg /kg, IV). Induction : When difficult airway or loss of airway is anticipated, inhalational induction with appropriate airway management equipment is indicated. Inhalational induction has become easier, faster and safer with the advent of sevoflurane and can be used after obtaining adequate seal with proper fitting face mask. It can also aid in calming and sedating the child before intravenous induction. Oxygen- nitrous oxide-sevoflurane (halothane) can be used for induction. Sevoflurane is less cardio-depressant and does not sensitize the myocardium to catecholamines and hence preferred over halothane. Intravenous line is established as the child falls asleep and intravenous fluids are started and appropriate monitors (discussed later) connected. With a ‘fit’ child, choice of induction technique and agents is not significant. Intravenous induction can be carried out using etomidate (0.5mg/kg), propofol (2 mg/kg), thiopentone (4-5 mg/kg) or ketamine (1-2 mg/kg). Presence of comorbidities, especially cardiac, can influence the choice of IV induction agents. Laryngoscopy and Intubation: Difficult laryngoscopy is expected with cleft palate (especially bilateral) and retrognathia. Difficult intubation should be anticipated in presence of retrognathia, micrognathia, cervical spine fusion, etc. seen in syndromic children. Presence of a pre-maxillary tab with cleft lip causes difficulty in intubation. Left sided cleft is more difficult to intubate. Muscle relaxants are


avoided if difficult intubation is anticipated. Succinylcholine or nondepolarizing relaxants such as vecuronium and rocuronium can be safely used. Laryngoscopy is generally straightforward in cleft lip patients; with cleft palate however, the laryngoscope blade can be trapped in the cleft. This is prevented by inserting a gauze pack or a dental roll in the cleft before laryngoscopy. In cleft surgeries, since upper lip and palate are involved, to maintain anatomical symmetry and avoid distortion, the ET tube is secured over the middle of the lower lip; mouth gags have recesses to accommodate the tube as it exits the mouth (fig.4).There is risk of the ET tube getting kinked, dislodged or even dragged out of its position during the positioning and surgery. Hence, specialized tubes such as Ring Adair Elwyn (RAE) tube, South Polar tube and Flexometallic / reinforced / kink resistant tubes have been used to overcome/prevent these problems. (fig.5) certain amount of experience is needed to insert and secure these tubes; stillettes are needed frequently.

The

ET

tube

may

even

be

sutured

over

the

lower

gum.

For cleft lip surgery, moistened ribbon gauze is inserted into pharynx. For cleft palate surgery, the surgeon inserts the gag before insertion of the pharyngeal pack. The tube position needs to be rechecked after gag and pack insertion for compression and ventilation. The Kilner Dott mouth gag and Dingman mouth gag (fig 4) have provision for the ET tube exit for stable fixation; they also protect against compression of tube. Position of ET tube must be checked frequently and good communication with the surgeon must be maintained as the surgeon and the anaesthesiologist have the same limited space to compete for. The eyeballs are lubricated and covered with gauze pads and taped. Orogastric tube may need to be passed before start of cleft palate procedure and removed after stomach contents are cleared. Jackson Rees Modification of Ayreâ&#x20AC;&#x2122;s T Piece (Maplesonâ&#x20AC;&#x2122;s F circuit) with minimal dead space, minimal resistance and being lightweight, is the circuit usually used. A paediatric circle absorber with soda lime can also be effectively used. Use of other airway techniques such as use of laryngeal mask airways (LMAs), fibreoptic intubation through a laryngeal mask airway, retrograde techniques have been reported but they have limited role in young children. Maintenance: Balanced anesthesia is ensured with oxygen- nitrous oxide-sevoflurane (isoflurane)-fentanyl and non- depolarizing relaxants. Controlled ventilation provides adequate oxygenation and avoids hypercarbia, which can precipitate arrhythmias if halothane and adrenaline containing local


anaesthetics are injudiciously used. It reduces bleeding and reduces risk and consequences of air embolism. Whichever the maintenance approach, the need is for a spontaneously breathing patient at the end of the repair for safe extubation. Narcotics need to be minimized at this time. Position: For cleft lip repair, child is supine with roll under shoulders and head moderately extended, resting on a head ring. Rose position (supine with head over the edge of the operating table) is often utilized. For adequate surgical exposure during cleft palate repair, child is positioned with maximum head extension; entire body is raised with folded blanket, allowing the head to drop back hyperextended into a stockinette head support. It also allows blood to drain from larynx and toward

the

nasopharynx

allowing

it

to

be

removed

by

suction.

Analgesia: Decision to use opioids or narcotics for analgesia is made based on the patient (as already discussed). If narcotics are used, they should be used judiciously, with proper titration and timing. Effective analgesia must persist /continue into post-operative period without risk of respiratory depression; non opioid analgesics can be very useful preoperatively (pre-emptive analgesia) and intra-operatively. (table 4) Regional Anesthesia /Analgesia: Infraorbital nerve block (5,7) (fig.6) : Infra-orbital nerve consists of four branches and provides sensory innervation to the upper lip, mucosa along upper lip, the vermillion, the lateral inferior portion of nose and lower eye lid. The nerve emerges beneath orbicularis oculi muscle from the infra-orbital foramen, and can be palpated along the inferior orbital rim at the infra-orbital notch (below the junction of medial and middle thirds of lower border of orbit) and can be blocked as it exits (Extra-oral or percutaneous approach). This point lies in the same vertical line as that passing over the pupil, the supra-orbital, the infra-orbital and the mental foramina. Since the foramen emerges in a caudad and medial direction, the needle is directed in a cephalad and lateral direction. There is also a vein that travels with it which can be traumatized causing a â&#x20AC;&#x153;black eye.â&#x20AC;? 1 ml. of 0.25% Bupivacaine or 1% lignocaine is injected with 26G or 27G needle; care is taken to avoid needle entry into the canal. The nerve can also be blocked by internal approach, from the alveolar sulcus subcutaneously. The needle is inserted lateral to lateral incisor, advanced upwards through the upper buccal


sulcus, towards the infra orbital foramen, stopping short of infra orbital rim, to avoid damage to the eye. By this approach, the benefit will not last as the area is dissected by the surgeon. Surgeons may infiltrate the palate with lignocaine and adrenaline to minimize bleeding during surgery but this may not have marked post-operative analgesic effects. Nasopalatine and palatine nerve block will provide palatal hard and soft tissue anesthesia. For nerve blocks, the dose of lignocaine can be stretched to 5-7 mg/kg with vasopressors. Epinephrine up to 10 µg / kg. can be used for hypocarbic or normocarbic patients. The concentration of adrenaline in solution should be limited to 1:2,00,000. FLUID AND BLOOD ADMINISTRATION The fluids are administered based on Holliday-Segar’s guidelines, taking into consideration the deficit, maintenance and replacement needs. Infants need dextrose as part of balanced salt solution (‘Isolyte-P’) whereas elderly children are well maintained on Ringer Lactate. Blood transfusion is not required for cleft lip repairs but has to be arranged for a palate repair, especially in a child with anaemia. The maximum allowable blood loss (MABL) can be calculated from estimated blood volume (EBV, table 5) and haematocrit values as below: MABL = EBV x (Child's pre-op. haematocrit - Minimum accepted haematocrit) Child's pre-op. hematocrit E.g. For a 5 kg. child, the EBV is: 5 kg x 80 mL/kg = 400 mL. With the child’s haematocrit as 35% and accepted final haematocrit as 25%, MABL = 400 x (35-25) = 114 mL 35 Based on Haemoglobin levels, MABL is estimated as below: MABL= EBV x (Child's pre-op. Hb - Minimum accepted Hb) Child's pre-op. Hb Acceptable Hb% may vary; normally 9gm% can be the minimum accepted. MONITORING DURING CLEFT LIP / PALATE SURGERY


Standard noninvasive monitoring should include heart rate, respiration, blood pressure, temperature, and oxygen saturation (pulse oximetry). A precordial stethoscope helps to monitor heart and respiration. The rate and tone of heart sounds help in identifying episodes of hypoxia (bradycardia) in younger age groups as cardiac output is determined more by heart rate and less by the stroke volume (the latter reflected by the tone, which is liable to come down due to cardiac depression and hypovolemia/ haemorhage / hypotension). An electrocardiogram is useful for assessing cardiac rate and rhythm. Capnography is useful for assessing ventilation and the unusual possibility of air embolism. Axillary or rectal temperature is monitored; hypothermia should be avoided with an aim to maintain thermo-neutral temperature (if necessary with warming blankets). For cases lasting over 4 hours, urinary catheter is advised. Other monitors as needed

may

be

used

for

comorbidities.

Blood loss is estimated by gravimetric methods (such as weighing swabs; 1gm swab weight gain= app.1 gm) and calorimetric methods (such as calibrated catchment trap in the suction line and suction container). It is important to estimate blood loss into surgical drapes, together with that pooling beneath the patient and onto the floor. Reversal and Recovery: The narcotics and relaxantsâ&#x20AC;&#x2122; administration must be timed and dosed such that no residual respiratory depressant effects are anticipated and spontaneous efforts set in at the end of the procedure. There should be no hurry to reverse the neuromuscular blockade till these objectives are met. A peripheral nerve stimulator may be used as a guide before administering neostigmine and atropine. Thorough but gentle suctioning of blood clots and secretions are needed before and after removal of pharyngeal pack. This may be done before removal of gag without using laryngoscope. Intact respiratory drive, full return of laryngeal protective reflexes, blood free airway and perfect analgesia should be the aim. Extubation at deeper planes is not advised. Extubation is carried out at the end of procedure in cleft lip repair and child placed in lateral position to allow for drainage of secretions / blood. Some patients after cleft palate repair and with ongoing airway obstruction problems may need delayed extubation and management in an ICU setting. POST OPERATIVE CONSIDERATIONS


A long traction suture is passed through the tongue and tied loosely. This clears the airway and stimulates respiration. The traction suture is removed after adequate recovery is confirmed. Airways, orally or nasally, are avoided as they could disrupt sutures. A Logan bow may be used to take the tension off the newly sutured lip and restraints are placed at the elbow before shifting the child to post-operative suite. (Fig.7) Post-operative position: Following palate surgery, the infant is placed in prone or lateral position with the head dependent, turned to the side, and hyperextended. This will allow blood or mucus to deposit in the dependent cheek or roll out of the mouth. Post operative monitoring : The intra-operative monitoring is continued into post-operative period for possible bleeding, airway obstruction and hypothermia. Post-operative analgesia: For cleft lip, the infraorbital block provides good analgesia post-operatively. Local anaesthetic infiltration used for cleft palate may help bring down systemic analgesic requirements. Non opioid analgesics such as rectal or parenteral paracetamol, diclofenac provide satisfactory pain relief. (table 4) Short acting and titratable opioid analgesics such as fentanyl can be used postoperatively in select cases. Patient-controlled analgesia (PCA), used for moderate to severe pain in children over 6 years old, is rarely needed for these procedures. Post-operative ventilation: Cleft palate surgeries complicated by bleeding, co-morbidities / syndromes, difficult and doubtful repairs, when airway maintenance is doubtful and respiratory depression may need ventilatory support.

COMPLICATIONS

Certain specific complications should be anticipated related to airway. In the majority of cases of cleft palate repair, it is easy to intubate but extubation is a riskier affair. Majority of the complications are more frequent in cleft palate repair as the duration of surgery and the surgical insult is more here as compared to cleft lip repair. These could include those related to the endotracheal tube such as auto-extubation and endo-bronchial intubation, kinking (due to


positional disturbances), or obstruction due to secretions/ blood. Airway insufficiency may be related to residual effects of sedatives, anaesthetic agents and relaxants. Obstruction could also be due to swelling of the tongue due to mouth gag placement during surgery. Surgical correction of the hard palate reduces the airway and this is worst in the first 24 hours postoperatively because of oedema. Bradycardia may occur due to parasympathetic reflexes during laryngoscopy and intubation, ET tube related hypoxia, surgical bleeding or due to drugs (suxamethonium and halothane). Hypothermia has potential to delay emergence and precipitate metabolic acidosis and respiratory and myocardial depression. Thermo-neutralilty of the child (360-380C) has to be maintained with warm blankets / aluminium foil / warmers; the temperature of the operating room, however, has to be in the comfort zone for the surgeon (240C). Air embolism is an unusual complication associated with these procedures. Severe bradycardia may lead on to cardiac arrest. Airway obstruction may result due to laryngospasm and laryngeal oedema. Bleeding with or without aspiration, pneumonia and hypothermia may be precipitated in the post-operative period. Intense post-operative monitoring needs to be continued in the post-operative period. The mortality rate has been reported to be less than 0.5%. Post intubation croup with acute laryngotracheobronchitis is an unusual complication. Humidified oxygen may reduce the incidence of tracheitis. SUMMARY Cleft lip and cleft palate are the most common congenital anomalies, frequently seen in association with some co-morbidities or syndromes. Repairs are normally performed in sequence keeping in mind the anatomical growth of the face with age. Feeding problems, recurrent nasal, ear and respiratory tract infections are seen, needing antibiotics. Sedative pre-medications are avoided to prevent respiratory depression and loss of airway reflexes in the post-operative period. Control of airway intra-operatively using preformed ET tubes allows unhindered surgical access and patent and secure endotracheal tube. Blood transfusion is not needed in cleft lip repair but has to be available in cleft palate repair in children with prior anaemia. Intra-operative monitoring should continue in post-operative period to guard against airway related problems and bleeding. Infra-orbital nerve block provides good analgesia in cleft lip repair.


REFERENCES:

1. Stoelting’s Anaesthesia and Coexisting disease. Ed. Roberta L Hines, Katherine E Marschall.5 th Edition. Churchill Livingstone; 2008; 612-13 2. Jayant K Deshpande. Kevin Kelly. Matthew B Baker. Anesthesia for pediatric plastic surgery.Ch.20.in Smith’s Anesthesia for Infants and Children.Eds.Etsuro K Motoyama, Peter J Davis. 7th Edition. Mosby Elsevier.2006.733-35 3. Barbara W Palmisano. Anesthesia for plastic surgery. In Pediatric Anesthesia.Ed. George A. Gregory. 3rd edition .Churchill Livingstone.1994.725-27 4. Robert S Holzman, Thomas J. Mancuso, David M. Polaner; A Practical approach to Pediatric Anesthesia.1 st edition, Lippincott Williams & Wilkins;2008;243-44 5. Deleque L, Rosenberg-Reiner S, Ghnassia L’intubation tracheale chez s enfants atteints de dysmorphie craniofaciales conigenitales. Anesthes Analges Reanimation.1980; 37: 133–138 6. Aarti Sharma.Cleft palate. In Yao and Artusio’s Anesthesiology. Problem Oriented Patient Management.6thEd.Lippincot Williams & Wilkins.2008;1049-60 7. Georges Peri and Jean-Michel Mondie. Blocks of the Head, Face and Neck. In Regional Anesthesia in Infants, Children and Adolescents. Ed. Bernard Dalens. First Ed.Williams & Wilkins;1993;431-32


Table (1) Congenital anomalies associated with cleft lip with or without cleft palate (2) Frequent

Occasional

Fetal hydantoin syndrome

Cri du chat syndrome

Mohr syndrome

Larsen's syndrome

Fetal trimethadione syndrome

Facioauriculovertebral anomaly

Orofaciodigital syndrome

Meckel-Gruber syndrome

Roberts' syndrome

Oculodentodigital syndrome

Trisomy 18 syndrome

Trisomy 18 syndrome

4 p-syndrome

Waardenburg's syndrome

Table (2) Sedatives and Sedative Analgesics DRUG

DOSAGE

Fentanyl

1 µg/kg

IV

15-20µg/kg

Fentanyl lollipop (oral transmucosal fentanyl)

2 µg/kg

Route / Forms Available

Transnasal

Morphine

0.05–0.1mg/kg

IV

Pethidine

1 mg/kg

IV

Codeine

1.5 mg/kg q4h

PO:15-mg,30-mg,60-mg tab;syrup 15 mg/mL

Oxycodone

0.15 mg/kg

PO:5-mg tablets; syrup 5 mg/mL


Midazolam

0.1 - 0.15 mg /kg 0.25 to 0.5 mg/kg

IM; 1 mg/ml Oral, from IV solution as a fruit-flavoured

0.2 to 0.3 mg/kg

syrup

0.3 mg/kg

Nasal Rectal

Diazepam

0.06-0.08 mg/kg Oral, 2mg/5 ml syrup

Ketamine

0.25 to 0.5 mg/kg 4-6 mg/kg

IV 10 mg/ml,50 mg/ml IM, from IV solution

Trichlofos Na

70-100 mg/kg Oral, 100mg/ml syrup (1/2 hr before)

Promethazine

0.5 mg/kg 0.35-0.5 mg/kg

Oral, 5 mg/5 ml (1/2 hr before) IV (25 mg/ml)

(IV, intravenous; IM, intramuscular; PO, by mouth)

Table (3) Fasting Guidelines

AGE

CLEAR FLUIDS

BREAST

FORMULA OR SOLIDS

MILK

COW'S MILK

Children

2

_

6

6

3â&#x20AC;&#x201C;12 months

2

4

6

6

<3 months

2

4

4

6

Table (4) Nonsedating Analgesics for Pediatric Use


DRUG

DOSAGE

FORMS AVAILABLE

Acetaminophen

10–15 mg/kg PO max.2,600 PO Tablets: 250 mg

(paracetamol)

mg/d

Syrup: 125 mg/5 mL (60 ml bottle)

30-40 mg/kg bolus rectal,

Rectal Suppo: 80 mg,170 mg

20mg/kg 12 hrly Diclofenac

IM 25 mg/ml,75 mg/3ml 1.0-1.5 mg/kg.

Aqueous 75 mg/ml Rectal Suppo.:12.5mg/100mg (Dicl.Na) 100mg (Dicl.K)

Ibuprofen

PO Tablets: 200, 400 mg 10–20 mg/kg 3-4 div. doses

Ketorolac

PO Syrup: 100 mg/5 mL (60 ml bottle)

IM / IV infusion (30mg /ml) 0.5

mg/kg

IV

to

load PO 10mg tab.

(maximum dose 30 mg) 0.5 mg/kg q8h Tramadol

IM or IV (limit use to 48 hr)

IV 50mg/ml

1-2 mg/kg.6 hourly

IV, intravenous; PO, by mouth; IM, Intramuscular; Suppo, suppository

Table (5) Estimated Blood Volume

Age

Circulating (ml/kg)

Preterm neonate

90 -100

Full term neonate

80 - 90

blood

volume


Infant

70 - 80

Child

70- 75

Obese child

60 - 65

Adult

65 - 70

Fig (1) and (2) Cleft Lip, Cleft Palate, Cleft Lip with cleft palate

Fig (3)

Development of Cleft palate


Fig (4) Dottâ&#x20AC;&#x2122;s and Dingman Mouth gag in cleft palate repair


Fig (5) RAE Tube, Polar Tubes and Flexometallic Tube

Fig (6) Infra-orbital nerve block (7)

Fig (7) Arm restraints and Loganâ&#x20AC;&#x2122;s Bow after cleft lip surgery (3)


ANTICOAGULANT THERAPY AND REGIONAL ANAESTHESIA Dr.J.Balavenkatasubramanian, Senior Consultant Anaesthesiologist, Ganga Medical Centre & Hospital, Coimbatore.

.

Introduction: The use of neuraxial anaesthesia and analgesia is increasing every passing day. Improvement in patient outcomes, including mortality, major morbidity, and patient-oriented outcomes, has been demonstrated with neuraxial technique due to the attenuation of the hypercoagulable response and the associated reduction in the frequency of thromboembolism after neuraxial blockade.

The development of standards for the prevention of perioperative venous thromboembolism (VTE), as well as the introduction of increasingly more potent antithrombotic medications, resulted in concerns regarding the heightened risk of neuraxial bleeding. Trends in patient management included not only in the avoidance of neuraxial techniques but also in the search for alternative therapies and likely played a prominent role in the resurgence of peripheral blockade. The American Society of Regional Anaesthesia has Published guidelines which would help the practising anaesthesiologist to follow certain safe protocols while administering Regional Anaesthesia in patients receiving Anticoagulants, Antiplatelets and Anti thrombotic medications. The following are excerpts from guidelines published by ASRA.

PERIOPERATIVE MANAGEMENT OF ANTITHROMBOTIC AND ANTIPLATELET THERAPY

Long-term anticoagulation with warfarin is often indicated for patients with a history of VTE, mechanical heart valves, and atrial fibrillation.


Perioperative Management of Patients on Warfarin

Preoperative 

Discontinue warfarin at least 5 d before elective procedure*

Assess INR 1 to 2 d before surgery, if >1.5, consider 1-2 mg of oral vitamin K

Reversal for urgent surgery/procedure, consider 2.5-5 mg of oral or intravenous vitamin K; for immediate reversal, consider fresh-frozen plasma

Patients at high risk for thromboembolism :

Bridge with therapeutic subcutaneous LMWH (preferred) or intravenous

UFH : Last dose of preoperative LMWH administered 24 hrs before surgery, administer half of the daily dose : Intravenous heparin discontinued 4 hrs before surgery 

No bridging necessary for patients at low risk for thromboembolism

Postoperative 

Patients at low risk for thromboembolism :Resume warfarin on postoperative day

Patients at high risk for thromboembolism (who received preoperative bridging therapy) : Minor surgical procedure resume- therapeutic LMWH 24 hrs postoperatively

:Major surgical procedure resume- therapeutic LMWH 48 - 72 hrs postoperatively or administer low-dose LMWH

Assess bleeding risk and adequacy of hemostasis when considering timing of the resumption of LMWH or UFH therapy.


Perioperative Management of Patients on Antiplatelet Therapy

Patients with coronary stents & Elective surgery postponed for the following durations if aspirin and thienopyridine (eg, clopidogrel) therapy must be discontinued

: Bare metal stents: 4-6 wk

: Drug-eluting stents: 12 months

If surgery cannot be postponed, continue aspirin throughout perioperative period

Patients at high risk for cardiac events (exclusive of coronary stents) 

Continue aspirin throughout the perioperative period

Discontinue clopidogrel at least 5 days (and preferably 10 days) before surgery

Resume clopidogrel 24 hrs postoperatively

Patients at low risk of cardiac events 

Discontinue antiplatelet therapy 7-10 days before surgery

Resume antiplatelet therapy 24 hrs postoperatively

Anesthetic Management of the Patient Receiving Thrombolytic Therapy Patients receiving fibrinolytic/thrombolytic medications are at risk for serious hemorrhagic events, particularly those who have undergone an invasive procedure. Recommendations are based on the profound effect on hemostasis, the use of concomitant heparin and/or antiplatelet agents (which further increase the risk of bleeding), and the potential for spontaneous neuraxial bleeding with these medications. •

In patients scheduled to receive thrombolytic therapy, we recommend that the patient be queried and medical record reviewed for a recent history of lumbar puncture, spinal or epidural anesthesia, or epidural steroid injection to allow appropriate monitoring. Guidelines detailing original contraindications for thrombolytic drugs suggest avoidance of these drugs for 10 days after puncture of noncompressible vessels (Grade 1A).

In patients who have received fibrinolytic and thrombolytic drugs, we recommend against


performance of spinal or epidural anesthetics except in highly unusual circumstances (Grade 1A). Data are not available to clearly outline the length of time neuraxial puncture should be avoided after discontinuation of these drugs. â&#x20AC;˘

In those patients who have received neuraxial blocks at or near the time of fibrinolytic and thrombolytic therapy, we recommend that neurological monitoring should be continued for an appropriate interval. It may be that the interval of monitoring should not be more than 2 hrs between neurologic checks. If neuraxial blocks have been combined with fibrinolytic and thrombolytic therapy and ongoing epidural catheter infusion, we recommend the infusion should be limited to drugs minimizing sensory and motor block to facilitate assessment of neurologic function (Grade 1C).

â&#x20AC;˘

There is no definitive recommendation for removal of neuraxial catheters in patients who unexpectedly receive fibrinolytic and thrombolytic therapy during a neuraxial catheter infusion. We suggest the measurement of fibrinogen level (one of the last clotting factors to recover) to evaluate the presence of residual thrombolytic effect and appropriate timing of catheter removal (Grade 2C).

UNFRACTIONATED INTRAVENOUS AND SUBCUTANEOUS HEPARIN Intravenous UFH Intraoperative heparinization typically involves injection of 5 to 10,000 U of heparin intravenously during the operative period, particularly in the setting of vascular surgery to prevent coagulation during cross clamping of arterial vessels. Neuraxial anesthetic techniques are often attractive for these patients because these techniques may provide reduced morbidity and improved postoperative analgesia. However, the use of neuraxial procedures in the presence of UFH may be associated with an increased risk of epidural hematoma, as demonstrated by case series, epidemiologic surveys, and the continued claims in the ASA Closed Claims database. Most published case series used similar guidelines for patient management, including exclusion of high-risk patients (preexisting coagulopathy) and performance of neuraxial procedure at least 1 hr before administration of heparin. Heparinization may be continued into the postoperative period. Prolonged intravenous heparin administration is usually performed with a constant intravenous infusion of heparin, usually with a goal of aPTT prolongation to 1.5 to 2 times the baseline level. The risk of any (spontaneous, surgical, or anesthesia-related) bleeding due to heparin in such an anticoagulated patient may be increased particularly if there is marked variation in the aPTT (regardless of the mean aPTT). ' Most


importantly, the initiation of systemic therapeutic heparin therapy for medical or surgical indications in the presence of a neuraxial catheter potentially increases the risk of hematoma formation during catheter removal. Thus, this analgesic technique remains controversial in that the risk seems too great for the perceived benefits. A review has recommended certain precautions to be taken to minimize the risk: (1)Neuraxial blocks should be avoided in a patient with known coagulopathy from any cause, (2)Surgery should be delayed 24 hrs in the event of a traumatic tap, (3)Time from instrumentation to systemic heparinization should exceed 60 mins, (4)Heparin effect and reversal should be tightly controlled (smallest amount of heparin for the shortest duration compatible with therapeutic objectives), (5)Epidural catheters should be removed when normal coagulation is restored, and patients should be closely monitored postoperatively for signs and symptoms of hematoma formation. These recommendations, as well as the practice of inserting epidural catheters 24 hrs in advance of surgery, have been used by most of the published case series. Validity of these and future recommendations will need to be determined. Subcutaneous UFH Low-dose heparin is commonly used for prophylaxis against development of VTE in general and urologic surgery. Administration of 5000 U of heparin subcutaneously every 12 hrs has been used extensively and effectively for prophylaxis against DVT. Anesthetic Management of the Patient Receiving UFH Anesthetic management of the heparinized patient was established more than 2 decades ago. Initial recommendations have been supported by in-depth reviews of case series, case reports of spinal hematoma, and the ASA Closed Claims Project. Recent thromboprophylaxis guidelines identifying more patients as candidates for thrice-daily subcutaneous heparin and the potential for increased bleeding with this therapy have prompted a modification of the previous ASRA guidelines. â&#x20AC;˘

We recommend daily review of the patient's medical record to determine the concurrent use of medications that affect other components of the clotting mechanisms. These medications include antiplatelet medications, LMWH, and oral anticoagulants (Grade IB).

â&#x20AC;˘

In patients receiving prophylaxis with subcutaneous UFH with dosing regimens of 5000 U


neuraxial bleeding may be reduced by delay of the heparin injection until after the block and may be increased in debilitated patients after prolonged therapy (Grade 1C). â&#x20AC;˘

The safety of neuraxial blockade in patients receiving doses greater than 10,000 U of UFH daily or more than twice-daily dosing of UFH has not been established. Although the use of thrice-daily UFH may lead to an increased risk of surgical-related bleeding, it is unclear whether there is an increased risk of spinal hematoma. We suggest that the risk and benefits of thrice-daily UFH be assessed on an individual basis and that techniques to facilitate detection of new/progressive neurodeficits (eg, enhanced neurologic monitoring occur and neuraxial solutions to minimize sensory and motor block) be applied (Grade 2C).

â&#x20AC;˘

Because heparin-induced thrombocytopenia may occur during heparin administration, we recommend that patients receiving heparin for more than 4 days have a platelet count assessed before neuraxial block and catheter removal (Grade 1C).

â&#x20AC;˘

Combining neuraxial techniques with intraoperative anticoagulation with heparin during vascular surgery is acceptable with the following recommendations (Grade 1A):

Avoid the technique in patients with other coagulopathies. Delay heparin administration for 1 hr after needle placement. Remove indwelling neuraxial catheters 2 to 4 hrs after the last heparin dose and assess the patient's coagulation status; re-heparin 1 hr after catheter removal. Monitor the patient postoperatively to provide early detection of motor blockade and consider use of minimal concentration of local anesthetics to enhance the early detection of a spinal hematoma. Although the occurrence of a bloody or difficult neuraxial needle placement may increase risk, there are no data to support mandatory cancellation of a case. Direct communication with the surgeon and a specific risk-benefit decision about proceeding in each case is warranted

Currently, insufficient data and experience are available to determine if the risk of neuraxial hematoma is increased when combining neuraxial techniques with the full antico-agulation of cardiac surgery. We suggest postoperative monitoring of neurologic function and selection of neuraxial solutions that minimize sensory and motor block to facilitate detection of new/progressive neurodeficits (Grade2C).


LOW-MOLECULAR WEIGHT HEPARIN The marked increase in the frequency of spinal hematoma in patients anticoagulated with LMWH prompted a reevaluation of the relative risks and benefits of neuraxial blockade. For example, ASRA guidelines have consistently recommended against the administration of twice-daily LMWH in a patient with an indwelling epidural catheter. Although once-daily LMWH dosing in the presence of an epidural catheter safe, caution was advised if the patient received an additional hemostasis-altering medications, including antiplatelet therapy. Anesthetic Management of the Patient Receiving LMWH Anesthesiologists in North America can draw on the extensive European experience to develop practice guidelines for the management of patients undergoing spinal and epidural blocks while receiving perioperative LMWH. Al consensus statements contained herein respect the labeled dosing regimens of LMWH as established by the FDA. Although it is impossible to devise recommendations that will completely eliminate the risk of spinal hematoma, previous consensus recommendations have seemed to improve outcome. Concern remains for higher dose applications, where sustained therapeutic levels of anti-coagulation are present. The anti-Xa level is not predictive of the risk of bleeding. We recommend against the routine use of monitoring of the anti-Xa level (Grade 1A). Antiplatelet or oral anticoagulant medications administered in combination with LMWH increase the risk of spinal hematoma. Education of the entire patient care team is necessary to avoid potentiation of the anticoagulant effects. We recommend against concomitant administration of medications affecting hemostasis, such as antiplatelet drugs, standard heparin, or dextran, regardless of LMWH dosing regimen (Grade 1A). The presence of blood during needle and catheter placement does not necessitate postponement of surgery. We suggest that initiation of LMWH therapy in this setting should be delayed for 24 hrs postoperatively and that this consideration be discussed with the surgeon (Grade 2C).

Preoperative LMWH Patients on preoperative LMWH thromboprophylaxis can be assumed to have altered coagulation. In these patients, we recommend that needle placement should occur at least 10 to 12 hrs after the LMWH dose (Grade 1C). In patients receiving higher (treatment) doses of LMWH, such as enoxaparin 1 mg/kg every 12 hrs, enoxaparin 1.5 mg/kg daily, dalteparin 120 U/kg every 12 hrs, dalteparin 200 U/kg daily, or tinzaparin 175 U/kg daily, we recommend delay of at least 24 hrs to


ensure normal hemostasis at the time of needle insertion (Grade 1C). In patients administered a dose of LMWH 2 hrs preoperatively (general surgery patients), we recommend against a neuraxial techniques because needle placement would occur during peak anticoagulant activity (Grade 1A). Postoperative LMWH Patients with postoperative LMWH thromboprophylaxis may safely undergo single-injection and continuous catheter techniques. Management is based on total daily dose, timing of the first postoperative dose and dosing schedule (Grade 1C). Twice daily dosing. This dosage regimen is associated with an increased risk of spinal hematoma. The first dose of LMWH should be administered no earlier than 24 hrs postoperatively, regardless of anesthetic technique, and only in the presence of adequate (surgical) hemostasis. Indwelling catheters should be removed before initiation of LMWH thromboprophylaxis. If a continuous technique is selected, the epidural catheter may be left indwelling overnight, but must be removed before the first dose of LMWH. Administration of LMWH should be delayed for 2 hrs after catheter removal. Single daily dosing. The first postoperative LMWH dose should be administered 6 to 8 hrs postoperatively. The second postoperative dose should occur no sooner than 24 hrs after the first dose. Indwelling neuraxial catheters may be safely maintained. However, the catheter should be removed a minimum of 10 to 12 hrs after the last dose of LMWH. Subsequent LMWH dosing should occur a minimum of 2 hrs after catheter removal. No additional hemostasis altering medications should be administered due to the additive effects. Oral Anticoagulants (Warfarin) Neuraxial Techniques in the Chronically Anticoagulated Patient Although no studies have directly examined the risk of procedure-related bleeding and the INR in patients recently discontinued from warfarin, careful consideration should be given before performing neuraxial blocks in these patients. Labelling of warfarin in the United States specifically lists spinal puncture and lumbar block anesthesia as contraindicated during warfarin therapy that is not interrupted before surgery


Timing of Neuraxial Catheter Removal During Warfarin Thromboprophylaxis The management of patients requiring long-term anticoagulation (with recent discontinuation of warfarin in anticipation of surgery) and patients receiving warfarin perioperatively for thromboprophylaxis remains controversial. Adjusted dose warfarin is the most common agent used for thromboembolism prophylaxis after hip and knee replacement surgery . Few data exist regarding the risk of spinal hematoma in patients with indwelling spinal or epidural catheters who are subsequently anticoagulated with warfarin. Bleeding may occur during catheter removal of the epidural catheter as a result of vascular trauma during catheter manipulation or dislodgment of an existing clot. The use of an indwelling epidural or intrathecal catheter and the timing of its removal in an anticoagulated patient are also controversial. Although the trauma of needle placement occurs with both single-dose and continuous catheter techniques, the presence of an indwelling catheter could theoretically provoke additional injury to tissue and vascular structures. Regional Anesthetic Management of the Patient on Oral Anticoagulants The management of patients receiving warfarin perioperatively remains controversial. Recommendations are based on warfarin pharmacology, the clinical relevance of vitamin K coagulation factor levels/deficiencies, case series, and the case reports of spinal hematoma among these patients. Caution should be used when performing neuraxial techniques in patients recently discontinued from long term warfarin therapy. In the first 1 to 3 days after discontinuation of warfarin therapy, the coagulation status (reflected primarily by factor II and X levels) may not be adequate for hemostasis despite a decrease in the INR (indicating a return of factor VII activity). Adequate levels of II, VII, IX, and X may not be present until the INR is within reference limits. We recommend that the anticoagulant therapy must be stopped (ideally 4-5 days before the planned procedure) and the INR must be normalized before initiation of neuraxial block (Grade IB). We recommend against the concurrent use of medications that affect other components of the clotting mechanisms and may increase the risk of bleeding complications for patients receiving oral anticoagulants and do so without influencing the INR. These medications include aspirin and other NSAIDs, ticlopidine and clopidogrel, UFH, and LMWH (Grade 1A). In patients who are likely to have an enhanced response to the drug, we recommend that a reduced dose be administered. Algorithms have been developed to guide physicians in the appropriate dosing of warfarin based on desired indication, patient factors, and surgical factors.


These algorithms may be extremely useful in patients at risk for an enhanced response to warfarin (Grade IB). In patients receiving an initial dose of warfarin before surgery, we suggest that the INR should be checked before neuraxial block if the first dose was given more than 24 hrs earlier or if a second dose of oral anticoagulant has been administered (Grade 2C). In patients receiving low-dose warfarin therapy during epidural analgesia, we suggest that their INR be monitored on a daily basis (Grade 2C). Neurologic testing of sensory and motor function should be performed routinely during epidural analgesia for patients on warfarin therapy. To facilitate neurologic evaluation, we recommend that the type of analgesic solution be tailored to minimize the degree of sensory and motor blockade (Grade 1C). As thromboprophylaxis with warfarin is initiated, we suggest that neuraxial catheters should be removed when the INR is less than 1.5. This value was derived from studies correlating hemostasis with clotting factor activity levels greater than 40%. We suggest that neurologic assessment be continued for at least 24 hrs after catheter removal for these patients (Grade 2C). In patients with INR greater than 1.5 but less than 3, we recommend that removal of indwelling catheters should be done with caution and the medication record reviewed for other medications that may influence hemostasis that may not effect the INR (eg, NSAIDs, ASA, clopidogrel, ticlopidine, UFH, LMWH) (Grade 2C). We also recommend that neurologic status be assessed before catheter removal and continued until the INR has stabilized at the desired prophylaxis level (Grade 1C). In patients with an INR greater than 3, we recommend that the warfarin dose be held or reduced in patients with indwelling neuraxial catheters (Grade 1A). We can make no definitive recommendation regarding the management to facilitate removal of neuraxial catheters in patients with therapeutic levels of anticoagulation during neuraxial catheter infusion (Grade 2C). Antiplatelet Medications Anesthetic Management of the Patient Receiving Antiplatelet Medications Antiplatelet medications, including NSAIDs, thienopyridine derivatives (ticlopidine and clopidogrel) and platelet GP Ilb/IIIa antagonists (abciximab, eptifibatide, tirofiban) exert diverse effects on platelet function. The pharmacologic differences make it impossible to extrapolate between the groups of drugs regarding the practice of neuraxial techniques. There is no wholly accepted test, including the bleeding time, which will guide antiplatelet therapy. Careful preoperative assessment of the patient to identify alterations of health that might contribute to


bleeding is crucial. These conditions include a history of easy bruisability/excessive bleeding, female sex, and increased age. Nonsteroidal anti-inflammatory drugs seem to represent no added significant risk for the development of spinal hema-toma in patients having epidural or spinal anesthesia. Nonsteroidal anti-inflammatory drugs (including aspirin) do not create a level of risk that will interfere with the performance of neuraxial blocks. In patients receiving these medications, we do not identify specific concerns as to the timing of single-shot or catheter techniques in relationship to the dosing of NSAIDs, postoperative monitoring, or the timing of neuraxial catheter removal (Grade 1A). In patients receiving NSAIDS, we recommend against the performance of neuraxial techniques if the concurrent use of other medications affecting clotting mechanisms, such as oral anticoagulants, UFH, and LMWH, is anticipated in the early postoperative period because of the increased risk of bleeding complications. Cyclooxygenase-2 inhibitors have minimal effect on platelet function and should be considered in patients who require anti-inflammatory therapy in the presence of anticoagulation (Grade 2C). The actual risk of spinal hematoma with ticlopidine and clopidogrel and the GP Ilb/IIIa antagonists is unknown. Management is based on labeling precautions and the surgical, interventional cardiology/radiology experience (Grade 1C).

On the basis of labeling and surgical reviews, the suggested time interval between discontinuation of thienopyridine therapy and neuraxial blockade is 14 days for ticlopidine and 7 days for clopidogrel. If a neuraxial block is indicated between 5 and 7 days of discontinuation of clopidogrel, normalization of platelet function should be documented. Platelet inhibitors ( GP IIb/IIIa) exert a profound effect on platelet aggregation. After administration, the time to normal platelet aggregation is 24 to 48 hrs for abciximab and 4 to 8 hrs for eptifibatide and tirofiban. Neuraxial techniques should be avoided until platelet function has recovered. Although GP Ilb/IIIa antagonists are contraindicated within 4 weeks of surgery, should one be administered in the postoperative period (after a neuraxial technique), we recommend that the patient be carefully monitored neurologically.


New Anticoagulants Anesthetic Management of the Patient Receiving Fondaparinux The actual risk of spinal hematoma with fondaparinux is unknown. Consensus statements are based on the sustained and irreversible antithrombotic effect, early postoperative dosing, and the spinal hematoma reported during initial clinical trials. Close monitoring of the surgical literature for risk factors associated with surgical bleeding may be helpful in risk assessment and patient management. Until further clinical experience is available, performance of neuraxial techniques should occur under conditions used in clinical trials (single-needle pass, atraumatic needle placement, avoidance of indwelling neuraxial catheters). If this is not feasible, an alternate method of prophylaxis should be considered. Oral Direct Thrombin and Activated Factor Xa Inhibitors in Development There are two (oral) medications intended for use as thromboprophylaxis after total knee and/or hip replacement that are in phase 3 clinical trials in the United States (and already released for use in Canada and Europe). These anticoagulants, dabigatran etexilate and rivaroxaban, inhibit thrombin and factor Xa, respectively. Dabigatran Etexilate Dabigatran etexilate is a prodrug that specifically and reversibly inhibits both free and clot-bound thrombin. The drug is absorbed from the gastrointestinal tract with a bioavailability of 5%. Once absorbed, it is converted by esterases into its active metabolite, dabigatran. Plasma levels peak at 2 hrs. The half-life is 8 hrs after a single dose and up to 17 hrs after multiple doses. It is likely that once-daily dosing will be possible for some indications because of the prolonged halflife. Because 80% of the drug is excreted unchanged by the kidneys, it is contraindicated in patients with renal failure. Dabigatran etexilate prolongs the aPTT, but its effect is not linear and reaches a plateau at higher doses. However, the ecarin clotting time and thrombin time are particularly sensitive and display a linear dose-response at therapeutic concentrations. Reversal of anticoagulant effect is theoretically possible through administration of recombinant factor Vila, although this has not been attempted clinically. Rivaroxaban Rivaroxaban is a potent selective and reversible oral activated factor Xa inhibitor, with an oral bioavailability of 80%. Phase 3 clinical trials have been completed in the United States. Like dabigatran etexilate, it is approved for use in Canada and Europe for thromboprophylaxis after total hip or knee replacement. Rivaroxaban is generally administered once daily for thromboprophylaxis. After administration, the maximum inhibitory effect occurs 1 to 4 hrs; however, inhibition is maintained for 12 hrs. The antithrombotic effect may be monitored with the PT, aPTT, and Heptest, all of which demonstrate linear dose effects. Rivaroxaban is cleared by the kidneys and gut. The terminal elimination half-


life is 9 hrs in healthy volunteers and may be prolonged to 13 hrs in the elderly owing to a decline in renal function (hence a need for dose adjustment in patients with renal insufficiency and contraindicated in patients with severe liver disease). Overall, clinical trials comparing rivaroxaban (5-40 mg daily, with the first dose 6 to 8 hrs after surgery) with enoxaparin (40 mg, beginning 12 hrs before surgery) demonstrate similar rates of bleeding and a comparable efficacy. A recent comparison of once-daily rivaroxaban 10 mg with enoxaparin reported superiority with the rivaroxaban regimen (and the simplicity of oral administration). Although a "regional anesthetic" was performed in more than half of the patients included in the clinical trials, no information regarding needle placement or catheter management was included. Although there have been no reported spinal hematomas, the lack of information regarding the specifics of block performance and the prolonged half-life warrants a cautious approach.

Risk of thrombosis • Most common congenital clotting disorder in women • 70%-90% lifetime risk of thrombosis • 60% chance of thrombosis during pregnancy and 33% during the puerperium • 10%—15% during pregnancy and 20% during puerperium in heterozygous • Risk of thrombosis increased >100-fold if homozygous • Mutation rate varies among ethnic groups • 5% during pregnancy and 20% during puerperium • 5% during pregnancy and 20% puerperium • Protein S declines during normal pregnancy • Risk of thrombosis in asymptomatic pregnant carrier is 0.5% • Homozygosity carries a significant risk of thrombosis

Summary The decision to perform spinal or epidural anesthesia/analgesia and the timing of catheter removal in a patient receiving antithrombotic therapy should be made on an individual basis, weighing the small, although definite risk of spinal hematoma with the benefits of regional anesthesia for a specific patient. Alternative anesthetic and analgesic techniques exist for patients considered an unacceptable risk. The patient’s coagulation status should be optimized at the time of spinal or epidural needle/catheter placement, and the level of anticoagulation must be carefully monitored during the period of epidural catheterization. Indwelling catheters should not be removed in the presence of therapeutic anticoagulation because this seems to significantly increase the risk of spinal hematoma. It must also be remembered that identification of risk factors and establishment of guidelines will not completely eliminate the complication of spinal hematoma. Vigilance in monitoring is critical to allow early evaluation of neurologic dysfunction and prompt intervention. Protocols must be in place for urgent magnetic resonance imaging and


hematoma evacuation if there is a change in neurologic status.We must focus not only on the prevention of spinal hematoma but also on rapid diagnosis and treatment optimize neurologic outcome.

References 1 Eriksson BI, Quinlan DJ, Weitz JI. Comparative pharmacodynamics and pharmacokinetics of oral direct thrombin and factor Xa inhibitors in development. Clin Pharmacokinet. 2009;48:1Y22. 2 Kopp SL, Horlocker TT. Anticoagulation in pregnancy and neuraxial blocks. Anesthesiol Clin. 2008;26:1Y22, v. Regional Anesthesia and Pain Medicine & Volume 35, Number 1, January-February 2010 Neuraxial Anesthesia and Anticoagulation 3 Gogarten W. The influence of new antithrombotic drugs on regional anesthesia. Curr Opin Anaesthesiol. 2006;19:545Y550. 4 Kelly ME, Beavis RC, Hattingh S. Spontaneous spinal epidural hematoma during pregnancy. Can J Neurol Sci. 2005;32:361Y365. 5 Karabatsou K, Sinha A, Das K, Rainov NG. Nontraumatic spinal epidural hematoma associated with clopidogrel. Zentralbl Neurochir. 2006;67:210Y212. 6 Finsterer J, Seywald S, Stollberger C, et al. Recovery from acute paraplegia due to spontaneous spinal, epidural hematoma under minimal-dose acetyl-salicylic acid. Neurol Sci. 2008;29:271Y273. 7 Litz RJ, Gottschlich B, Stehr SN. Spinal epidural hematoma after spinal anesthesia in a patient treated with clopidogrel and enoxaparin. Anesthesiology. 2004;101:1467Y1470. 8 Wu CL, Perkins FM. Oral anticoagulant prophylaxis and epidural catheter removal. Reg Anesth. 1996;21:517Y524. 9 Wu CL, Perkins FM. Oral anticoagulant prophylaxis and epidural catheter removal. Reg Anesth. 1996;21:517Y524.


INTENSIVE CARE MANAGEMENT OF SEVERE TRAUMATIC BRAIN INJURED PATIENT Dr Venkatesh H.K Professor & HoD, BGS Global Hospitals, Bangalore

Traumatic brain injury is an important cause of death and disability in the civilian population. Mortality is as high as 30% in organized centers. Some of the neurologic injury that occurs at the moment of traumatic impact is irreversible. Over the past few decades advances in monitoring and intervention with better understanding has helped to reduce mortality and morbidity in severe traumatic brain injury (TBI) victims. Head injury is classified based on mechanism of injury, severity, pathology and CT scan findings. Closed head injuries form about 82% of all severe head injuries.1 A simple classification of head injury: primary injury and secondary injury. Primary injury occurs at the time of impact, which includes skull fractures and or intracranial lesions like epidural hematomas, subdural hematomas, intra cerebral hematomas and cerebral contusions. Based on severity of injury, head injury can be classified as: Mild (GCS 13-15), Moderate (GCS 9-12) and Severe (GCS < 8). Secondary injury results following the primary insult which refers to intracranial and systemic factors that cause ongoing and reversible or preventable injury. Hypotension, and hypoxia are systemic factors and raised intracranial pressure (ICP), seizures, expanding lesions and hyperthermia are the secondary factors that has been shown to influence the outcome.2 All neurological damage from severe TBI does not occur at the time of primary injury, but evolves over hours and days. Improved outcome has been observed when secondary insults are prevented or adequately treated. The trend in the reduction of mortality is the result of implementation of TBI guidelines that emphasize the importance of monitoring and resuscitation.3

Pathophysiology

For better management of the head injured, understanding pathophysiology is necessary.


Cerebral Blood Flow and Metabolism Normal cerebral blood flow is 45-55 ml/100g/min. Cerebral metabolic rate of oxygen (CMRO2) is 3.5-4.5 ml/100g/min. Disturbances of the cerebral circulation play an important role in the pathophysiology of head injury. Ischemia has been the single most important determinant of outcome.Cerebral metabolic rate Oxygen (CMRO2) is reduced by 50% in severe head injured patients (GCS < 8). Several factors have been implicated in the causation of the posttraumatic ischemia which include increased ICP, arterial hypotension, vasospasm and intracranial mass lesions. Mitochondrial dysfunction has also been postulated for ischemic injury. 4,5Martin et al.,6have described three distinct hemodynamic phases following head injury (fig.1). Phase I: Hypoperfusion (day 0), Phase II: Hyperemia (days 1-3) and Phase III: Delayed hypoperfusion (Vasospasm) (days 4-14). In a prospective study the lowest blood flows were observed on the day of injury (Day 0) and the highest CBF were documented on postinjury Days 1 to 5.7Thus, phase I requires maintenance of cerebral perfusion pressure (CPP), normal oxygenation and normal hematocrit. Hyperventilation is to be avoided during this phase.

Figure 1: The time course of posttraumatic CBF observed after severe head trauma. (Mean CBF values are represented). Autoregulation of cerebral blood flow


Cerebral blood flow is maintained constant between a MAP of 50-150 mm Hg (fig.2). Cerebral autoregulation is usually disturbed following head injury. CBF not only is impaired when associated with a high ICP or low Arterial blood pressure (ABP), but it can also be disturbed by too high a Cerebral perfusion pressure (CPP) (CPP = MAP â&#x20AC;&#x201C; ICP).8 Most studies have associated preservation of autoregulation with good outcome. It is necessary to maintain blood pressure in the autoregulatory range in these patients. The interaction between systemic pressure and cerebral dynamics will determine the cerebral perfusion. Hypotension and hypertension both aggravate brain perfusion and secondary injury.

Fig.2 Normal regulatory control of cerebral blood flow

Vascular response to carbon dioxide in head injured patients CBF changes by 3% for every mmHg change in PaCO2 between 20-80 mm Hg (fig.2). Hyperventilation causes vasoconstriction and reducing the CBF and thus ICP. Cerebral blood flow response to changes in PaCO2 is preserved following Traumatic brain injury (TBI).Absence of response to changes in PaCO2 carries poor prognosis and is indicative of vasomotor paralysis.


Intracranial pressure (ICP) ICP is elevated in as many as 72 % of the patients following head injury. The correlation between high ICP and a poorer outcome is well established by several groups.9The causes of raised ICP are brain edema, hyperemia, intracranial lesions such as hematomas, contusions.

Biochemical changes Following head injury, a wide range of biochemical and metabolic changes takes place. Detailed discussion of these is beyond the scope of this topic. However, in brief, these changes are: i) release of excitatory aminoacids â&#x20AC;&#x201C; Glutamate and aspartate

ii) intracellular calcium

accumulation iii) increased levels of free radicals which cause lipid peroxidation and cell destruction iv) cytokines v) apoptosis which is programmed cell death in the areas of secondary injury.

Intensive care management Primary considerations in the management of severe head injured patients are to maintain gas exchange, blood pressure, temperature, ICP, glucose and electrolytes. Every patient with severe head injury (GCS <8) should have definitive airway, maintain oxygenation, and optimal ventilation. The pathway for management is outlined below.

Severe Head Injury GCS < 8 Diagnostic Evaluation Trauma Evaluation Intubation Oxygenation Sedation Yes

Deterioration?

CT Scan Yes

ICU

ICP monitor and Treatment

Surgical Lesion

Evacuation


Initial resuscitation of the severe head injury patient Systemic effects in head injured patients

The systemic effects are diverse involving every system. The systemic effects are tabulated in table 1

Cardiovascular

Shock Arrhythmias Hypotension / hypertension Respiratory Airway obstruction Respiratory disturbances â&#x20AC;&#x201C; tachypnea, irregular breathing Aspiration Pneumonia Pulmonary edema Fluid and electrolyte disturbances Sodium disturbances â&#x20AC;&#x201C; hypo and hypernatremia Hyperglycemia Hematologic Coagulopathy Infection

Table. 1 Systemic effects following traumatic head injury

Monitoring The mainstay of neurologic monitoring is continuous assessment of GCS, pupillary reactivity, and hemodynamic status. Oxygenation, Central venous pressure, Invasive, blood pressure, Electrolytes and glucose, ICP, and

CPP

are routinely monitored.

Other

specialized

monitors

include

CBF and

electrophysiological studies are practiced in few centres.

Blood Pressure and Oxygenation Blood pressure management plays an important role in the outcome of these patients. Hypoxemia and hypotension are the two secondary factors which strongly predicts outcome.10Many studies


have confirmed that hypoxemia in patients with SHI following trauma is associated with higher mortality.11-13 Both prehospital and in-hospital hypotension have a deleterious influence on outcome from severe TBI.14Based on the current evidence, oxygen saturation should be maintained > 90% and SBP > 90 mm Hg. Aggressive attempts to maintain cerebral perfusion pressure (CPP) (CPP = MAP â&#x20AC;&#x201C; ICP) above 70 mm Hg with fluids and pressor should be avoided because of the risk of adult respiratory distress syndrome (ARDS). CPP of <50 mm Hg should be avoided. The CPP value to target lies within the range of 50â&#x20AC;&#x201C; 70mm Hg. Patients with intact pressure autoregulation tolerate higher CPP values. CPP of 60-70 mm Hg is recommended in TBI patients. Adequate intravascular volume and CVP of 6-8 mm Hg is ideal. Phenylephrine, Dopamine and or noradrenaline are used to maintain adequate CPP of 50-70 mm Hg. The effects of blood pressure and ICP on CPP are enumerated below (fig.3):


Fig.3 Vasodilator and vasoconstrictor cascade

Cerebral venous oxygen saturation (SjvO2) provides a global measure of balance between CBF and CMRO2. Normally, there exists a coupling between CBF and CMRO2. SjvO2 can be obtained by intermittent sampling of blood from the catheter placed in the jugular bulb or continuously using fibreoptic catheter. Normal range of SjvO2 is 55-75%,> 90% is considered as hyperemia and < 50% as ischemia or hypoperfusion. Episodes of desaturation are frequently associated with increased morbidity and mortality.15 Monitoring SjvO2 helps to optimize ventilation during raised ICP management without the risk of ischemia. Cerebral ischemia is one of the most important causes of secondary insults following acute brain injury. Monitoring brain tissue oxymetry not only allows the detection of impending cerebral


ischemia, but also be used as a "surrogate end point" to evaluate putative therapies, targeting therapy towards improved cerebral oxygenation. Brain tissue oxygenation correlates closely with outcome. 16-18 Patients treated with ‘PO2–guided therapy’ to maintain a PbrO2>25 mmHg had a lower mortality rate than a historical group of patients treated with ‘ICP/CPPguided therapy’ alone. Jugular venous saturation<50% or brain tissue oxygen tension <15 mm Hg are treatment thresholds.

Transcranial Doppler is a noninvasive monitoring modality for indirect measurement of CBF. Changes in the flow velocities reflect changes in the blood flow and thus aids in the management of head injured patients.

Intracranial Pressure (ICP) Intracranial pressure is increased in severe head injured patients. Monitoring ICP has helped in early recognition of expanding intracranial lesion and thus early intervention and treatment. Patients who had persistent elevation of ICP had poor outcome compared to patients whose ICP was controlled.19-20 Intracranial pressure (ICP) should be monitored in all salvageable patients with a severe traumatic brain injury (TBI; Glasgow Coma Scale [GCS] score of 3–8 after resuscitation) and an abnormal computed tomography (CT) scan. An abnormal CT scan of the head is one that reveals hematomas, contusions, swelling, herniation, or compressed basal cisterns. ICP monitoring is indicated in patients with severe TBI with a normal CT scan if two or more of the following features are noted at admission: age over 40 years, unilateral or bilateral motor posturing, or systolic blood pressure (BP) <90 mm Hg.

There are various devices for ICP monitoring: Ventricular catheter device Parenchymal devices Subdural bolts Intra parenchyma catheters


Treatment should be initiated with intracranial pressure (ICP) thresholds above 20 mm Hg.Management algorithm is outlined below Fig.4. A systematic multimodal approach to manage ICP has been found to be effective and improved outcome.

Hyperventilation Hyperventilation causes hypocapnia and results in vasoconstriction. This reduces the CBF and thus the ICP. The advantage of reduction in the ICP is offset by the risk of ischemia. Moderate hyperventilation may exacerbate pre-existing impairment of cerebral blood flow and metabolism in TBI patients and should be therefore carefully used under appropriate monitoring. Prophylactic hyperventilation (PaCO2 of 25 mm Hg or less) is not recommended. Hyperventilation is recommended as a temporizing measure for the reduction of elevated intracranial pressure (ICP). Hyperventilation should be avoided during the first 24 hours after injury when cerebral blood flow (CBF) is often critically reduced. If hyperventilation is used, jugular venous oxygen saturation(SjvO2) or brain tissue oxygen tension (PbrO2) measurements are recommended to monitor oxygen delivery.

Hyperosmolar therapy Currently Mannitol and hypertonic saline are used for the treatment of raised ICP.It has two distinct effects in the brain.14 1. One effect is an immediate plasma expandingeffect, which reduces the hematocrit, and thereby reduces bloodviscosity, increases CBF, and increases cerebral oxygendelivery. 2. The osmotic effect of mannitol is delayed for 15â&#x20AC;&#x201C;30min while gradients are established between plasmaand cells. Its effects persist for a variable period of90 min to 6h, depending upon the clinical conditions. Arterial hypotension, sepsis, nephrotoxic drugs, or preexisting renal disease place patients at increased risk for renal failure with hyperosmotictherapy. It has been observed that use of hypertonic saline (HTS) as small volume resuscitation fluid is useful in poly trauma patients with head injury. HTS is used as bolus or continuous infusion.21 The advantages of HTS over Mannitol is its hemodynamic stability, no rebound phenomenon and its efficacy in refractory intracranial hypertension. The dose for continuous infusion is 0.1 â&#x20AC;&#x201C; 1 ml/kg /h. serum sodium levels should be monitored at regular intervals.


Mannitolis usedin patients with signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial causes.

Analgesia and Sedation Sedative and analgesic agents are used routinely in the ICU to alleviate pain and agitation.All patients on ventilator should be well sedated as part of the ICP management protocol.

Fluid and Electrolyte Management Isotonic fluids like 0.9% saline, colloids are preferred. Lactated ringerâ&#x20AC;&#x2122;s solution with osmolarity of <270 mOsmol/l is avoided as this can increase cerebral edema. Daily maintenance volume of 2500 â&#x20AC;&#x201C; 3000ml/day sufficient to maintain CVP 6-8 mm Hg. The common metabolic disturbances observed are hyponatremia or hypernatremia and hyperglycemia. Hyperglycemia is frequently seen in head injured patients and persistent hyperglycemia has been associated with poor outcome. Blood sugar should be monitored frequently to maintain at < 150 mg/dl.

Hypothermia Hypothermia has been shown to be effective in the management of raised ICP in severe TBI. Pooled data indicate that prophylactic hypothermia is not significantly associated with decreased mortality when compared with normothermic controls.

Infection Fever following infection is of concern as this increases the metabolic requirement and CBF, thus ICP. Catheter-related bloodstream infections are associated with significant morbidity, mortality, and costs. Infection prophylaxis can be divided into several aspects of care, including external ventricular drainage (EVD) and other ICP monitoring devices, and prophylaxis to prevent nosocomial systemic infections. Peri-procedural antibiotics for intubation should be administered to reduce the incidence of pneumonia. Early tracheostomy should be performed to reduce mechanical ventilation days. However, it does not alter mortality or the rate of nosocomial pneumonia. Early extubation in qualified patients can be done without increased risk of pneumonia.


Deep Vein Thrombosis Prophylaxis Deep venous thrombosis is perhaps the single most significant preventable cause of morbidity and mortality in the neurosurgical patients and the incidence of DVT is approximately 25%.22The risk of developing deep venous thrombosis (DVT) in the absence of prophylaxis was estimated to be 20% after severe TBI. Mechanical devices to reduce the incidence of DVT in SHI patients have found to be effective though not to the extent of pharmacologic prophylaxis. Considering the risk of hematoma in these patients mechanical devices seems to be more appropriate in the initial period than anticoagulation prophylaxis. At present, use of graduated compression or IPC stockings placed for DVT prophylaxis for patients with severe TBI and use of prophylaxis with low-dose heparin or LMWH for prevention of DVT in patients with severe TBI is acceptable.

Nutrition Nuitrition is widely accepted as an important component in the management of critically ill patients. Patients who receive early nutritional support with good calorie intake have improved outcome.23 Calorie intake is achieved with 15-20% from proteins, 60-70 % carbohydrates and remaining with fats. The total calorie requirement is 140 % and 100% the BEE in non-paralysed and paralysed ventilated patients respectively. Vitamins, Minerals, should be supplemented. Zinc has been found to be one of the important supplements which improve visceral proteins.Patients should be fed to attain full caloric replacement by day 7 post-injury.

Antiseizure Prophylaxis Posttraumatic seizures (PTS) are classified as early, occurring within 7 days of injury (incidence of about 30 % in SHI and 1% in mild HI), or late, occurring after 7 days following injury (1013% after SHI).24It is desirable to prevent both early and late PTS. However, it is also desirable to avoid neurobehavioral and other side effects of medications, particularly if they are ineffective in preventing seizures. These risk factors for occurrence of post traumatic seizures (PTS) include the following: Glasgow Coma Scale (GCS) Score <10 Cortical contusion Depressed skull fracture


Subdural hematoma Epidural hematoma Intracerebral hematoma Penetrating head wound Seizure within 24 h of injury

A loading dose of 20 mg/kg of phenytoin sodium is administered followed by 5 mg/kg/d q8h. If administered for prophylaxis, to be tapered after 1 week.In penetrating injury, late onset PTS, prior h/o seizures, and following craniotomy, should be continued for a period of 6-12 m.

Steroids There is no role for steroids in SHI. Studies have shown that steroid treated group had higher mortality and morbidity compared to controls.25-26

Conclusion As in all areas of clinical medicine, the optimal plan of management for an individual patient may not fall exactly within the recommendations of these guidelines. This is because all patients, and in particular, neurotrauma patients, have heterogeneous injuries, and optimal management depends on a synthesis of the established knowledge based upon Guidelines, and then applied to the clinical findings in the individual patient, and refined by the clinical judgment of the treating physician.An increasing body of evidence shows that brain multimodality monitoring (BMM) â&#x20AC;&#x201C; including intracranial pressure, brain oxygen (PbtO2), cerebral microdialysis, regional cerebral blood flow and quantitative electroencephalography, helps ICU physicians to examine individual response to several routine therapeutic interventions in neurocritical care (e.g. hemodynamic augmentation, management ofcerebral perfusion pressure, blood transfusion, insulin therapy) and may improve the management of secondary brain injury.

Interested readers can refer to recent guidelines in the management of traumatic brain injury. www.braintrauma.org and pediatric guidelines @ PediatrCrit Care Med 2012 Vol. 13, No. 1 (Suppl.).


Insert ICP monitor

Maintain CPP > 70 mmHg

YES

Intracranial Hypertension ?*

NO

Ventricular drainage (if available)

YES

Reconsider repeating CT scan

YES

Intracranial Hypertension ?*

Carefully withdrawICP treatment

Hyperventilation to PaCO2 30-35 mm Hg

Intracranial Hypertension ?*

Mannitol (0.25-1 g/kg IV)

YES

NO

Intracranial Hypertension ?*

NO May repeat 3% saline if ICP refractory to treatment NO

YES

Surgical Decompressive therapy

High dose Barbiturate <30 mmHg â&#x20AC;&#x201C;

Hyperventilation to PaCO2Craniectomy

MonitoringSjO2, AVDO2, PbtiO2 and/or CBF recommended Second Tier Therapy

* Threshold of 20-25 mm Hg may be used. Other variables may be substituted in individual conditions.

Fig.4Critical pathway for treatment of intracranial hypertension in the severe head injury patients.


References: 1. Foulkes M, Eisenberg HM, Jane JA, et al: The traumatic coma data bank: design, methods, and baseline characteristics, J Neurosurg 1991; 75 (suppl): S8 2. Chesnut RM, Marshall LF, Klauber MR, et al: The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34: 216-222 3. Hesdorffer D, Ghajar J, Iacono L. Predictors of compliance with the evidence-based guidelines for traumatic brain injury care: a survey of United States trauma centers. J Trauma 2002; 52: 1202–1209 4. Verweij BH, Muizelaar JP, Vinas FC, et al. Impaired cerebral mitochondrial function after traumatic brain injury in humans. J Neurosurg 2000;93:815-820 5. Early Mitochondrial Dysfunction after Cortical Contusion Injury. Lesley K. Gilmer, Kelly N. Roberts, Kelly Joy, Patrick G. Sullivan, and Stephen W. Scheff.Journal of Neurotrauma. August 2009, 26(8): 1271-1280 6. Martin NA, Dobestein C, Alexander M, et al: Posttraumatic cerebral arterial spasm: transcranial Doppler ultrasound, cerebral blood flow, and angiographic findings. J Neurosurg 1992; 77: 583 7. Kelly DF, Martin NA, Kordestani R, et al. Cerebral blood flow as a predictor of outcome following traumatic brain injury. J Neurosurg. 1997 Apr;86(4):633-41 8. Czosnyka M, Smielewski P, Piechnik S, et al: Cerebral Autoregulation following head injury. J Neurosurg 2001; 95: 756-763 9. Saul TG, Ducker TB: Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. J Neurosurg 1982; 56: 498 10. Manley G, Knudson M, Morabito D, et al. Hypotension, hypoxia, and head injury: frequency, duration, and consequences. Arch Surg 2001;136:1118–1123 11. Struchen MA, Hannay HJ, Contant CF, et al. The relation between acute physiological variables and outcome on the Glasgow Outcome Scale and Disability Rating Scale following severe traumatic brain injury. J Neurotrauma 2001;18:115–125 12. Stochetti N, Furlan A, Volta F. Hypoxemia and arterial hypotension at the accident scene in head injury. J Trauma 1996;40:764–767 13. Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34:216–222


14. Muizelaar JP, Lutz HA, Becker DP. Effect of mannitol on ICP and CBF and correlation with pressure autoregulation in severely head injured patients. J. Neurosurg. 1984;61: 700–706 15. Gopinath SP, Roberson CS, Contant CF, et al. Jugular venous desaturation and outcome after head injury. J NeurolNeurosurg Psychiatry 1994;5:717-23 16. Mazzeo AT, Bullock R. Monitoring brain tissue oxymetry: will it change management of critically ill neurologic patients? J Neurol Sci. 2007;261(1-2):1-9 17. Meixensberger J, Renner C, Simanowski R, Schmidtke A, Dings J, Roosen K. Influence of cerebral oxygenation following severe head injury on neuropsychological testing. Neurol Res 2004; 26:414–417 18. Stiefel MF, Spiotta A, Gracias VH, et al. Reduced mortality rate in patients with severe traumatic brain injury treated with brain tissue oxygen monitoring. J Neurosurg 2005; 103:805–811 19. Howells T, Elf K, Jones P et al. Pressure reactivity as a guide in the treatment of cerebral perfusion pressure in patients with brain trauma. J Neurosurg 2005;102:311–317 20. Lane PL, Skoretz TG, Doig G, et al. Intracranial pressure monitoring and outcomes after traumatic brain injury. Can J Surg 2000;43:442–448 21. Battison C, Andrews PJ, Graham C, et al. Randomized, controlled trial of the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury. Crit. Care Med. 2005;33: 196–202 22. Agnelli G, Piovella F, Buoncristiani P, et al: Enoxaparin plus compression stockings compared

with

compression

stockings

alone

in

the

prevention

of

venous

thromboembolism after elective neurosurgery. N Engl J Med 1998; 339:80–85 23. Young B, Ott L, Twyman D, et al. The effect of nutritional support on outcome from severe head injury. J Neurosurgery 1987; 67:668-676 24. Yablon SA: Posttraumatic seizures. Arch Phys Med Rehabil 1993;74:983–1001 25. Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10,008 adults with clinically significant head injury (MRC CRASH trial): randomized placebo controlled trial. Lancet 2004;364:1321–1328. 25 26. Watson NF, Barber JK, Doherty MJ, et al. Does Glucocorticoid administration prevent late seizures after head injury? Epilepsia 2004;45:690–694


IS THERE A ROLE FOR DOPAMINE OR DIURETICS IN ACUTE RENAL FAILURE Dr Akkamahadevi.P Professor of Anaesthesiology, JSS Medical College, Mysore.

Edwin Wou et al in 2002 said that role of dopamine in renal dysfunction was more a fiction than science. Daryl Jones in 2005 thought renal dose of dopamine began as hypothesis, became a paradigm, a dogma later, a myth and finally a superstition. Likewise the benefit of using diuretics for treating acute renal failure is also being questioned.

What is acute renal failure (ARF)? There is no consensus in the definition of Acute Rena Failure. There more than 30 different definitions. It can be defined as 

Sudden inability of the kidneys to vary urine volume and content appropriately in response to homeostatic needs.

There is an increase in blood urea nitrogen (40mg/dl or higher) or a sustained rise in serum creatinine.

There are 3 major types of ARF. Prerenal failure which is due to acute circulatory problem, is reversible if circulatory status improves. The renal cause may be due to primary or secondary renal disease, toxins and pigment. It is a serious pathology and requires vigorous treatment. Post renal failure is due to obstruction of urinary tract and can be treated by early removal of obstruction. It is the oliguric phase of acute renal failure due to renal cause where the physician thinks of using a diuretic or dopamine which is supposed to result in enhanced renal effects. Dopamine is a Neurotransmitter in both Central and Peripheral Nervous system, described by Barger and Dale in 1910. It is a catecholamine with dose dependent effect. α receptor stimulation at higher doses(10-20µg/kg/min) causes systemic vasoconstriction, β receptor stimulation at lesser dose (5-10µg/kg/min) increases cardiac index and Dopamine receptor stimulation at low dose (< 5µg/kg/min) causes renal vasodilatation. Dopamine receptors are present along the


nephron, maximum in proximal tubules. D 1 family receptor stimulation causes vasodilation as suggested by Gurd in 1937. This theory is in practice for last several decades.

Low dose Dopamine: The dosage of dopamine less than 5µg/kg/min, which stimulates the D1 receptor and causes vasodilation, is the “renal dose” or “low dose” dopamine. The perceived useful effects of low dose dopamine in preventing and treating ARF are Increased cardiac output  Natriuresis through enhanced renal perfusion  Decreased tubular metabolic activity  Diuresis Because of these properties Dopamine has been used to improve and treat acute oliguric renal 

failure in various clinical conditions. It is supposed to be useful prophylactically to preserve renal function following Cardiac and vascular surgeries, liver transplantation, Contrast induced nephropathy and high risk groups like hypertension, diabetes and left ventricular dysfunction.

But the BEST EVIDENCE says that Renal dose dopamine is not useful to treat or prevent ARF. Meta analysis by Kellum JA et al and Jan O Friedrich et al showed that Dopamine had no effect in preventing mortality or need for renal replacement. On the contrary, it caused adverse events like arrhythmias, myocardial, limb and skin ischaemia. They recommended that low dose dopamine should be eliminated from routine clinical use. The same is supported by many authors.

The reasons for the inefficacy are 

Etiology is multifactorial, contribution of hypovolemia and decreased renal perfusion is unknown

Interindividual variation in the pharmacokinetics, poor correlation between blood levels and administered dose

Complexity of dopamine action, overlap of doses during infusion

Increased plasma renin activity

Tolerance to prolonged use, 2 to 48 hrs, desensitises receptors

Increases medullary oxygen demand in the distal tubular cells leading to risk of ischemia


Bad effects of low dose dopamine

The low dose of Dopamine is not only ineffective but also harmful. 

Sepsis needs fluid resuscitation, diuresis harms by removing the fluid

Worsens splanchnic mucosal ischemia GI ischemia - translocation of endotoxin and microorganism into portal circulation Hepatic ischemia- increases production and decreased clearance of pro inflammatory cytokines. There is sepsis and multiple organ failure

Harms endocrine system. The hypophysiotropic property may suppress the circulatory concentration of all anterior pituitary hormones except cortisol.

Affects immunological system, suppresses T-lymphocyte function

Blunts the ventilatory drive

High plasma level accentuates α and β agonist action causing arrhythmias, myocardial, limb and cutaneous ischemia

Diuretics: Diuretics like furosemide and mannitol were also used in combination with low dose dopamine to prevent and treat ARF. Assumed benefit in ARF 

Convert oliguric state to non oliguric state (false assumption of improved renal function)

Improves intrarenal circulation by vasodilation.

Plasma expansion by increasing ventricular preload, cardiac output, renal blood flow, glomerular hydrostatic pressure and glomerular filtration rate.

Washing out of luminal debris and proteinacious material

Mannitol also decrease in renin release

Increments of urine volume ameliorate the dangers of congestive heart failure due to intravenous fluid therapy.

Reduces the effect of hydroxyl and other free radicals and protects against ischemia reperfusion injury


But yet again the best evidence says that diuretics in ARF are not proved beneficial and are over prescribed to oliguric patients without any material benefit. Mehta et al cohort study showed that patients with high dose diuretics had higher odds of death or non recovery. John Kellum et al review says that diuretics neither reduce the need for renal replacement therapy or dialysis nor reduces hospital mortality.

HARMFUL EFFECTS OF DIURETICS 

Direct toxic effects due to high dose causing intrarenal vasoconstriction

Initial extra cellular fluid expansion causing pulmonary edema( mannitol), later, depletion of volume may cause further hypovolemia

Temporary deafness and tinnitus (loop diuretics)

Electrolyte disturbance

Indirect ill effects by delaying the initiation of dialysis

Scientific Evidence shows that the role of low dose dopamine or diuretics in preventing or treating ARF is a fiction. Ravindra Mehta warns the physicians to be aware that even small changes in the kidney function can have deleterious effects. They need to recognize it early and consider immediate dialysis as the first treatment of choice. HAEMODIALYSIS is the only answer in an established case of ARF due to a renal cause. However to those who are still skeptical, “The obscure we see eventually, the obvious takes a little longer.’ -FR Murrow References: 1. Ho KM, Power BM: Benefits and risks of furosemide in acute kidney injury. Anaesthesia 65: 283–293, 2010 2. Agarwal RC, Jain RK, Yadava A. Prevention of Perioperative Renal Failure. Indian J Anaesth 2008;52:38 3. Anil K Saxena. “Dopamine – Renal Dose” – Does it really exist?. American College Of Chest Physicians, 2008 4. Friedrich JO, Adhikari N, Herridge MS, Beyene J. Meta-analysis: low-dose dopamine increases urine output but does not prevent renal dysfunction or death. Ann Intern Med 2005;142:510-24. 5. Jones D, Bellomo R (2005) Renal-dose dopamine: from hypothesis to paradigm to dogma to myth and, finally, superstition? J Intensive Care Med 20: 199–211. 6. E.B.C. Woo et al. / European Journal of Cardio-thoracic Surgery 22 (2002) 106–111


7. Mehta RL, Pascual MT, Soroko S, et al. Diuretics, mortality and nonrecovery of renal function in ARF. J Am Med Ass 2002; 288:2547-2553. 8. Lameire N et al. Loop diuretics for patients with acute renal failure: Helpful or harmful?JAMA 2002 Nov 27: 288: 2599-601 9. Kellum JA, Decker M, Janine RN. Use of dopamine in ARF: A Meta-analysis. Crit Care Med 2001; 29:1526-1531.


VIDEO SESSIONS


LOWER EXTREMITY PERIPHERAL NERVE BLOCKS Dr. J.Balavenkatasubramanian, Senior Consultant Anaesthesiologist, Ganga Medical Centre & Hospital, Coimbatore, India.

Introduction The last couple of decades has seen resurgence of Regional Anaesthesia. It is becoming increasingly evident that Regional Anaesthesia offers enormous benefit to the patient in the perioperative period. This resurgence has led to tremendous advancements in laboratory and clinical research. These has led to enhancement of success rates in the peripheral blocks and an enhanced safety profile.

The upper extremity blocks are extremely useful as sole anaesthetic

technique. However the lower extremity blocks are more useful for providing excellent analgesia and at times for anaesthesia. Lowerâ&#x20AC;?Extremity Peripheral Nerve Anatomy Lowerâ&#x20AC;?extremity PNB requires a thorough understanding of the neuroanatomy of the lumbosacral plexus. Anatomically, the lumbosacral plexus consists of 2 distinct entities: the lumbar plexus and the sacral plexus. There is some communication between these plexi via the lumbosacral trunk, but for functional purposes these are distinct entities. The lumbosacral plexus arises from at least 8 spinal nerve roots, each of which contains anterior and posterior divisions that innervate the embryologic ventral or dorsal portions of the limb. With the exception of a small cutaneous portion of the buttock (which is supplied by upper lumbar and sacral segmental nerves), the innervation of the lower extremity is entirely through branches of the lumbosacral plexus. The nerves to the muscles of the anterior and medial thigh are from the lumbar plexus. The muscles of the buttocks, the posterior muscles in the thigh, and all the muscles below the knee are supplied by the sacral plexus. There are a multitude of approaches to each peripheral nerve block described for the lower extremity.


Lumbar Plexus Anatomy The lumbar plexus is formed within the psoas muscle from the anterior rami . The branches of this plexus, the iliohypogastric, ilioinguinal, genitofemoral, lateral femoral cutaneous, and femoral and obturator nerves emerge from the psoas laterally, medially, and anteriorly . Of these, the femoral, lateral femoral cutaneous, and obturator nerves are most important for lower窶親xtremity surgery. Femoral Nerve The femoral nerve is formed by the dorsal divisions of the anterior rami of the second, third, and fourth lumbar nerves. The femoral nerve emerges from the psoas muscle in a fascial compartment between the psoas and iliacus muscles, in which it gives off articular branches to the hip. It enters the thigh posterior to the inguinal ligament. There it lies lateral and posterior to the femoral artery. This relationship to the femoral artery exists near the inguinal ligament, but not after the nerve enters the thigh. As the nerve passes into the thigh, it divides into an anterior and a posterior division and quickly arborizes . At the level of the inguinal ligament, there are dense fascial planes, the fascia lata, and fascia iliaca. The femoral nerve is situated deep to these fascial planes. The femoral artery, vein, and lymphatics reside in a separate fascial compartment medial to the nerve. The anterior division of the femoral nerve gives off the medial and intermediate cutaneous nerves that supply the skin of the medial and anterior surfaces of the thigh. The muscular branches of the anterior division of the femoral nerve supply the sartorius muscle and the pectineus muscle and articular branches to the hip. The posterior division of the femoral nerve gives off the saphenous nerve, which is the largest cutaneous branch of the femoral nerve, and the muscular branches to the quadriceps muscle and articular branches to the knee. The terminal nerves of the posterior division of the femoral nerve, the saphenous and the vastus medialis nerves, continue distally through the adductor canal. After leaving the adductor canal, the saphenous nerve emerges from behind the sartorius muscle, in which it gives off an infrapatellar branch and then continues distally to supply the cutaneous innervation of the anteromedial lower leg down to the medial aspect of the foot.


Obturator Nerve The obturator nerve is a branch of the lumbar plexus formed within the substance of the psoas muscle from the anterior division of the second, third, and fourth lumbar nerves. It is the nerve of the adductor compartment of the thigh, which it reaches by piercing the medial border of the psoas and passing straight along the sidewall of the pelvis to the obturator foramen. After entering the thigh through the obturator groove, the nerve divides into an anterior and posterior division. The anterior division has three branches including the muscular branches to the adductor muscles, an articular branch to the hip joint, and a cutaneous branch to the medial side of the thigh. The posterior division of the obturator nerve descends with the femoral and popliteal artery to the knee joint, and forms 2 branches: a muscular branch to the external obturator and adductor magnus muscles and an articular branch to the knee. The divergence of the obturator nerve from the femoral nerve begins as they emerge from the substance of the psoas muscle. At the level of the inguinal ligament, the obturator nerve lies deep and medial relative to the femoral nerve and is separated from it by several fascial compartments. This separation at the level of the inguinal ligament is obvious in anatomic dissections and has also been shown both radiographically with contrast and by magnetic resonance image.

Lateral Femoral Cutaneous Nerve The lateral femoral cutaneous nerve is formed by union of fibers from the posterior division of the anterior primary rami of L2 and L3. It emerges from the lateral border of psoas major below the iliolumbar ligament, passing around the iliac fossa on the surface of the iliacus muscle deep to the iliac fascia. Above the inguinal ligament, it slopes forward and lies inside the fibrous tissue of the iliac fascia. It perforates the inguinal ligament approximately 1 cm from the anterior superior iliac spine from where it enters the thigh. The lateral femoral cutaneous nerve supplies the parietal peritoneum of the iliac fascia and the skin over a widely variable aspect of the lateral and anterior thigh. It has no motor innervation.


Sacral Plexus Anatomy The sacral plexus is formed within the pelvis by the merger of the ventral rami of the fourth and fifth lumbar and the first 3 or 4 sacral nerves. The fourth and fifth lumbar ventral rami are common to both the lumbar and the sacral plexus and the lumbosacral trunk. Of the 12 branches of the sacral plexus, 5 are distributed within the pelvis and the other 7 emerge from the pelvis to distribute to the buttock and the lower extremity. The sacral plexus provides motor and sensory innervation to portions of the entire lower extremity including the hip, knee, and ankle. The most important components of the sacral plexus for lowerâ&#x20AC;?extremity surgery are the sciatic and the posterior cutaneous nerves and their terminal branches. Sciatic Nerve The lumbosacral trunk (L4â&#x20AC;?L5) and anterior divisions of the sacral plexus (S1â&#x20AC;?S3) merge to form the tibial nerve, whereas the posterior divisions merge to form the common peroneal nerve. These 2 large mixed nerves of the sacral plexus are initially bound together by connective tissue to form the sciatic nerve. At this level, the tibial component is medial and anterior, whereas the common peroneal component is lateral and slightly posterior . The superior gluteal artery is immediately superior and medial to the sciatic nerve at the level of the piriformis. Doppler identification of the superior gluteal artery has been used to help identify appropriate needle insertion site during sciatic nerve block. The sciatic nerve exits the pelvis via the greater sciatic notch below the piriformis muscle. At this level, it lies lateral and posterior to the ischial spine. As it enters the thigh and descends toward the popliteal fossa, it is posterior to the lesser trochanter of the femur, on the posterior surface of the adductor magnus muscle within the posterior medial thigh compartment deep to biceps femoris. There is no artery after a similar course because the chief blood supply to the thigh is through the anterior femoral artery. The popliteal artery and vein, the continuation of the femoral artery and vein, reach the popliteal fossa by passing through the adductor hiatus and continue downward with the artery anterior to the vein. In the upper part of the popliteal fossa, the sciatic nerve lies posterolateral to the popliteal vessels. Specifically, the popliteal vein is medial to the nerve, whereas the popliteal artery is anterior, lying on the popliteal surface of the femur . The sciatic nerve usually divides into its component nerves, the tibial and common peroneal nerves, at the upper aspect of the popliteal fossa.


Tibial Nerve In the popliteal fossa, the tibial nerve lies posterior and lateral to the popliteal vessels . In the lower part of the fossa, it sends branches to the major ankle plantar flexors, the gastrocnemius, and soleus muscles. The tibial nerve then courses on the posterior surface of the tibialis posterior muscle, along with the posterior tibial vessels. At the ankle, the nerve and vessels enter a compartment beneath the flexor retinaculum . As it passes to the plantar aspect of the foot, it gives off the lateral and medial plantar nerves. Of the digital nerves, those to the medial 3ツス toes are supplied by the medial plantar nerve, whereas those of the lateral 1ツス toes are supplied by the lateral plantar nerve

Peroneal Nerve The common peroneal nerve diverges laterally leaving the popliteal fossa by crossing the lateral head of the gastrocnemius. It lies subcutaneously just behind the fibular head, in which it can be easily traumatized. As it rounds the neck of the fibula, the common peroneal nerve divides into its terminal branches, the deep peroneal nerve and the superficial peroneal nerve. The deep peroneal nerve continues distally, accompanied by the anterior tibial artery, on the interosseus membrane. Nerve and artery emerge on the dorsum of the foot between the extensor hallucis longus and tibialis anterior. At this level, the deep peroneal nerve is lateral to the dorsalis pedis artery. The deep peroneal nerve innervates the extensor (dorsiflexor) muscles of the foot and the first webspace. The superficial peroneal nerve descends in the lateral compartment, between the peroneus longus and brevis muscles. After supplying these ankle evertors innervates, it emerges between them to innervate the skin of the lower leg and foot. Posterior Femoral Cutaneous Nerve The posterior femoral cutaneous nerve is a purely sensory nerve derived from the anterior rami of S1窶心3.14 It travels with the sciatic nerve out of the pelvis and into the upper thigh. While deep to the gluteus maximus, it gives off the inferior clunial nerves (sensory nerves to the lower buttock) and perineal branches (sensory to the external genitalia). It emerges from the lower edge of the gluteus maximus to lie in subcutaneous tissue and continues down the posterior aspect of the thigh and the leg giving off, in succession, femoral and sural branches (sensory branches to


the back of the thigh and the calf). It becomes superficial near the popliteal fossa where its terminal branches often anastomose with the sural nerve.

Sural Nerve The medial and lateral sural nerves are pure sensory nerves derived from the tibial and common peroneal nerves, respectively, at the level of the knee joint. Together, they supply the posterolateral aspect of the leg and ankle and the dorsal surface of the foot.

Approaches to the Lower Extremity

Nerve Blocks of the Lumbar Plexus: Psoas Compartment Block The psoas compartment block was first described by Chayen et al.15 in 1976. It can be performed as a singleâ&#x20AC;?injection technique or with a catheter placed for prolonged analgesia. It has been used to provide anesthesia for thigh surgery. In combination with parasacral nerve block, it has been used for hip fracture repair. It is successfully used for analgesia after total hip arthroplasty (THA) or total knee arthroplasty (TKA) It has also been used in the treatment of chronic hip pain. The psoas compartment block is a deep block of the lumbar plexus from a posterior approach. Traversing from posterior to anterior at the level of L4â&#x20AC;?L5, the following structures would be encountered: posterior lumbar fascia, paraspinous muscles, anterior lumbar fascia, quadratus lumborum, and the psoas muscle. The common iliac artery and vein are situated anterior to the psoas muscle, which is inside a fascial sheath, the psoas compartment . Because the final positioning of the needle is within the body of the psoas muscle through which the lumbar plexus traverses, it is thought to be the most consistent approach to block the entire lumbar plexus with a single injection. It is useful for providing consistent anesthesia in the distributions of the femoral, lateral femoral cutaneous, and the obturator nerves

Several descriptions of the needle entry site for the psoas compartment blocks have been described. All rely on bony contact with the transverse process as a guide to depth of needle


placement. They estimated the distance from the skin to the lumbar plexus to be 8.35 cm in men (range 6.1â&#x20AC;?10.1 cm) and 7.1 cm in women (range 5.7â&#x20AC;? 9.3 cm). The depth of the lumbar plexus correlated with gender and body mass index. Importantly, the distance from the transverse process to the lumbar plexus was extremely consistent at a distance of less than 2 cm. This relationship of transverse process to the lumbar plexus was independent of body mass index or gender. Thus, contact with the transverse process provides a consistent landmark to avoid excessive needle penetration during psoas compartment block.

The depth of needle insertion is emphasized because of the complications associated with excessive needle depth including renal hematoma, pneumocele, total spinal anesthesia, and unintended intraâ&#x20AC;?abdominal, and intervertebral disk catheter placement. To ensure the proper position of the needle during psoas compartment block and avoid excessive needle insertion, it is highly recommended that the transverse process be intentionally sought. Epidural spread of local anesthetic is another common side effect of psoas compartment block, occurring in 9% to 16% of adult patients. This side effect is usually attributed to retrograde diffusion of the local anesthetic to the epidural space when large volumes of local anesthetic are used (greater than 20 mL). In most cases, there is residual lumbar plexus blockade apparent after the resolution of the contralateral block. However, there are case reports of total spinal anesthesia occurring during lumbar plexus blockade and vigilance must be maintained during the management of this block.

Continuous Psoas Compartment Blocks Continuous techniques have been described to provide analgesia after a variety of operations including THA, TKA, open reduction and internal fixation of acetabular fractures, open reduction and internal fixation of femur fractures, and anterior cruciate ligament reconstruction. Interest in this block developed as practitioners sought alternatives to neuraxial techniques that could provide consistent analgesia after hip, femur, and knee surgery. One theoretical advantage of psoas compartment block over other continuous approaches to the lumbar plexus is the decreased likelihood of catheter dislodgement because of the large muscle mass that must be traversed to reach the lumbar plexus. The muscle mass anchors the catheter.


Femoral Nerve Block Indications for single‐injection femoral nerve block include anesthesia for knee arthroscopy in combination with intra‐articular local anesthesia and analgesia for femoral shaft fractures, anterior cruciate ligament reconstruction (ACL), and TKA as a part of multimodal regimens.Their use in complex knee operations is associated with lower pain scores and fewer hospital admissions after same‐day surgery. The femoral nerve divides into the posterior and anterior divisions shortly after it emerges from under the inguinal ligament and undergoes extensive arborization. Commonly, the anterior branch of the femoral nerve will be identified first. Vloka et al. reported this to be the first motor response elicited 97% of the time. Stimulation of this branch leads to contraction of the sartorius muscle on the medial aspect of the thigh and should not be accepted, as the articular and muscular branches derive from the posterior branch of the femoral nerve. The needle should be redirected slightly laterally and with a deeper direction to encounter the posterior branch of the femoral nerve. Stimulation of this branch is identified by patellar ascension as the quadriceps contract.

Defining the 3‐in‐1 Block During femoral nerve block, it has been advocated to use a higher volume of local anesthetic and apply firm pressure just distal to the needle during and a few minutes after injection to block the femoral, lateral femoral cutaneous, and obturator nerves, the so‐named “3‐in‐1 block. However, despite many efforts to consistently produce a 3‐in‐1 block, the effectiveness of these maneuvers has not been shown. In most reports, the femoral nerve is the only nerve consistently blocked with this approach.Blockade of the lateral femoral cutaneous nerve occurs through lateral diffusion of local anesthetic and not through proximal spread to the lumbar plexus.8 The obturator nerve is less frequently anesthetized during 3‐in‐1 block than the lateral femoral cutaneous (LFC), which is not surprising given the number of fascial barriers between these structures at the level of the inguinal ligament. Despite the lack of scientific support for the term 3‐in‐1, many authors still continue to refer to the anterior femoral nerve block as a 3‐in‐1 block. Within this text, we will refer to this approach as a femoral nerve block.


Continuous Femoral Nerve Block Continuous femoral nerve block has been shown to improve outcome after major knee and vascular surgery of the lower extremity compared with intravenous narcotic therapy or continuous infusion or injection of analgesics. It provides equivalent analgesia with fewer side effects than epidural analgesia The role of stimulating versus nonstimulating catheters for continuous peripheral nerve blocks to improve success rate is an active area of research at this time.

Fascia Iliacus Block Dalens et al. originally described the fascia iliacus block in children. The indications for its use are the same as those for single‐injection femoral nerve block. Advocates believe its utility lies in the double pop technique for applying this block. The double pop refers to the sensation felt as the needle traverses the fascia lata then the fascia iliaca . Penetration of both layers of fascia is important for successful fascia iliacus blockade. To facilitate the appreciation of the “clicks” or “pops,” the use of a short bevel or pencil tipped needle has been advocated to provide more tactile feedback than cutting needles. This technique does not employ the use of a nerve stimulator. Although transient femoral neuropathy has been reported after fascia iliacus block, this appears to be a rare occurrence. The needle entry site for the fascia iliacus block is determined by drawing a line between the pubic tubercle and the anterior superior iliac crest and dividing this line into thirds. The needle entry point is 1 cm caudal to the intersection of the medial two thirds and lateral one third along this line. This site is well away from the femoral artery, making this useful for patients in whom femoral artery puncture is contraindicated.

Continuous Fascia Iliacus Blocks Continuous fascia iliacus blocks have been described for analgesia after femur fracture and repair, femoral elongation procedures, skin graft harvesting, ligamentous knee reconstruction, and TKA. Much like femoral continuous catheters, the degree of analgesia seems to be highly correlated with the final position of the catheter.


Obturator Nerve Block Indications for a single窶進njection obturator nerve block are generally limited to diagnostic indications or therapeutic relaxation of the adductor muscles of the thigh. Despite the significant amount of literature that has been devoted to anesthetic sparing of this nerve with many approaches to the lumbar plexus, only 2 studies have examined the effect of the addition of an obturator nerve block to improve analgesia after major knee surgery. Both studies reported a decrease in opioid consumption and pain scores in patients undergoing TKA receiving obturator nerve block in addition to a femoral or femoral and sciatic nerve block.

LFC Nerve Block The LFC nerve of the thigh is a purely sensory nerve that supplies a large but variable area from the inguinal ligament to the knee on the lateral aspect of the thigh. LFC nerve block is most commonly used as the sole anesthetic during diagnostic muscle biopsy and harvesting of split thickness skin grafts. It has also been used to provide analgesia in elderly patients undergoing hip fracture repair. However, in a study comparing LFC nerve block, femoral nerve block, and patients receiving no block following femoral neck repair, LFC nerve block was not as effective at controlling postoperative pain as femoral nerve block. Typically, this block is done as a fan technique with variable success. Whether this is because of variability in the distribution of innervation or to poorly localizing the nerve is not known.

Saphenous Nerve Block The saphenous nerve follows the saphenous vein to the medial malleolus and supplies the cutaneous area of the medial aspect of the calf and foot to the level of the midfoot. The saphenous nerve block is often combined with a sciatic block to provide anesthesia and analgesia for surgery involving the medial aspect of the lower leg and foot. The saphenous nerve is a purely sensory nerve and does not contribute to the bony innervation of the foot. Approaches to the saphenous nerve along its entire course, from the adductor canal to the ankle, have been described. Success rates vary widely between techniques. For example, successful block is reported in 33% to 65% of cases with a field infiltration performed medially at the level of the


tibial plateau, 70% to 80% of cases with the trans sartorial approach, 95% to 100% of cases with femoral paracondylar approach and near 100% of cases with the paravenous approach.

Continuous Psoas Compartment Blocks Versus Epidural Analgesia Advantages of continuous psoas compartment block compared with epidural block include unilateral analgesia and motor block, lack of impairment of bladder function, and improved risk/benefit ratio in patients anticoagulated after surgery. These advantages must be weighed against the disadvantages of incomplete blockade for anesthesia and the need for supplementation in a balanced analgesic regimen for effective analgesia.

Nerve Blocks of the Sacral Plexus Parasacral Block The parasacral nerve block (PSNB) described by Mansour76 in 1993 has been described as more than an isolated sciatic nerve block. It has been used to provide analgesia following major foot and ankle reconstruction. Parasacral block will consistently block both components of the sciatic nerve and the posterior cutaneous nerve of the thigh. Spread of local anesthetic may also anesthetize other branches of the sacral plexus including the superior and inferior gluteal and pudendal nerves. The pelvic splanchnic nerves (S2窶心4), the terminal portion of the sympathetic trunk, the inferior hypogastric plexus, and the obturator nerve all lie in close proximity to the elements of the sacral plexus and may all be anesthetized with this approach. For procedures about the knee, this may provide an advantage over more distal approaches to the sciatic nerve. For procedures below the knee, the adductor weakness from the obturator and superior gluteal nerve block may actually be disadvantageous for mobilization of the patient. The sympathetic nerve supply to the bladder is also in close proximity but problems with voiding and the need for bladder catheterization after PSNB have not been reported. A notable difference from other approaches to the sciatic nerve is the type of muscle response deemed acceptable as an endpoint for injection. Mansour76 described contraction of the hamstring muscles (biceps femoris, semitendinous) above the knee as the endpoint for PSNB with most consistent success.


Sciatic Nerve Block: at the Level of the Gluteus Maximus The sciatic nerve, the largest nerve derived from the sacral plexus, innervates the posterior thigh and almost the entire leg below the knee. The most common indications for sciatic nerve block are anesthesia and analgesia for foot and ankle surgery. There are a variety of approaches to the sciatic nerve block and their success rate is widely variable, ranging from 33% to 95%. Gaston Labat83 first described, at the beginning of the 20th century, the sciatic nerve block that is now referred to as the Classic Approach of Labat. This approach is based on the bony relationship of the posterior superior iliac spine and the greater trochanter with the patient positioned in a modified Sims position. Winnie was the first to modify the original description, adding in an additional landmark, the sacral hiatus to greater trochanter distance, to more precisely account for varying body habituses. Difficulty identifying these landmarks led Chang and colleagues84 to describe a transrectal method of identifying the ischial spine. Franco described a simple approach to the sciatic nerve block in the prone position. The needle entry site is perpendicular to the floor 10‐cm lateral from the middle of the intragluteal sulcus regardless of the patient's gender or body mass index. The sciatic nerve was found by trainees in ≤3 passes in 85% of the cases reported. Whether the success of this simple approach will be replicated in a larger sample size remains to be seen.

Subgluteal Approaches to the Sciatic Nerve Raj et al.described a supine approach to the sciatic nerve in the flexed hip position, initiating the block at the midpoint between the greater trochanter of the femur and the ischial tuberosity. The positioning of the patient was thought to be advantageous compared to the classic approach of Labat by “thinning the gluteus maximus muscles, making the sciatic nerve more superficial.” However, identifying these bony landmarks in very obese patients is sometimes difficult and the patient position requires additional personnel to maintain.

A lateral subgluteal approach to the sciatic nerve using the greater trochanter of the femur as a landmark was first described by Ichniyanagi in 1959.86 Other investigators have described a high success rate using this high lateral approach with a slightly more caudal entry point. Notably, when using this approach the success rate of the blockade of the posterior cutaneous nerve of the thigh was 83%. Although theoretically the posterior cutaneous nerve should reliably


be blocked in most proximal approaches to the sciatic nerve, the success rate of blockade is not usually reported. The anterior approach to the sciatic nerve has the appeal of supine positioning and a single prep of the patient for combined femoral and sciatic nerve blocks. Its popularity had long been limited by its low success rate and relatively painful use of the femur as a deep landmark. Chelly and Delaunay described a nerve stimulating technique positioning the needle at the level of the lesser trochanter as originally described by Beck. Vloka et al. described the importance of internal rotation of the leg if the path to the sciatic nerve is obstructed by the lesser trochanter. A magnetic resonance imaging study of the anatomy of this area found that in 65% of patients the sciatic nerve is inaccessible from the anterior approach at the level of the lesser trochanter. These authors suggested needle placement 4 centimeters lower where obstruction to the sciatic nerve occurred in only 5% of the patients. Sciatic Nerve Block at the Level of the Popliteal Fossa Popliteal fossa block is chiefly used for foot and ankle surgery.Short saphenous vein stripping may also be performed under combined popliteal and posterior cutaneous nerve block. The block has also been successfully used in the pediatric population. Popliteal fossa block anesthetizes the entire leg below the tibial plateau save the skin of medial aspect of the calf and foot (i.e., saphenous nerve distribution). Potential advantages of popliteal block over ankle block are improved calf tourniquet tolerance and immobile foot. The components of the sciatic nerve may be blocked at the level of the popliteal fossa via posterior or lateral approaches. Patient positioning—prone, lateral (operative side nondependent), or supine (with leg flexed at the hip and knee)—may determine the optimal approach for an individual patient. The classic posterior approach to the popliteal fossa is accomplished with the patient positioned prone . Traditionally, the sciatic nerve is located 5 cm above the popliteal crease. However, to block the sciatic nerve before its division, a 7‐ to 10‐cm distance has been recommended. With a large‐volume single‐injection technique, inversion is the motor response that best predicts complete neural block of the foot. A lateral approach to blockade of the sciatic nerve in the popliteal fossa has been described. Because the common peroneal nerve is located more superficially than the tibial nerve, the stimulating needle encounters it first. Success rate with all approaches is typically 90% to 95%, with approximately 5% of patients requiring supplemental general anesthesia. It is believed that incomplete block is the result of


poor diffusion (because of the size of the sciatic nerve), the separate fascial coverings of the tibial and peroneal nerves, or blockade of only a single component of the sciatic nerve.

Continuous Sciatic Nerve Blocks Continuous sciatic nerve blockade can theoretically be achieved at any place along the course of the sciatic nerve. These blocks have been used for analgesia after major foot and ankle reconstruction, ankle fracture fixation, and below the knee amputation. Several studies have been published on the use of continuous popliteal blocks for analgesia after extensive foot and ankle surgery. All studies reported excellent analgesia with few side effects. Compared with intravenous analgesia or placebo infusion, a continuous infusion of local anesthetic via a popliteal catheter reduces pain scores and opioid consumption, and decreases sleep disturbances. Successful catheter placement has been reported with both lateral and posterior approaches. The only consistent problem reported with popliteal catheters is a high incidence (15%â&#x20AC;?25%) of kinking or dislodgement.

Ankle and Foot Block Indications for blockade of the terminal nerves of the lumbosacral plexus distally, at the ankle and midtarsal levels, include anesthesia for surgery to the foot. Diagnostic block has also been described. The peripheral nerves blocked at these levels are terminal branches of both the sciatic (posterior tibial, superficial peroneal, deep peroneal, and sural) and femoral (saphenous) nerves. The 5 peripheral nerves that supply the foot are relatively easy to block at the ankle . There are no important variants in the innervation of the distal musculature. However, there is considerable variation in the branching and distribution of the sensory nerves of the foot. For this reason, blockade of all 5 nerves has been advocated. Neural blockade of the posterior tibial nerve has been described at the supramalleolar, midmalleolar, subcalcaneal, and midtarsal levels with no evidence of superiority of any technique.


Comparisons of Nerve Localization Techniques Nerve Stimulation Versus Paresthesia Techniques for Lower‐Extremity PNB There are few studies directly comparing success rate with paresthesia techniques versus peripheral nerve stimulation (PNS) techniques in lower‐extremity PNBs. However, PNS provides a success rate comparable to earlier reports of paresthesia techniques. In addition, it may improve patient comfort during block performance. However, its biggest advantage may be the redirection cues that are provided to the operator. Redirection Cues Lower‐extremity PNBs generally tend to be deeper blocks than most approaches to the brachial plexus. Perhaps one of the most compelling reasons for using PNS during lower‐extremity PNB is the valuable “redirection cues” obtained during initial unsuccessful passes of the needle. For example, when performing a sciatic nerve block in the gluteal region, one may observe knee flexion as a result of stimulation of the superior gluteal nerve. This likely indicates that the needle is posterior, lateral, and cephalad to the sciatic nerve and should be repositioned appropriately. Imaging Aids Several investigators have examined the use of imaging technology to improve localization of both the lumbar plexus and the femoral nerve. Kirchmair and colleagues showed the usefulness of ultrasound in localizing the psoas major using a curved array transducer at low (4‐5 MHz) frequency. The location of the lumbar plexus is then inferred. It is not possible to distinguish peripheral nerves from tendon fibers with the ultrasound technology currently commercially available. The main limitations to visualization in this volunteer study were obesity and occasional high riding iliac crests in male patients.. Marhofer et al. compared the use of ultrasound guidance to nerve stimulation during femoral nerve blocks. These investigators found that ultrasound guidance was superior to nerve stimulation because it allowed the use of a smaller volume of local anesthetic and shorter latency period. The authors attributed this difference to the ability to visualize the administration of the local anesthetic during injection. They used ultrasound to reposition the needle when the local anesthetic spread out of the fascial plane and away from the nerve. It should be noted that ultrasound failed to identify the femoral nerve in a small number of patients in each of these studies.


Local Anesthetic Choices and Dosing of Lower‐Extremity PNB Pharmacologic Considerations Selection of a local anesthetic solution for lower‐extremity blocks differs somewhat from that of upper‐extremity approaches because of the indications and applications of each. For example, upper‐extremity blocks are commonly performed as the intraoperative anesthetic. In addition, pain after surgery to the upper extremity may not be as severe or protracted. As a result, intermediate‐acting local anesthetics and local anesthetic mixtures are frequently selected for surgery to the arm. These principles may not apply to lower‐extremity surgery in which peripheral blockade is often supplemented with a neuraxial or general anesthetic intraoperatively, and the need for sustained postoperative analgesia is achieved with long‐acting amides administered either as single injections or continuous infusions. Finally, although the use of adjuvants such as clonidine, opioids, and ketorolac is common during lower‐extremity peripheral techniques, their efficacy in improving the quality or duration of blockade has not been consistently shown.

Local Anesthetic Selection Few randomized studies have compared local anesthetics for lower‐extremity block. Fanelli et al.evaluated the onset and duration of combined femoral‐sciatic block performed with 0.75% ropivacaine, 0.5% bupivacaine, or 2% mepivacaine. Ropivacaine had an onset similar to that of mepivacaine but with a duration of analgesia between that of bupivacaine and mepivacaine. Connelly et al. reported no significant clinical differences between 0.75% ropivacaine and 0.5% bupivacaine for sciatic nerve blockade. When equipotent (rather than equivalent) concentrations were compared, onset times for the 2 local anesthetics showed no differences in onset times for sensory and motor block. However, the times to block regression and first analgesia were slightly longer with bupivacaine. In a single comparative study of sciatic block, levobupivacaine has block characteristics similar to ropivacaine.


Epinephrine Epinephrine prolongs the duration and quality of most local anesthetics used for lower‐extremity peripheral block. The effects are the result of vasoconstriction of the perineural vessels, which decreases uptake and thereby increases the neural exposure to the local anesthetic. However, the difference is only somewhat dose dependent. The addition of epinephrine 5 µg/mL (1:200,000 dilution) significantly increases the duration of lidocaine from 186 minutes to 264 minutes. Although epinephrine 2.5 µg/mL (1:400,000 dilution) prolongs the block to nearly the same extent (240 minutes), it has no effect on nerve blood flow. The addition of epinephrine to local anesthetics with vasoconstrictive properties, such as ropivacaine, may not increase block duration but would still facilitate detection of intravascular injection. The decision to add epinephrine (and the dose of epinephrine) is based on the concerns related to cardiac or neural ischemia versus the ability to discern an intravascular injection. In general, because seizures related to intravascular injection were highest in patients undergoing peripheral nerve block,the benefits of adding epinephrine outweigh the risks. However, the nearly equivalent effects on block quality and duration reported with epinephrine 2.5 versus 5.0 µg/mL suggest that the lower concentration is optimal, particularly in patients theoretically at risk for nerve injury (diabetics, patients with chemotherapy‐induced neuropathy.

Bicarbonate The addition of bicarbonate has been recommended to increase the speed of onset of peripheral and plexus blockade. However, most studies that have shown statistically significant differences used commercially prepared epinephrine‐containing solutions of local anesthetics (which have a much lower pH due to the addition of antioxidants) compared with plain local anesthetic solutions. A recent review of the literature involving brachial plexus block concluded that there was little reason to add sodium bicarbonate with plain local anesthetics or those with freshly added epinephrine. These results were substantiated in a study by Candido et al. which reported no difference in the onset or duration of combined lumbar plexus‐sciatic block in patients that received 0.5% bupivacaine with alkalinization compared with those who received a non‐alkalinized solution.


Clonidine Clonidine has been extensively investigated as an adjuvant for brachial plexus block. Prolongation of analgesia after the addition of clonidine is most likely peripherally mediated and dose dependent. During intravenous regional anesthesia, clonidine 150 µg may improve tourniquet tolerance. Side effects such as hypotension, bradycardia, and sedation do not occur with a dose less than 1.5 µg/kg or a maximum dose of 150 µg. Clonidine as an adjuvant for lower‐extremity block is much less defined. The limited data for lower‐extremity techniques validates those of previous upper‐extremity reviews. The results are most notable with intermediate‐acting agents. Opioids To date, there are no comparative studies evaluating the effect of opioids as adjuvants to lower‐extremity single‐dose or continuous techniques. Despite this lack of data, opioids, including

morphine, sufentanil, and

fentanyl,

are

often

added

to

lumbar

plexus

infusions.Investigations involving the brachial plexus report no difference in block onset, quality, or duration when opioids are added to the local anesthetic solution. A recent review concluded that the role of opioids in peripheral nerve block is not clinically relevant.

Other Adjuvants Most studies investigating adjuvants such as neostigmine, hyaluronidase, and tramadol involve upper‐extremity blocks. A single study evaluating the efficacy of nonsteroidal antiinflammatory drugs as adjuvants reported that the addition of ketorolac to lidocaine for ankle block resulted in longer duration and improved analgesia after foot surgery compared with intravenously administered ketorolac. In summary, selection of a local anesthetic solution for lower‐extremity peripheral blockade requires thoughtful consideration and is based on the duration of surgery, analgesic requirements, and anticipated rehabilitative efforts. The lowest effective dose and concentration should be used to minimize local anesthetic systemic and neural toxicity. Likewise, the addition of 1:200,000 or 1:400,000 epinephrine is recommended to facilitate detection of intravascular injection, as well as decrease local anesthetic levels. The role of other adjuvants is less defined; additional studies are required to determine the efficacy of clonidine, opioids, tramadol, and nonsteroidal antiinflammatory drugs in single‐dose or continuous lower‐extremity techniques.


Complications of Lower‐Extremity Peripheral Nerve Blocks Complications associated with peripheral nerve blockade are not common. Auroy and colleagues prospectively evaluated serious complications after PNBs in a 5‐month period in France. Using a 95% confidence interval, they estimated the potential for serious complications per 10,000 PNBs to be 0 to 2.6 deaths, 0.3 to 4.1 cardiac arrests, 0.5 to 4.8 neurologic injuries, and 3.9 to 11.2 seizures. There is a paucity of reports of complications specifically associated with lower‐extremity PNBs as compared with upper‐extremity PNBs. This is most likely related to their less common application rather than to inherent safety of the techniques.

Local Anesthetic Systemic Toxicity The potential for systemic local anesthetic toxicity would seem to be very high for lower‐extremity PNBs. Relatively large doses of local anesthetic are used for combined femoral and sciatic nerve blocks to anesthetize the entire lower extremity. However, there are only a few case reports of local anesthetic toxicity associated with lower‐extremity PNBs. For instance, in Fanelli and colleagues' series of 2,175 patients undergoing femoral sciatic combined blocks, there were no systemic adverse local anesthetic reactions reported. The apparent margin of safety seems to vary with individual block techniques. For instance, there are no case reports of toxicity after popliteal sciatic blockade, whereas there are several case reports of severe toxicity following lumbar plexus and proximal sciatic blocks. Anatomic differences in the anatomy, primarily in the vascularity and presence of deep muscle beds in the area of blockade, are the most likely explanation for this discrepancy. Severe toxic reactions typically occur during the injection or immediately thereafter. This suggests that the mechanism of these events is commonly an unintentional intravascular injection of local anesthetic into the circulation, rather than absorption. A forceful, rapid injection of local anesthetic carries a much higher risk of local anesthetic toxicity than a slow, gentle injection. This is because the mean dose of local anesthetic that elicits the signs of central nervous system toxicity is much less during rapid intravascular injection as compared with that associated with slower absorption after appropriate deposition. After a lower‐extremity peripheral nerve block, local anesthetic levels peak at approximately 60 minutes after deposition. Perhaps this slow time to peak blood levels offers an explanation for the low incidence of toxic complications associated with absorption. Important measures to decrease the risk of severe toxicity include the use of


epinephrine as an intravascular marker, slow methodical injection while avoiding high窶進njection pressure, frequent aspiration, constant assessment of the patient and vital signs, and prudent selection of local anesthetic concentration and volume.

Proximal Spread (Neuraxial Block) A potential needle misadventure of proximal peripheral nerve blocks is intrafascicular spread of the local anesthetic proximally toward the spinal cord, resulting in neuraxial blockade.This is a particular concern with block techniques that involve needle placement at the level of the nerve roots or spinal nerves, such as paravertebral, and psoas compartment block. Forceful, fast injections within the dural cuffs or perineurium can result in unintentional spinal or epidural anesthesia. Hemorrhagic Complications Several approaches for PNBs of the lower extremity involve deep needle penetration. These approaches include the psoas compartment approach to the lumbar plexus, the obturator nerve block, and the parasacral and classical approaches to the sciatic nerve. Despite the proximity of these deep nerves to vascular and hollow viscous structures, there are relatively few reports of needle misadventures. Retroperitoneal hematoma formation after psoas compartment block has been reported by several investigators. To reach the lumbar plexus, the needle must transverse multiple muscle and other tissue layers. The combination of its deep location and inability to apply pressure after an inadvertent puncture of deeply situated blood vessels supplying the local muscles and other structures may make this block less suitable in the setting of anticoagulation as compared with other more superficial lower extremity nerve blocks. Conservative management of retroperitoneal hematoma is recommended unless the patient develops hypotension unresponsive to volume resuscitation. Infectious Complications There are no case reports of infection after single窶進njection, lower窶親xtremity PNBs. Cuvillon et al.reported on the incidence of bacterial complications associated with the use of continuous femoral nerve blocks. Two case reports of psoas abscess requiring drainage and intravenous antibiotic therapy has been reported in patients who received a continuous femoral nerve block. Neurologic Complications


Neurologic complications after lower‐extremity PNB can be related to a variety of factors related to the block including needle trauma, intraneuronal injection, and neuronal ischemia. However, a search for other causes should include surgical factors such as positioning, retractor injury, and hematoma formation. In many instances, the neurologic injury may be a result of a combination of these factors. Tourniquet Neuropathy Tourniquet‐induced neuropathy is well documented in the orthopedic literature and ranges from mild neuropraxia to permanent neurologic injury.The incidence of tourniquet paralysis has been reported as 1 in 8,000 operations. A prospective study of lower‐extremity nerve blockade suggested that higher tourniquet inflation pressure (>400 mm Hg) was associated with an increased risk of transient nerve injury. Current recommendations for appropriate use of the tourniquet include the maintenance of a pressure of no more than 150 mm Hg greater than the systolic blood pressure and deflation of the tourniquet every 90 to 120 minutes.Even with these recommendations, post tourniquet application neuropraxia may occur, particularly in the setting of preexisting neuropathy.

Discharge Criteria The ability to ambulate independently is an important consideration for patients receiving lower extremity PNBs. Klein et al.have examined the controversy of long‐lasting analgesia versus potential complications from insensate extremities after PNB in ambulatory surgery patients. They prospectively studied 1,791 patients receiving either upper‐ or lower‐extremity nerve block with ropivacaine 0.5% and being discharged home the same day. There was a single complication related to a fall after combined femoral and sciatic nerve blocks. The authors attributed the low rate of complications to the immobilization related to the surgical procedure and generally cautious nature of postsurgical patients.


AN APPROACH TO DIFFICULT AIRWAY Dr. Raveendra U.S. Professor & HOD K.S.Hegde Medical Academy, Mangalore.

American Society of Anaesthesiologists defines difficult airway (DA) as a â&#x20AC;&#x153;clinical situation where a conventionally trained anaesthesiologist experiences difficulty with face mask ventilation of the upper airway, or with difficulty in tracheal intubation or both.â&#x20AC;? Difficult airway has two major components: difficult mask ventilation (DMV) and difficult tracheal intubation (DI) (further subdivided into difficulty in laryngoscopy and intubation). The availability of supraglottic airway devices (SGAD) has changed the significance of these definitions in such a way that even patients identified to have difficult intubation can be managed safely. Assessment and identification of difficult airway Routine assessment of airway, done in detail, should lead to identification of difficult airway. Temporomandibular joint movement, mouth opening, size and proportion of mandible and maxilla, oral cavity, teeth, submental space, size, shape, circumference and movement of neck and weight of the patient are the important parameters used to predict difficult airway. The objective measurements like mouth opening, thyromental distance (TM), neck circumference to TM ratio, sternomental distance are also used in the prediction of difficulty. Upper lip bite test is used to assess the ability to prognathicate the mandible. Various scoring systems have been proposed, studied and validated. They include Modified Mallampati (class I to IV), Wilsons scoring system (weight, head, neck and jaw movements, mandibular recession and buck teeth), Intubation difficulty score (IDS), LEMON (Look, Evaluate, Mallampati, Obstruction, Neck mobility) etc. The scoring systems vary in their specificity and sensitivity. None of them can completely identify the presence of difficult airway or all the components of difficult airway. In addition to the identification of the anatomical abnormality of each component of airway, it is important to identify the functional abnormality which could be present in an anatomically normal or difficult airway. Examples are obstructive sleep apnoea (OSA) and risk of aspiration. In this context, two related terms, compromised airway and obstructed

1


airway should be remembered. They are different from each other but can co exist in the same patient eg: a patient with a long standing huge goitre with stridor.

Finally, the assessment should include few other aspects in a patient with DA. They are (a) cooperation of the patient (b) feasibility of nerve blocks (c) ability to perform the procedures through the neck [tracheostomy, transtracheal jet ventilation (TTJV),cricothyoidotomy] and (d) ability to tolerate period of apnea (cardio-respiratory reserve) Review of records: Previous records should be reviewed for details whenever available. Investigations: Whenever required investigations are helpful. These include X-ray cervical spine (AP, lateral and open mouth), neck (AP and lateral views), chest x-ray (if retrosternal extension of thyroid is suspected), CT, MRI, indirect laryngoscope, and awake fiberoptic evaluation.

Predictors of difficult Intubation

Predictors of difficult Mask ventilation Obesity

History of difficult intubation

Beard

Relatively long upper incisors

Edentulousness

Inter incisor distance Less than two finger breadth or less than 3 cm

Skin sensitivity (burns, epidermolysis bullosa, fresh skin grafts)

Maxillary incisors override mandibular incisors

Age older than 55 years

Cannot touch chin to chest or cannot extend

Large tongue

neck

Poor atlanto-occipital extension

Thyromental distance less than three finger

Pharyngeal pathology

breadths (less than 6 cm)

Facial dressings

Mallampati III/Samsoon IVâ&#x20AC;&#x201D;relatively large

Facial burns

tongue, uvula not visible

Facial deformities

Short, thick neck

2


Common syndromes associated with difficult airway 1.

Pierre Robin syndrome

Micrognathia, hypoplastic mandible with glossoptosis, cleft palate

2.

Treacher-Collins syndrome

Mandibulofacial dysostosis, micrognathia, maxillary and mandibular hypoplasia, microstomia

3.

Goldenhar syndrome: Oculo-auriculo-

unilateral facial hypoplasia, micrognathia with

vertebral syndrome

unilateral cleft defect, unilateral maxillary hypoplasia, cervical vertebral defects.

4.

Apert’s syndrome:

craniosyntosis and micrognathia

Acrocephalsyndactyly 5.

Golz-Gorlin syndrome: Focal dermal

Dental and facial asymmetry and stiff neck

hypoplasia 6.

Klippel-Feil syndrome

Congenital fusion of cervical vertebrae, cleft palate

7.

Meckel-Gruber syndrome

Microcephaly, encepahlocoele, micrognathia, cleft palate

8.

Mobius syndrome

Congenital facial diplegia, micrognathia

9.

Trisomy 13 :Patau syndrome

Microcephaly, microognathia, cleft palate

10. Trisomy 18 Edward’s syndrome

Micrognathia

11. Trisomy 21 : Down’s syndrome

Microcephaly, atlantoaxial instability, hypotonia

12. Turner’s syndrome

Micrognathia with short webbed neck

Approaches to difficult airway Detailed plan should be made with attention to details. Primary plan should include what is going to be done first to achieve control and protection of the airway. Backup plan should be ready to implement if primary plan fails. Also, should be included in the planning, are the rescue techniques to maintain oxygenation when intubation and ventilation are difficult or when the “can’t ventilate, can’t intubate 3


(CVCI)” is reached. These include tracheostomy, cricothyroidotomy (needle and surgical) and transtracheal jet ventilation (TTJV). Algorithms are useful in devising the plan.ASA and Difficult Airway Society (DAS) algorithms are the two most commonly used algorithms.ASA difficult airway algorithm helps in selecting the plan by considering different options: 1) Awake vs. after intubation 2) Spontaneous vs. after relaxant 3) Non-surgical vs. surgical Planning should also include a method to continuously administer oxygen throughout the procedure and appropriate equipment. In addition, the feasibility of regional anaesthesia should always be considered, even while preparing for airway management.

Techniques for difficult mask ventilation If mask ventilation is difficult even after using proper size mask and application of triple manoeuvre, consider: 

Two hand ventilation

Insertion of oral or nasal airway

Two person ventilation

Application of Continuous Positive Airway Pressure(CPAP)

Endotracheal Intubation by conventional technique of using a Macintosh blade after induction of anaesthesia may not be feasible in DA. Hence alternate techniques should be considered in both primary and backup plan.

Optimization of laryngoscopy and intubation: When the intubation fails in the first attempt, following changes and manoeuvres may be considered: 

Change in position of the patient

4


Change in size and type of blade and laryngoscope: straight blade, Mcoy’s blade, polio blade, TruView scope etc

Use of Boogie

Use of Video laryngoscope

Optimal External Laryngeal Manipulation (OELM) by backward, upward, right and posterior pressure (BURP). OELM is different from Sellick manoeuvre.

Alternate techniques for intubation in difficult airway 

Awake Fiberoptic nasotracheal intubation under direct vision

Fiberoptic

nasotracheal

intubation

under

direct

vision under

spontaneous

breathing/paralysis 

Indirect techniques of fiberoptic assisted intubation; nasal and oral, using alternate nostril, boogie, guide wire etc

Blind nasal intubation under airway blocks

Retrograde intubation

Intubation using video laryngoscopes

Intubation using optical stylet

Intubation using laryngeal mask airway (LMA) and other SGAD: blind, fiberoptic guided or using intubation assist devices. Advantage of intubation through SGAD is that ventilation can be easily provided.

Anaesthesia of the airway can be achieved by using lignocaine spray or jelly for the nostrils, gargle (4% viscous) for the oral cavity, superior laryngeal nerve (SLN) block and transtracheal injections. Alternatively lignocaine nebulization can be used. Take care of the total dose of local anaesthetic to prevent toxicity.

Alternates to Endotracheal intubation Intubation with a cuffed ETT is gold standard of airway management. However, in many situations alternate devices can be used for airway management especially in DA. They include:

5


LMA: Classic (cLMA sizes:1,1.5,2,2.5,3,4,5 and 6, reusable and disposable versions are available, selection based on weight)

Other SGAD:I-Gel (pre-inflated cuff, sizes 1,1.5,2,2.5,3,4 and 5,colour coded, easy to insert),Cobra Perilaryngeal Mask Airway(PLMA), Air Q mask, Tulip Airway (two sizes to fit into all patients)etc

Laryngeal tube(LT) and Laryngeal tube Suction(LT-S) Role of alternate devices and techniques in DA management

Primary ventilation device for surgery in anticipated DA

Alternate ventilation device when primary plan fails

Conduit for intubation

Emergency ventilation device

Rescue device when mask ventilation is difficult or in CVCI situations

Pre hospital airway management

Extubation in DA In DA, extubation should be as planned as intubation. Extubation has additional risk of airway complications compared to intubation: a) Often it is not included in planning b) Changes in airway anatomy c) Presence of blood secretions and edema and d) Effect of residual anaesthetics and residual paralysis Following are the important considerations for extubation in DA:  Ensure complete reversal and recovery. Extubation in lighter plane should be avoided  When the anatomy is altered it is safer to extubate later in the post operative ward using airway exchange catheter.  Clear the airway before extubation

Special situations in airway management 1. Paediatric patients 2. Trauma 3. Obstetrics

6


4. Burns: acute, contractures 5. ICU Paediatric airway: Anatomical differences between adult and children should be remembered. Specific aspects of DA management in children: (a)

Lack of cooperation: awake techniques are difficult.

(b)

Airway blocks are difficult and risk of LA toxicity.

(c)

Small infants are obligatory nasal breathers.

(d)

Association with syndromes.

(e)

DMV is managed with airway insertion, lateral position, 2 hand ventilation and use of CPAP.

(f)

A roll under the shoulder is useful.

(g)

Age appropriate equipment should be used.

(h)

SGAD should always be considered.

(i)

Repeated attempts should be avoided

Obstetric Difficult Airway Here 2 lives are at risk and detailed planning is very important. Unique features of obstetric DA are: 

Anatomical changes in the airway related to pregnancy, super added to DA; smaller size of endotracheal tube may be required

Increased incidence of bleeding during airway manipulations

Rapid onset of hypoxia

Need for Rapid Sequence Induction(RSI) in view of full stomach

If it is an emergency caesarean section, waking up is not a good option

Airway management in burns Airway management in acute phase of burns: Difficulty arises because of DMV, lack of cooperation, full stomach (?) and airway oedema. Neck contracture after burns is a DA situation. Anaesthetic implications are a) No neck extension possible. Hence, both DMV and DI could be present b) Airway blocks may not be 7


possible due to contracture induced changes in anatomy c)Emergency procedures through neck are not possible.Options available include:a)awake fiberoptic intubation b)Insertion of LMA awake and induction of anaesthesia c)Release o contracture under tumescent anaesthesia etc. Nebulization of airway with lignocaine can be used for awake technique. Airway in trauma Trauma airway management is complicated by a) full stomach b) Actual/potential cervical spine injury c) Hemodynamic instability d) head injury e)Rib fracture, lung contusion and pneumothorax and f)physical injury to airway Again, awake fiberotic intubation is the best technique. Presence of blood and restless patient reduce the chance of success. ILMA can also used s a temporarizing measure. In transection of trachea, distal segment can be directly intubated. Lastly, in gross facial injury or where endotracheal intubation is difficult, tracheostomy can be the best choice. Clinical “Do” s and “don’t” s for DA management 

Always identify the nature of DA.

Plan meticulously

Use techniques and equipment which are familiar only

Have facilities for continuous oxygen administration

Have expert assistant, colleague with you

Call for help early in case of anticipated difficult airway

Consider regional anaesthesia as an option

Consider awake technique

Always consider whether waking up patient and rescheduling will be an option

Avoid multiple attempts at intubation and prevent CVCI

Consider using SGAD

If DMV is not there, muscle relaxants can be used.

Succinyl choline can still be used, but the contraindications must be remembered.

Always confirm intubation with end tidal carbon dioxide

Extubation should be planned

Details of airway management should be documented and copy handed over to patient.IDS is used to quantify the difficulty

8


Topics not covered in this article, but important for understanding of DA 

Details of assessment criteria and their significance

Details of fiberoptic aided airway management

LMA and other supraglottic devices

Role of rescue techniques

DA and need for Double lumen tubes

DA in ICU

Common case scenarios for DA for PGs and important aspects Massive thyroid: Size, duration and retrosternal extension. Compression of trachea and presence of compromised or obstructed airway. Involvement of vocal cords. Difficulty with procedures through neck. Preoperative fiberoptic evaluation and awake fiberoptic intubation may be required. Evaluation of vocal cord movement before extubation. Cleft lip and palate :Problems related to age, respiratory tract infection,syndromes etc.Could have DMV and DI or only DI.Awake techniques are difficult nor required.Relaxant can be used after confirming mask ventilation.Laryngoscopy difficulty due to cleft palate,left side laryngoscopy reported to be useful.Before extubation,rule out tongue edema.

9


10


References 1. American Society of Anesthesiologists Task Force on Management of the Difficult Airway: Practice guidelines for management of the difficult airway. Anesthesiology 2003; 98:1269-1277.An updated report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway 2. Crosby E: The unanticipated difficult airway—evolving strategies for successful salvage. Can J Anaesth 2005; 52:562-567 3. American Society of Anesthesiologists Task Force on Management of the Difficult Airway : Practice guidelines for management of the difficult airway: A report. Anesthesiology 1993; 78:597-602. 4. Benumof's airway management : principles and practice/[edited by] Carin A. Hagberg.—2nd ed.p. cm.Rev. ed. of Airway management. 1996 5. Gupta Sunanda, Sharma Rajesh, Jain Dimpel: Airway assessment : predictors of difficult airway. Indian J. Anaesth.2005;49(4):257-262 6. Kheterpal S, Han R, Tremper KK, et al: Incidence and predictors of difficult and impossible mask ventilation. Anesthesiology 2006; 105:885-891. 7. Combes X, Le Roux B, Suen P, et al: Unanticipated difficult airway in anesthetized patients: Prospective validation of a management algorithm. Anesthesiology 2004; 100:1146-1150. 8. Crosby E: The unanticipated difficult airway—evolving strategies for successful salvage. Can J Anaesth 2005; 52:562-567. 9. William Rosenblatt : Awake intubation made easy! ASA volume 37 10. U S Raveendra. Teaching and training in fibreoptic bronchoscope-guided endotracheal intubation. Indian J Anaesth. 2011 Sep;55(5):451-5

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12


PG DEBATES


PROSEAL LMA IN LAPAROSCOPIC SURGERIES Post graduates: Dr Nidhi Dr Pooja Shah JNMC, Belgaum

Moderator: Dr P.F.Kotur, Professor, JNMC, Belgaum

For 

Designed by Dr Archie Brain based on classic LMA, was introduced in 2000

Although endotracheal intubation is the gold standard in laparoscopic surgeries done under general anaesthesia, ProSeal LMA proved to be an equally effective airway tool in laparoscopic surgeries in terms of adequate ventilation & oxygenation with minimal intraoperative &postoperative complications

Attenuation of haemodynamic response-ProSeal LMA being a supraglottic airway device does not require laryngoscopy & is atraumatic to insert without any injury to vocal cords as in case with endotracheal intubation.

Increase in Heart rate & MAP was observed 10 seconds after intubation & persisted till 3 minutes after intubation & during the time of extubation in ETT group.

However statistically significant (p<0.05) increase in Heart rate & Mean Arterial Pressure in ProSeal LMA group was seen only 10 seconds after insertion.

ProSeal LMA has built in drain tube(DT) that allows expelled gastric contents to bypass the pharynx. This specific design feature decreases the risk of aspiration


Unlike the ET Tube or gastric tube, ProSeal LMA channels gastric fluid away & also permits gastric access during extended cases where ETT is not appropriate.

The gastric drain tube allows simple & rapid decompression of stomach if required. Time taken for successful passage of Nasogastric Tube in ProSeal LMA was 9.77 s(6-16 sec) & 11.5 s(8-17) s in ETT.

Insertion of Nasogastric Tube is less traumatic with ProSeal LMA than ET Tube. Success rate of Nasogastric Tube in 1st attempt with ProSeal LMA (90%) was higher than via nasal route in intubated patients (66.7%).

ProSeal LMA achieves a higher seal pressure 30-35 cm of H20 with no increase in mucosal pressure supporting good ventilation.

The Peak Airway Pressure did not increase beyond oropharyngeal pressures throughout the surgery.

It decreases likelihood of throat irritation & post extubation coughing. Intracuff pressure lower & airway seal pressure higher. The pressure exerted on mucosa is below that considered critical for mucosal perfusion. Therefore ProSeal LMA forms a more effective seal without an increase in mucosal pressure.

Incidence of sore throat in intubated patients (20%) is higher than ProSeal LMA (10%) group.

ProSeal LMA has a dorsal cuff in addition to peripheral cuff which pushes the mask anterior to provide a better seal around the glottic aperture & permits high airway pressures without leak. Its use is permitted during controlled ventilation.

The overall insertion rates of ProSeal LMA is similar to ETT insertion. The use of introducer tool might increase insertion success further,


Its use has been suggested in cases of failed intubation with difficult ventilation after Rapid sequence induction (RSI) - controlled ventilation & ability to drain stomach desirable.

In difficult RSI-use of Gum elastic bougie in passage of ETT when vocal cords are partially visible is not advisable & ProSeal LMA can be used as an early rescue...

In obese patients allows ventilation with higher airway pressures & less gastric insufflation.

During peritoneal insufflation, endobronchial displacement is more common with ETT.

ProSeal LMA offers an airway that bridges the gap between classic LMA & ETT.

Against: The ProSeal LMA is a developed version of laryngeal mask airway -A supraglottic airway device developed by Archie Bain in the late 1990’s. Having gone through the various advantages, let us now identify its shortcomings/disadvantages. 

At insertion, one requires adequate training to use it. In a study conducted by Mahender Nath and colleagues, it was found that first attempt success rate was 88% as compared to 100% success in placement of ET Tube. Repeated attempts did manage to secure the airway, but would definitely amount to some degree of oropharyngeal injury.

As with other supraglottic airway devices, restricted mouth opening, h/o oral surgeries(cleft palate repair), presence of oral and pharyngeal pathology like enlarged tonsils pose a problem to insertion and proper positioning of the device.

Coming to the issue of malposition, it is necessary to ensure proper placement of the device before we can proceed with IPPV under GA.


Foldover malposition can occur very frequently with the device, (3% incidence) recognition of which is essential to ensure safety. In a case report published by Brimacombe, a patient for laparoscopic cholecystectomy was maintained on IPPV with airway secured with ProSeal LMA, where an unidentified foldover malposition led to aspiration of the regurgitant gastric fluid. He mentions that, in presence of the foldover malposition, ventilation was maintained and seal was normal in 98% of the cases, which is what we check usually for proper placement, thus exposing the patient to the risk of aspiration of gastric contents.

Maltby and co-workers, presented a study that compared the safety of the LMA and the ETT as an airway during gynecologic laparoscopic surgery, in non-obese and obese (BMI > 30 ) patients. The LMA Classic (LMA-C) was used for the non-obese patients and the ProSeal LMA was used for the obese. Of interest, they did not exclude patients with a history of gastroesophageal reflux or hiatus hernia if their symptoms were controlled at the time of the study. They found that oxygenation and ventilation were comparable whether the airway was secured with an ETT or a LMA. Still, this study raised concerns in some circles. For instance, expressing a concern about possible regurgitation and aspiration, Cooper noted that while the LMA "has an impressive safety record" we must "be certain that we are not compromising patient safety by using the LMA because it can be used, rather than should be used. Despite other reports of safe use of ProSeal LMA in large series, there still is concern about the safety of this practice. Many of the studies are not adequately powered to conclude that the ProSeal LMA is a safe and suitable alternative as compared with ETT where pulmonary aspiration of gastric contents is concerned. ď&#x201A;ˇ

Sore throat incidence is seen even with LMA. In a study done by Burgard and colleagues showed that, A significant increase in cuff pressure is seen during the first 60 minutes. Three minutes after insertion of the laryngeal mask, cuff pressure can significantly be reduced without any major gas leakage. Postoperative sore throat can be reduced when cuff pressure is continuously monitored and kept on low-pressure values.


THIRD SPACE: THE HISTORY AND MYSTERY OF IT…. Post Graduates: Dr Subramanian.V.V, Dr Bhagirath.S.N. JSSMC, Mysore

Moderator: Dr Uma.G Lecturer, JSSMC, Mysore

Fundamental changes in the approach to intraoperative fluid management in recent years have stemmed forth from radically altered perceptions of the role of fluid shifts and vascular physiology in determining intraoperative conditions and post operative outcomes. Many accepted notions, some based not entirely on firm evidence, now stand challenged thanks to new evidence or often the lack of it. ! One such contention in dispute is the existence of third space. Many new findings are particularly instrumental in altering our concepts about third space and fluid management. A short sketch of such inherited precepts is outlined first to lend a better perspective on evolving changes.

The tendency to generously administer I.V. fluids intraoperatively on the premise of making up for the patient’s deficits including and most importantly the third space loss was quintessentially a dogmatic approach that faltered, when the very foundation on which it stood was questioned. We discuss here in some detail, such a foundation (the idea of a third space….!), its veracity and its inevitable influence on our day to day anaesthetic practices.

Fluid therapy intraoperatively is aimed at making up for patient losses, as varied as the cause for the loss may be. One straightforward approach adopted hitherto was the supplementation of I.V. fluids to replace the deficit that occurred secondary to keeping the patient nil by mouth. This was subsequently complemented by a replacement proportional to the intraoperative loss that accrued due to the surgery per se. These surgical losses, if one can term them as such, were in turn computed on the actual blood loss, the evaporative (insensible perspiration) losses that ensued and specific to our discussion the third space losses. While the third space loss is seen here to be a vital pillar on which fluid replacement therapy stands, the very existence of such a space is in question. So, if it all, such a space were not to exist, where then was all the fluid administered going to..? On the other hand if such a space did exist, then why was it so difficult to quantify it with a measurable amount of success..? These are questions, which we shall attempt at answering. . ..

The History of Third Space… The need for replacement with fluids, especially those with specific quantities of salts and other constituents to suffice for the perceived surgical loss was for the first time shown by Moore1. As innocuous as this may seem to us now, this simple assertion served to mould our ideas regarding intraoperative surgical management in a more scientific manner over the next few decades. 1


Figure 1 Body Fluids Compartments

2


Where this administered fluid went inside one’s milieu was anybody’s guess for quite some time. While the divisions shown in Fig 1 served to illustrate in some clarity the compartmentalisation of fluids in vivo, the intricacies of such divisions remained gray. For instance, the extracellular fluid shown to constitute 1/3rd of the body weight was speculated to divide itself between the interstitium and the vascular channels. That which was in the interstitium, it was believed was further segregated into a defined anatomical space and an ill defined non anatomical space. This assertion first conceptualised by Tom Shires2 in the early 1960’s was embraced with a great deal of enthusiasm from different scientific quarters and was further emboldened by contemporaneous findings by Boba3 and Hoye4, which served to illustrate Shires’ idea in as much as showing that there were clear perceptible deficits, often acute, in the extracellular space in animals during shock and in man during surgical trauma; a finding that lent some credence to the possible existence of such a third space. The existence of such an all consuming third space encouraged generations of anaesthesiologists to pour fluids to make up for such a deficit5.

This accepted notion of a third space, convenient as it may be for fluid computations, was questioned as early as the mid 1970s. The initial challenge crept up in the form of corrections to the accepted levels of fluid loss accruing from fasting, insensible perspiration and third space. Contrary to established precepts, fasting was not shown to cause a fluid deficit as significant as was thought before6. Furthermore, fluid loss due to insensible perspiration was also shown to be overestimated7. This overcorrection manifested as perioperative weight gain often in excess of 10 kgs8, 9. This implied the simple yet glaring fact that overestimated deficits led to an overcorrection, which caused more harm than good to the patient. Yet, strangely enough, this overcorrection seldom gets reflected in terms of an increase in intravascular volume, which leaves us with only one other option as to where the fluid can go – the interstitium. Even more discordant a fact was that successive measurements failed to show a substantial accumulation in the discernible anatomical interstitium, thereby leading one to suppose that most of the fluid was going into the non anatomical interstitium i.e. the so called third space; a definitive feather in the cap for the traditional school of thought which championed the existence of the third space. And yet, this non anatomical interstitium has repeatedly evaded detection.

The Mystery behind Third Space…

But for indirect computations, direct evidence has been woefully lacking in showing the existence of the elusive third space. Many an attempt has been in vain at this endeavour. A few such attempts are discussed hereunder. The use of tracers for assessment of the third space was pioneered by Brandstrup and colleagues in 200610, 11

. These tracer dilutions which heralded some success were predominantly done with either sulphate or 3


bromide ion tracers. However, tracer dilution techniques brought with them a plethora of ambiguities which did not help further the point they set out to prove in the first place.

These being:

a. The selection of a suitable tracer which distributed exclusively in the third space

b. How long one ought to wait till the tracer has distributed exclusively in the third space before it begins redistributing elsewhere?

c. How does one validate the method adopted to quantify this third space?

d. The requirement of a steady state condition necessary for a tracer to function optimally rules out states of hemodynamic shock or even surgical stress which defeats the purpose wholly.

e. Settings of hypotension or hypovolemia prolong equilibration of the tracer causing more of it to remain in the plasma rather than the third space.

f. Sequestration of the above preferred tracers inside the erythrocytes, plasma components and subsequent accumulation in liver and kidney further alienates its efficacy.

g. The final salvo being the results of the bromide tracer technique. Notwithstanding the above shortcomings, the bromide tracer techniques showed an expanded fECV not accounted for by the calculated fluid balance12, 13, 14.

Does it have something to do with the vascular barriers..?

Fluid administered to a normovolemic patient was previously thought to remain exclusively within the vascular channels thereby leading to normovolemic hemodilution. But this does not happen in practice. This is explained as under.

i.

There exists a gradient across the vessel and the interstitium, with the intravascular compartment having a high hydrostatic pressure as opposed to a low hydrostatic pressure in the Interstitium. 4


ii.

This calls for a substantial inwardly acting colloidal osmotic pressure intravascularly to counter the hydrostatic pressure gradient.

iii.

In this setting, if one were to transfuse iso-oncotic colloids, they would not change the intravascular colloid osmotic pressure.

iv.

On contraireâ&#x20AC;&#x2122;, if one were to transfuse crystalloids, since they would not exert any colloid osmotic pressure, there is no inwardly acting force to keep them trapped within the vascular compartment. i.e. crystalloids readily cross the vascular barrier into the interstitium as opposed to their colloidal counterparts.

v.

Administration of crystalloids in a normovolemic patient does not therefore increase the intravascular volume.

vi.

Consequently, preloading a patient prior to anaesthesia with crystalloids ill serves the purpose of preventing intraoperative hypotension secondary to anaesthesia15, 16.

vii.

In summary, in a normovolemic patient â&#x20AC;&#x201C; infused colloid tends to remain intravascularly and infused crystalloid tends to cross over into the interstitium.

How long does this dictum hold goodâ&#x20AC;Ś?

viii.

After a certain limit, once infusion of colloids leads to a relative state of hypervolemia, strangely enough, the colloidal fluid hitherto trapped intravascularly begins to cross over into the interstitium.

Why does the vascular barrier give way to colloids under conditions of hypervolemia?

5


Figure 2 Cartoon illustrating non - circulating glycocalyx fluid volume and the circulating plasma volume

ix.

Damage to the endothelial glycocalyx (Fig 2) secondary to hypervolemia, ischemia/reperfusion17, 18, proteases19, Tumor Necrosis Factor â&#x20AC;&#x201C; Îą20, low density lipoprotein21 and Atrial Natriuretic Peptide (ANP)22 has been shown to be the prime factor in increased permeability to colloids by the vascular membrane.

Figure 3 Glycocalyx before and after overloading with fluids x.

While surgical stress is predominantly to blame for most of the above listed endothelial irritants23, 24, ANP release is secondary to perioperative hypervolemia25, 26. 6


xi.

Disinclination towards a fluid overload in the tissue and the interstitium stems from an awareness of its less desired effects namely â&#x20AC;&#x201C; anastomotic leakage, tissue edema, pulmonary edema and reduced tissue oxygenation.

xii.

In summary, avoiding damage to the vascular barrier (endothelial glycocalyx), minimising preloading a patient prior to administration of anaesthesia and a judicious choice of colloid versus crystalloid - serves to limit the extent of transfused fluid crossing over to the interstitium.

xiii.

Points worth remembering: a) Volume depletion secondary to normal preoperative fasting is insignificant b) Volume depletion secondary to fasting is significant only if a bowel wash has been administered, dehydrated patients and hypovolaemic patients. c) Preloading with crystalloids before administration of anesthesia as routine practice is best reconsidered. d) Generous fluid replacement intraoperatively does more harm than good to the patient. e) Volume replacement based on only urinary output is best avoided. f) Use colloids judiciously.

So why is this fluid shift mechanics important to this discussion..?

The endothelial glycocalyx layer appears to have a major role in fluid exchange. Protection or restoration of this endothelial glycocalyx might be an important therapeutic goal.

To prevent perioperative fluid shifting, carefully maintain homeostasis of all fluid compartments by judicious use of crystalloids and colloids as necessary. Avoid hypervolemia as well as hypovolemia thereby avoiding third space shifting.

Conclusion As anaesthesiologists, our immediate concern lies not in the answers to afore raised questions, but more so with the perioperative fluid management involving a â&#x20AC;&#x153;goal directedâ&#x20AC;? strategy based on hemodynamic parameters.

7


References: 1. Moore, F. D.: Metabolic Care of the Surgical Patient. Philadelphia and London, W. B. Saunders Company, 1959. 2. Shires T, Williams J, Brown F. Acute change in extracellular fluids associated with major surgical procedures. Ann Surg 1961; 154: 803±10 3. Boba, A.: Support of Blood Volume During Operation without Blood Transfusion. Surg. Forum, 17:61, 1966. 4. Hoye, R. C.: Blood and Fluid-Volume Deficits Following Extensive Surgery. Surg. Forum, 17:55, 1966. 5. Kaye AD & Kucera AJ. Fluid and electrolyte physiology. In Miller RD (ed.). Anesthesia. Philadelphia: Churchill Livingston, 2005, pp. 1763–1798. 6. Jacob M, Chappell D, Conzen P et al. Blood volume is normal after preoperative overnight fasting. Acta Anaesthesiologica Scandinavica 2008; 52: 522–529. 7. Lamke LO, Nilsson GE & Reithner HL. Water loss by evaporation from the abdominal cavity during surgery. Acta Chirurgica Scandinavica 1977; 143: 279–284. 8. Dawidson IJ, Willms CD, Sandor ZF et al. Ringer’s lactate with or without 3% dextran-60 as volume expanders during abdominal aortic surgery. Critical Care Medicine 1991; 19: 36–42. 9. Virgilio RW, Rice CL, Smith DE et al. Crystalloid vs. colloid resuscitation: is one better? A randomized clinical study. Surgery 1979; 85: 129–139. 10. Brandstrup B. Fluid therapy for the surgical patient. Best Practice & Research. Clinical Anaesthesiology 2006; 20:265–283 11. Brandstrup B, Svensen C & Engquist A. Hemorrhage and operation cause a contraction of the extracellular space needing replacement – evidence and implications? A systematic review. Surgery 2006; 139: 419–432. 12. Reid DJ. Intracellular and extracellular fluid volume during surgery. British Journal of Surgery 1968; 55: 594– 596. 13. Breckenridge IM, Digerness SB & Kirklin JW. Validity of concept of increased extracellular fluid after open heart surgery. Surgical Forum 1969; 20: 169–171 14. Breckenridge IM, Digerness SB & Kirklin JW. Increased extracellular fluid after open intracardiac operation. Surgery Gynecology & Obstetrics 1970; 131: 53–56. 15. Jackson R, Reid JA & Thorburn J. Volume preloading is not essential to prevent spinal-induced hypotension at caesarean section. British Journal of Anaesthesia 1995; 75: 262–265. 16. Rout CC, Akoojee SS, Rocke DA & Gouws E. Rapid administration of crystalloid preload does not decrease the incidence of hypotension after spinal anaesthesia for elective caesarean section. British Journal of Anaesthesia 1992; 68: 394–397. 17. Chappell D, Jacob M, Hofmann-Kiefer K et al. Hydrocortisone preserves the vascular barrier by protecting the endothelial glycocalyx. Anesthesiology 2007; 107: 776–784. 18. Rehm M, Zahler S, Lotsch M et al. Endothelial glycocalyx as an additional barrier determining extravasation of 6%hydroxyethyl starch or 5% albumin solutions in the coronary vascular bed. Anesthesiology 2004; 100: 1211–1223.

8


19. Adamson RH. Permeability of frog mesenteric capillaries after partial protease digestion of the endothelial glycocalyx. The Journal of Physiology 1990; 428: 1–13. 20. Chappell D, Hofmann-Kiefer K, Jacob M, et al. TNF-a induced shedding of the endothelial glycocalyx is prevented by hydrocortisone and antithrombin. Basic Research in Cardiology 2009; 104: 78–89.

21. Vink H, Constantinescu AA & Spaan JA. Oxidized lipoproteins degrade the endothelial surface layer: implications for platelet-endothelial cell adhesion. Circulation 2000; 101: 1500–1502. 22. Bruegger D, Jacob M, Rehm M et al. Atrial natriuretic peptide induces shedding of endothelial glycocalyx in coronary vascular bed of guinea pig hearts. American Journal of Physiology. Heart and Circulatory Physiology 2005; 289:H1993–H1999. 23. Desborough JP. The stress response to trauma and surgery. British Journal of Anaesthesia 2000; 85: 109–117. 24. Wilmore DW. Metabolic response to severe surgical illness: overview. World Journal of Surgery 2000; 24: 705–711. 25. Kamp-Jensen M, Olesen KL, Bach V et al. Changes in serum electrolyte and atrial natriuretic peptide concentrations, acid-base and haemodynamic status after rapid infusion of isotonic saline and Ringer lactate solution in healthy volunteers. British Journal of Anaesthesia 1990; 64: 606–610. 26. Schutten HJ, Johannessen AC, Torp-Pedersen C et al. Central venous pressure – a physiological stimulus for secretion of atrial natriuretic peptide in humans? Acta Physiologica Scandinavica 1987; 131: 265–272.

9


CAN REGIONAL ANESTHESIA BE GIVEN IN A PATIENT WITH DIFFICULT AIRWAY Postgraduates: Dr Usha.N.K Dr Amita Mahesh

Moderators: Dr Radha.M.K, Professor & HoD, AIMS, B.G.Nagar

Dr Raveendra.U.S, Professor & HoD, KSHEMA, Mangalore

For: The anticipated technical difficulties and the success rate affect the decision of the anaesthesiologist to use a regional technique in a patient with difficult airway.

It is mandatory in all cases of anticipated difficult airway management to consider the balance between four different factors: 1. Technique success rate. 2. Minor / major surgery. 3. Patient position during surgery and duration of operation. 4. Intraoperative complications.

For minor / intermediate surgical procedures in the patient with anticipated difficult airway it is safer whenever possible to choose a neuraxial technique.

Maternal risks of general anaesthesia include increased incidence of pulmonary aspiration of gastric contents and failed endotracheal intubation which are major causes of maternal mortality and morbidity.

In an emergency, where there is a need to swiftly provide anaesthesia, regional anaesthesia is not a contraindication in the hands of an experienced anaesthesiologist. It is important to select a technique that minimizes the potential complications. Neuraxial blockade can be used in severe preeclampsia as it avoids the undesirable effects of general anaesthesia.


Improved needle catheter technology, successful placement by nerve stimulation technique, recent introduction of long acting local anaesthetic agent, variety of opioid and non-opioid adjuvants to local anaesthetics, development of local anaesthetic encapsulated in lipophilic membrane, allowing for sustained release, have improved the success rates with neuraxial anaesthesia.

Spinal anaesthesia provides excellent surgical conditions for most orthopaedic surgeries on lower limbs, gynaecological, urological, perirectal and inguinal procedures.

Regional anaesthesia provides an awake patient which helps in early detection of complications eg: stroke in carotid endarterectomy, TURP syndrome in TURP patients.

Obesity and COPD are two challenging conditions to the anaesthesiologist. In patients with COPD- deleterious effects of general anaesthesia are worsening of V/Q ratio, attenuation of HPV, exacerbated bronchospasm along with sedative effects of general anaesthetics and opioids which increase the intraoperative and post operative pulmonary complications. For minor intermediate surgical procedures in patients with anticipated difficult airway it is safer wherever possible, to choose peripheral nerve block. A number of regional anaesthetic techniques can be used for day care surgeries. These techniques involves little physiological trespassing compared to GA, so they are particularly suited for ever growing population of high risk elderly patients presenting for day care procedures. In ambulatory orthopaedic surgery, regional anaesthesia techniques are utilized extensively. It provides excellent analgesia with reduced risk of opioid side effects such as nausea, vomiting, drowsiness In relation of site of surgery, upper limb nerves can be blocked with various techniques. A combined block of lower extremity offers many advantages over spinal / epidural


anaesthesia like less hypotension, no retention of urine, post spinal headache and a few concerns regarding bleeding status of patients on anticoagulants.

IVRA (intravenous regional anaesthesia) is suitable for operations of the distal extremities (below elbow, below knee) in situations where it is safe and easy to apply an occlusive tourniquet. Cervical epidural has been used with good results in thoracic surgery, shoulder and upper extremity surgery, in carotid artery surgery, parathyroid surgery, neck dissection for head and neck cancers.

Achondroplasia is traditionally considered to have difficult airway and was earlier considered a contraindication for regional anaesthesia. But, several recent studies have reported success of epidural anaesthesia with few complications. Evidences supporting the benefit of intraoperative neuraxial anaesthesia: Decreasing the length of hospital stay, decreased incidence of thrombo embolic events, lower perioperative blood loss, early mobilization, cognitive function retainment, attenuation of metabolic stress response of surgery and anaesthesia, reduced incidence of cardiac events in patients with known coronary artery disease undergoing major vascular and cardiac surgery and reduced morbidity and mortality. In conclusion, regional anaesthesia is not a contraindication in anticipated difficult airway patients however the risk benefit ratio for a particular patient has to be optimized.


Against: Airway management is most important part of patient management in anaesthesia. Any compromise in ventilation or oxygenation can result in unacceptable, irreversible cerebral damage. Hence it is safe to secure airway before opting for any other technique in difficult airway scenario. Considering regional anaesthesia for surgery is not a substitute for managing patients with anticipated difficult airway. Most regional techniques have a failure rate of 1-10% even in the hands of expert anaesthesiologists.

Therefore securing an airway is necessary even when regional

technique is sufficient for that procedure. There are many indications which require the conversion of regional anaesthesia to general anaesthesia and the need for endotracheal intubation: Untoward complication of regional anaesthesia like high spinal which requires endotracheal intubation Extension of surgery beyond the duration of action of the regional anaesthetic drugs. Inadequacy of the level of block Improper action of the drug Any local anaesthetic toxicity resulting in cardiopulmonary arrest Impatient surgeon

Even though endotracheal tube is the gold standard among airway devices there are newer airway devices like ProSeal LMA which provide reasonably adequate airway protection even in an anticipated difficult airway but without the stress response.

Airway in an obstetric patient is considered to be difficult owing to the various anatomical and physiologic changes. Management is often stressful because of the


urgency of the case, and the consequences of emergency intubations are more serious. Prediction of difficulty with the airway is notoriously inaccurate.

Pre-eclampsia is common and results in oedema which may be marked. Itâ&#x20AC;&#x2122;s better to manage eclampsia patients by securing airway rather than regional technique to avoid and manage the intra operative complications like convulsions, pulmonary edema, and cerebral edema.

Airway management is a principal anesthetic concern in thyroid surgery because of the following advantages: -bleeding well controlled -anatomical landmarks are well defined -unnecessary movement of the patient is avoided -prevents aspiration -over sedation which can lead to respiratory depression or inability to keep the airway patent because of the compressing mass is avoided

Blood pressure should be maintained as close to baseline as possible throughout in patient undergoing vascular surgeries including major surgeries like carotid surgeries which is well obtained with administration of GA. ANAESTHEISA FOR OCCULAR SURGERIES General anaesthesia is the technique of choice for the following procedures: 1) Paediatric age 2) Perforating globe injuries 3) Emergency penetrating eye injuries 4) For the surgeries which requires proper maintenance of IOP. CONCLUSION:


REGIONAL ANAESTHESIA should not be considered in patients who have been judged to have a DIFFICULT AIRWAY. The decision to proceed with regional anaesthesia because the airway cannot be assessed or has been proven to be difficult to manage must be considered in terms of risk and benefits. The ASA closed claims database projects has identified failure in regional anaesthesia as a source of serious error when no airway strategy was prophylactic ally considered. REFERENCES: 1) American society of anaesthesiology task force on management of difficult airway. Practice guidelines for management of difficult airway Anesthesiology 2003;98:1269-77. 2) European Journal of Anaesthesiology: June 2006 - Volume 23 - Issue - p 260 3) Martin F, Buggy J: Newer airway equipment: opportunities for enhanced safety. BJA 2009; 102(6): 734-8. 4) Hugh Gilbert: complications and controversies in regional anaesthesia: ASA chapter 6: vol 31. 5) John C. Drummond, Piyush M. Patel: neurosurgical anaesthesia: millerâ&#x20AC;&#x2122;s anaesthesia 7th editon. Chapter 63. 6) Textbook of core topics in airway management by Ian calder, Adrian pearce. 7) Robert A, peter freund: Endocrine anaesthesia: Textbook of Anesthesiology by David E Longnecker. 8) Textbook of clinical Anaesthesia, Barash 6th edition.


CLINICAL CASE DISCUSSIONS


A PATIENT WITH BRONCHIECTASIS POSTED FOR LEFT LOWER LOBE LOBECTOMY Dr C L Gurudatt Professor and Head, Mysore Medical College and Research Institute, Mysore

Dr.Mahantesh Sharma Professor of Anaesthesiology JJM Medical College Davangere.

A 35year old woman presented with history of fever, cough with purulent sputum and progressively worsening dyspnea since 2 months. She has history of pulmonary tuberculosis 6 years ago, for which antituberculous therapy was given. Subsequently, she was diagnosed to have left lower lobe Bronchiectasis. She was also treated for left lower lobe pneumonia 2 months ago. She has no other medical illness. O/E: Her height is150 cms & weight is 52 kgs. She is mildly dyspnoeic with accessory muscles of respiration in use. On auscultation there are bronchial breath sounds on the left side with basal coarse crepitations. Chest X Ray revealed honey combing appearance in the left lower zone.CT scan revealed bro nchiectasis involving left lower lobe PFT revealed on FEV1 of 65%.All other blood investigations were normal and sputum for AFB is negative.Patient is on bronchodilator therapy by nebulization and is posted for left lower lobe lobectomy.

1.What is bronchiectasis? Bronchiectasis is a disease classified under chronic obstructive pulmonary diseases. It is also considered as a wet lung disease as the patient will bring out copious secretions. It is characterized by -Persistent and irreversible dilatation and distortion of medium sized bronchi by more than 2 mm caused by repeated cycles of airway infection and inflammation. -Involved bronchi are inflamed and easily collapsible, resulting in airflow obstruction and impaired clearance of secretions -It may require surgery if it causes haemoptysis or recurrent pneumonia. The other diseases under COPD are chronic bronchitis, emphysema and cystic fibrosis.


2. What are the causes for Bronchiectasis? Approximately one third of patients with bronchiectasis have an infectious trigger, usually years before the onset of the disease. Childhood viral infections, such as pertussis and bacterial infection, can cause permanent damage to the airways, leading to bronchiectasis years after the initial infection. Mycobacterial tuberculosis is an important cause, with its resultant granulomatous inflammation of the airway, lung parenchyma, and lymph nodes can cause subsequent bronchiectasis Direct lung injury due to acid or particulate matter aspiration or recurrent pneumonia may lead to bronchiectasis. Patients with human immunodeficiency virus infection have a higher prevalence of bronchiectasis than individuals with a normally functioning immune system. Bronchiectasis is an increasingly recognized complication of collagen vascular diseases, particularly rheumatoid arthritis.

3. When do you say cough is productive? •

When the sputum production is > 100 ml/ day

Seen in conditions like Bronchiectasis, lung abscess, empyema rupturing into bronchus, necrotizing pneumonia, alveolar cell carcinoma and chronic bronchitis.

4. Why colour and odour of the sputum are important? Based on the colour of the sputum one can approximately diagnose the causative factor

Colour of the sputum

Conditions

Yellow ( purulent)

Bacterial infection

Greenish

Pseudomonas

Black Red currant jelly

Aspergillosis, Coal Pneumoconiosis Klebsiella pneumonia

Rusty

Pneumococcal pneumonia

Pink frothy

Pulmonary oedema

Blood stained

Haemoptysis

Anchovy sauce like

Ruptured amoebic lung abscess

workers’

White Mucoid, viral Odour of the sputum is offensive and foetid in – Lung abscess, Bronchiectasis and Anaerobic bacterial infections


5. How do you grade respiratory dyspnoea? Roizen’s classification is a simple method of grading the severity of dyspnoea. ROIZEN’S CLASSIFICATION Grade of dyspnoea caused by respiratory problems (assessed in terms of walking on a level surface at a normal pace) Category Description 0

No dyspnoea while walking on a level surface at a normal pace( no limitation of distance or pace)

I

Unlimited distance with limited pace “I am able to walk as far as I like, provided I take my time”

II

Limited pace and distance - Specific (street) block limitation (“I have to stop for a while after one or two blocks”)

III

Dyspnea on mild exertion (“I have to stop and rest while going from the kitchen to the bathroom”)

IV

Dyspnea at rest

Higher the grade of dyspnoea more severe will be the disease, decreased cardiopulmonary reserve and increased incidence of post operative pulmonary complications.

6. What concurrent medications the patient can be on and anaesthetic importance of the same? Patient can be on bronchodilators, steroids, mucolytic and mucokinetic agents and may also be on digoxin and diuretics if he/she has chronic cor pulmonale.

BRONCHODILATORS: 1) Beta 2 agonists eg. Salbutamol, terbutaline Chronic use can produce hypokalemia (beta 2 agonists push the potassium in to the cell), there by prolonging the duration of non depolarizers and induce dysrhythmias. Systemically administered beta 2 agonists can lead to dysrrhythmias 2) Xanthines (theophyllines) Interaction with halothane can produce dysrrhythmia. CNS stimulation can lead to a) increased seizure activity and b) lighter planes of anaesthesia


3) Steroids There can be suppression of adreno cortical axis if the patient is on Prednisolone of > 10mg taken for > than 10 days within 10 months. These patients require supplemental doses of steroids before induction. Chronic use can also produce Cushing’s syndrome and all the problems associated with the same.

ANTIBIOTICS : Aminoglycosides antibiotics can prolong the duration of action of NDMRs by blocking the fast calcium channels in the pre junctional nerve ending.

7. Why history of previous tuberculosis disease is important? •

Sputum for AFB to be sent

If positive the patient will be in active infectious stage of tuberculosis. Surgery to be postponed till the patient becomes sputum negative. If emergency surgery has to be done, regional anaesthesia is the preferred choice. If GA has to be given, disposable breathing circuits are to be used.

If patient is on anti tubercular treatment, liver function tests are required as both isoniazid and rifampicin can produce hepatotoxicity.

8. What details would you like to ask regarding previous admission for pneumonia? •

Treatment history-especially h/o management with invasive mechanical ventilation.

If such history is there, then patient may have tracheal narrowing. Hence a history of any post extubation stridor or difficulty in breathing should be taken.

A neck X-ray, AP and lateral view may be taken to know the site and extent of narrowing.

Smaller sized endotracheal tubes may have to be kept ready.

9. Anything important in personal history? H/o Smoking to be taken especially in male patients. Duration and number of cigarettes per day are more important which is expressed as pack years. •

PACK YEARS : number of packs of cigarettes/day × number of years of smoking One pack = 20 cigarettes

> 40 pack years is high risk for post operative pulmonary complications


SMOKING INDEX : number of cigarettes /day × total duration in years – SI <100 mild smoker – SI 100-300 moderate smoker – SI >300 heavy smoker

Anaesthetic importance of smoking – Post operative pulmonary complications are very common and severe in smokers and can lead to increased morbidity and mortality. •

Smoking increases the carboxy haemoglobin levels due to increased carbon monoxide inhalation. Increase in carboxy haemoglobin levels (a) decrease the oxygen carrying capacity of haemoglobin, (b) shift the OD curve to the left and decrease the oxygen release to the tissues, (c) produce spuriously high pulse oximetry readings (oxy haemoglobin and carboxy haemoglobin have the same wave length of 940 Nm and hence pulse oximeter reads carboxy haemoglobin also as oxy haemoglobin. Only Co-oximeter can differentiate between the two and can give the correct saturation readings). The half life of carboxy haemoglobin is 4-6 hours and stopping smoking for 24 hours is enough to reduce the problems associated with it. Normal carboxy haemoglobin levels is < 2% in non-smokers. Whereas it can be as high as 10% in smokers.

Smoking produces hypertrophy and hyperplasia of mucus secreting glands

Impairs ciliary motility and mucociliary transport mechanism leading to infection, atelectasis and collapse.

Inhibits the function of alveolar macrophages and suppresses immune mechanism

Increases airway resistance due to bronchoconstriction

Makes the airways hyperactive.

Increases postoperative pulmonary complications

Induces coronary vasoconstriction producing decreased coronary blood flow.

8 weeks of abstinence from smoking is enough to reduce the above problems.

10. What are the main points to be considered in general physical examination? •

Body Mass Index :


-obesity (BMI >30kg/m2) decreases FRC with relative increase in CC producing increase in intra pulmonary shunts and decrease in pulmonary reserve. - Also decreases thoracic and lung compliance producing restrictive lung disease and exaggerating the problems associated with obstructive disease. - Increased postoperative pulmonary complications due to hypoventilation. -In elective surgeries, obese patient is asked to reduce body weight preoperatively in order to reduce postoperative pulmonary complications. In this patient BMI is 23kg/m2 and hence normal. •

Signs of respiratory distress: Tachypnoea, use of accessory muscles of respiration, and cyanosis.

Pallor – anaemia can exacerbate the respiratory problems by increasing the work of breathing due to anaemic hypoxia.

Cyanosis If cyanosis is present, the arterial haemoglobin saturation with oxygen is 80% or less (Pao2 <50 to 52 mm Hg), which indicates an increased ventilation perfusion mismatch and limited margin of respiratory reserve. It may also indicate the presence of respiratory failure and requirement of oxygen therapy/ mechanical ventilatory support.

Pedal oedema and raised JVP - indication of right heart failure as a result of cor pulmonale.

Clubbing – may be present and should be graded

VITALS •

Fever: indicates infection

Pulse rate: may be irregularly irregular if the patient is in atrial fibrillation and missed beats which can occur as a result of chronic hypoxia.

Blood pressure- postural hypotension if on diuretics for failure.

11. What important findings you would like to get from systemic examination? Respiratory system – Position of trachea If collapse or fibrosis of the lung is present, the trachea may be pulled to the same side. It is likely in this patient as she had pulmonary tuberculosis.


– Respiratory rate and pattern Rate more than 30 with use of accessory muscles of respiration indicates respiratory distress.

-Measurements of chest- barrel chest in emphysematous patients. Chest expansion is normally 5 cms which can be reduced to < 2cms in COPD patients. -obliteration of liver dullness on percussion may be present.

– Breath sounds Bronchial breath sounds may indicate pneumonic consolidation or cavity. Distant sounds are an indication of emphysema Decreased breath sounds heard over fibrosis, collapse, pleural effusion, and pneumothorax. – Added sounds •

Wet sounds (crackles /coarse crepitations) are usually caused by excessive fluid in the airways and indicate sputum retention or edema. Commonly heard over the areas of bronchiectasis.

Dry sounds (wheezes/ rhonchi) are produced by high-velocity gas flow through narrowed bronchi and are a sign of airway obstruction.

Cardiovascular system – Pulmonary hypertension to be ruled out, signs of which include a palpable P2, narrowly split second heart sound, increased intensity of the pulmonary component of the second heart sound, and parasternal heave( right ventricular hypertrophy). If present can be a bad prognostic sign.

Per abdomen In right heart failure - epigastric pulsations, tender hepatomegaly, hepatojugular reflex

12. What investigations should you ask for this patient? Laboratory tests -haemoglobin, total count and differential count, absolute eosinophilic count (>2000/cmm –in tropical eosinophilia, >300/cmm in asthmatics indicate increased risk of peri op


bronchospasm), random blood sugar, blood grouping, typing and cross matching, urine routine, renal function tests, 12 lead ECG to look for P-pulmonale ( P waves with height of > 3 small squares or 0.3 Mv amplitude) and RVH(R/S ratio >1 in V1 and V2), chest x-ray to rule out pneumonic consolidation, sputum for culture and sensitivity and for AFB, Pulmonary Function Tests (PFT) – bed side tests & using spirometry

13. What findings you will look for in the x-ray chest? 

Emphysematous changes like horizontally placed ribs with wide intercostal spaces, flattened domes of the diaphragm, hyper lucent lung shadows and tubular heart will be present.

X ray chest should not be taken to confirm these changes as one can expect these changes after clinical examination alone.

Main aim is to rule out pneumonitis or malignancy.

14. What ECG findings may be present? •

Features of right atrial and right ventricular hypertrophy with strain.

Low-voltage QRS complex due to lung hyperinflation and poor R-wave progression across the precordial leads.

An enlarged P wave (“P pulmonale”) of amplitude > 3 small squares in standard lead II is diagnostic of right atrial hypertrophy. Right ventricular hypertrophy, R/S ratio of greater than 1.0 in lead V1 and V2 (i.e., R-wave voltage exceeds S-wave voltage).

15. Enumerate the static and dynamic lung function tests STATIC TESTS Force is not used by the patient and not time based •

Divided into 4 lung volumes and 4 lung capacities.

2 or more lung volumes together comprise a capacity


Lung volumes

Lung capacities

1.Tidal volume

1.Vital capacity

2.Inspiratory reserve volume

2. Total lung capacity

3.Expiratory reserve volume

3.Functional residual capacity

4.Residual volume

4. Inspiratory capacity

DYNAMIC TESTS Force is used and they are time based. Includes •

Maximum breathing capacity, Forced vital capacity, Forced expiratory volume in first second (FEV1), Maximum mid expiratory flow rate, Peak expiratory flow rate, Respiratory muscle strength

16. Describe the bed side lung function tests? 1) SABRASEZ BREATH HOLDING TEST: This is done mainly to test the cardio pulmonary reserve of the patient. Patient is asked to take deep inspiration and hold the breath as long as possible. Listen by keeping a stethoscope over the trachea to identify early expiration normal > 40 secs; <25 secs indicates decreased ventilatory capacity; <15 secs – poor cardiopulmonary reserve 2) SNIDER’s MATCH BLOWING TEST : Mainly reveals expiratory capacity and maximum breathing capacity of the patient. A lighted candle is kept in front of the patient at a distance of 6 inches. Patient is asked to blow the candle with the mouth open without pursing the lips. If patient can’t blow out the candle at 6 inches, MBC< 100 lts/min and FEV1 <1.6 litres •

Can also be done by keeping the lighted candle at 9 inches and 3 inches

If the patient can blow at 9 inches, MBC > 150lts/min

If the patient can blow at only 3 inches then MBC is 50lts/min

3) DE BONO’S WHISTLE Used to calculate the PEFR of the patient. •

It is a whistle with adjustable diametered aperture. Patient is asked to blow the whistle with the aperture maximally open.


If not possible then the aperture size can be reduced and patient is again asked to blow the whistle. The size of the aperture at which the patient can blow the whistle is noted. For each size of the aperture PEFR values are given on the whistle.

4) AUSCULTATION OVER THE TRACHEA : •

performed during a forced expiration

normal is 3 to 4 secs

> 6 secs indicates obstructive airway disease

5) WRIGHT’S RESPIROMETER For measuring tidal volume and minute volume. 6) WRIGHT’S PEAK FLOW METER For measuring PEFR. 17. What are the three legged stool assessment of pulmonary function? Tests are done to assess the respiratory mechanics, parenchymal functions of the lung and cardiopulmonary reserve of the patient.

3 legged stool Prethorocotmy respiratory assessment

Lung mechanics FEV1 (ppo > 40%) MVV FVC RV/TLC

Pulmonary parenchymal functions DLCO (ppo >40%) Pao2 >60 Paco2<45

Cardiopulmonary reserve VO2max >15ml/kg/min Stair climbing >2 flights 6 min walk test Exercise SPO2 <4%

18. Based on PFT, how do you assess the severity of COPD patients? Stages Stage 0 At risk Stage 1 Mild Stage 2 Moderate

Characteristics Normal spirometry Chronic symptoms ( cough, production) FEV1/FVC < 70% FEV1> 80% predicted With or without symptoms FEV1/FVC < 70% FEV1 50-80% predicted

sputum


Stage 3 Severe Stage 4 Very severe

With or without symptoms FEV1/FVC < 70% FEV1 30-50% predicted With or without symptoms FEV1/FVC < 70% FEV1<30% predicted or FEV1 <50% with chronic respiratory failure With or without symptoms

19. What is Shapiro et al scoring system for respiratory disease patients posted for thoracic and upper abdominal surgeries? PARAMETER 1. EXPIRATORY SPIROGRAM a. % FVC + FEV1 /FVC > 150 b. % FVC + FEV1 /FVC 100 -150 c. % FVC + FEV1 /FVC < 100 d. Preoperative FVC < 20ml/kg e. Post bronchodilator FEV1/FVC <50% 2. CVS a. normal b. controlled HTN, recent MI without sequel > 2yr

SCORING 0 1 2 3 3 0 0

c. signs of CCF 1 3. CNS a. normal 0 b. confusion, disoriented, obtunded, spasticity, agitation, 1 bulbar malfunction c. significant muscle weakness, paraplegia, hemiplegia 1 4. ABG a. normal 0 b. PaCO2 >50, PaO2 <60 1 c. ph >7.5 or <7.3 1 5. POST OP AMBULATION a. within 36 hours 0 b. bed confinement >36hours 1 Pre operative score zero - minimal incidence of post op pulmonary complications Score 1 to 2 â&#x20AC;&#x201C; moderate risk, require post op supplemental oxygen and incentive spirometry. Score >3 â&#x20AC;&#x201C; high risk patient, requires management in the intensive care unit post operatively, with intensive monitoring and assisted with pulmonary toileting at least for 24 hours.

20. How ABG analysis will help in this patient?


Arterial blood gas data such as PaO2 less than 60 mm Hg or PaCO2 greater than 45 mm Hg have been used as cut off values for pulmonary resection

It also helps in pre operative preparation and deciding about post operative care regarding supplemental oxygenation / mechanical ventilation as per Nunn and Milledge classification.

21. What is the importance of ppo FEV1? •

Patients with a ppo FEV1 greater than 40% are at low risk for post resection respiratory complications.

The risk of major respiratory complications is increased in the subgroup with a ppo FEV1 less than 40% (although not all patients in this subgroup develop respiratory complications)

Patients with a ppo FEV1 less than 30% are at high risk of major respiratory complications

22. How do you calculate the predictive post operative FEV1 and the functional lung tissue to be removed? PPO FEV1 = pre op FEV1 X (1 - % functional lung removed/100) % Functional lung removed = number of sub segments removed / total sub segments X 100 In this patient: After left lower lobectomy with a pre operative FEV1 (or DLCO) 65% of normal would be expected to have a predictive post operative FEV1 = 65% × (1 - 24/100) = 50%.

23. What is the importance of VO2 max, 6 min walk test and staircase climbing? •

Formal laboratory exercise testing is currently the “gold standard” for assessment of cardiopulmonary function, and the maximal oxygen consumption (VO2 max) is the most useful predictor of post-thoracotomy outcome.

The risk of morbidity and mortality is unacceptably high if the preoperative VO2 max is less than 15 mL/kg/min.

Post resection exercise capacity can be estimated based on the amount of functioning lung tissue removed. An estimated ppoVO2 max less than 10 mL/kg/min may be an absolute contraindication to pulmonary resection. (mortality 100%)

The distance that a patient can walk during a 6-minute walk test (6MWT) also shows an excellent correlation with VO2 max and requires little or no laboratory equipment.


A 6 MWT distance of less than 2000 ft (610 m) correlates to a VO2 max less than 15 mL/kg/min

Stair climbing is done at the patient's own pace but without stopping and is usually documented as a certain number of flights.

There is no exact definition for a “flight”, but 20 steps at 6 inches /step is a frequent value.

PERFORMANCE

VO2

MAX INTERPRETATION

EQUIVALENT > 5 FLIGHT OF STAIRS > 20 ml/kg/min

FEV1 >2L – low mortality after pneumonectomy

>3 FLIGHT OF STAIRS >15 ml/kg /min

FEV1 of 1.7l – low mortality after lobectomy

<2 FLIGHT OF STAIRS <12ml/kg/min

Correlates with high mortality

< 1 FLIGHT OF STAIRS <10ml/kg/min 6min walk test 610m

15ml/kg/min

24. How do you prepare this patient for surgery? RESPIRATORY PREPARATION MANEUVERS 1. Abstinence from smoking : cessation for > 4-8wks - ↓incidence of postoperative complications - 12-48hrs ↓ CO Hb concentration - ↑O2 carrying capacity & ODC shifted back to right. Beneficial effects of smoking cessation & time course TIME COURSE

BENEFICIAL EFFECT

12 – 24 hr 48 – 72 hr

↓ CO & nicotine levels CO Hb levels normalized , ciliary function improves ↓ sputum production PFT’S improve Immune function & metabolism normalizes ↓ overall postoperative morbidity & mortality

1-2 wk 4 – 6 wk 6 -8 wk 8 – 12 wk


2. Dilating airways: a. Bronchodilators & sympathomimetics b. Parasympatholytics c. PDE inhibitors Aminophylline – Loading dose 5 mg/kg, Smokers 7mg/kg( smokers require increased doses as there will be hepatic microenzyme induction and hence increased metabolism), Under GA reduce by 2mg/kg( under GA there is a reduction in the hepatic blood flow and hence decreased requirement.) Infusion – 0.5 mg/kg/hr, smokers -- 0.7 mg/kg /hr, under GA reduce by 0.2mg/kg/hr Therapeutic concentration 10-20 mg/L Advantages 

Stimulates respiratory centre and improves respiration.

Increases the contractility of the diaphragm

Direct bronchodilatory effect

Bronchodilatation through PDE inhibition and increasing cAMP and also by increasing the endogenous catecholamine levels by anti adenosine effect

Improves the inotropy of the heart and decreases the peripheral vascular resistance, thereby improving the cardiac output and decreasing the dead space.

Disadvantages 

By increasing the endogenous catecholamine levels by anti adenosine effect, increases the automaticity of the heart and increases the incidence of dysrhythmias.

Interacts with halothane producing cardiac dysrhythmias. Halothane can be safely used 4 hours after the last dose of Aminophylline.

Aminophylline is not routinely used as a bronchodilator nowadays due to its dysrhythmogenic effect.

Steroids

Cromolyn sodium as a prophylactic drug.

3. Loosening secretions: a. Mucolytics: N- acetyl cysteine, potassium iodide b. Airway hydration c. Humidification by ultrasonic nebulizers d. Systemic hydration to correct hypovolemia and electrolyte imbalance

4. Removing secretions: a. Postural drainage b. Coughing c. Chest percussion & vibration d. Forced expiration technique


5. Adjunct medications: a. Antibiotics after culture & sensitivity b. Antacids – H2 blockers or proton pump inhibitors – if symptomatic reflux is present.

6. Measures to motivate: Psychological preparation b. Preoperative pulmonary care training -incentive spirometry -secretion removal maneuver c. Pre op exercises, d. Weight loss/gain e. Stabilize other medical problems

7 Prophylaxis against AF/Flutter: Dysrrhythmias like atrial flutter and fibrillation are common during the peri operative period due to hypoxemia. Drugs commonly used to prevent these area. A. Digoxin. b. Calcium channel blockers - Diltiazem – currently best c. Beta blockers d. Amiodarone

25. Why is airway assessment in a patient requiring one lung ventilation important? Patient’s airway must be assessed for the ease of intubation with double lumen endotracheal tube. A difficult airway is a relative contra indication for introduction of a double lumen endotracheal tube. Other things to be considered are 

At the time of the pre operative visit, there may be a history or physical findings that lead to suspicion of difficult endobronchial intubation (previous radiotherapy, infection, prior pulmonary or airway surgery)

The most useful predictor of difficult endobronchial intubation is the plain chest radiograph.

Distal airway problems not detectable on the plain chest film can sometimes be visualized on the CT scan.

A side-to-side compression of the distal trachea, the so-called saber-sheath trachea, can cause obstruction of the tracheal lumen of a left-sided DLT during ventilation of the dependent lung for a left thoracotomy.

Similarly, extrinsic compression or intraluminal obstruction of a mainstem bronchus that can interfere with endobronchial tube placement may be evident only on CT.


An anaesthesiologist should always look at the CT scan of the thorax of the patient to complete the assessment of the airway.

The major factors in successful lower airway management are anticipation and preparation based on the pre operative assessment.

26. What are the indications for one lung ventilation? ABSOLUTE 1. Isolation of each lung to prevent contamination of a healthy lung Infection (abscess, infected cyst), massive hemorrhage a. Control of distribution of ventilation to only one lung Bronchopleural fistula, bronchopleurocutaneous fistula, unilateral cyst or bullae, major bronchial disruption or trauma b. Unilateral broncho pulmonary lavage c. Video-assisted thoracoscopic surgery d. Differential broncho spirometry (split lung function tests)

RELATIVE 1. Surgical exposure—high priority - Thoracic aortic aneurysm, pneumonectomy, lung volume reduction, minimally invasive cardiac surgery, upper lobe lobectomy

2. Surgical exposure — low priority - Esophageal surgery, middle and lower lobectomy, mediastinal mass resection, thymectomy bilateral sympathectomies 27. What are the different methods of the lung separation? •

Three types of devices available

1. Double lumen tubes (DLT’s): The most common technique 2. Bronchial blockers: Involves blockade of a main stem bronchus to allow lung collapse distal to the occlusion. These bronchial blockers can be used with a standard endotracheal tube or contained within separate channel inside a modified SLT such as the Univent tube. Ex: Arndt, Cohen, Fuji


3. Endobronchial tubes with single lumen (SLTs): Advanced into the contra lateral main stem bronchus, protecting this lung while allowing collapse of the lung on the side of surgery.

28. What are the different double lumen tubes you know? Robertshaw tubes both right sided and left sided. Made of either red rubber-reusable or PVC single use - most commonly used, Carlen’s tube with a carinal hook (left sided), Carlen’s right sided – White’s tube Bryce Smith-left sided, Salt- right sided

29. How the right and left sided double lumen tubes are identified? The DLT is held with the concavity of the tracheal portion facing anteriorly, the direction with which the endobronchial portion faces is the side of the tube. The right sided DLT also has Murphy’s eye in the cuff of the endobronchial portion for ventilation of the right upper lobe bronchus.

30. What is the method of insertion of double lumen ETT? Two techniques are used commonly when inserting and placing a DLT.

(A) BLIND TECHNIQUE: The DLT is introduced with the direct laryngoscopy with the concavity of the endobronchial portion facing anteriorly .Once the endobronchial portion crosses the glottis the DLT is turned 90 degrees to the side to which it belongs and then pushed till a resistance is encountered. The DLT should pass the glottis without any resistance. The optimal depth of insertion for a left-sided DLT is strongly correlated with the patient's height in average-sized adults. In adults, depth measured at the teeth, for a properly positioned DLT will be approximately 12 + (patient height/10) cms.

(B)USE OF FIBRE OPTIC BRONCHOSCOPE TO INSERT DLT The direct vision technique uses bronchoscopic guidance, in which the tip of the endobronchial lumen is guided into the correct bronchus after the DLT passes the vocal cords using direct vision with a flexible fiberoptic bronchoscope. The cuff of the endobronchial portion appears as brilliant blue with FOB.

31. How do you select Double-Lumen Tube size based on adult patients’ sex and height?


Height

Sex

(cm)

Female

Size (Fr)

<160 (63 35 in.) *

Female >160

37

Male

<170 (67 39 in.) †

Male

>170

41

For females of short stature (< 152 cm or 60 in.), examine bronchial diameter on CT scan and consider 32 Fr.

For males of short stature (<160 cm or 63 in.), consider 37 Fr

Size 25 Fr is also available for young adults and children

32. What is the position adopted for lung surgery and the associated complication? Lateral decubitus position is always adopted for lung surgeries. •

Neurovascular complications Brachial plexus – commonly injured, compression injury of dependant arm, stretch

injury of non-dependant arm Factors Contributing to Brachial Plexus Injury in the Lateral Position •

Dependant arm (compression injuries)

- arm directly under thorax, pressure on clavicle into retroclavicular space, cervical rib, caudal migration of thorax padding into axilla •

Non-dependant arm (stretch injuries)

- lateral flexion of cervical spine, excessive abduction of arm (>90 ͦ), semiprone or semisupine repositioning after arm fixed to a support Other injuries •

Dependent eye, dependent ear pinna, cervical spine in line with thoracic spine , dependent and nondependent suprascapular nerves, nondependent leg: sciatic nerve dependent leg: Peroneal nerve

33. What drugs are used for premedication before lung surgeries?


On the day before surgery a. Anxiolytics b. H2 receptor blockers c. Continue bronchodilator nebulization d. Continue steroids

On the day of surgery – Steroid supplementation: if the patient is on steroids before.

1. For minor surgery 100mg hydrocortisone IV one hour before induction and 100 mg infusion over 24 hours 2. For major surgery 100 mg one hour before induction and 100mg 8th hourly for 48 hours. –Bronchodilators: 2 puffs of inhalations before shifting onto the operating table. The same bronchodilator device to be kept near the patient for use during surgery if required. –Opioids: Long acting drugs like morphine to be avoided as they produce post operative respiratory depression. Short acting drugs like fentanyl 1-2 µg/kg body weight given intravenously before induction. –Benzodiazepines: Diazepam 10 mg oral previous night, Midazolam 0.01 to 0.05 mg/kg I.V. before induction –Anticholinergics: to be avoided as they increase the viscosity of the secretions and also increase the dead space. They may also produce unwanted tachycardia and dry mouth.

34. What induction agents are used and their advantages and disadvantages? PROPOFOL Advantages: Rapid onset, airway reflexes obtunded, direct bronchodilator, reduces post operative nausea and vomiting, antiarrhythmic, suppression of intubation responses Disadvantages: Pain on injection, hypotension, bradycardia KETAMINE Advantages: Profound analgesia, good bronchodilator, maintains HR, BP, decreases post operative shivering Disadvantages: Increased secretions, airway reflexes exaggerated, emergence delirium, hypertension and tachycardia. Increased systemic and pulmonary vascular resistance, increased O2 demand by the myocardium worsening the coronary artery disease, dysrhythmias

THIOPENTONE SODIUM Advantages: Rapid onset, no pain on injection, cost effective


Disadvantages: Sensitises airways (bronchospasm) under lighter planes of anaesthesia, no bronchodilation, hypotension, no supression of intubation response

INHALATIONAL INDUCTION Used in children and in patients with difficult airway. Potent inhalational anaesthetics may prevent development of bronchospasm by -Blocking airway reflexes, Direct relaxation of smooth muscles of airway, Inhibition of mediator release Halothane and sevoflurane are preferred

35. What are the monitors used for this patient? Non invasive monitors Pulse oximetry, ECG, end tidal CO2, NIBP, temperature, and neuromuscular monitoring. A chest stethoscope may be placed over the dependent hemithorax to assess dependent lung ventilation. Pulse oximetry, which is a standard of care, is especially valuable during thoracic surgery because hypoxemia may occur during OLV.

Invasive monitoring – Direct arterial line, central venous pressure and transoesophageal echocardiography may be required in major surgeries like pneumonectomy, and lung transplant and also in patients with cardiovascular compromise

36. How do you diagnose and manage peri operative bronchospasm? Diagnosed by a sudden increase in resistance to ventilation or peak inspiratory pressure on ventilator. Other causes which mimic a bronchospasm with increased resistance to ventilation or increase in peak air way pressure should be ruled out before diagnosing bronchospasm. (a) Lighter plane of anaesthesia- deepening with additional doses of volatiles, I.V. anaesthetics, opioids and muscle relaxants will decrease the resistance and PIP. (b) Obstruction of the tube – either kinking, obstruction by foreign body or secretions, bevel of the tube abutting against the tracheal wall – passing a suction catheter easily will rule out this problem.


(c) Endobronchial intubation if a single lumen ETT is used. – pulling out the tube will relieve the problem. (d) Tension pneumothorax – absence of breath sounds, decreased chest movement and hyper resonance on the side of tension pneumothorax with hypotension and desaturation will clinch the diagnosis. A 16G needle passed through 2nd intercostal space in the mid-clavicular line as a life saving measure will relieve the tension pneumothorax. (e) Aspiration of stomach contents – more common in full stomach patients. (f) Pulmonary oedema – crepitations, cyanosis and pink frothy sputum through the tube – common in cardiac patients. Management of bronchospasm– - cut off N2O, - give 100% O2 - deepening the plane of anaesthesia with volatile agents and muscle relaxant top up dose If bronchospasm persists, institution of bronchodilator therapy •

Subcutaneous terbutaline, Corticosteroids, Xanthines If bronchospasm still persists, then

Inj Lignocaine – 1mg/kg I.V. bolus with 1mg/kg/hr infusion

Ketamine infusion – 0.5mg/kg I.V. bolus with 0.5 mg/ kg/ hr infusion MgSO4 - 2gm I.V. bolus

37. How do you ventilate this patient during one lung ventilation? PARAMETERS

SUGGESTED

GUIDELINES/EXCEPTIONS

TIDAL VOLUME

5 – 6 ml/kg

Maintain peak airway pressure

<35cm

H2O Plateau pressure< 25 cm of H2O PEEP

5cm of H2O

With COPD, not added

RR

12 bpm

Maintain normal PaCO2 (30-40 mm hg)

MODE

VCV/PCV

PCV for patients with risk of lung injury (bullae, spontaneous pneumothorax)


38. How do you treat desaturation during one lung ventilation? THERAPIES FOR DESATURATION DURING OLV Severe or precipitous desaturation: Resume two-lung ventilation (if possible). Gradual desaturation: 1. Ensure that delivered FiO2 is 1 2. Check position of DLT or blocker 3. Ensure that cardiac output is optimal, decrease volatiles to < 1 MAC 4. Apply recruitment maneuver to the ventilated lung 5. Apply PEEP – 5cm H2 O to ventilated lung 6. Apply CPAP – 1-2cm H2 O to non-ventilated lung 7. Partial ventilation techniques 8. Intermittent re-inflation of non-ventilated lung 9. Mechanical restriction of blood flow to the non-ventilated lung

39. How do you time the extubation based on ppo FEV1 of the patient?

40. How do you provide post operative analgesia? 1. SYSTEMIC ANALGESIA a. opioids - Intermittent IM /IV, continuous IV infusion, subcutaneous infusions, PCA, Transdermal, fentanyl & Sufentanil, sublingual buprenorphine b. NSAIDs –Acetaminophen – 4g/day, orally/rectally c. Ketamine – low dose IM or 1mg, IV infusion d. Alpha 2 agonists -Dexmedetomidine 0.3-0.7µg/kg/hr, clonidine - 150µg IV infusion 2. INTRAPLEURAL ANALGESIA -produce multi-level intercostal block, less reliable 3. TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION


4. CRYOANALGESIA - 20 ͦc – degeneration of nerve axons 5. EPIDURAL ANALGESIA -Thoracic epidural T3 – T8, Bupivacaine, Opiates combined with LA, Fentanyl, dimorphine, Sufentanil, morphine are effective, Bupivacaine – 0.0625 – 0.125%, Morphine – 0.050.1mg/ml, Fentanyl – 2µg/ml, Mixed agonist/antagonist like butorphenol, buprenorphine & nalbuphine also used 6) PARAVERTEBRAL BLOCK - catheter can be placed in the paravertebral space either percutaneously or directly when chest is open.

41. What are the common post operative complications? 1. PULMONARY COMPLICATIONS •

Infections – atelectasis, pnuemonia, empyema & mediastinitis

Pnuemothorax & tension pneumothorax

Postpnuemonetomy pulmonary edema

Torsion of residual lobe, Postoperative respiratory failure

2. CARDIOVASCULAR COMPLICATIONS •

Right sided heart failure, dysrhythmias, right – left shunting through foramen ovale

Myocardial ischemia & infarction, postoperative hypertension, herniation of heart

3. ANATOMICAL STRUCTURE INJURIES •

Phrenic nerve, recurrent laryngeal nerve, spinal cord, brachial plexus,

Thoracic duct, injuries related to lateral decubitus position

4. WOUND INFECTION & SEPSIS

42. What are the causes of post operative hypoxemia? 1.

Diffusion hypoxia or Fink effect

2. Increased V/Q mismatch – anaesthesia produces a reduction in FRC as a result of decrease in the tone of the diaphragm and diaphragm rests high in the thorax due to relative increase in the intra abdominal pressure. The consequences of this are more in the elderly and smokers. There is an increase in closing capacity which will be higher than FRC which increases intrapulmonary shunt. 3. Reduced cardiac output – causes decrease in the oxygen flux which may be insufficient to meet the patient’s O2 demand especially if he is shivering. The fall in mixed venous PO2 will then produce a fall in arterial PO2 with further reduction in O2 flux. The situation will be made worse if the patient is anaemic as well.


4. Hypoventilation (a)

Drugs – most anaesthetic drugs depress ventilation. The residual effects of premedicants, induction agents, maintenance agents, and analgesics can produce post op hypoventilation .Opioids and muscle relaxants are the most common causes of drugs causing post op hypoventilation.

(b)

Obstruction - Partial respiratory obstruction in the post op period is often not recognized immediately.

(c)

Pain – may prevent from deep breathing and also from coughing. This causes both hypoventilation as well as atelectasis and collapse of the alveoli.

(d)

Intra operative hyperventilation – producing considerable total body deficit of CO2

producing

hypoventilation

when

patient

is

made

to

breathe

spontaneously. (e)

Tight abdominal binders after abdominal surgeries.

ACKNOWLEDGEMENT I sincerely thank my post graduates Dr Shwetha K.M. and Dr Shalini for their help in preparing this manuscript


A DIABETIC PATIENT FOR BELOW KNEE AMPUTATION Dr Madhusudhan.U Professor & HoD, Kasturba Medical College, Mangalore

Dr Ravikumar.C Professor of Anaesthesiology, JJM Medical College, Davangere.

58 year old female, diabetic for past 20 years, is on irregular treatment presented with wound in the right foot for the past 2 months. O/E: Patient is dehydrated, febrile PR= 110/min, BP=100/60 Investigations: Blood Sugar= 450 mg/dl; Blood urea= 67 mg/dl; Serum creatinine= 1.8 mg/dl Serum Na+= 140 mEq/l, Serum K+=4.5 mEq/l Urine ketone bodies= positive X- ray leg showed osteomyelitis of tibia lower end Patient is posted for emergency below knee amputation

Points for discussion:  Discuss microvascular and macrovascular complications of DM, and their anesthetic implications  Tests for autonomic neuropathy  Patient optimization pre op and anesthetic management for emergency and elective surgery  Different insulin regimes  DKA, HHS  Briefly discuss gestational diabetes mellitus


Questions: 1

How do you classify DM etiologically?

2

What is the mechanism of release of insulin from beta cells?

3

Name the tissues which require insulin and which do not require insulin?

4

Discuss the pathophysiology of type I DM

5

Discuss the pathophysiology of type II DM

6

Difference between type I and II DM

7

Criteria for diagnosis of DM

8

Acute and chronic complications of DM

9

Pre operative evaluation and airway assessment tests for autonomic Neuropathy, investigations 10 Pre operative optimization of elective surgery 11 Pre operative optimization of emergency surgery 12 Choice of anaesthesia 13 Anticipated intra operative complications 14 Types of insulin regimens NTCR/ TCR 1 and TCR 2 15 Pathophysiology of DKA 16 Principles of management of DKA in ICU 17 Difference between DKA and HHS 18 Treatment goals of DM 19 Define gestational diabetes and pathophysiology 20 Intra operative complications of gestational DM


PATIENT WITH END STAGE RENAL DISEASE FOR RENAL TRANSPLANTATION Dr Sunita.U, Professor and HoD, Vaidehi Institute of Medical Sciences, Bangalore

Dr Sanikop.S, Professor & HoD, JNMC, Belgaum

32 Year old, male patient, known case of CRF due to membranoproliferative glomerulonephritis. C/O Generalized weakness and vomiting on and off for the past one year. Patient is undergoing hemodialysis for the past 3 months three times a week. O/E patient is thin built, anemic and has pitting pedal edema. Investigations Hb-6.8%, PT/INR-1.2 Patient is on oral Amlodipine 2.5mg OD and tab Atenolol 25mg BD, patient is planned for renal transplant , donor being his wife.

Questions:

1. What are the salient signs, symptoms and investigation which suggest the diagnosis in this patient. 2. What are the organ systems involved in CRF and their influence on anesthetic management 3. What do we mean by pre-operative optimization. 4. Pre-operative evaluation of recipient posted for renal transplant. 5.

What pre-operative medications these patients are on and its anesthetic implications.

6. Can we post pone renal transplant case and under what circumstances? 7. Differences between live donor and deceased donor kidney. 8. What monitoring would be appropriate for renal recipient?


9. How GA varies in renal recipient when compared to ASA grade 1 patient receiving GA 10. How RA is different in transplant patient when compared to ASA grade 1 patient receiving RA 11. Does technique of Anesthesia has any bearing on post op outcome or controversial issues of RA and GA for renal recipient 12. What are the common incidental surgeries in patients with CRF. 13. Does post-transplant recipient kidney differ any way from what it was in donor and does it make sense to Anesthesiologist. 14. What are the commonly encountered pitfalls while anesthetizing CRF patients either for transplant or for incidental surgical procedures 15. Carry home messages.


PRIMIGRAVIDA WITH PREGNANCY INDUCED HYPERTENSION Dr Kodandaram.N.S, Prof & HoD, ESIC - PGIMSR, Bangalore

Dr Rangalakshmi, Prof & HoD, Sri Raja Rajeshwari Medical College, Bangalore.

30 years old primigravida with 36 weeks amenorrhea was admitted to the hospital with history ofheadache. She is diagnosed to have PIH from 28 weeks of gestation and is on tab methyldop a 250 mg thrice daily since then. O/E: She is moderately built, anaemic, pitting pedal edema is present. PR= 108 bpm. BP= 160/110 Patient is evaluated for PIH profile Hb-7.8 g%; SGPT- 183 IU/ml; SGOT- 210 IU/ml; platelet=1 lakh/ cumm

Points for discussion:  Pathophysiology of PIH/Anesthetic Implications/ Complications of PIH  Anaesthetic management for elective/ emergency caesarean section  Labour analgesia in this patient  Briefly discuss anaemia in pregnancy


Questions

Pregnancy induced hypertension 1. Classify hypertensive disorders in pregnancy. 2. What are the criteria to diagnose pre-eclampsia- eclampsia ? 3. What is the significance of proteinuria in pregnancy ? 4. Outline pathogenesis & pathophysiology of pre-eclampsia- eclampsia 5. What is hellp syndrome, partial hellp syndrome & their differential diagnosis 6. How will you manage hellp syndrome ? 7. When will you plan for delivery of the baby in pih 8. What drugs are used / not to be used to treat htn in pregnancy? 9. What are the precautions taken while using mgso4 ? 10. What is the optimum fluid therapy in pih;what types of fluid should be used and how

will you monitor hydration status of the patient ?

Anaesthesia in patients with PIH for LSCS

1. How will you manage general anesthesia in a patient with preeclampsia ? 2. What is the role of epidural anaesthesia ? can we conduct spinal ? 3. What are the anaesthetic problems in pih ? 4. How do you manage eclampsia ? 5. What measures are advised to ensure fetal maturity in pih ?

Anaesthesia for elective LSCS

1.

What are the physiologic changes in the normal course of a pregnancy ?

2.

How conducting neuraxial blockade is different in pregnant patients from non-pregnant women?

3.

What are the airway concerns in anaesthetising a pregnant lady ?

4.

What is tunstall drill?

5.

List the complications of epidural anaesthesia.


6.

Name post-op complications that may land a lady into icu after delivery despite an apparently normal antenatal history.

Anemia in pregnancy

1. What is physiological anemia of pregnancy ? 2. What is bohr’s shift & double bohr’s shift ? 3. Effect of maternal anemia on foetus ? 4. What is common cause of anemia in pregnancy ? 5. Total dose iron infusion ?

Labour analgesia

1. Why is labour analgesia important ? 2. Differentiate first from second stage pain. 3. What is differential block ? 4. Enumerate pain pathways in labour & corresponding technics to block them. 5. What is entonox ? what is poynting effect ? 6. What are possible drawbacks of lumbar epidural block from obstetrician’s view ? 7. Which local anaesthetics are preferred for labour analgesia & why ? 8. Timing of epidural initiation ? 9. Contraindications to lumbar epidural block ? 10. Use of narcotics in epidural block. what is “walking epidural” ?


A PATIENT WITH OBSTRUCTIVE JAUNDICE FOR LAPAROSCOPIC CHOLECYSTECTOMY Brig. (retd.) Dr C.V.R.Mohan, Prof & HoD, M.S.Ramaiah Medical College and RI, Bangalore.

Dr Chidananda Swamy, Senior Consultant, BGS Global Hospital, Bangalore

A 50 year old female patient presents with history of jaundice 3 months ago and pain in the right hypochondrium with anorexia and nausea since 1 month. She is diagnosed to have Gallstones and is posted for a laparoscopic cholecystectomy.

Points for discussion: Anaesthetic implications Investigations and pre operative optimization of the patient Anaesthetic management for laparoscopic cholecystectomy Brief discussion on liver transplant in cirrhotic patient and post operative jaundice o Halothane hepatitis o o o o

Questions: •

Please sum up the case.

What are the symptoms of liver disease?

What are the types of jaundice?

How do you clinically differentiate them?

What is your clinical impression?

What are the routine and specific tests done?

What is your clinical diagnosis?

What is the differential diagnosis?

What is the aetiopathogenesis of viral hepatitis?


What is the treatment of infective hepatitis?

What other viruses cause hepatitis?

What is drug induced hepatitis?

Which enzyme is a sensitive marker to mild post –op hepatitis?

What is the cause?

Immune Mediated (Halothane) Hepatitis •

What is the incidence?

What is the aetiopathology?

Which inhalational agent is safe in this regard?

And why?

How do you investigate a post op hepatic dysfunction?

Anaesthetic implications of cholestasis •

What are the anaesthetic implications of cholestasis?

What are the anaesthetic implications of cholestasis?

Management •

What are the treatment options for cholelithiasis?

What are the advantages of Lap Cholecystectomy over open cholecystectomy?

Investigations •

What investigations are mandatory pre-operatively?

Scoring the Hepatic dysfunction •

What are the various scores to evaluate the liver dysfunction?

How do you optimize the patient with liver dysfunction before surgery?


A PATIENT WITH IHD AND HYPERTENSION FOR RIGHT HEMICOLECTOMY Dr. Murali.R.Chakravarthy, Chief Consultant, Fortis Hospital, Bangalore

Dr. Gangadhar.S.B Professor & HoD, Siddhartha Medical College, Tumkur

A 60 years old male is posted for right hemicolectomy for colon cancer. Patient is a known hypertensive for past 10 years. Past history also reveals post PTCA status (1 year back). Patient is on regular medication with clopidogrel, aspirin, metaprolol, isosorbide and nifedipine. O/E: PR= 60 bpm, BP=140/90 mm Hg ECG= Q waves in lead II, III, aVF & T wave inversions V5 & V6 Echo= global hypokinesia of heart with ejection fraction 38%

Points for discussion:  Preoperative optimisation and perioperative management of the above patient coming for 1. elective upper abdominal surgery, 2. emergency upper abdominal surgery [Duodenal ulcer perforation] 3. DHS for fracture neck of femur 

Investigations and treatment of IHD

Transfusion trigger in an IHD patient

Anesthetic implications and ACC/AHA guidelines

Postoperative pain management


Questions:

1. For elective surgeries with patient on multiple antihypertensive medications what blood pressure do you take it as acceptable 2. What class of antihypertensive medications is to be continued and what to be stopped prior to the surgeries 3.How does the type of stent placed during PTCA important in the management of this patient 4.What are the pre op investigations you would like to ask . 5. what are the intra op monitors you would like to ask 6. Induction agent of choice for this case in elective and emergent surgeries 7. Maintenance of anaesthesia - inhalational agents of choice. 8. Analgesia preffered intra op and post operative period 9. What emergency drugs would you like to keep available inside OR 10. ASRA guidelines. 11. PA catheterisation in this case and its importance. 12. Intra – op fluid therapy – what to use. 13. How to prevent intra – op and post – op hypothermia and shivering 14. How to prevent and treat intra – op arrhythmias 15. What other details of his previous CAG and current 2D-echo is important for this case management 16. How to prevent intra op blood loss during DHS surgery 17. Post op analgesia in emergency surgeries 18. Post op troponin measurement and its importance. 19. Post operative chest physiotherapy and its importance 20. Post – op oxygen therapy.


PATIENT WITH GRAVES DISEASE POSTED FOR THYROIDECTOMY

Dr. Safia Shaikh, Professor & HoD, KIMS, Hubli

Dr.Ragavendra Rao, Professor & HoD, SDM College of Medical Sciences & Hospital Dharwad

36 yrs old female complains of neck swelling for the past one year with size of the mass grad ually increasing. Patient has history of dyspnoea, dysphagia , weight loss, palpitations, heat intolerance and oligomenorrhoea. O/E: patient is thin built with prominent eyeballs PR= 120 bpm, BP= 160/100 ECG revealed sinus tachycardia TFT values are depicting moderate hyperthyroid state Hb = 9 gm% with Hematocrit 27% Antithyroid antibodies is positive. The case is diagnosed as Grave’s disease and is posted for near total thyroidectomy. Points for discussion: ●Anaesthetic implications of hyperthyroidism ●Preoperative preparation and peri operative Anesthetic management ●Intraoperative and postoperative complications ●Postoperative pain management ●Discuss in brief Anaesthetic implications of hypothyroidism


Questions: 1. What is the diagnosis of the above clinical scenario? 2. How is the thyroid hormone synthesised in the body? How is its synthesis regulated? 3. What is the role of thyroid hormone in maintaining vital organ system physiology? 4. What is the normal daily secretion of thyroid hormone and their normal serum values? 5. What are the causes of hyperthyroidism? 6. What are the clinical symptoms and signs of thyroid disease? 7. What specific things are you seeking in the examination of a patient with neck swelling? 8. How do you assess airway obstruction clinically due to thyroid swelling? 9. What is retrosternal goitre? What are the types? 10. What is superior vena caval syndrome? How will you diagnose it? 11. Describe thyroid function tests. How will you interpret? 12. Which investigations to be ordered to rule out airway obstruction in this patient? 13. How will you medically optimise this patient preoperatively to euthyroid state? 14. What is the role of beta blockers in this patient? 15. When can this patient be taken for elective surgery? 16. How will you prepare this patient coming for emergent surgery? 17. What are the implications of pregnancy in hyperthyroidism? 18. How would you differentiate hyperthyroidism, thyrotoxicosis and thyroid storm? 19. Is there a role of regional anaesthesia for thyroid surgery? 20. How do you premedicate this patient? In which patients premedication should be avoided? 21. What are the parameters to be monitored intra operatively in this patient? 22. How will you prepare yourself if difficult intubation is suspected? 23. What are the strategies to be considered while intubating this patient? 24. What are the problems associated with positioning for thyroid surgery? 25. How do you maintain anaesthesia in this patient? 26. What are the possible intra operative problems and how will you manage it? 27. What is thyroid storm and how will they present intra operatively? Describe its management.


28. When will you extubate this patient? 29. What are the major post operative complications and its management? 30. Which patients require ICU care post operatively? 31. How will you manage post operative pain in this patient? 32. What are the signs and symptoms of hypothyroidism? 33. How will you treat hypothyroidism medically? 34. What is myxedema coma? How will they present? 35. Describe the anaesthetic implications of hypothyroidism. 36. What specific aspects will you consider if a hypothyroid patient presents for emergency surgery?


Hailing from the city of Vizag in the State of Andhra Pradesh, this Anaesthesiologist’s name has today come to be common parlance among budding anaesthesiologists and veterans in the field alike, the world over. His simple, yet novel system of assessing a patient’s ease of intubation, just by asking the patient to open his or her mouth to study the visibility or the lack of it of oro-pharangeal structures serves to anticipate and plan for difficulties in securing an airway – a basic premise on which General Anaesthesia literally stands… Dr Sheshagiri Mallampatti Rao

While today’s rave parties may seem a new phenomenon, history can’t help but repeat itself. . ! This early 19th century illustration from the popular “Strand” magazine depicts in some Victorian candour these medical school students having a gala time inhaling Ether, thus getting a stupurous high, so to speak – An Ether Frolick…if you will..!

The Earliest Rave Party

A stone inscription at the Massachusetts General Hospital, Boston, U.S.A in honorarium of that wonderful inhalational drug which by its effect caused insensibility to pain, indeed a momentous discovery in all of Anaesthesia. The relief in stone on top depicts in some illustrative detail the administration of such a wonder drug to a patient in pain to set him free from the ails of life and humanity, that being pain…

A Monument to Ether


PG EXCEL 2012 A leap beyond excellence

CME PROGRAMME IN ANAESTHESIOLOGY JSS Medical College, Mysore On Saturday, 21st July 2012 and Sunday 22nd July 2012 Evaluation of Speakers and Moderators EVALUATION FORM FOR PARTICIPANTS General Information 1. NAME:___________________________________________________________________________ 2. College: __________________________________________________________________________ 3. Phone number: __________________________________________________________________ 4. Designation: _____________________________________________________________________

Evaluation of lectures/speakers Evaluation is to be done to assess 1) Quality of presentation 2) Content 3) Usefulness to you. In evaluating quality please take into account speed and style of delivery of speech and quality of slide, besides other characteristics that appeal to you. In evaluating content, consider whether the material presented was factual, relevant and up to date.

Evaluation is to be done as below GRADES 4

3

2

1

EXCELLENT

VERY GOOD

GOOD

AVERAGE


Interactive Clinical Case Discussions TOPIC

Quality of presentation 4/3/2/1

Contents 4/3/2/1

Usefulness 4/3/2/1

1) A Patient with Bronchiectasis posted for left lower lobe lobectomy Dr.Gurudatt, (Mysore) Dr.Mahantesh Sharma, (Davanagere) 2) A Diabetic patient for below knee amputation Dr.Madhusudhan U (Mangalore) Dr.Ravikumar C (Davanagere) 3) A Patient with End Stage Renal Disease for Renal Transplantation Dr.Sunita.U, (Bangalore) Dr.Sanikop (Belgaum) 4) Primigravida with pregnancy induced hypertension Dr.Kodandaram.N.S (Bangalore) Dr.Rangalakshmi (Bangalore) 5) A Patient with Obstructive Jaundice for Laparoscopic Cholecystectomy Dr.CVR Mohan,(Bangalore) Dr.Chidanandaswamy, (Bangalore) 6) A Patient with IHD and Hypertension for right hemicolectomy Dr.Murali Chakravathi (Bangalore) Dr.Gangadhar (Tumkur) 7) Patient with Graves disease posted for Thyroidectomy Dr. Safia Shaikh (Hubli) Dr.Ragavendra Rao (Dharwad)

Focus sessions TOPIC 1. Application of gas laws in Anaesthesiology Dr.P.N.Viswanathan (Mysore) 2. The Electrical Activity of the Heart â&#x20AC;&#x201C; ECG Dr.Muralidhar K (Bangalore) 3. Vaporizers Dr. Aruna Parameswari (Chennai)

Quality of presentation 4/3/2/1

Contents 4/3/2/1

Usefulness 4/3/2/1


4. Examination of the CVS Dr.Lakshmi Kumar (Cochin)

5. Anaesthesia Workstation Dr.Ramkumar Venkateswaran (Manipal) 6. Acid-Base Physiology Dr.Laxmi kumar (Cochin) 7. X-Ray for Anaesthesiologists Dr.Saraswathi (Bangalore)

Video Sessions Quality of presentation 4/3/2/1

TOPIC

Contents 4/3/2/1

Usefulness 4/3/2/1

Contents 4/3/2/1

Usefulness 4/3/2/1

1. Lower extremity Peripheral nerve blocks Balavenkatasubramanian J (Coimbatore) 2. An Approach to Difficult Airway Dr.Raveendra (Mangalore)

Expert opines TOPIC 1. Anaesthetic Management of a patient with Bronchial Asthma Dr. Harsoor S.S (Bangalore) 2. A Neonate for Herniotomy Dr.Aruna parameswari (Chennai) 3. An Obese Patient for Bariatric Surgery Dr. Radhika Dhanpal (Bangalore)

4. Anaesthesia for Cleft Lip and Cleft Palate repair Dr.Balabhaskar (Bellary) 5. Anticoagulant therapy and Regional Anaesthesia Balavenkatasubramanian J (Coimbatore) 6. Intensive Care Management of Severe Traumatic Brain Injury Patient Venkatesh.H.K (Bangalore)

Quality of presentation 4/3/2/1


PG Debate TOPIC

Quality of presentation 4/3/2/1

Contents 4/3/2/1

Usefulness 4/3/2/1

1. ProSeal LMA in Laparoscopic surgeries Dr.P.F.Kotur (Belgaum) 2. Third Space: The History and Mystery of it Dr.Uma (Mysore) 3. Can regional anaesthesia be given in a patient with difficult airway? Dr.Radha.M.K (Bellur) Do feel free to comment: _____________________________________________________________________________________ _____________________________________________________________________________________ _____________________________________________________________________________________ Evaluation of the programme as a whole: 1. Was there adequate time for discussion

Yes/No

2. Did the topics selected cover all the important aspects of the specialty

Yes/No

3. Improvement in your understanding and skills

Yes/No

4. Were the arrangements made by organizers for:

Excellent

Good

Satisfactory

Registration Conduct of CME programme

Suggestions for future programmes: _____________________________________________________________________________________ _____________________________________________________________________________________ _____________________________________________________________________________________


Comrades in arms Scientific Committee

Dr Anup.N.R

Dr Subramanian.V.V

Dr Bhagirath.S.N

Dr Caroline Sheryl Kuruvilla

Dr Vishnuvardhan.V

Reception & Inauguration

Dr Tulsi.T

Dr Nishanth Baliga

Dr Arpitha.A

Dr Sowmya.H.P

Dr Attarde Viren Bhaskar

Dr Gayathri Devi.B.U

Registration Committee

Dr Prajwal

Dr Sowmya.N

Dr Praveen Kumar

Dr Shwetha.M.Reddy

Dr Yashoda.C

Transportation and Accomodation Committee

Dr Chowdary Sriram Basappa

Dr Mahendra Kumar S.N.M

Dr Sharan Basappa Bevoor

Catering Committee

Dr Mohammed Shahid

DrJitendra. V.Kalbande

Dr Ajay

Dr Hitendra

Entertainment Committee

Dr Varun Reddy.P.J

Trade & Exhibition Committee

Dr Shashidhar.M

Dr Poorna.M.S

Dr Mohamed Mohseen

Dr Prashanth.R.P

Audiovisual Committee

Dr Santosh.M.O

With Many Thanks

Somesh – Cover Designer – Undergraduate Whizkid

Madhu – P.A. to Dept of Anaesthesia



PG Excel 2012 CME Volume