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Published by The Fiji School of Medicine Flexible & Distance Learning Unit 1st edition 2010 2nd edition 2011 Principal Author & Editor-in-Chief Prof. Craig Callan Adams BMedSci (Hons.) MBBS (Hons) MD Head, Discipline of Clinical Skills (FSMed) Contributing Authors: Dr. Gerard Ahern MBBS (Clinical Anatomy) A/Prof. Maurice Brygel MBBS FRACS (General Surgery) A/Prof. Norman Eizenberg MBBS (Medical Education) Advisory Panel: Dr. Karl Alexander MBBS FRANZCA (Anaesthetics) Prof. Suzanne Anderson MBBS FRANZCR (Medical Imaging) Dr. Justin Bowra MBBS FACEM (Emergency Medicine) Prof. Gary Browne MBBS FACEM (Emergency Medicine) Dr. John Fatiaki MBBS (General Practice) A/Prof. Ray Garrick MBBS FRACP (Neurology) A/Prof. Nigel Hope MBBS FRACS PhD (Orthopaedics) Professor Alex Pitman MBBS FRANZCR (Medical Imaging) Prof. Julie Quinlivan MBBS FRANZCOG PhD (Obstetrics & Gynaecology) A/Prof. Jacob Sevastos MBBS FRACP PhD (Nephrology) Dr. Sitiveni Vudiniabola MBBS MMed (General Surgery) Dr. Ifereima Waqainabete MBBS MMed (General & Vascular Surgery) Acknowledgements Professor Graham W. Boyd (Cardiology) and the late Dr. Keith Millingen (Neurology) (Royal Hobart Hospital, Australia) for developing the concepts & teaching the fundamental principles of how to formulate a meaningful clinical (bedside) diagnosis. The late Professors Peter Lisowski (Anatomy) and Arthur Cobbold (Physiology) for their medical science genius. special thanks to: Ms. Janine Hanson for her invaluable assistance typing and proof-reading the text. Mr. Gerard Williams & Mr. Jese Tema for the photography, digital image manipulations, artwork and HD video/audio editing. and our models for the images/movies: Tim Squires; Sophie McGilvray (UNDA medical students) Illustrations on cover and on pages throughout the book: Selections from the anatomical drawings of ANDREAS VESALIUS. Copies of copyright material in this compilation of student notes have been made in accordance with the provisions of Section 53B of the Copyright Act for the teaching purposes of the University. “FOR USE ONLY BY STUDENTS ENROLLED IN THE STUDY OF MEDICINE”




Part I THE LOGIC OF CLINICAL METHOD introduction method synthesizing the complete diagnosis general comments hierarchic approach to diagnosis an example of the suggested approach Part II HISTORY TAKING general approach to the patient the present illness background history beginnings of a diagnostic synthesis writing up and presenting your history example of a written history presentation conclusion cardinal symptoms of four major systems Part III introduction


SYSTEMS cardiovascular respiratory alimentary (GIT) nervous (central & peripheral) haematopoietic/lymphatic rheumatological endocrine genito-urinary (& urinalysis) REGIONS eyes (& ophthalmoscopy) ENT analysis of a mass/lump breast pregnant abdomen (& PV) hernia (& PR) orthopaedic check-lists emergency medicine check-list EMERGENCY MEDICINE &TRAUMA (Dr. A,B,C,D,E, F) Danger Response Airway Breathing Circulation Disability Exposure (to metabolic insults) Fractures Part IV Full Physical Examination (head to toes) Part V MSAT clinical exams Part VI Conclusions


RECOMMENDED ACCOMPANYING TEXTBOOKS Anaesthesia & Resuscitation  Textbook of Anaesthesia – Aitkenhead et al 5th edition, Churchill Livingstone Elsevier  Fundamentals of Anaesthesia – Smith et al 3rd edition Cambridge Medicine  Respiratory Physiology - the Essentials. West 8th edition Wolters Kluwer, Lippincott Williams & Wilkins Basic Medical Science  Anatomedia – Eizenberg, Adams et al., McGraw-Hill, 2007  Acland‟s DVD Atlas of Anatomy, Wolters Kluwer, Lippincott Williams & Wilkins, 2003  Last‟s Anatomy Regional & Applied – McMinn 9th edition Churchill Livingstone Elsevier  Color Atlas of Anatomy – Rohen & Yokochi 7th edition Wolters Kluwer, Lippincott Williams & Wilkins  Review of Medical Physiology – Ganong 23rd edition, McGraw-Hill 2003  Robbins Basic Pathology – Kuma et al., 8th edition Saunders/Elsevier; 2007 Clinical Skills  Clinical Method – Adams, 1st edition, McGraw-Hill, 2012  Clinical Examination – Talley & O‟Connor 6th edition, Churchill Livingstone/Elsevier  Macleod's Clinical Examination - Douglas et al 12th edition, Churchill Livingstone General Practice  Murtagh‟s General Practice – 4th edition McGraw-Hill 2007 Medicine  Clinical Medicine - Kumar & Clark 7th edition, Elsevier/Saunders 2009  Davidson's Principles & Practice of Medicine - Boon et al. 20th edition, Churchill Livingstone  UpToDate (online, College Library)  Therapeutic Guidelines (soon to become available online, College Library) Obstetrics & Gynaecology  Dewhurst‟s Textbook of Obstetrics & Gynaecology - edited by K D Edmonds. 7th edition. Blackwell. 2007  Obstetrics, Gynaecology and Women‟s Health - O‟Connor V. and Kovacs G., Cambridge Press, Sydney, 2003 Paediatrics  Practical Paediatrics - Roberton D.M & South M., 6th edition. Churchill Livingstone/Elsevier 2006  Paediatric Handbook, Staff of the Royal Children‟s Hospital Melbourne, Australia. 8th edition Blackwell 2010 Psychiatry  Review of General Psychiatry - Goldman 5th edition McGraw-Hill  Kaplan & Saddock‟s Synopsis of Psychiatry - 10th edition Wolters Kluwer, Lippincott Williams & Wilkins  Management of Mental Disorders - World Health Organisation, Collaborating Centre for Evidence in Mental Health Policy. Sydney 4th edition 2004  General Practice Psychiatry - Blashi G, Judd F, Piterman L., McGraw Hill. 2007  Diagnostic & Statistical Manual of Mental Disorders- DSM-IV-TR – American Psychiatric Association 2000 Surgery  Clinical Surgery - Henry & Thompson 2nd edition Elsevier/Mosby/Saunders  Textbook of Surgery - Tjandra et al 3rd edition Wiley-Blackwell  Schwartz‟s Principles of Surgery – Brunicardi et al 8th edition McGraw-Hill  Principles & Practice of Surgery - Garden et al 5th edition Churchill Livingstone  Current Surgical Diagnosis & Treatment - Lawrence Way 11th edition McGraw-Hill  Concise Textbook of Surgery – S. Das, 5th edition  Scott: An Aid To Clinical Surgery – Williamson & Waxman 6th edition Churchill Livingstone 1998  Lecture Notes on General Surgery - Ellis et al 11th edition Blackwell  Essential Surgery: problems, diagnosis & management - Burkitt & Quick 3rd edition Churchill Livingstone  Essential General Surgical Operations - Kirk & Winslet. 2nd edition Churchill Livingstone  Apley‟s System of Orthopaedics & Fractures – Louis Solomon et al 8th edition. Oxford University Press  Neurosurgery in the Tropics - Rosenfeld & Watters Macmillan Education  Essential Neurosurgery - Andrew Kaye 3rd edition Blackwell  Plastic Surgery Secrets - Jeffrey Weinzweig Elsevier  Pathology for Surgeons in Training – Gardner & Tweedle 3rd edition Hodder Arnold


“Discard in the first instance all attempts to identify or to name, and try instead to read the malady, tracing the symptoms to the seat of their cause, and discerning the nature of the morbid process by their character and course.” Gowers, 1892

Part I - The Logic of Clinic Method INTRODUCTION In the absence of any clearly defined logic of clinical method, the most common road by which you learn (and we teach) is through recognition of patterns of disease. And there is no doubt that this works fairly well for the experienced physician. But it takes time to accumulate knowledge of these patterns, and now that we are introducing you to clinical aspects of medicine much earlier in your course, there is a need to delineate some guidelines to help you make clinical assessments, independent of any knowledge about disease patterns. Indeed with the rapid increase in medical knowledge and the increasing complexity of diseases, some sort of method of seeing the wood through the trees is fast becoming necessary even for the relatively experienced clinician. In addition, pattern-recognition can never work if one is confronted by a new disease, or disease variant. Even with the commoner conditions each patient is an individual so that there is a real danger in forcing them into some pigeon-hole of disease especially if they have any important deviation from its typical form Despite all that has been said about clinical logic, it has never actually been defined. It is said that most good clinicians work by „hypotheticodeductive‟ reasoning, i.e. as clinical data is accumulated during the interview and physical examination, different ideas of their meaning spring to mind and further evidence is then sought for or against the proposal which is then either rejected or accepted depending on the outcome. But for the student without much knowledge of disease the real difficulty with this method is: “Which hypothesis?” Those who have written on this subject suggest that any hypothesis is reasonable to begin with. But time is short and there must be something more than a random process involved. In that some hypothesis must occur to us as more probable than others if this method is to work. In the absence of a means by which „good‟ hypotheses about clinical data can be identified, particularly in the early undergraduate years when medical knowledge is slight, this approach may not be particularly valuable.

anatomy, physiology, general pathology, etc. with which to approach clinical data. THE METHOD When embarking on any process of detection, the first question in one‟s mind should be those which group information into broad categories, rather than those aimed at levels of detail. For example, the question: “Is there anything wrong with the cardiovascular system?” is a much more important initial question than “Does the patient have mitral stenosis?” in the detection of why a particular patient is suffering from shortness of breath. In general, we can use our knowledge of anatomy, physiology and general pathology to group information along various lines, and this is quite capable of getting us very close to a diagnosis even where we do not have any prior knowledge of the various specific disease processes concerned. There are four important questions which should be considered quite separately when you analyse clinical information, viz. WHERE, WHAT, HOW & WHY. Where is the problem?

Anatomical diagnosis

What (in general terms) is it‟s nature?

Pathological diagnosis

How does it affect the patient?

Physiological diagnosis

Why did this patient get this particular condition?

Aetiological diagnosis

The value of this approach is that it allows you to focus down within each category on much less than the total body of information, and thereby gives you a much greater chance of reaching the correct conclusion. Secondly, each of these aspects does indeed contribute importantly to clinical diagnosis and, when taken together, the four categories severally describe all the elements of clinical diagnosis. By contrast, when the „pattern recognizer‟ pins some „offthe-rack‟ diagnostic label on a patient, it so often lacks one or other of these categories, particularly the physiological and aetiological ones. Thus we often hear that a patient has had an acute myocardial infarct (anatomical & pathological diagnosis) but where is the comment about how this has affected them functionally (did they have secondary heart failure or ventricular dysrhythmias for example – important in treatment as well as diagnosis) and what were the longterm factors predisposing to his condition, and the more recent ones precipitating it (aetiological diagnosis).

What we have to do is find some guide to structuring and synthesising clinical data, and what follows is a suggestion of how this may be done, given that you already have a PBL course which integrates the basic groundwork of


The important point here is that by using this approach you can „tailor-make‟ a diagnosis to the individual patient as you go along, rather than force them into some preconceived diagnostic pigeonhole read about in a text book or happened upon on Wikipedia. Like Kipling, we are trying to learn by structure & simplification: “I keep six honest serving men, They taught me all I knew. Their names are What and Why and When, And How and Where and Who” R. Kipling “Just So Stories” Essentially what we are trying to do here is to hone down on particular categories of diagnosis at any given time and in this way not be overwhelmed by the information we have so painstakingly collected. And as we shall see, although we may still no doubt do a certain amount of pattern-recognition, there are principles we can build up within each of our four categories as very helpful guidelines to reach a diagnosis in a more logical or problem-solving way.

pressure (tending to reduce lung compliance) in early heart failure will be aggravated by lying flat. Similarly the distribution of referred pain can often give us a clue to the system or organ involved, provided we know our neurosome innervation, particularly in relation to referred pain. Indeed, neurophysiology is vital for localising the anatomical site of any trouble in the central nervous system. Actually our knowledge of function often turns out to be even more important than direct anatomical knowledge in deciding an anatomical diagnosis, especially in the relatively „hidden‟ organs such as the nervous system, lungs, heart and to a certain extent the abdominal organs. In that case, it is the symptom itself, its quality, its radiation, aggravating and relieving factors, which often give the most important clues to the anatomical site, system or organ involved in the disease process, as illustrated above.

In some respects, this is much more like solving a jigsaw puzzle where we realize that certain pieces are clearly related to sky, others to trees, and others to people, houses, etc., and which can all be put together and solved as subunits before going on to the solution of the overall puzzle itself.

Physical examination also adds to Anatomical Diagnosis by giving us direct evidence about the organ involved, particularly if we understand the anatomical relationships of the various organs and their surface anatomy, e.g. respiratory signs over the right lower chest anteriorly indicate involvement of the right middle lobe by some process. (The precise nature of this process is not considered when addressing this Anatomical category of diagnosis, but separately as indicated below, under Pathological Diagnosis).

Actually in that respect, once you have solved the problem in each of the four categories, you will sometimes see that they can be put together in different ways.

Of course physical examination is particularly important in defining the anatomical site of conditions visible to our eyes or palpable to the touch, such as skin and joint disease.

And now that you only have a limited number of combinations to deal with, you will often be able to see that interesting possibilities arise.

But so often, in less accessible systems, examination findings are few, and the history becomes of the utmost importance.

For example, one may see hypertension associated with renal disease and this can be looked at both ways around i.e. as hypertension causing renal disease, or being its effect.

Note also that some conditions will not appear to be confined to any one region or organ-system, raising the possibility that we are dealing with a multi-system disease (however, see also 3 below).

And here is lesson #1, which you should never forget, namely, when you are in a quandary in such respects, always look for what came first in time, and this is one way in which careful history taking can be so important.

2. PATHOLOGICAL DIAGNOSIS - WHAT is the general pathological nature of the lesion, independent of its site?

1. ANATOMICAL DIAGNOSIS – WHERE is the lesion? Throughout the history-taking and physical examination one should be listening and looking for evidence of which region or system is involved. In the history we often get clues from this not only by our knowledge of anatomy, but from physiology, because disturbed function may give us an important clue to the anatomical system involved, e.g. shortness of breath, which gets worse when the patient lies flat is probably due to impairment of left heart function rather than a respiratory cause, because increased pulmonary venous

Here we consider only the general areas of clinical pathology and not specific histopathological processes. Thus we wish to know whether the problem is inflammatory, neoplastic, traumatic degenerative, hereditary, immunological, atrophic, ischaemic, etc. the most important data to answer this question come from the history, namely the time-intensity relationships of the major symptom or symptoms involved. It is largely for this reason that it is so important to have a clear and accurate history from the patient, particularly that which relates to the circumstances of onset and timecourse of progression of the symptoms.


All good histories should start with a clear account of this. When the onset of the symptoms is dramatic, occurring within seconds, it is most usually due to rupture or obstruction of a hollow tube somewhere within the body, for example, a perforated peptic ulcer, a spontaneous pneumothorax (rupture of the lung into the pleural cavity) or an acute coronary artery occlusion. Note that in many organs such as the brain, heart, etc, the only hollow tubes are vascular ones, and this allows the diagnosis to be narrowed much more than in the case of the abdomen, where the distinction between, say, obstruction of the gut and blood vessels may be more difficult on these grounds alone. Note, too, that in organs where the only hollow tubes are vascular, a sudden onset not only gives us information about pathology but also anatomy, e.g. an acute „stroke‟ involving the parietal cortex suggests involvement (probably obstruction) of the middle cerebral artery. To distinguish between rupture and obstruction of a hollow tube may be difficult, but if the symptoms pass off within minutes, or at the most hours, the condition is very unlikely to be rupture, and far more likely to be (reversible) obstruction such as embolism or arterial spasm. Of course, other acute events include mechanical and traumatic ones. When a patient has less acute onset of symptoms, i.e. occurring over days or a week or so, the condition is more likely to be inflammatory, toxic, allergic or immunological condition. Again we need to ask broad questions first so as to identify which of these processes is most likely. It is for this reason that we ask about both general (shivers and sweats, fever, peripheral blood neutrophilia) and local (purulent secretions from the organ concerned) evidence of inflammation, both in the history and on physical examination. Once we know this, we can then go on to further detail about whether it is infective, and if so, whether bacterial, viral or secondary to necrosis from other cause as in alcoholic „hepatitis‟, acute myocardial infarction, pulmonary infarction, etc. Note the importance of the question: “Is there any sort of inflammatory disorder?” before considering more detailed questions such as: “Is this viral?” I would emphasise, too, the importance of separating considerations of the pathological nature of the lesion from any analysis of its anatomical site, at least in the first instance, just as Gowers advocated. Clues about an allergic nature to any process will be found in the history as well as on examination. But if not we may have to go to other investigations such as serum complement, analysis of blood for immunoglobulins, antigen-antibody complexes, toxins etc (and particularly drugs) must be remembered as a

potential cause of disease, and a useful clue here apart from the drug-history, is that such agents normally affect the body symmetrically. Thus a peripheral nerve lesion localised to one leg is likely to have a local cause, and unlikely to be primarily toxic as in, say, arsenic poisoning. Chronic conditions - i.e. coming over months or years. These include the neoplasms, chronic inflammation, chronic immunological disorders, degenerative diseases, and hereditary conditions. Again, clues about chronic inflammatory lesions are often indicated by fever and local purulent secretions, but may also be accompanied by weight loss. Weight loss (and anorexia) in the absence of fever in a chronic progressive process over months suggests neoplasia. (But be careful to ask about decrease in appetite, because weight loss despite increase appetite could be due to increased fuel loss in the urine as in diabetes mellitus, maldigestion or malabsorption of ingested food, or increased body metabolism as in thyrotoxicosis). Remember that what you are first looking for in any category of disease, pathological or otherwise, is the broad or general sort of disease process involved, not some specific histopathological entity. In relation to local secretions, enquire not only about evidence of inflammation, but also about the presence of blood or serum, because this could give the clue to a vascular or ulcerative nature of the underlying pathological process. In determining clinical pathology the history is often of the utmost importance, particularly in relatively „hidden‟ organs such as the brain, but also in the cardiovascular system (especially the heart) and to some extent in the respiratory system. Actually, in any of the organ systems where there is an intermittent disorder which you are not lucky enough to observe at the time, the history is the only information you have to go on in making a pathological diagnosis. In more accessible and less evanescent conditions, clinical examination can also provide useful information about pathology. This is most obvious in the skin and joints, where the evidence of inflammation (local heat, redness, swelling, pain and loss of function) and deformity are usually obvious. (heat & redness less obvious in the shoulder & hip due to the muscle coverings). The same holds true to a lesser extent in at least some of the internal organs, particularly the abdomen, where masses may be palpable to the examining hands. Then, the consistency, shape, size, degree of tenderness and presence of any overlying bruits, can add usefully to discerning the nature of the pathological process. For example, a grossly enlarged, hard „knobbly‟ liver with an irregular surface and edge would suggest secondary


carcinoma; a uniformly enlarged firm liver without irregularity would suggest some other chronic process (e.g. some condition of infiltrative type, or perhaps cirrhosis of the liver in the stage before atrophy had ensued to diminish liver size). In sorting this particular situation out, the presence or absence of splenic enlargement is useful (because splenic involvement and enlargement is rare in secondary carcinoma). When examining the abdomen define not only the anatomical relationships of palpable organs, but note changes in position, size, shape, consistency, tenderness, irregularity, pulsatile nature and the presence of vascular bruits, because this may give you important information about the pathological nature of the lesion concerned. Also remember that rectal examination will give you useful information about the macroscopic appearance of the stool, including the presence of any blood, altered, occult or otherwise. In the respiratory system, you will also sometimes obtain useful information about pathology from your physical examination, including examination of the sputum, and in this respect, you must be able to distinguish between consolidation and collapse of the lung, pleural fluid, pneumothorax and chronic obstructive airways disease. At the extreme, the central nervous system rarely gives you any direct evidence on clinical examination about the pathological nature of the process involved, (except where there are vascular bruits etc. to be heard). It is in such cases that you are so dependent on a good history for this diagnostic aspect. At the end of these two questions “WHERE?” and “WHAT?” we should be in a position to know whether the disease is local or general, anatomically, and if local, which organ or system is involved. We should also have a fairly clear idea of the pathological nature of the process involved, particularly whether it is a hyper-acute (dramatic onset) acute, subacute or chronic process. If we have listened to the patient carefully during our history-taking and collected the information completely and accurately during our clinical examination, we should be able to synthesise the anatomy and pathology of the problem fairly accurately and hence be very close to a diagnosis indeed. For example, in a patient who has had an onset of shortness of breath, with cough, yellow sputum and fever over a 24 hour period, and who on examination has the signs of consolidation over the right lower chest anteriorly, we can say without any prior knowledge of names of diseases that he or she has an acute inflammatory lesion involving the middle lobe of the right lung. (And if they have a high white cell count in the peripheral blood with increased neutrophil polymorphs, it is more likely that this inflammation is bacterial than viral). Thus, without any knowledge of names such as „pneumonia‟, etc. we have come very close to our

diagnosis already and merely on a basic knowledge of general anatomy, physiology and pathology. Indeed, „pneumonia‟ merely describes an acute inflammation of the lung parenchyma and the name is only shorthand for what we have found ourselves, nothing more. You may be better off not naming names initially at all, in the same way as Gowers has advised, since this sometimes carries subtle connotations leading you in wrong directions subconsciously. Thus, the diagnosis „lobar pneumonia‟ is most usually due to the organism strep. Pneumoniae, and tends to imply this if you use diagnostic labels without careful thought. You may still sometimes fall into the trap of trying to stick labels on patients, regardless of what has been said, so let me say, further, that whenever you do, please analyse each of the syllables within that label, and make sure they are relevant to the individual patient confronting you (e.g. if your label is acute viral hepatitis, is it really acute, is it really the liver that is involved and, if so, is it inflamed, and what is the evidence that the inflammation is due to a virus?). 3. PHYSIOLOGICAL DIAGNOSIS - HOW does the condition affect the patient? As already noted, in many situations, the functional manifestations, sequelae and/or complications of a disease process are dominant in allowing us to make our anatomical diagnosis. In addition, by the time we have addressed this category of diagnosis we usually have most of the clinical information available about the present illness to begin to synthesise it to a more complete diagnosis. In this respect, we sometimes have several groups of symptoms that could either be seen as primary causative events, or secondary functional consequences, and this can create difficulties. Hypertension associated with impairment of renal function is a good example, because hypertension could be either the cause or the effect of the latter. Similarly, paroxysms of tachycardia could either be the cause (low diastolic coronary perfusion time/pressure) or the effect, of myocardial ischaemia. And when one merely assembles the data together at the end of the physical examination, unravelling cause and effect in such cases can be very difficult. The important principle here is not just to look at the data itself, but for which came first in time. Clearly, if a patient describes palpitations first, followed by chest pain, then it is likely that the palpitations are primary, and the myocardial ischaemia secondary. As general point, you should get used to the idea of stating your anatomical and pathological diagnosis (e.g. acute myocardial infarction) and following it with whatever functional consequences are involved in the


individual patient confronting you, including any secondary effects, sequelae, and/or complications of his disease. This is the area where traditional textbook diagnoses are so deficient (and of course if you think about it, no textbook or „off the rack‟ diagnosis could describe the functional sequelae or complications in any individual patient). The functional aspects of disease bear not only on the diagnosis but on the patient‟s management. The severity of the condition has obvious importance in treatment. For example, a patient who has a very low arterial and central venous pressure with rapid (reflex) tachycardia after a haematemesis needs blood transfusion before any further consideration can be given to other categories of the clinical diagnosis. Similarly in a patient with severe „asthma‟ and consequent severe central cyanosis, oxygen is needed before we should make any attempts to understand further details of the process involved. The same holds true for all other emergency situations. There, we have to act appropriately to treat obvious and severe functional disturbances before delving into aspects of the condition of lesser urgency. Functional consequences or sequelae of disease processes may also have an important bearing on the treatment of chronic conditions (although there, not usually until other aspects of the diagnosis have been discerned). For example in treating patients with hypertension, the case of anti-hypertensive medication is stronger when there is evidence of its secondary effects such as left ventricular hypertrophy, retinal arteriolar narrowing, etc. 4. AETIOLOGICAL DIAGNOSIS - WHY did the patient get the condition in the first place? What we first aim to do in taking a clinical history and examining the patient is define the nature and anatomical site of the present illness confronting us, together with its functional sequelae and/or complications. But once we have answered those questions we must next ask: “Why did the patient develop this condition in the first place?” In this regard, if the time-intensity relationships are chronic, we will want to know the long-term predisposing factors which might have been involved (e.g. whether there are the „risk factors‟ of cigarette smoking, high blood pressure, diabetes, elevated cholesterol, obesity etc. present in a case of chronic angina due to coronary atherosclerosis).

superimposed thrombosis and consequent heart attack, we will want to find out both the long-term factors predisposing to the atherosclerosis and the acute factors precipitating the recent events. Finding out about predisposing and/or precipitating factors to disease usually comes from the second phase of our history, namely the background to the illness. You must therefore ask your patient about this background, leaving him initially to tell his own story, and only later asking more specific questions. If you are still at a loss in this respect, always ask the patient what he thought brought the condition on - they may be wrong, but patients often supply interesting and useful insights into their disease process, even if only in a general way. When you have elucidated the aetiological background to the illness as well as its anatomical site its pathological nature and its functional consequences, effects sequelae and/or complications, then you should have a complete diagnosis, e.g. acute (pathology) viral (aetiology) hepatitis (liver inflammation = anatomical, pathological), with secondary impairment of liver function. The diagnosis in some other patient might be acute (pathology) myocardial (anatomical) infarction (pathology), with secondary left ventricular impairment and episodic ventricular tachycardia (functional), the acute precipitating factors being uncertain, but the longterm aetiological risk factors including cigarette smoking, high blood pressure, diabetes and „repressed hostility‟. SYNTHESIZING THE COMPLETE DIAGNOSIS Note that once you have identified these various categories of disease they may not always fit together as neatly as the above, but at least now you will only have four sub-conclusions from which to synthesise your diagnosis, and that makes the evidence a lot easier to handle than a whole mass of unprocessed data. Getting the four categories in their correct order and perspective can be difficult at times but remember, as emphasised above, that what is cause and what is effect can usually be determined by elucidating which came first in time. Remember, too, that some organ diseases can have multiple effects on different systems, so that what may appear to be a multi-system disorder can often turn out to be a single organ problem with secondary manifestations elsewhere.

Along the same lines, if the condition is acute, we must enquire about the precipitating factors, such as some change in the patient‟s life-style or some important lifeevent, exposure to toxins, infectious agents, unusual environment etc.

The first principle here (Occam‟s razor) is to try first to make the simplest diagnosis possible i.e. to see if the condition can be viewed as primarily due to an abnormality of one system with secondary manifestations elsewhere (e.g. primary liver impairment with secondary (functional) effects in other organs, primary renal failure with secondary hypertension, oedema, pulmonary congestion, etc).

And, of course, when we have an acute-on-chronic process such as chronic coronary atheroma with sudden

Sometimes, of course, you will indeed be dealing with a multi-system disorder, such as a „collagen‟ disease (e.g.


systemic lupus erythematosis), but in approaching any information, you should only think of such disorders after having excluded the simpler possibility that the widespread nature of the condition is due to single organ failure with secondary manifestations elsewhere.


The four categories of diagnosis are not always mutually exclusive but this can sometimes allow them to interact in useful ways.

You may think it slightly odd that we have talked so much about dissecting clinical information before mentioning how it should be collected, but I have done this deliberately so that you may understand the framework in which to collect information.

For example, if a patient presents with right hemiparesis affecting the arm, more than leg, together with dysphasia, the likelihood is that it is the left parietal cortex involved, anatomically. But if, when we turn to our considerations of pathology, we find that the condition was of sudden onset, (i.e. in our terms obstruction or rupture of hollow tubes) then, in the brain, this means that it was vascular, so we can go back to our anatomical diagnosis and extend it by considering it in terms of vascular anatomy, and in the present case this would lead us to the conclusion that the patient had a lesion (probably obstruction through thrombosis or embolism) of the left middle cerebral artery. Secondly, we have already seen how important functional diagnosis can be in localising the anatomical site of the lesion, particularly in relatively „remoteâ€&#x; organs. For example, in a patient presenting with chest pain not typical of myocardial ischaemia, the finding of impairment of left ventricular function would add some weight to the notion that the pain might indeed be of cardiac origin. In a similar way, the aetiological diagnosis may interact with the diagnosis of the present illness (anatomical, pathological and functional diagnosis).

The thrust of this exercise has been to try and give you guidelines for making clinical diagnoses without prior knowledge of medical conditions.

Unless you have some insight into that, your data collection will be unstructured and your diagnoses correspondingly confused. For example, we usually advise taking all aspects of a clinical history before doing the physical examination, but it must be said that unless we can get a very good idea of the anatomy and pathology of the general problem in the history before we come to the examination, we will not be in a very good position to ask all relevant questions about the background aetiology (e.g. past history, family history, social history, drug history, etc) leading up to the condition. In such cases, one often finds that the most important question one asks in relation to aetiology occur to the consciousness only after the physical examination, and hence in practice we often have to go back over the history, looking for factors or events which may have predisposed to, or precipitated, the event. It is for these sorts of reasons that you have to know the structure of the clinical method we use, and the guidelines involved, before you can really go about collecting information to greatest advantage.

Thus, if the above patient with a typical chest pain and left ventricular impairment was 52 years of age and had a long history of hypertension, cigarette smoking, obesity and diabetes, this would be the right context for a predisposition to vascular disease, and hence would support the general notion that the pain was indeed myocardial ischaemia. On the other hand, if the aetiological background setting was all wrong in relation to the preliminary diagnosis of the presenting illness, one would have to rethink the anatomical, pathological and functional aspects of the diagnosis. For example, if the above patient presenting with chest pain and cardiac enlargement was aged 15 and had no evident background risk factors predisposing to myocardial infarction, then the whole diagnosis should be rethought - perhaps he has pericarditis with pain due to that, and apparent rather than real cardiac enlargement due to fluid in the pericardium? These interactions between the various diagnostic categories, though relative, can be very useful in piecing the information together to the best possible final clinical diagnosis.


HIERARCHIC APPROACH TO DIAGNOSIS There is a final important aspect of your approach to collecting information, namely that you ask broad questions which allow you to group information within the various categories, before moving to finer levels of detail. For example, in a patient with muscular weakness, there is no point in looking for a primary muscular cause if there is good evidence of neurological involvement, e.g. the presence of sensory symptoms and signs. This hierarchic approach of going from broader to more narrow levels allows you to „corner‟ the diagnosis at all stages, but it is one of the most difficult aspects of the dissecting and synthesising clinical information, and there is no substitute for practice on individual patients to achieve success. No amount of book-reading can make you competent in building diagnoses for individual patients in this way. Another useful hint is to try playing the game of „Twenty Questions‟, i.e. see if you can build up the correct diagnosis in one of your colleague‟s patients by asking him a series of up to twenty questions. This will force you to ask broader questions before more detailed ones. As an example when a patient is found unconscious (or when your car suddenly stops) you need to know rapidly which of the major systems is at fault; (in the case of your patient, is it lack of oxygen supply, lack of blood supply, sudden drop in glucose fuel levels etc?).

When you play your game of „Twenty Questions‟ try not to use more, and again heed Kipling‟s advice: „But different folks have different views, I know a person small, She keeps ten million serving men, Who get no rest at all. She sends „em abroad on her own affairs, From the second she opens her eyes One million How‟s, Two million Where‟s, And seven million Why‟s!‟ From Kipling‟s „Just So Stories‟ I want you to use the method described as a guideline to help you reach diagnoses. As far as possible, try to avoid the pattern-recognition approach, which can be both difficult at your stage of knowledge, and misleading unless you are dealing with anything other than a very classical case - and each patient being an individual means that this rarely happens. As Horace said (65 B.C.): „If you know any better methods than these, be frank and tell them; if not use these with me‟. With this method, you may not always finish up with a tidy diagnosis, but it will usually be a fairly accurate one. And even if you haven‟t identified the diagnosis totally in all its four categories, you will at least have „cornered‟ it and pointed to the areas or diagnostic categories where more information (e.g. more history and/or investigations) is needed.

In this respect, there is usually one point (at the end of the line, as it were) where each system can quickly be checked, especially in emergencies. For example, in our ailing car, if the spark crosses the spark-plug gap (end of the ignition system line) when the starter motor is turned over, there is nothing wrong with the ignition system and the fault must be elsewhere (? fuel system). If there is no spark, then you have localised the trouble to the ignition system. Thus, the first questions must be those where both the answers „yes‟ and „no‟ will give useful information. Only when you have localised the system involved by this means should you go on to dissect the problem in more detail. Again, in our unconscious patient, if there is no recordable carotid pulse or blood pressure, you will have localised the problem to the cardiovascular system, and you must then find out whether this drop in blood pressure is due to sudden drop in peripheral arteriolar resistance in the circulation or to a reduction in cardiac output; if the latter, is this due to an altered heart rate or a reduced stroke volume, and if the latter, is it that the heart „can‟t‟ (e.g. valve rupture) or „won‟t‟ (e.g. primary heart muscle failure) pump, and so on down the line. The broad, HIERARCHIC approach to diagnosis is one I strongly advise you to follow.


AN EXAMPLE OF A LOGICAL APPROACH TO CLINICAL DIAGNOSIS A 14 year old boy presents with a one week history of gradually increasing malaise, shivers, lethargy, mild bilateral loin pain, and the passage of decreased amounts of „smoky‟ urine, beginning a week or so after the onset of a sore throat. There has been no dysuria or other urinary symptoms, and apart from occasional headache, no symptoms relevant to other systems. There is no relevant background past history, family history, social history, psychological history or drug history. On examination he has some facial and ankle „puffiness‟, a blood pressure of 150/90 mmHg, a reduced urinary output, temperature 38 degrees C, and mild loin tenderness. Urine examination reveals proteinuria (3.0 grams per 25 hours) red cells and red cell casts in the urine, with some of the red cells having unusually fragmented appearances. There are also some white blood cells in the urine. According to our guidelines, we would construct the diagnosis as follows: (1) Anatomical site of the lesion Both history and examination point to the renal system, although we would have to be careful that the high blood pressure was not primary and the renal impairment secondary. However, the blood pressure is only moderately elevated, making the latter unlikely. So, taking the hierarchic approach we have first defined the system involved and now we can try to localise the anatomical problem a little further. The „smoky‟ urine suggests the presence of red cells, which is confirmed on examination, and the presence of red cell casts means that the blood has passed through the tubules, so that the bleeding must have come from somewhere in the nephron itself rather than the collecting system (pelvices, ureters, bladder, etc). The renal tenderness is consistent with this conclusion. Just how high up the nephron is the next problem in our hierarchic approach to anatomy. In this respect, odd-shaped red cells usually mean that the cells have been squeezed through damaged glomerular capillaries. Proteinuria of more than 2 grams per day also points to a glomerular site of the lesion (normally less than 0.5 grams per day is filtered by the glomerulus, so this would be the maximum amount we could expect in the urine from any tubular lesion with secondary failure of reabsorption of normally filtered protein). Moreover, there is hypertension, and from our knowledge that renin is released from the juxtaglomerular apparatus in the afferent arteriole this, too,

would be consistent with a glomerular site of the lesion. In addition, there is oliguria and fluid retention (oedema) and this could be related to a reduced glomerular filtration rate. All of these features point strongly to the lesion having a glomerular site. It is important to note that we have been led to our anatomical diagnosis just as much by indirect information relating to derangements in kidney function (hypertension, oedema, oliguria, etc) as by the more direct examination findings (loin tenderness, red cell casts, etc) relating to anatomy per se. (2) General pathological nature of the process Clearly this is an acute process, and probably an inflammatory one in view of the fever and presence of white cells in the urine. Whether this inflammation is due to necrosis, or bacterial or viral infection, or an inflammatory response to allergic or other damage will need more evidence - for example a high neutrophil white cell count in the urine and circulating blood would be more in keeping with a bacterial than viral inflammation. An allergic component might be indicated by further history revealing a background tendency to allergies in the past, and this would point the way to a need for such measurements as serum complement, immunoglobulins and other immunological factors in our investigation of the disease. (3) Functional diagnosis i.e. HOW does the disease affect the patient? Our functional diagnosis has already been very important to us in building our anatomical diagnosis. But, as discussed above, it has also been helpful by making us address the question of whether the hypertension has been the cause or effect of the renal disorder. Finally, it will also be important to treatment (e.g. is the degree of impairment of renal function sufficient to warrant dialysis). (4) Aetiological diagnosis The question „Why?‟ leaves us to go back and ask about the background to this illness. In this case, the early sore throat may give a clue, but we might also do well to ask further about allergies etc. in the past. Without much knowledge of medical conditions, we have therefore built a diagnosis of an acute post-sore-throat glomerulitis (inflammation of the glomeruli) of uncertain cause, with moderate secondary impairment of glomerular function. Actually once you get to recognise patterns of disease in later years, you will see this as classical „acute poststreptococcal glomerulonephritis‟, but you can also see that the two diagnoses are not very far apart, and ours may even be better suited to the individual patient than the „off the rack‟ textbook label.


Thus, our diagnosis includes a statement about the presence and degree of impaired renal function. And are nephron segments other than the glomeruli involved in the patient confronting us as the textbook label implies? Also, is there really evidence that it is caused by a streptococcus? Again, if you ever do put textbook labels on your patients as you no doubt will occasionally, at least analyse each syllable, to see whether it does actually fit your individual patient, and whether it is complete (especially in its functional and aetiological aspects). This method of clinical synthesis is designed to help you build up clinical diagnoses in real patients by using your knowledge of physiology, anatomy and general pathology in a very broad and simple way. If you know your anatomy, particularly surface markings of organs, neurosome distributions, neurophysiology, attachments and relationships of the various abdominal organs etc. and if you have trained yourself to group information around the four broad categories suggested, you will hopefully find this approach not only simple, but helpful, even in quite difficult cases, and even where you have little knowledge about the pattern of the disease concerned. INVESTIGATION In the first three years of the course you will be taught principles of investigation only. As indicated above, when you are lacking in some diagnostic aspect in an individual patient, the important further information you must seek first should be more history and/or examination. The next important principle is that any tests should be done with a purpose and not as a „routine‟. If you approach clinical diagnosis through the categories suggested, you will soon see where you need to investigate further, because you will recognise which of the various categories is incomplete. Thus, in a patient where you are not sure of the origin of chest pain, an x-ray of the chest may be helpful in elucidating the anatomical diagnosis. On the other hand, you may be fairly certain that the chest pain is cardiac, but pathology may be your difficulty, e.g. you may need to take blood for analysis of „cardiac‟ enzymes to help determine whether the episode was a reversible ischaemic one, or an irreversible infarction of the cardiac muscle. The other important principle is always to do simple non-invasive 10 tests before more invasive 20 or 30 ones. Finally, when faced with having to do very invasive investigations ask yourself whether you are really looking for a cure (i.e. reversibility) or alleviation because if the latter, your invasive tests may be unjustified.

10 Investigations (available in Fiji/PI‟s, cheap, noninvasive, will answer a specific question re: Dx; staging; prognosis; management)  haematology (Hb; WBC‟s; differentials; platelets; FBE; clotting profile; blood typing/cross-matching etc)  biochemistry (UEC; Hb1Ac; cardiac enzymes; LFT‟s; TFT‟s)  microbiology (wound swabs; MSU; blood films; sputum; FOB; etc)  pathology (ECG)  radiology (diagnostic U/S) 20 Investigations (available, moderately expensive, moderately invasive, will answer a significant question re: Dx; staging; prognosis; management)   

immunology (tumour markers etc) radiology (plain films/tomography) biopsy (FNAB)

30 Investigations (available, expensive &/or invasive, will answer important questions re: Dx; staging; prognosis; management)    

radiology (IVP; angiography; CT/MRI) endoscopy (gastroscopy; colonoscopy etc) biopsy (tru-cut/incisional/excisional) nuclear medicine (bone scan etc)

TREATMENT The important principle of treatment which has not changed through the centuries is: „First do no harm‟. Another over-riding principle is to follow a set structure in your approach to each patient:: 1. resuscitate/ameliorate 2. stabilize 3. optimize Consider & treat all four categories of the disease. Always look for reversible conditions, even in situations where they seem unlikely. Treatment regimens should be:  readily available  affordable (for both patient & MoH)  proven (evidence-based) to be effective Also, in these days of increasing specialisation, don‟t ever forget to treat your patient as a person, and with dignity. Especially remember that: „To know what kind of person has a disease is as essential as to know what kind of disease a person has‟ (Francis Scott Smythe). Think about non-drug treatment, particularly regular exercise (e.g. walking 30 mins/day) healthy diet and psychological aspects, before leaping in with potentially dangerous drugs. And if the disease outlook is gloomy, at least try to give your patient some hope; instil some faith in them and you will be surprised how even patients with incurable illnesses respond.


Part II - History Taking General approach to the patient Be well-dressed and clean always! Introduce yourself. Show that you are friendly! Be alert to elements of the history told in parentheses i.e. as asides, and by nonverbal means of communications such as body language. Avoid appearing hurried. Take only jottings for notes and write the history up more completely subsequently. Otherwise you will distract your patient. Be observant while taking a history, particularly observe the patient‟s general demeanour, including any anxiety etc, and observe carefully their face, eyes, and hands which often hold a host of clues to the underlying problem. THE PRESENT ILLNESS Patient‟s account of the current illness Let the patient tell their own story, and get them to do so from the beginning, for example by asking: „Now please tell me about your trouble from the beginning‟. Initially, try not to interrupt, or only do so when the patient starts to get off the track (e.g. by spending a long time telling you what their neighbours thought was the trouble); even then your questions should remain broad and very general, and in eliciting answers, you should avoid asking about specific symptoms at this stage. Do not use medical terms, and if your patient uses them get them to explain what they mean by them in terms of his symptoms. By the end of this stage you should have a good idea of all of the major symptoms the patient complains of, and the way in which they unfolded in time. This stage of general questioning needs no medical knowledge at all, nor should it be allowed to intrude. Specific interrogation The next phase aims first to determine more about the major symptom or symptoms involved - specifically the onset, severity, time-intensity relationships, precipitating factors for each episode, relieving factors, quality or character of the symptom, associated phenomena, and in the case of pain, its precise site and any radiation.

If you can only think of yes/no alternatives to ask, then frame the question so as to include both aspects equally, to avoid giving the patient any impression that the answer should be „Yes‟; for example: „Was the pain made better by sitting forward, or did that make no difference at all‟. Comment The reason for going into the principal symptom or symptoms in this way is to obtain an idea about two quite separate aspects of the condition facing you. 1. WHERE in the body, anatomically, is the condition localised? At the very least we want to know if possible which system is involved, so that we can give that particular attention during our clinical examination. In this respect, the site of the symptom, its radiation (if pain), its quality, precipitating, aggravating, and relieving factors, are particularly important. Thus, a knife-like stabbing right lower anterior chest pain aggravated by inspiration and coughing and relieved by holding the chest firmly, suggests an involvement, anatomically, of the pleura overlying the middle lobe of the right lung. „Crushing‟ central retrosternal chest pain radiating to the left arm, precipitated by exercise and relieved by rest, suggests disease of the coronary arteries. On the other hand, central chest pain worse in some positions and better in others, suggests that it may be stemming from a pericardial site. Yet other chest pain made worse on swallowing indicates an oesophageal origin. 2. WHAT, in general pathological terms, is the nature of the lesion? This is mainly given by the precise mode of onset, and the subsequent time-intensity relationships of the symptoms. This is discussed more fully below, but you should note that the onset is particularly important, i.e. whether hyperacute, acute, subacute or chronic. Systems enquiry This should not just be a mindless collection of a long check-list of all possible symptoms but should be approached from the perspective of clues already obtained.

In eliciting answers to these aspects, you should again ask only general questions, at least to begin with - for example it is far better to ask: „Did you notice anything which made the pain worse?‟ than to ask: „Was the chest pain made worse by exercise?‟ The latter immediately reveals your own bias, and is a loaded question, which should always be avoided.

Particularly go into the other symptoms in the main system you suspect to be involved, e.g. cough, sputum, haemoptysis, shortness of breath, pain in the chest, weight loss, fever, in the respiratory system; shortness of breath on exertion, shortness of breath at night, orthopnoea, swelling of the ankles, chest pain, palpitation, faintness etc, in the cardiovascular system.

Only if your general questions do not elicit satisfactory answers should you be more specific. Even here, in doing so you should avoid loading the question or showing your own bias. One way to do this is to give a list of alternatives, e.g. „Was the pain throbbing, burning, cutting, stabbing, pressing, squeezing, gripping etc, in nature?‟

It is true that you must ask about other systems, but only emphasise the positive and relevant negatives in your presentation. Never forget in the systems enquiry to ask about fever and weight loss, because these are of great importance in making your general pathological diagnosis.


Also ask about any change in secretions (e.g. discoloured sputum etc). Information from a third party This is especially necessary in the young, or where the patient is a poor historian, intoxicated or unconscious. (N.B. Never imply criticism of some other doctor or hospital when discussing a patient‟s previous management on hearsay evidence from a third party. This is a very common cause of litigation and may get you into deep trouble). BACKGROUND HISTORY Ask about the factors which led up to the illness, because these may give you important clues to what predisposed to or precipitated it, relevant to the aetiological diagnosis (see below). In doing so, again ask only general questions, at least initially. If specific questions do come into your mind (as they should), by all means ask them, but only after the general ones, and even then, do so in such way as to not reveal that you have any particular answer in mind. There are a number of categories of questioning relevant to the underlying aetiological background of the disease, as follows: Previous illnesses Knowing about these can be very helpful. However, in discussing them, don‟t accept medical terms such as „duodenal ulcer‟, „angina‟, „gout‟. Clarify all such statements from the patient by going into the symptoms precisely. When a febrile illness is involved, always ask about travel abroad. Ask also about previous chest x-rays and results of previous insurance examinations (for example blood pressure) where appropriate. Family history Particularly that which might be relevant to the patient‟s present condition. Social history Include occupation, alcohol, tobacco, other „recreational‟ drugs, home circumstances, interests, habits (including any dietary habits or fads), pets, hobbies, etc. Psychological history It is best to broach this only towards the end of the enquiry when you have the patient‟s confidence. Indeed, obtaining a full history in the many cases where stress seems to be a feature may require coming back at a later stage. Drug history An increasingly important problem, both in terms of selfadministration and medically prescribed drugs. If the patient is taking medically prescribed drugs, ask about any side-effects, and the degree of compliance with therapy.


THE BEGINNINGS OF A DIAGNOSTIC SYNTHESIS AFTER HISTORY-TAKING At the completion of the history you should have gained a very good idea about which system is involved (i.e. the beginnings of an anatomical diagnosis), and a good idea about the nature of the general pathology. You should also have an idea of who the condition affects the patient because this is relevant to our third or „Functional‟ category of diagnosis. You may very well have good information about the background aetiology as well, but remember that dissecting this adequately depends on your having a good idea of the anatomical and pathological nature of the lesion to begin with. This may not become absolutely clear until after the clinical examination, so you will often have to return to these background aspects of the history after completing your physical examination. Never forget that your first line of further „investigation‟ should be a more complete history. 1. Anatomical diagnosis You should, by the end of the history, have an idea of the system involved. Again, the quality, site, radiation, aggravating and relieving factors are most important in this respect. A further example is that shortness of breath made worse by lying flat and relieved by sitting upright is generally of cardiac origin (left heart failure with pulmonary congestion). This example illustrates another aspect of making an anatomical diagnosis, namely that it is often functional consequences (i.e. the „Functional‟ category of diagnosis) which give you the clue to anatomy. Thus shortness of breath does not point directly to cardiac involvement, but only indirectly through pulmonary congestion. Again, much of our anatomical diagnosis is dependent on a knowledge of basic normal physiology - e.g. the nerve neurosome distribution for pain, particularly referred pain, the physiology of the circulation with posture (redistribution of blood volume on lying flat is important in the pathogenesis of left heart failure), etc. This is discussed more fully in Part I of this booklet.

onset conditions there give the clue not just to pathology, but to the anatomical structures involved (and in this case, to the segment of artery involved). (b) Acute conditions These are ones that come on over a few days or up to about two weeks. If associated with fever, almost certainly an inflammatory condition (this is not to say that it is necessarily infective, because any dead or damaged tissue, e.g. area of infarction, may cause secondary inflammation). (c) Subacute, say coming on over 2-6 wks. (d) Chronic - i.e. coming on over months. In this case, the time-intensity relationships become very important. If relentlessly progressive, and particularly if associated with weight loss and no fever, neoplasia is likely. If associated with fever (with or without weight loss), then chronic inflammation is likely. In the latter case, look for confirmatory evidence of local inflammation in the system involved, both in the secretions (diarrhoea, purulent sputum, nasal discharge, vomiting etc) or, if the region is accessible to touch and the patient‟s sensitivities, pain, tenderness, heat, redness, swelling, loss of function etc., i.e. the hallmarks of local inflammation. Define the time-intensity relationships carefully, as this may tell you whether the disease is an acute remitting and relapsing process (such as so-called „chronic‟ duodenal ulcer) or whether it is a chronic progressive one (like neoplasia). (e) Long-term chronic condition When the symptoms have been present a very long time, neoplasia is unlikely, and the condition is more likely to be degenerative (e.g. emphysema), very chronic inflammatory (e.g. bronchiectasis), „autoimmune‟, „constitutional‟, hereditary, familial etc. These aspects of clinical pathology are also discussed fully in part I. Comment Thus, even at the end of history-taking you should have some idea of what is going on in each of our four categories of diagnosis, particularly the first two.

(a) Hyperacute onset Conditions which come on within a few seconds or minutes are called hyperacute, and are usually brought about by rupture or obstruction of some hollow tube somewhere within the body.

If you are lucky your diagnosis may almost be complete but, mostly, it will be very tentative at this stage. It should be written down in its four categories as far as possible, e.g. (i) Myocardial (anatomical), ischaemia (pathological) (ii) With secondary angina, left heart failure, and atrial fibrillation (functional diagnoses) (iii) Predisposed to by the background „risk factors‟ of heavy cigarette consumption, high blood pressure, and diabetes

If the symptom goes away within a few minutes or hours, it is more likely to be obstruction than rupture.

However, again, predisposing factors (iii) may be particularly difficult to define at this stage.

In some areas such as the abdomen there are many hollow tubes which can be obstructed or ruptured, including gut, blood vessels, gall bladder, ureter, etc, but in others such as the brain there are very few, and sudden

Finally, having done this tentative diagnostic exercise, think about what further questions you should ask in the light of it, to help better define each of its diagnostic categories, before going on to the physical examination.

2. General pathological diagnosis


WRITING UP AND PRESENTING A HISTORY In writing up and presenting your histories you should observe the following rules: Presentation First present a head-line, including a brief statement to put the patient‟s background in context and a succinct comment on his/her presenting complaint - e.g.: the patient is a 43 year old stressed housewife with six children who presents with a history of sudden onset of severe central chest pain radiating to the left arm, lasting for one hour, a week before admission, and five similar episodes since, all coming on out of the blue. Present illness This should begin at the beginning and give a chronological account of the problem(s). By all means present a brief background at this stage if you wish, but get to the major symptom early on and elucidate the way it unfolded in time (time-intensity relationships), followed by the other aspects of that particular symptom as already discussed, i.e. its site, radiation, quality, severity and precipitating, aggravating and relieving factors. Then obtain the history about other symptoms related to the system which seems to be involved, (e.g. in the case of cough: shortness of breath (including positional variation), sputum, haemoptysis, chest pain, weight loss, fever etc). In this respect, it is just as important that you comment on the absence of potentially associated symptoms, as their presence. Only after this should you go into the enquiry of other systems. Most students spend far too much time on the latter and far too little on the main problem, so that the history loses its perspective. At each stage of the presentation you should pause and give yourself an opportunity to elucidate any important points that have come up because of the information already obtained (e.g. if you think the patient has pericardial pain for some reason, then it is important to comment on the presence or absence of aggravation of the chest pain by posture).

EXAMPLE OF A WRITTEN/ORAL HISTORY PRESENTATION The following is a sketch of a possible history, put forward to amplify the above. It is not meant to be complete, but to indicate the framework you should use. Presentation The patient is a 42 year old housewife with six children, who smokes 60 cigarettes per day, and presents with a history of five episodes of severe central chest pain in the past week. Present illness The patient had been well until a week before admission. At that time, on a Saturday evening, and after having „a few drinks‟ at home with friends, she noticed the sudden onset, over a few minutes, of an increasingly severe „heavy‟ central chest pain, spreading over the next few minutes to involve the left shoulder and the upper aspect of the left arm, where it felt not only „heavy‟ but „numb‟. That particular episode passed within five minutes, and she gave no further thought to it until two days later, when it recurred, this time whilst she was hanging out her washing on the Monday morning. This episode was more severe than the last, and caused her to sit down, after which it slowly eased over the next 15 minutes. Over the next five days there were several more episodes, each about the same as the second in site and radiation, but varying from 10 minutes to half an hour in length. She noticed no precipitating factors (in particular, there was no relation to effort), and no factors which aggravated the pain once it had commenced. Nor could she do anything in particular which would bring relief. In between attacks, she felt perfectly well. There were no associated symptoms, either during or between the attacks, except for rapid palpitation and shortness of breath soon after the start of one attack. There was no other shortness of breath, either on exertion or at night, no discomfort on lying flat, no palpitations, no faints, no swelling of the ankles, and no blackouts.

Background history: As above.


Systems enquiry revealed very little. specific interrogation were as follows:

The results of

Cardiovascular system As above. In addition, no claudication; no history of varicose veins. General No tiredness, loss of energy, weight loss, loss of appetite, or change in sleep pattern. No shivers or sweats. Respiratory No cough, sputum, haemoptysis, chest pain, shortness of breath, or wheeze. Alimentary system No loss of weight or appetite, no difficulty in swallowing, no indigestion, no abdominal pain or vomiting, no disturbance of bowel habit, no PR bleeding or jaundice. Urinary system No increased frequency of micturition, no nocturia, no dysuria, no haematuria. Genital system Periods normal. Six previous pregnancies - all full term and normal children of normal weight. The patient had been taking oral contraceptive therapy for the past three years.

Past history Past history of high blood pressure, during all pregnancies. No history of diabetes. Family history Mother died 56 years of a „stroke‟ (had high blood pressure). Father died 61, of „heart attack‟ (also hypertensive). One sister (younger) on treatment for high blood pressure. Married, 6 children. Social history Husband an alcoholic. Many family difficulties. Patient complains of a great deal of anxiety and worry, particularly over the welfare and future of her children. Normally smokes 20-25 cigarettes per day, but up to 60 in recent weeks, when domestic problems increased. She had recently started drinking up to two bottles of beer per day. Psychological history As above. Drug therapy Oral contraceptive pill for three years.

Haemopoietic system No anaemia, spontaneous bruising or bleeding episodes. Endocrine system No thirst, polyuria, pigmentation, goitre, weakness Skin No rashes, pustules or boils Locomotor system No joint pain or swelling. No weakness. Nervous system No headaches, „turns‟, fits, visual speech or hearing disturbances, no weakness, imbalance, or sensory symptoms, normal sphincter control. No recent change in behaviour or mood.




Thoughts on diagnosis at this stage could be jotted down as follows:

Make your history show the wood through the trees. Avoid medical jargon in presenting it.

1. Anatomical diagnosis: site, radiation, quality and nature of the pain suggests a myocardial infarction.

Be clear and concise both in writing up and presenting your histories.

2. Pathological diagnosis: this is an acute relapsing and remitting process (i.e. reversible ischaemia, at least so far).

Always avoid bias, not only in your questioning, but in interpreting the symptoms.

3. Physiological diagnosis: functionally, there seem to be very few consequences, except for possible secondary dysrhythmia and left heart dysfunction in one attack. 4. Aetiological diagnosis: the background upon which these symptoms have arisen (perhaps relevant to underlying aetiology) is a past history and family history of hypertension, heavy cigarette smoking, oral contraceptive therapy; and an unusually high amount of psychological stress recently as a possible precipitating factor. Of course, no diagnosis could be complete at this stage, and must await more information from the clinical examination. Even then, more history may be needed for a full clinical diagnosis (especially in the aetiological category). N.B. When any patient seems to have two or more clearly different and unrelated problems it is sometimes better to obtain and present the history related to each quite separately, and discuss the diagnostic aspects of each within the framework of a problem list. (But always be on guard that you may be dealing with multiple manifestations of single organ or system disease).

Use the clinical information in each individual patient to draw conclusions. Don‟t jump to conclusions on the basis of small pieces of evidence and then try to justify them by some theoretical knowledge you may have. Knowledge of anatomy & physiology is to be used in interpreting the individual patient‟s symptoms, not in making the patient fit your preconceptions! (See accompanying lecture notes on clinical symptoms & signs). Observe courtesies to patients and staff. Don‟t discuss problem medical areas in front of patients. Avoid using terms like „cancer‟, „Ca‟, „malignancy‟, „neoplasia‟ etc in front of patients. (the euphemism „mitotic disease process‟ may be better). Earn your patient‟s confidence, make them feel appreciated; be helpful and unhurried, and always remember Ericson‟s truism: „The best kind of history-taking is at the same time the best kind of psychotherapy‟


Part III - PHYSICAL EXAMINATION OF THE VARIOUS BODY SYSTEMS & REGIONS INTRODUCTION The purpose of this section is to give you a framework to approach the physical examination so that you may collect all the relevant information, and do so accurately, thoroughly and completely. CATEGORY A (LEFT COLUMN)


The order of performance of the physical examination within each of the various systems and regions. This will be shown in the left column of each section, and is most important. It relates to the techniques which students must be able to master, and the order in which we recommend they be performed within each system or region.

Physical signs or conditions which the student should be able to elicit and interpret at the bedside.

These are the ordinary basic routines of physical examination. They must be mastered by the end of your second year. At that time, students should be able carry out all of these techniques competently, without hesitation, and without leaving anything out. Of course, in subsequent years, we expect you to be able to perform more than just the routine so that, like having learnt the routine of driving a car, your senses can become free to observe and interpret other relevant information along the way. Even that can present a problem in a patient with a lot of physical findings, so remember to pause at the end of each phase of the physical examination of each system (e.g. after examining the hands routinely, ask what more, in the light of information already gathered, you should be looking for). It has to be said that the layout within category A tends to be somewhat artificial. In that we are approaching examination of different systems separately. This is done to fit in with the ways we teach you various aspects of the physical examination during your early years. Eventually you will have to learn to do a complete physical examination, and because of that, the broad routine of this process, which covers all of the systems & regions, is outlined at the end of this section.

Experience has shown that students approaching their final examination in MBBS often have a good knowledge about medical & surgical conditions, yet be far from competent in carrying out a physical examination and diagnosing various clinical conditions. One of the problems in this respect is that students are not always aware of just how far they fall short of the expected standard in relation to clinical signs, and this category aims to improve this by stating the minimum standard and range of clinical diagnostic abilities required. Students should be able to diagnose all of the common reversible conditions from physical signs by the end of Third Year, and diagnose them all as a minimum standard for Fourth and Fifth Year. This section should be used as a checklist and space is provided for the students to tick off various signs which they have seen, felt, heard or diagnosed. Every effort should be made to fill in any gaps, and the aid of your medical & surgical registrars & consultants should be sought in this respect. Various computer-assisted learning resources are also being developed within the Medical Education Unit & associated Teaching Hospitals to help with less commonobserved, but still reversible conditions. But in the end there is no substitute for seeing patients on the wards - including on an independent self-directed basis. It is really up to you.

CATEGORY C The techniques of physical examination within each of the various systems and regions. Lecture notes and multiple media explaining and demonstrating how the physical examination should be performed, with particular emphasis on the relevant clinical anatomy & physiological principles involved.


PRELIMINARIES (FOR ALL SYSTEMS & REGIONS) INTRODUCTION 1. wash hands (before and after seeing every patient) 2. smile, look patient in the eye, shake hands and introduce yourself (this introduction would obviously have already been done prior to taking the history, but when practicing short cases, make sure you spend time getting to know the patient first before you ask permission to examine them) 3. explain (in non technical terms) what you would like to do and ask permission. This is „informed consent‟ (mandatory). Also ask if there is any particularly tender areas to avoid, movements they cannot do or postures they cannot comfortably achieve &/or maintain. 4. obtain adequate exposure (clothes removed where necessary, but maintaining patient dignity with underwear or folded sheets/towels) 5. position patient appropriately for the system/region to be examined (patient lying supine with head on one pillow/at ~45 degrees/sitting up/standing etc) BUT make sure the patient is comfortable with the position you are asking them to make and maintain. GENERAL INSPECTION ENVIRONMENT Begin by observing the patient‟s „environment‟ from the foot of the bed. While your patient is undressing and positioning themselves look around the bedside and take careful note of: 1. what is going on? any special aids; devices; equipment; orthotic/prosthetic devices; written instructions/signs over the bed from nursing or medical staff; cards, flowers etc from family/friends (assessing social support from loved ones) 2. what is going in? O2; IV drips; CVC; meds/drugs; NGT; PEG‟s etc 3. what is coming out? examine sputum; vomitus; stool samples; look for any drain tubes/catheter bags/NGT & examine contents 4. vital signs? check temperature chart (febrile above 38 deg.) BP; HR; RR; O2 saturation

GENERAL INSPECTION PATIENT Then look carefully at your patient from the foot of the bed and ask yourself the following initial questions: 1. how sick does the patient look? (e.g. reduced conscious state; neoplastic, respiratory or cardiac cachexia; dyspnoea; central cyanosis, etc) Don‟t underestimate the importance of initial clinical impression. There is still some „art‟ and „intuition‟ left in medicine & surgery ... otherwise computers would have replaced us years ago! ;-) 2. urgent medical intervention required? (DRABCDE‟s of resuscitation, pain relief) or can we continue with our full examination? 3. obvious syndrome evident? (eg Cushing‟s; Grave‟s; Marfan‟s, Down‟s, Turner‟s etc) 4. postural abnormalities? (characteristic hemiparesis of stroke; shortened & externally rotated leg in #NOF; loss of deltoid bulge in dislocated shoulder etc) 5. abnormal movements or pulsations? (fasciculations/tremor/choreo-athetoid movements; neck or praecordial pulsations etc) or lack of movements? (stroke; spinal pathology etc) 6. muscle wasting? left c.f. right; upper limb c.f. lower limb; flexor c.f. extensor; proximal c.f. distal (LMN lesions; disuse atrophy; neoplastic/cardiac cachexia etc) 7. skin changes? central cyanosis; jaundice; anaemia; scars from previous or current surgery or trauma? obvious skin lesions/bruises/rashes; pigmentation abnormalities; discharging fistulae/sinuses etc Note that in a long case or in real cases, you would make many of these general observations while taking the history, but remember to review again when you have adequate exposure. Now, once you have completed the preliminary general inspection focus on the appropriate system or region determined by your history and provisional working diagnosis/problem list and begin your specific inspection.

Note: use all of your senses not just your eyes – consider unusual smells, sounds ... use the Sherlock Holmes type of attitude!






GENERAL EXAMINATION routine, from foot of the bed – consider x7 categories in your check-list as previously described

GENERAL EXAMINATION conscious state; colour, including especially central cyanosis, anaemia etc. dyspnoea/hyperventilation. pulsations: particularly in neck, praecordium and epigastrium. malar flush of mitral stenosis.

HANDS examine both hands together: check dorsum & palms once only (avoid repeatedly turning the hands over). comment on important CVS signs and in order of diagnostic importance. PULSE 1. rate (count for 15 sec then x4; unless irregular then full 1 min) 2. rhythm (regularity) (radio-radio delay; radio-femoral delay; collapsing pulse etc if deemed appropriate) RESPIRATION convenient to assess respiratory rate after taking the pulse (count for 15 sec then x4). BLOOD PRESSURE brachial artery is just medial to the biceps tendon (take sitting and standing). JUGULAR VENOUS PULSE (JVP) (a) look with patient‟s neck relaxed (looking straight ahead) locate the JVP between 2 heads of SCM &/or along the anterior & posterior borders of SCM.

(b) confirm that it is venous by any two of the following:

double impulse (compared with carotid pulse) not palpable, filling from above, obliteration with slight pressure; and variation in height with inspiration, upright posture, and hepatojugular reflux.

HANDS state of perfusion (colour, temperature, capillary return); cyanosis (central versus peripheral); stigmata of bacterial endocarditis (splinter haemorrhages. Osler‟s nodes. Janeway lesions) palmar crease pallor (? anaemia); tar stains (smoking); clubbing of nails. PULSE arrhythmias, including sinus arrhythmia, atrial fibrillation, extra-systoles, coupled beats (pulsus bigeminus). also pulsus paradoxus (in severe asthma, constrictive pericarditis). pulsus alternans (severe hypertension). collapsing pulse (at wrist) in A.I. slow-rising plateau pulse (best felt at neck). bisferiens pulse of aortic stenosis combined with incompetence. tortuous visible arteries (eg locomotor brachialis). BLOOD PRESSURE recognise response to standing (including increased pulse rate) i.e. baroreceptor JUGULAR VENOUS PULSE (JVP) measure and interpret height of any raised JVP noting any exaggeration of „a‟ or „v‟ waves; timing and interpretation of these (absent „a‟ wave in atrial fibrillation; large or giant „v‟ wave in TI; intermittent „cannon‟ waves in complete heart block. signs of obstruction of SVC. Kussmaul‟s sign in constrictive pericarditis, pericardial tamponade, tension pneumothorax, right ventricular infarction.

(c) measure height above the sternal angle - if JVP elevated go on to feel for pulsation in the liver, particularly if prominent „v‟ wave. also look for enlarged spleen, ascites and for sacral & peripheral (ankle) oedema.

(d) assess character of the JVP (see opposite) CAROTIDS locate laryngeal prominence of thyroid cartilage in the midline. walk finger to inferior edge. locate cricoid cartilage (cricothyroid membrane in between) retract SCM and push common carotid artery against carotid tubercle of C6. particularly noting: 1. 2. 3. 4.

pulse volume/amplitude pulse character (wave-form) feel for thrills & tenderness of the carotid triangle listen for bruits.

MEDIASTINUM define if midline (tracheal position - define by pressing middle finger straight back above sternal notch).

CAROTIDS slow upstroke/plateau pulse/slow downstroke in aortic stenosis (AS); low-pitched bruit radiating from base of heart in AS collapsing pulse in AI high frequency thrill &/or high-pitched long loud localised bruit (upper border of thyroid cartilage) in internal carotid artery stenosis. distinguish arterial bruits from venous hum. tenderness of the carotid triangle (with a history of sore throat followed by neck tenderness? – consider Lemierre's syndrome – a septic thrombophlebitis of the internal jugular vein). MEDIASTINUM




HEART (a) inspection. for evidence of a pacemaker; any abnormal left or right parasternal pulsations, visible apex beat.

HEART (a) inspection visible pulsations.

(b) palpation. not just of the apex, but pulsation elsewhere. also thrills. n.b. if in doubt, here or in any other category (a-d) (especially auscultation), ask the patient to stop breathing for a few moments.

(c) percussion. usually not helpful

(b) palpation

apex beat. characteristic thrust at apex in LV hypertrophy; left parasternal heave in RV hypertrophy. abnormal pulsations elsewhere (e.g. cardiac aneurysm). thrills, including where maximal, and timing.

(c) percussion. (except perhaps when apex beat impalpable, and where pericardial fluid suspected)

(d) auscultation. firstly heart sounds. (d) auscultation

First listen to 1st and 2nd heart sounds (time with carotid pulse) with bell at apex (pressing only very lightly) Next listen to 2nd sound at base with diaphragm, and define its split with inspiration Now listen for added heart sounds at apex and left parasternal area, especially with bell for 3rd heart sounds, 4th sounds Then listen for murmurs (ask patient to stop breathing - in mid expiration - if you are having difficulty), first over the whole precordium (including left infraclavicular region) with both bell and diaphragm in a general way. then listen specifically for:

(i) apical murmurs. systolic ones with the diaphragm. (ii) basal murmurs. most heard best with diaphragm. also

listen in neck. (iii) diastolic. listen for murmur of mitral stenosis (with bell), especially if a loud first heart sound or an apical systolic murmur is heard. also listen (with diaphragm, para-sternally) for aortic incompetence. Remember with all murmurs to describe:  site  where maximum  radiation  quality  pitch  intensity  position & duration in the cardiac cycle  manoeuvres that alter intensity.

Not usual to be able to detect split first sound Recognise split second sound, increased split during inspiration Third heart sound in normal children, and with cardiac dilatation in adults (volume overload) Fourth heart sound in ventricular hypertrophy. murmurs Be able to diagnose classic murmurs of: mitral stenosis; mitral incompetence aortic stenosis; aortic incompetence tricuspid incompetence; tricuspid stenosis pulmonary stenosis; pulmonary incompetence patent ductus; ASD; VSD also friction rubs (pericardial, pleuro-pericardial). pansystolic murmurs include: mitral incompetence; tricuspid incompetence (increased by inspiration); VSD ejection systolic murmurs include: aortic & pulmonary valve stenosis. diastolic murmurs include: mid-diastolic at apex in mitral stenosis; early diastolic at left sternal edge in AI (also, rarely, pulmonary incompetence). Be able to comment on the haemodynamic significance of all valve lesions. Use of Valsalva, handgrip, respiration, and other manoeuvres in bringing out particular murmurs (see also „making basic sciences work in clinical diagnosis‟cardiovascular section).

Make two postural manoeuvres on routine auscultation: 1. first, patient on the left side and listen at the apex for mitral stenosis (with bell) 2. then with the patient sitting up and breathing out, listen at the left lower parasternal edge, in full expiration, for the early diastolic (high-pitched blowing) murmur of aortic incompetence. this latter should be the last part of the cardiac examination, for the patient is now sitting up and we can then conveniently go on to the next stages. Know how to perform Valsalva manoeuvre, handgrip etc. which may help bring our some murmurs.




LUNG BASES Percuss both bases and listen for breath sounds and inspiratory crepitations

LUNG BASES Detect fine, late inspiratory crepitations of early pulmonary oedema, and distinguish from „normal‟ (the latter sometimes present in immobile or elderly patients, but are cleared by coughing or deep breaths).

When describing breath sounds always describe all of the following: 1. quality 2. intensity 3. presence or absence of added sounds If crepitations present, define their: 1. position anatomically 2. position in respiratory cycle 3. cleared by coughing? SACRAL OEDEMA ideally “one finger in one spot for one minute” – (not recommended in MSATs, a few secs is enough!) look for this especially in patients confined to bed.

SACRAL OEDEMA Pitting versus non-pitting. Unilateral oedema and calf tenderness in DVT.

THE PERIPHERAL VASCULAR SYSTEM Palpate aorta. Listen for abdominal bruits in hypertension. Feel for radio-femoral delay. Examine femoral, popliteal, and foot pulses (anterior & posterior tibials; dorsalis pedis, perforating peroneal). Look & feel for ankle oedema, calf tenderness. Examine state of perfusion of legs - colour, temperature, capillary return. Buerger‟s test where indicated.

THE PERIPHERAL VASCULAR SYSTEM State of veins (including varicose veins). Skin temperature, atrophy, nail and hair growth (reduced in peripheral vascular disease).

NECK Listen in the neck for bruits, especially over carotid bifurcation, if you have not already done so. OPTIC FUNDI Examine the retinal vasculature, noting particularly arterial calibre and regularity, and light reflex; A-V nipping, haemorrhages, exudates, papilloedema. COMMENT This should be the order of a complete routine physical cardiovascular examination. However, at the end of each step you should pause to ask what in addition you should look for in the light of the history and/or other clues in this particular patient. e.g. listen particularly for a pericardial friction rub in any patient with chest pain aggravated by lying flat and eased by sitting forward. As each stage of the routine examination is completed, ask yourself whether there are particular things you should look for in this way. Also, at the end of the examination, are there any more questions you wish to ask in the history related to any of the four categories of diagnosis, viz. Anatomical, Pathological, Functional, Aetiological, particularly the latter?

NECK thrills/bruits Distinguish carotid artery stenosis, from aortic valve stenosis (with radiation of the murmur to the neck). OPTIC FUNDI note:  a/v ratio, particularly arterial narrowing (look along the artery to see whether this is uniform or irregular)  increased light reflex from arteries, e.g. „copper wiring‟ or „silver wiring‟  haemorrhages of different types (blot, dot, flameshaped, sub-hyaloid) and their origins  „hard‟, and „soft‟ exudates (retinal infarcts)  optic atrophy  papilloedema COMMENT Be able to diagnose:  congestive cardiac failure (high and low output), left and right ventricular hypertrophy/failure  myocardial infarction; aortic dissection  cardiac arrhythmias  cardiac valvular lesions/shunts  hypertension (incl. hypertension shock - with and without peripheral vasoconstriction)  sub-acute bacterial endocarditis  vena caval obstruction, superior & inferior  constrictive pericarditis  cardiac tamponade


SECTION C - notes on CVS History & examination cardinal CVS symptoms:  tiredness/lethargy/malaise  pre-syncope & syncope  chest pain  palpitations  shortness of breath „sob‟ (rest/exercise/work)  orthopnoea  paroxysmal nocturnal dyspnoea „pnd‟  swelling of ankle/legs „soa‟  intermittent claudication


hands - dorsum

wrists – radial pulse (palpate radial artery b/w brachioradialis & FCR tendons)

hands – palms report on:  state of perfusion (colour, temperature, capillary return)  cyanosis (central versus peripheral)  stigmata of bacterial endocarditis: (splinter haemorrhages. Osler‟s nodes. Janeway lesions)  tar stains (smoking)  palmar crease pallor (? anaemia)  tendon xanthomata  clubbing of nails

report on:  rate (beats/min)  rhythm (sinus; AF) wrists - respiratory rate  breaths /min


radio-radial delay & radio-femoral delay

arms – BP

eyes conjunctivae - should be pink (suspect anaemia if particularly pale) sclerae - should be white (jaundice if yellow) also look for xanthelasma (subcutaneous cholesterol deposits around eyelids)

use obliteration of radial pulse to estimate systolic BP


ophthalmoscopy (optic fundi) note:  a/v ratio, particularly arterial narrowing (look along the artery to see whether this is uniform or irregular)  increased light reflex from arteries, e.g. „copper wiring‟ or „silver wiring‟  haemorrhages of different types (blot, dot, flameshaped, sub-hyaloid) and their origins  „hard‟, and „soft‟ exudates (retinal infarcts)  optic atrophy  papilloedema


face look for the characteristic „malar flush‟ of mitral stenosis

mouth most important sign is central cyanosis (bluish tinge of tongue (+/- mucous membranes/lips) also check for high arch palate (but not in someone 158 cm) and assess for dental hygiene.

1. patient relaxed looking straight ahead (turning head to the left tenses the sternocleidomastoid muscle (SCM) and the investing layer of the deep cervical fascia and may make it more difficult to see) 2. from in front of the patient look for the double impulse flicker of the right jugular venous pulse (JVP) 3. look between the 2 heads of SCM (manubrio-sternal & clavicular) and along the anterior & posterior borders of SCM (the internal jugular vein is deep to the SCM muscle and therefore you are looking for the transmitted impulse coming out from behind the muscle)

JVP – CONFIRM 1. double impulse flicker timed with carotid pulse (only single impulse in AF) 2. not palpable 3. occluded by soft pressure 4. IJ vein fills from above 5. changes height with: -respiratory cycle -posture 6. hepato-jugular reflux


V, a positive deflection due to filling of the right atrium against the closed tricuspid valve during ventricular contraction Y, a negative deflection due to emptying of the right atrium upon ventricular relaxation two particular conditions for a student not to miss: giant „v‟ waves of tricuspid incompetence – occur with every beat cannon „a‟ waves – irregular occurrence with various types of heart block

JVP – MEASURE patient usually at 450 measure height (cm) of the impulse above sternal angle with two straight edges should be less than 3-4 cm and usually seen just above the clavicles in young healthy people An elevated JVP is the classic sign of venous hypertension (e.g. right-sided heart failure). JVP elevation can be visualized as jugular venous distension, whereby the JVP is visualized at a level of the neck that is higher than normal. The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the Kussmaul sign, and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes: constrictive pericarditis, restrictive cardiomyopathy, pericardial effusion, and severe right-sided heart failure.

carotids trying to assess (clinically) left ventricular function and aortic valve stenosis/regurgitation. palpate:  on one side at a time!  at level of cricoid cartilage  retract SCM muscle  pressing common carotid artery back against the carotid tubercle of C6 assess: 1. amplitude/volume 2. wave-form or character 3. thrills (? turbulent flow due to atherosclerosis)

JVP - CHARACTER A, a positive wave due to contraction of the right atrium C, a positive deflection due to bulging of the tricuspid valve toward the atria at the onset of ventricular contraction X, a negative deflection due to atrial relaxation


carotid bruits auscultate for bruits (turbulent flow due to atherosclerosis). a carotid bruit is characteristically loudest at the neck and dissipates towards the praecordium. whereas the murmur of AS is characteristically loudest in aortic area and dissipates towards the neck). plus correlate with the carotid pulse.

trachea check for position (should be TML) useful to ascertain whether a displaced apex beat is really due to cardiac enlargement or actually a misleading mediastinal shift (is something pushing e.g. pneumothorax or pulling – chronic, severe pulmonary fibrosis) possible causes of such a shift ?  tension pneumothorax  tumour (e.g. lung cancer)  lymph node enlargement  fibrotic change in lung



palpate both sides of sternum for heaves/thrusts/thrills. If the hand is actually lifted off the chest wall with each beat suspect right ventricular hypertrophy. (remember that due to anti-clockwise rotation of the heart during development, most of the anterior surface of the heart is formed by the right ventricle).

thrills may indicate turbulent blood flow due to valvular pathology or ASD/VSD

look closely for scars, deformities look & feel for subcutaneous pace-makers


apex beat – look look for the position of the apex beat … “the most inferior and lateral point that you can see &/or feel the pulsation of the heart during systole” look tangentially across chest wall. in certain female patients you may need to lift left breast to obtain clear view

heart chambers 1. 2. 3. 4. 5. 6. 7. 8.

right atrium right auricle left auricle coronary sulcus right ventricle left ventricle apex of heart anterior interventricular sulcus

count down the rib interspaces starting at the second costal cartilage at the sternal angle normal position is the 5th intercostal space ~ 1cm medial to the mid-clavicular line (5th ICS MCL) apex beat – feel place fingers between the ribs in the intercostal spaces and feel for the most inferior & lateral point that you can feel the beating of the apex of the left ventricle assess: 1. position 2. size 3. character

great vessels 1. 2. 3. 4. 5. 6. 7. 8.

aortic arch brachiocephalic a L common carotid a L subclavian a R brachiocephalic v L brachiocephalic v superior vena cava inferior vena cava


cardiac auscultation listen: with your stethoscope over the cardiac areas & along sternal edges with both diaphragm & bell use diaphragm for high frequencies bell for lower frequencies report: 1. 2. 3. 4. 5.

number of heart sounds intensity of heart sounds any changes of these sounds (spit S2) with inspiration added sounds murmurs

any added sounds ? any murmurs ? (if yes then describe fully) ? need for postural manoeuvres &/or exercises to accentuate murmurs check for carotid bruits if not already done so

murmurs originating from flow abnormalities in these valves are not usually best heard directly over them!

heart valves Pulmonary Aortic Mitral Tricuspid


aortic area

tricuspid area(s) pulmonary area

mitral area


two routine postural manoeuvres

lung bases – percussion cardiac auscultation – left lateral position (MS) brings the apex of the heart closer to the chest wall use the bell to listen for the mid-diastolic (low pitched) murmur of mitral valve stenosis

lung bases – auscultation

cardiac auscultation – sitting up (AI) use the diaphragm at the lower left sternal edge with the patient in full expiration to listen for the early diastolic (high pitched) murmur of aortic valve incompetence

sacral oedema


peripheral vascular examination acute arterial occlusion the six „P‟s: 1. painful 2. pale 3. pulseless 4. paralysed 5. paraesthesia 6. perishingly cold ! inspection  skin colour (white, blue, black)  decubitus ulcers  ischaemia/gangrene  trophic changes (skin, nails onychogryphosis)  loss leg hair (? contentious sign) where to palpate/auscultate the arteries? aorta & coeliac trunk bruits

abdominal aorta (AAA) palpate deeply in the midline (or slightly to the left of the midline) between xiphisternum and umbilicus.

SMA bruits

note: should be ~2-3 cm > 6cm is suggesting an AAA aortic bruits (don‟t forget to auscultate the major arteries for bruits. especially: aorta, coeliac trunk, origin of SMA, renal aa and origin of IMA)

left renal artery bruits


right renal artery bruits

femoral pulse (femoral artery is found 2 cm below an imaginary point midway between ASIS and symphysis pubis i.e. mid inguinal point) palpate for thrills auscultate for bruits

IMA bruits


popliteal pulse (palpate in the middle of the diamondshaped popliteal fossa. however often easier to feel at the proximal angle (between the hamstring insertions) or at the distal angle (between two heads of gastrocnemius) of the popliteal fossa).


„pedal pulses‟

posterior tibial artery (palpate between medial malleolus & medial border of tendo-calcaneus or „Achilles tendon‟)

dorsalis pedis artery (continuation of the ant. tibial – runs from between the medial & lateral malleoli to the first toe cleft). May be felt anywhere along this path. Classically, described as being at the apex of the first toe cleft between extensor hallucis longus tendon & the extensor digitorum tendon of the second toe. note: occasionally the dorsalis pedis is small or absent (and unable to be palpated).

anterior tibial artery (palpate between medial & lateral malleoli). Due to the thick fibrous superior & inferior extensor retinacula, it may be helpful to move your finger proximally or distally a few cm to find the gap between them where the arterial pulsations can be more easily felt. perforating peroneal artery (palpate 1-2 cm medial to the lateral malleolus). This artery supplies a variable amount of the dorsum of the foot and may be the major supply. To be considered if a dorsalis pedis pulse is weak or absent but there are no symptoms or signs of ischaemia.


Buerger‟s test - for occlusive arterial disease:

ankle oedema (ideally: “one finger in one spot for one minute” – but not under exam conditions!)

calf tenderness (squeeze and assess for clinical evidence of a DVT, particularly in the venous sinuses of the deeper situated soleus muscle)

 elevate leg for 1 min & observe increase pallor  exaggerated if patient exercises foot (eg repetitive dorsi-plantar flexion)

 bring leg back to horizontal (or hang over edge of bed)  reactive hyperaemia delayed, venous filling time prolonged (relative to normal limb) purple cyanotic hue occurs if arterial supply impaired


normal CXR

bronchial tree

cardiac shadow

lungs & pleurae


congestive cardiac failure radiologically:  cardiomegaly  pulmonary congestion  upper lobe vessels more prominent  pulmonary oedema  alveolar oedema  indistinctness of perihilar vessels  bilateral basal interstitial septal oedema (horizontal linear opacities – Kerley B lines)  pleural effusions






GENERAL EXAMINATION From the end of the bed (with clothes removed at least above the waist). First open-mindedly looking for any abnormality at all; then with a more closed mind looking for respiratory distress: central cyanosis, tachypnoea, use of accessory respiratory muscles, asymmetrical chest movements etc.

GENERAL EXAMINATION Respiratory distress. central cyanosis. use of accessory muscles of respiration. expiratory wheeze (audible). inspiratory stridor. asymmetry of chest movement. increased A-P diameter in COPD

HANDS Particularly for finger-clubbing, cyanosis, state of skin perfusion, metabolic flap (asterixis).

HANDS central vs. peripheral cyanosis. clubbing. signs of CO2 narcosis.


FACE/TONGUE cyanosis – central/peripheral.


NASAL SINUSES detect fluid/inflammation in maxillary and frontal sinuses.


VOICE hoarse/husky voice in recurrent laryngeal nerve paralysis. nasal voice of palatal paralysis.


COUGH moist/productive or dry. „brassy‟ or bovine‟, weak cough in recurrent laryngeal nerve paralysis.

SPUTUM examine.

SPUTUM mucoid, mucopurulent, purulent, blood-stained.

TRACHEA Position and length of trachea above sternal notch.

TRACHEA Normally slightly deviated to right. Very little trachea above sternal notch in chronic obstructive airways disease.

LYMPH NODES inspect & palpate: axillary, cervical, supraclavicular. (maybe even supratrochlear, and inguinal).

LYMPH NODES Define any enlargement; also consistency, matting of nodes, size, number distribution etc.




CHEST (a) Inspection  degree and symmetry of movement  type of respiration (patient at 45 degrees)  degree of resting inflation (patient sitting upright)

CHEST (a) Inspection shape of chest: barrel chest; kyphoscoliosis. asymmetry of chest movement

(b) Palpation Chest movement (especially testing with hands & thumbs for asymmetry of chest expansion) Overall chest expansion with a tape-measure (at the nipple line). Remember to palpate anteriorly in three positions, placing hands symmetrically: (i) under the clavicles (ii) in the mid-chest anteriorly, over the breasts, and (iii) laterally, under the breasts. Vocal fremitus (or use stethoscope and check for vocal resonance) (c) Percussion  compare each side as you go along  perform with „follow-through‟ action  percuss para-sternally, then laterally  including axillae  light and heavy percussion  define normal liver and cardiac dullness  remember to percuss apices & clavicles (d) Auscultation most use stethoscope diaphragm, but use bell in hairy patients. comment on: 1. intensity of breath sounds 2. quality of breath sounds (vesicular or bronchial) 3. added sounds (eg. crackles/crepitations & wheezes/rhonchi) If added sounds present: i) where anatomically? (R or L; UL or LL etc) ii) where in respiratory cycle (insp/exp/pan) iii) cleared by coughing? Also vocal resonance If added sounds present, determine type, effect of coughing & position in respiratory cycle.

Recognise changes in respiration:  increase rate and/or depth  use of accessory muscles of respiration  in-drawing of intercostal spaces in severe airways obstruction  grunting respiration of pneumonia with pleurisy  Kussmaul respiration  Cheyne-Stokes respiration  stridor of tracheal stenosis or obstruction. Other: recognise lobar surface markings abnormal veins on chest, colour transition in SVC obstruction (b) Palpation  alterations in movement  asymmetry  vocal fremitus  rib lumps; rib tenderness, local or on compression (with fractures, pleurisy)

(c) Percussion

Degree of dullness Movement of percussion borders on inspiration (e.g.liver dullness).

(d) Auscultation (i) breath sounds Normal breath sounds are vesicular, and produced by airways rather than in alveoli; intensity related to total and regional airflow. Reduced breath sounds: occur with obstruction of regional airflow (e.g bronchial occlusion ) or attenuation at an interface (e.g. pleural effusion ), emphysema. Increased breath sounds: (bronchial breathing, aegophony, whispering pectoriloquy) occur with reduction of normal regional attenuation of breath sounds (e.g. in consolidation, dense pulmonary fibrosis). (ii) vocal sounds Vocal resonance. Produced and altered above.

Remember axillae & apices.






(d) Auscultation (contd).

(iii) Added sounds note type, pitch, intensity and position in respiratory cycle.

SPECIAL TESTS FET tidal volume spirometry

crepitations or crackles Coarse creps: in large airway secretions, inspiratory and expiratory, cleared by coughing (thus distinguished from pleural rub). Fine creps produced by sudden opening of peripheral airway units. Late high - pitched basal inspiratory creps suggest alveolar involvement (e.g. pulmonary oedema). Early inspiratory and late expiratory creps suggest origin from small to medium airways, e.g. in bronchitis/bronchiolitis. rhonchi or wheezes Produced by oscillation of opposing airway walls with significant narrowing. Pitch determined by physical properties of airway rather than airway size. Monophonic wheeze in local obstruction; polyphonic in wide spread obstruction. Rhonchi usually expiratory; inspiratory wheeze implies significant airway narrowing (as does pulsus paradoxus therefore check for this where appropriate, e.g. severe asthma). pleural rib - distinguish from coarse rales (ask patient to cough).

GENERAL COMMENTS Often helpful to examine chest with patient straddling a chair/stool. Remember to examine the lateral aspects of chest. Especially in axillae (hands-on-head helps).

GENERAL COMMENTS Know the surface markings of the major lung lobes. Know accurately the physical signs of collapse (with and without an obstructed bronchus), pulmonary consolidation, plural effusion, pulmonary embolism, and cor pulmonale. Be aware of normal increase in breath sounds at right apex (due to trachea being slightly to the right).


notes on the respiratory examination





Pembertonâ€&#x;s test/sign



percussion note type



hollow viscus




normal lung


consolidation collapse fibrosis


consolidation collapse pleural thickening

stony dull

pleural effusion






GENERAL-make sure all clothes are removed, down to underpants only.

How sick does the patient look? present?

GENERAL INSPECTION (from end of bed) Skin, face, abdomen.

GENERAL INSPECTION State of nutrition, hydration, any tremor or restlessness, jaundice, pigmentation, hair loss, spider naevi, bruising, gynaecomastia, parotid enlargement.

HANDS Including palms, nails.

HANDS Inspect palmar creases as an index of anaemia (and confrim by looking at conjunctivae, tongue, areolae). Koilonychia in chronic iron deficiency. Leuconychia, finger-clubbing, palmar erythema, bruising, Dupuytren‟s contracture in chronic liver disease. „Metabolic flap‟ in hepatic failure (also seen with CO2 narcosis, renal failure).

MOUTH Including throat, tongue, teeth, gums.

Any syndromes

MOUTH Pigmentation of the buccal mucosa in Addison‟s disease of the adrenal glands. Pigmentation of the lips in Peutz Jegher‟s syndrome. Koplik‟s spots in measles. Petechiae over the junction of hard and soft palate in infectious mononucleosis. Dry tougue in dehydration (also mouth breathing). Glossitis in nutritional deficiencies, pale tongue in anaemia. Atrophic tongue also in most anaemias (not just B12 deficiency). Large tongue in amyloid disease, acromegaly.

SALIVARY GLANDS Parotids, submaxillary glands especially. Also inspect and palpate parotid duct orifice.

SALIVARY GLANDS Enlargement from lymphocytic infiltration in lymphoma etc. Enlargement in Sjogren‟s syndrome (also dry eyes). Parotid enlargement in alcoholic liver disease.

ABDOMEN Lie patient flat, remove blankets, turn down sheet to level of symphysis pubis. (a) Inspection - respiration, symmetry, contour, swellings, distension, etc. Looking tangentially across abdomen during quiet respiration often helps define subtle masses at this stage.

ABDOMEN (a) Inspection. Observe any alteration in contour, particularly fullness in the flanks (fluid?), other masses, asymmetry. Look for any visible scars, marks, striae, visible peristalsis or pulsation; abnormal veins including caput medusa (veins spreading from the umbilicus in portal hypertension). Also jaundice, loss of hair and female distribution of bodily hair in chronic liver disease.

look for swellings; distension or other alterations in abdominal contour – especially on quiet inspiration: 1. fat 2. fluid 3. flatus 4. faeces 5. fetus 6. „fantom‟ pregnancy (pseudocyesis) 7. filthy big tumour   

scars, striae visible peristalsis or pulsations superficial veins (caput medusa)






(b) Palpation. Ask patient if they have any tender or

(b) Palpation. Observe any tenderness, guarding or

painful spots, then palpate in each quadrant, starting away from any area of pain with warm hands. first lightly then more firmly/deeply. Keep observing patient‟s face & eyes for any signs that you may be hurting them. perform with your interphalangeal joints extended, flexing at MCP joints. imagine the structures underlying your hands and state them as you proceed: Note guarding, rigidity, tenderness, release (rebound) tenderness; masses; pulsations.

release tenderness. Observe any masses and describe their anatomical localisation and physical characteristics including contour, regularity, smoothness, firmness, tenderness, etc. (see also Category A). Then look specifically for liver edge (if felt, is it displaced or enlarged, ie. Percuss from upper to lower border- normal percussion span 12 cms), spleen enlargement (particularly in lymphoproliferative and myeloproliferative disorders, portal hypertension, severe CCF). Enlarged Kidneys (especially in polycystic disease). Palpable pulsatile aorta (also listen for overlying bruit). Gall bladder - if enlarged, often easier to see than feel, especially by looking tangentially across the abdomen when the patient takes a deep breath (alternatively try standing at the patients right shoulder and feeling with the cupped right hand over the patient‟s right hypochondrium during inspiration). Remember Courvoisier‟s law if gall bladder enlarged; also Murphy‟s sign. Recognise palpable sigmoid colon, caecum, with constipation. Demonstrate gastric splash in upper intestinal obstruction. Remember the seven f‟s in any abdominal distension (fat, fluid, flatus, faeces, fetus, phantom pregnancy! filthy big tumour).

COMMENTS 1. If any mass felt by palpation, then determine its anatomical localisation, namely whether it is attached to the diaphragm and whether it is an anterior or posterior organ. Attachment to the diaphragm given by movement (and direction of movement) on inspiration; anterior v‟s posterior organ given by (i) where dull to percussion (anteriorly or posteriorly). (ii) whether you are able to ballott the mass from the loin (if so probably posterior, but large anterior masses sometimes also ballottable). 2. If you can only feel a vague mass on initial examination always go on to do bi-manual examination, including ballottment. This especially helps with posterior masses. Routine palpation of organs. Feel specifically for liver, spleen, kidneys, (aorta, gall bladder). Bi-manual helps define liver edge better. Getting the patient relaxed, both your hands in position (and keeping them still) and succeeding to get the patient to take deep breaths with an open mouth are vital to tipping a spleen. Also, don‟t palpate too laterally for a spleen. It may be felt more medially than you expect, especially if moderately large. Right lateral position may help in feeling a difficult spleen. Bi-manual examination with ballottment at the very end of inspiration is the way to feel for enlarged (or displaced) kidneys.

(c) Percussion Routine, and over all palpable organs. Remember to percuss upper and lower limits of liver dullness (< 12 cm is normal span in MCL); also percuss bladder where appropriate. Demonstrate resonance in flanks; shifting dullness if fluid suspected.

(d) Auscultation over any mass; bowel sounds, bruits

(c) Percussion

liver dullness, splenic dullness (not normally dull any further anteriorly than the left midaxillary line). shifting dullness in ascites, also fluid thrill in tense ascites (where you may have to use a bi-manual „dipping‟ technique to feel any enlarged organs)

(d) Auscultation increased bowel sounds in gut obstruction, absent in ileus. Vascular bruits including aortic, femoral, renal and other arterial obstructions. Hepatic bruits (over vascular secondaries, hepatoma). Splenic friction rubs.





HERNIAL ORIFICES Always inspect hernial orifices. inguinal & femoral

INGUINAL LYMPH NODES GENITALIA Always inspect as part of the routine examination. RECTAL EXAMINATION Including stool inspection and test for faecal occult blood. LEGS

(review surface landmarks)

INGUINAL LYMPH NODES feel for enlarged inguinal lymph nodes: superficial: horizontal & vertical chains and deep: along femoral vein. describing their consistency, size, degree, of matting etc. GENITALIA Testicular atrophy in chronic liver disease, etc. RECTAL EXAMINATION Rectal masses, enlarged prostate (benign versus malignant). Haemorrhoids, tenderness (eg. pelvic abscess or other inflammation). Recognise stool in malabsorption, melaena, iron therapy, obstructive jaundice, ulcerative colitis. LEGS

bruising; oedema; peripheral neuropathy GENERAL COMMENT Always give a statement about the:

(i) Anatomical localisation of the organ, before

naming it, eg. This mass moves downwards with respiration, is resonant to percussion anteriorly and ballotts from the loin, therefore is a posterior mass attached to the diaphragm, and most likely kidney. Do not do the reverse of jumping to a conclusion and trying to justify that by subsequent examination. If you do, one day you will find a mass which does not fit your preconceptions and be confused eg. a central abdominal mass which is mobile, does not move with respiration but is dull to percussion anteriorly is, using your anatomical knowledge, probably a mensenteric mass (small bowel mesentery, omentum, transverse colon); however the pattern-recogniser will find it difficult and usually makes a mistake.

GENERAL COMMENT Be familiar with the external and general manifestations of failure of the major intra-abdominal systems including chronic hepatic failure, chronic renal failure, chronic malabsorption. Also recognise conditions which may cause infiltration, particularly of liver, spleen, and lymph nodes, without overt clinical signs of chronic failure of the organ concerned. Recognise and be able to differentiate firm, smooth enlargement of an infiltrated liver from the moderate irregular enlargement of cirrhosis, and this in turn from the large craggy hard nodular enlargement of secondary carcinoma of the liver. Know the signs of hepatic failure, ulcerative colitis (including acute toxic megacolon) and of obstructive jaundice (remember to examine urine as well as stool).

(ii) Pathology - apart from major information on

anatomy, you can also often get some indication of the pathology involved by the character of the mass, ie. whether cystic or solid, irregular, hard, craggy, ulcerated etc. In this respect you should also look at secretions, in this case the faeces; for example blood suggests ulceration, the presence of neutrophils microscopically provides important evidence of (bacterial) infection. Always look in any system for both general (fever) + local (heat, redness, swelling, pain and tenderness, loss of function, purulent secretions) evidence of inflammation in the abdomen the latter includes rigidity, guarding, tenderness, release tenderness, and/or (purulent) diarrhoea.






GENERAL First inspect and palpate the area indicated by the history to be involved, to decide which system to examine in more detail.

GENERAL including state of consciousness. face and limbs: looking in the latter particularly for muscle atrophy, fasciculations, tremor or other involuntary movements (choreo-athetoid, spasms, tics, convulsions).

For example, in a patient with leg weakness, do not assume that you are dealing with a central nervous system problem. Inspection and palpation might reveal muscle tenderness and wasting more compatible with primary muscular inflammatory disorder, for example (if there is doubt, you should ask about sensory disturbances, which would clinch a central nervous system rather than a primary muscular cause).

General inspection should include skin, hair distribution, pigmentation. Also skull: inspection, palpation, percussion; auscultation (especially over orbits, carotid bifurcations). Inspection under load, e.g.; fatigue under load in myasthenia gravis, etc.).

Alternatively, there may be serious joint disease with secondary wasting and weakness of muscle, so be aware of this. Another important principle is to examine the affected part both at rest and under load, because this may bring out the symptom, e.g. weakness of the legs, arms, or ocular muscles under load in myasthenia gravis. This principle of examination under load is one you should also bear in mind with the examination of other systems (for example exertion may bring out obvious signs of heart failure not present at rest in borderline cases). HIGHER FUNCTIONS state of consciousness and mood comprehension, insight and self-awareness).


intellectual function Orientation in time, place and person Memory short term memory, including Babcock sentence (normal should get it right after you repeat it three times); contemporary events; popular figures; seven digits forwards; five digits backwards; a sentence which includes a name, address, and an object should be retained for at least five minutes. Arithmetic ability serial 7‟s from 100; monetary calculations.

note: Babcock sentence is: “One thing a nation must have to become rich and great is a large secure supply of wood”

HIGHER FUNCTIONS state of consciousness and mood Abnormal levels of consciousness, e.g. dulled, stuporose, comatose. Alternatively, increased activity e.g. in hyperthyroidism; hypomania; anxiety; agitation of alcohol withdrawal in delirium tremens. Altered mood includes emotional change, confusion, illusions, hallucinations, delusions, flights of ideas, depression, euphoria, anxiety, indifference, catatonia. intellectual function Orientation Memory short term memory related to problems in learning new information, so often best tested by getting the patient to recall a number of unusual words associations (use yourself as a control, without cheating!). Arithmetic calculation be aware of the patient‟s background before setting standards. As with other aspects of intellectual function, if in doubt enquire from relatives about any deterioration they may have noticed.




Abstract reasoning Ask meaning of proverbs; e.g. patient to explain differences between, say, a child and a dwarf; other analogies

Abstract reasoning Proverbs are useful, but many people know their meaning anyway, and other analyses of concepts, particularly using analogy, can be helpful e.g. „Why is the heart likened to a pump?‟

Language and articulation Dysphasia. Determine whether left or right handed; ability to understand spoken words; ability to express in speech; ability to understand written words or commands; ability to express in writing. Distinguish dysphasia from dysarthria.

Language and articulation Recognise the difference between fluent aphasia (often containing jargon which the patient does not have insight into) in receptive dysphasia. And on the other hand, the non-fluent nature of expressive dysphasia. Note that nominal expressive dysphasia does not particularly help in distinguishing anatomically between Broca‟s and Wernicke‟s area lesions.

Dyspraxia Get patient to demonstrate how they might light a cigarette, comb their hair, wink or blow a kiss, wave goodbye, put out the tongue, imitate speech.

Dyspraxia recognisable particularly in non dominant hemisphere lesions and need to be brought out by asking the patient to perform complicated movements such as dressing and drawing. Dyspraxia can also occur with dominant hemisphere lesions, but to be demonstrable there must not be any confusion, dysphasia, motor weakness, or incoordination; therefore usually tested later with spinal motor system (see below)

Agnosia Recognition of a watch or other familiar other objects by sight, touch, hearing. Differentiation of right from left (parietal neglect or inattention). Before we can really test for dyspraxia, we must know if there is normal strength and comprehension. Similarly, before we can test for agnosia, we must know whether peripheral sensation is intact.

Agnosia also usually tested later with the spinal sensory system, because we must first know whether ordinary peripheral sensation is intact.

Visuo-spatial orientation

Visuo-spatial orientation




CRANIAL NERVES I. olfactory first inspect each nostril with otoscope or torch, then check air entry of each nostril, then test smell


II. optic

II. optic

 visual acuity (Snellen chart)  visual fields: test each eye separately: red hat pin in the middle of each quadrant for retinal lesions (ophthalmological); red hat pin slowly brought in from periphery through middle of each quadrant for visual pathway lesions (neurological / neurosurgical) (see added notes below)  visual attention/inattention  visual orientation (recognise thumbs up/down)  pupils (size, shape, equality, colour)  pupillary light reflex (afferent arc)  Marcus Gunn or „swinging light‟ response  colour vision (Ishihara chart)  optic fundi (ophthalmoscopy) including optic disc, vasculature, macula & peripheral retina

recognise:  visual field defects: hemianopias / quadrantanopias; visual acuity abnormalities  papilloedema, optic atrophy physiological pitting of disc versus glaucomatous cupping  vascular narrowing, irregularity, increased light reflex, AV nipping, haemorrhages, exudates in hypertension; also papilloedema, macular star in malignant hypertension;. Recognise optic atrophy. Other haemorrhages, e.g. blot, dot, vitreous haemorrhages in diabetes; sub-hyaloid haemorrhage associated with subarachnoid haemorrhage. Exudates including hard exudates in diabetes; soft „cotton wool‟ exudates in hypertension (micro-infarcts). Venous engorgement, particularly in polycythaemia. Venous „cattle-trucking‟ in hyperviscosity syndromes


III, IV, VI. recognize isolated lesions to all three nerves:

       

eyelids (ptosis) exophthalmos (proptosis)/enophthalmos pupils: colour, size, shape/irregularity pupillary light reflex (efferent arc of direct & consensual) position of eye at rest ocular movements - pursuit (asking patient to follow red hat pin) & saccadic (asking patient to look: up, down, left, right on request) nystagmus (check at rest and especially at extremes of eye movements) accommodation response (bilateral convergence & pupillary constriction)

look for:  nasal D/C: mucus; blood; pus  foreign body  rhinorrhoea (anterior cranial fossa lesion, #cribriform plate of ethmoid) tumour, etc. test for anosmia

III ptosis, fixed dilated pupil, laterally deviated, unable to move at all IV normal position at rest, reduced depression with adducted eye VI medially deviated at rest, unable to abduct recognize:  squints - paralytic, concomitant  ophthalmoplegia (internuclear)  Horner‟s syndrome  Argyll-Robertson pupils  Holmes-Adie pupil  afferent pupil defect (APD)  nystagmus of different types: unilateral, bilateral, horizontal, vertical rotational; ocular bobbing etc




V.  motor: muscles of mastication (temporalis; masseter; lateral pterygoid, medial pterygoid)  sensory: test sensation over all three divisions, comparing left with right (may be only subjective e.g. different feeling during shaving etc.) use different modalities to test the three trigeminal nuclei which span the length of the brainstem (spinal; principal & mesencephalic nuclei)  afferent arc of corneal reflex (this test is most unpleasant, only perform if absolutely indicated)  general sensory to anterior two-thirds of tongue via lingual nerve (not taste)  jaw jerk

V. If corneal reflex absent, distinguish whether due to V or VII lesion by asking the patient whether they can feel the touch of the cotton wool on their cornea, or by asking them to voluntarily close their eyes tightly

VII. first look for:  atrophy of frontalis (loss of forehead lines)  loss of nasolabial folds  drooping of mouth (food debris)

VII. Paralysis or paresis - distinguish upper motor neuron from lower motor neuron lesion. (sparing of frontalis in UMN). Need to protect eye(patch & artificial tears) if efferent arc of corneal reflex &/or input to lacrimal gland is affected by a CN VII lesion.

then test strength of:  frontalis (eyebrow lifting)  orbicularis oculi (eye closure)  orbicularis oris (mouth closure)

VIII. Distinguish middle ear deafness from nerve deafness.

parasympathetic visceromotor to all of the glands of head & neck (except for parotid gland - IX) special sensory. taste to anterior 2/3 of tongue via nervus intermedius component of the facial n. consider nerve to stapedius ( intolerance to loud noise) VIII. first use otoscope to view EAC & tympanic membrane. test hearing in both ears. Tuning fork tests (Rinne‟s test, Weber‟s test). caloric testing IX. pharyngeal „gag‟ reflex – afferent arc  bilateral soft palate elevation (ask if they can feel stimulus) taste & general sensation to posterior third of tongue X & cranial XI. efferent arc of gag reflex (say “Ahh”) vocalisation swallowing/deglutition cough reflex (afferent & efferent arcs) XI. (spinal) - strength of SCM & trapezius XII. motor innervation of tongue. observe tongue at rest (atrophy, fasciculation) and during protrusion (deviation, spasticity, tremor); rapid alternating movements (coordination); test power with tongue in each cheek in turn. NECK Know how to test for neck stiffness.

IX, X & cranial XI. Recognise bulbar palsy, pseudo-bulbar palsy. Be able to assess a patient who may be at risk of aspiration pneumonia – neurological compromised patient only able to eat/drink if all of the following are NAD:    

normal gag clear voice clear cough spontaneous swallow (observe for one min  should see at least 1-2 swallows)  check & clear CN‟s VII & XII  also percuss & auscultate lungs (esp. right apico-basal & middle lobe bronchopulmonary segments)  if in doubt test formally with video fluoroscopy during swallowing (or coloured gel if tracheostomy in-situ)

XI. SCM & trapezius: muscle atrophy & weakness. XII. coating atrophy, spasticity, fasciculation, tremor tongue deviation and its interpretation rapid alternation movements of protruded tongue distinguish dysarthric from dysphasic speech. NECK recognise neck stiffness & meningism detect carotid bruits.






LIMBS spinal motor system

LIMBS spinal motor system

do this completely through as outlined below (comparing each side as you go along), first with upper limbs, then moving to the lower limbs.

inspection wasting fasciculation involuntary movements: spasms, tics, convulsions, seizures; choreo-athetoid. tremors: including rest tremors, action or postural tremors, intention tremors, asterixis (metabolic „flap‟). also observe under load, e.g. patient‟s ability to maintain posture with eyes closed (upper limbs, arms outstretched; lower limbs - Romberg test). gait.

inspection - at rest; and under load e.g. arms outstretched

palpation tone important to get the patient to relax and let you control the process. Use full range of movement and once patient relaxed, increase the velocity of stretch to increase sensitivity. You are testing abnormalities in the muscle‟s resistance to stretch.

palpation muscle tenderness. palpation of nerves. tone types or rigidity/spasticity

power test all muscle groups

power grade any reduced strength

reflexes including reinforcement. abdominal reflexes, plantar reflexes. know how to elicit clonus in hyper-reflexive states.

reflexes. hyperactive, reduced, pendular (cerebellar). delayed relaxation phase in myxoedema. pout reflex in frontal lobe lesions. finger jerk in upper motor neuron lesions.uknow spinal cord segments involved in reflexes as follows: deep tendon reflexes: biceps (C5, 6) & brachioradialis (C5,6) triceps (C6,7) knee (L3,4) ankle (L5,S1) superficial reflexes: bulbo-cavernosus (S2-4) anal & bladder reflexes (S2-4) special reflexes include Kernig‟s reflex rigidity. also know vascular reflexes, viz. normal blood pressure response to the Valsalva manoeuvre, upright posture, mental arithmetic; potency etc.

co-ordination & gait including rapid movements (hand & finger tapping) rapid alternating movements (dysdiadokokinesis) finger-thumb apposition, ataxia including finger-nose test, heel-knee test, Romberg test, past-pointing, heel-toe test. note: muscle power and vision must be adequate to interpret co-ordination dyspraxia – test where appropriate

co-ordination & gait  cerebellar ataxia - particularly ataxic gait (truncal ataxia)  dyskinesia & festination in Parkinsonism  hemiplegic gait  high-stepping gait with foot-drop  other jerky uncoordinated gaits with chorea, hemiballismus, hysteria etc dyspraxia - parietal lesions.




LIMBS spinal sensory system  light touch & pressure touch  cutaneous pain & temperature  pressure pain (tendon squeeze)  joint position sense & two-point discrimination  vibration sense

LIMBS spinal sensory system Know sensory neurosome & dermatome distribution to spinal cord. pain & temperature - anterolateral spinothalamic tract  crosses over at (or near) the level of entry into the spinal cord  contralateral spinal cord  contralateral brainstem  contralateral VPL thalamus  contralateral posterior limb of the internal capsule  contralateral sensory cortex (post central gyrus) discriminative touch (two-point discrimination) & proprioception (joint position sense)  psilateral spinal cord (posterior funiculi)  ipsilateral gracile/cuneate nuclei  crosses over as the medial lemniscus in the caudal medulla  contralateral brainstem  contralateral VPL thalamus  contralateral posterior limb of the internal capsule  contralateral sensory cortex (post central gyrus) note: that soft touch & vibration may travel up both pathways and therefore these sensory modalities may be less discriminating with spinal cord lesions.

cortical Stereognosis (i.e. tests of agnosia including dysgraphaesthesia, astereognosis, left/right perception/attention, two-point discrimination, tactile localisation). GENERAL COMMENT At the end of the routine examination, pause as usual to consider what special things you should be looking for, before leaving the bedside. Then make, quite separately, anatomical and pathological diagnoses, e.g. slow onset of hemiparesis would not suggest „stroke‟ from a cerebrovascular cause, but perhaps tumour or some chronic inflammation depending on other features. Once you have made your initial anatomical and pathological diagnoses, ask further questions relating to special pathology, and then to aetiology e.g. about cigarette smoking, oral contraceptives, migraine, alcohol in say, a young woman presenting with an acute cerebral infarct within the territory of the middle cerebral artery supply.

cortical Recognise:  agnosia  neglect  sensory inattention. GENERAL COMMENT Be able to diagnose the following lesions: cerebral infarction, haemorrhage, embolism, space occupying lesions; subarachnoid, subdural, extradural haemorrhage. Flaccid and spastic hemiparesis. Parkinson‟s disease. Brain stem and cranial nerve lesions. Cerebellar lesions. Cord compression. Lower motor neuron versus upper motor neuron paralysis. Peripheral neuropathy. Peripheral isolated nerve lesions including ulnar, radial, median (including carpal tunnel syndrome) and lateral popliteal nerve palsy.


NOTES ON CRANIAL NERVES visual field testing At the bedside it is possible to obtain a rough assessment of the visual fields by the technique of confrontation. This is based on a direct comparison of the patient's visual fields with those of the examiner as they look into each otherâ&#x20AC;&#x;s eyes from a distance of about one metre. After an initial assessment made with both eyes open, the examiner shuts one eye and the patient covers the opposite so that the left visual field will correspond to the examiner's right and vice versa. The examiner, throughout the test, monitors the fixation of the patient's gaze since if the patient looks away from the examiner's eye the test is invalidated. The clinician then proceeds to test the outer limits by bringing a target into the field of vision from the periphery at several points on the circumference. The direction of approach should be distributed over upper and lower quadrants and nasal and temporal aspects of the visual fields. A satisfactory way to test each of the four quadrants is to advance the target towards the centre of gaze along lines at 45° to the vertical and horizontal axes of the field. The test object should be moved on a plane mid-way between the patient and the examiner.

When the patient, as the result of disturbed consciousness or because of a dysphasic defect is unable to cooperate at all, it is possible to demonstrate gross defects in the visual fields by rapidly moving one hand towards the patient's face from the side. This menacing stimulus will usually evoke reflex blinking when it is perceived from a normal visual field but the patient will not blink when menaced from a hemianopic side. A patient suffering from a lesion in a parietal lobe may see the test object perfectly well when presented in isolation in each visual half field but will consistently fail to perceive an object in one half of the visual field when stimuli are presented simultaneously and bilaterally. This is called an inattention hemianopia and is an example of perceptual rivalry. Clearly this test cannot be performed in patients with significant visual field loss. In most cases confrontation will map out visual defects with sufficient precision for clinical purposes but the method does not define the full extent of the lateral aspects of the normal visual fields. When minor defects are present (partial quadrantanopias) or when the shape of the visual defect is important in localisation, the visual fields should be mapped out more accurately (in the ophthalmology Dept.) by using a tangent (Bjerrum) screen and a perimeter.

A finger is a satisfactory target but a more accurate assessment may be made by using a pin with a large head (e.g. a red hat pin). This has the advantage of enabling an estimate to be made of the extent of the visual fields to different coloured objects by using pins with white, red and green heads.

Although tests of colour vision are not carried out routinely, they may reveal subtle defects of the retina or optic nerve. The most commonly used method is to present, to each of the patient's eyes separately, plates made up of coloured dots containing numerical shapes (Ishihara plates). The patient is asked to discern the numbers shown in each pattern.

The visual fields for coloured objects are concentric with, but smaller than, those for white objects.

internuclear ophthalmoplegia

A red hat pin can also be used to plot gaps in the central areas of the fields (scotomas) and detect enlarged blind spots. If the patient is unable to cooperate by fixing on the examiner's eye, other techniques may be used roughly to map out hemianopic or quadrantic field defects. The patient may be asked to look at the examiner's nose with both eyes open. The examiner then stretches out both arms and moves the fingers asking the patient to point to the moving hand


NOTES ON NERVOUS SYSTEM EXAMINATION Holmes-Adie syndrome Dilated pupil due to loss of parasympathetic postganglionic innervation (Adie's tonic pupil) Loss deep tendon reflexes Diaphoresis Holmes‟ rebound phenomenon Raising both arms up and stopping suddenly in front of face - looking for over & under shooting Strange pathways  trochlear nerve crosses over from the nucleus to the contralateral eye !!  medial striae of olfactory nerve crosses over to contralateral temporal cortex via ant. commissure  LMN fibres of oculomotor nerve destined for superior rectus cross over in midbrain and pass to contralateral eye!!



periorbital regions – look/feel for trauma (lacs, abrasions, bruising, oedema, bony deformities); xanthelasma (subcutaneous cholesterol deposits) eyelids – ptosis; lid retraction; trachoma (eversion required of upper & lower eyelids); eyelashes not inverted eyeball – no proptosis, exophthalmos, (enophthalmos) pupils – black (not opaque, yellow, red) round, equal (between 2-4 mm) reacting to light (direct & indirect) and accommodation (Arygll Robertson) cornea – clear (no scarring) sclera – white (not yellow with jaundice; not red with haemorrhages) palpebral conjunctivae – pink (not pale suggestive of anaemia) formally check CN‟s II; III; IV & VI corneal reflex (afferent arc is ophthalmic division trigeminal; efferent arc is facial nerve)

Transparency of the cornea, lens and vitreous humour permits the physician to directly view arteries, veins, optic nerve and the retina. Direct observation of the structures of the fundus through an ophthalmoscope may show disease of the eye itself or may reveal abnormalities indicative of disease elsewhere in the body. Among the most important of these are vascular changes due to diabetes or hypertension and swelling of the optic nerve head due to papilloedema or optic neuritis. In this sense, the eye serves as a window through which many valuable clinical evaluations may be made. When a preliminary diagnosis of an imminently dangerous eye condition, such as acute glaucoma or retinal detachment, is made by the examiner, prompt referral to an ophthalmologist may prevent irreversible damage. Or, when distressing but less urgent conditions, such as visual impairment due to cataract or vitreous floater, are recognized, the patient can be reassured and referred. THE OPHTHALMOSCOPE Ophthalmoscopy has been accepted as a valuable addition to diagnostic procedures for over a hundred years. The literature is replete with findings made with ophthalmoscopic examinations. Yet little has been written giving the medical student detailed instructions on the use of the instrument. Because the examination can give the physician so much information about a patient's well being, correct use of the ophthalmoscope makes it one of the most valuable tools available for diagnostic use. A. Small aperture: Provides easier view of fundus through un-dilated pupil. Always start examination with this aperture, proceed to large aperture as pupil adapts to light. B. Large aperture: Standard aperture for dilated pupil and general examination of the eye.

C. 4OO0oK aperture: Provides highest colour temperature available for accurate tissue colour, yet light intensity is reduced, which is helpful for sensitive eyes. The high colour temperature is retained even if the examiner uses the rheostat to lower the light intensity. D. Fixation aperture: The pattern of an open centre and thin lines permits easy observation of eccentric fixation without masking the macula. The graduated cross hairs can be used to estimate either the amount of eccentric fixation relative to the macula or the size or location of a lesion on the retina or choroid. E. Fixation star: Serves the same functions as the fixation aperture. However, the open centre and thin line pattern is replaced by a star pattern with an open centre, which still allows the macula to be viewed without difficulty. F. Red-free light: Excludes red rays from the examination field; this is superior to ordinary light in viewing slight alterations in vessels, minute retinal haemorrhages, illdefined exudates and obscure changes in the macula. The nerve fibres become visible and the observer may note the disappearance of such fibres, as in optic nerve atrophy. The background appears gray, the disc appears white, the macula appears yellow, the fundus reflex is intense and the vessels appear almost black. This aperture is also used to help distinguish veins from arteries ... veins stay relatively blue, but oxygenated arterial blood makes arteries appear blacker. This makes differentiation easier for the examiner. G. Slit or streak: Helpful in determining various levels of lesions, particularly tumours and oedematous discs. H. Cobalt filter: The cobalt blue filter is extremely helpful in eliciting fluorescence from the dye, fluorescein. The magnification afforded by the + 20 or the + 40 lens on the ophthalmoscope permits visualization of small corneal lesions with ease, and in combination with the cobalt blue filter, permits otherwise difficult lesions, such as herpes simplex dendrites and small corneal abrasions, to be identified and diagnosed with ease. CHOICE OF APERTURES AND LENSES There is a wide range of practical apertures to select from: small spot, large spot, 4000oK, fixation, fixation star, red-free, slit and cobalt. This selection of apertures covers all the physician's needs in an ophthalmologic examination. You also have a wide choice of 23 viewing lenses, ranging from-25° to + 40 dioptors, with fast, accurate, one-hand selections. This helps compensate for patient or doctor refractive error, the position of the ophthalmoscope and the changes in viewing requirements necessitated by focusing on different points within the eye. ADDITIONAL USES FOR THE OPHTHALMOSCOPE In addition to examination of the fundus, the ophthalmoscope is a useful diagnostic aid in studying other ocular structures. The light beam can be used to illuminate the cornea and the iris for detecting foreign bodies in the cornea and irregularities of the pupil. By placing the +15.00 lens in the scope and looking at the pupil as in fundus examination [2 inches (5cm) distance


from patient], the physician may verify doubtful pupillary action. Lens opacities can also easily be detect by looking at the pupil through the +6 lens setting at a distance of 6 inches (15cm) from the patient. In the same manner, vitreous opacities can be detected by having the patient look up and down, to the right and to the left. Any vitreous opacities will be seen moving across the pupillary area as the eye changes position or comes back to the primary position. HOW TO USE THE OPHTHALMOSCOPE In order to conduct a successful examination of the fundus the examining room should be either semidarkened or completely darkened. It is preferable to dilate the pupil when there is no pathologic contraindication, but much information can be obtained through the un-dilated pupil.

8. To examine the extreme periphery instruct the patient to: a) look up for examination of the superior retina b) look down for examination of the inferior retina c) look temporally for examination of the temporal retina d) look nasally for examination of the nasal retina. This routine will reveal almost any abnormality that occurs in the fundus. 9. To examine the left eye, repeat the procedure outlined above except that you hold the ophthalmoscope in the left hand, stand at the patient's left side and use your left eye.

The following steps will help the physician obtain satisfactory results: 1. For examination of the right eye, sit or stand at the patient's right side. 2. Select "0" on the illuminated lens dial of the ophthalmoscope and start with small aperture. 3. Take the ophthalmoscope in the right hand and hold it vertically in front of your own right eye with the light beam directed toward the patient and place your right index finger on the edge of the lens dial so that you will be able to change lenses easily if necessary. 4. Dim room lights. Instruct the patient to look straight ahead at a distant object. 5. Position the ophthalmoscope about 15cm in front and slightly to the right (25째) of the patient and direct the light beam into the pupil. A red "reflex" should appear as you look through the pupil. 6. Rest the left hand on the patient's forehead and hold the upper lid of the eye near the eyelashes with the thumb. While the patient holds their fixation on the specified object, keep the "reflex" in view and slowly move toward the patient. The optic disc should come into view when you are about 3-5cm from the patient. If it is not focused clearly, rotate lenses into the aperture with your index finger until the optic disc is as clearly visible as possible. The hyperopic, or far-sighted, eye requires more "plus" (black numbers) sphere for clear focus of the fundus; the myopic, or near-sighted, eye requires "minus" (red numbers) sphere for clear focus. 7. Now examine the disc for clarity of outline, colour, elevation and condition of the vessels. Follow each vessel as far to the periphery as you can. To locate the macula, focus on the disc, move the light approximately 2 disc diameters temporally. You may also have the patient look at the light of the ophthalmoscope, which will automatically place the macula in full view. Examine for abnormalities in the macula area. The red-free filter facilitates viewing of the centre of the macula, or the fovea.


OVERCOMING CORNEAL REFLECTION One of the most troublesome barriers to a good view of the retina is the light reflected back into the examiner's eye by the patient's cornea-a condition known as corneal reflection. There are three ways to minimize this nuisance: 1.0n the ophthalmoscope shown in this book, the dust cover/polarizing filter may be used. The filter reduces corneal reflection by 95%. It is recommended that the polarizing filter be used when corneal reflection is present. 2. Use the small spot aperture. However, this reduces the area of the retina illuminated. 3. Direct the light beam toward the edge of the pupil rather than directly through its centre. This technique can be perfected with practice. USE OF FIXATION TARGET Direct the patient to focus on the centre of the fixation target projected within the light beam. Simultaneously, the doctor should check the location of the pattern on the fundus. If the centre of the pattern does not coincide with the fovea, eccentric fixation is indicated. In this procedure the polarizing filter is especially useful since it dramatically reduces reflections caused by the direct corneal light path.


THE EAR Since symptoms of ear disease are relatively few in number and frequently non-specific, a clinical examination of the ear is important in the management of ear disorders. When a patient complains of ear pain, examination of the ear is indicated to differentiate whether the patient's disorder is an ear infection or a disorder originating in adjacent structures, such as the temporomandibular joint, the teeth or the tonsils. As the only window into the middle ear, the appearance and behaviour of the tympanic membrane offers valuable information about possible disease within the middle ear. Fortunately, the ear provides easy access for examining and diagnosing disorders of the complex and interrelated ear, nose and throat system. The otoscope, when used correctly, is the single most important diagnostic tool .available to the practitioner for determining whether the ear is the source of the patient's complaint. HOW TO USE THE OTOSCOPE 1. Carefully inspect the pinna and post auricular skin. Gently palpate the pinna to determine if any tenderness exists. 2. Inspect the entrance to the ear canal for debris or pus which might interfere with further examination. 3. Choose the largest speculum which can comfortably be inserted into the ear canal. Straightening the outer ear canal makes insertion of the speculum easier.

PNEUMATIC OTOSCOPY Pneumatic otoscopy provides physicians with a simple method for determining tympanic membrane mobility and helps them recognize many middle ear disorders. It is the pneumatic capability and insufflator attachment of the otoscope which enables the examiner to assess the mobility of the intact tympanic membrane. This first requires that you use a speculum sufficiently large to fit snugly into the ear canal in order to establish an airtight chamber between the canal and the interior of the otoscope head. Gently squeezing the small rubber ball of the pneumatic attachment produces small changes in the air pressure of the canal. By observing the relative movements of the tympanic membrane in response to the induced changes pressure, the physician can obtain valuable diagnostic data about the mobility of the tympanic membrane. When fluid is present in the middle ear, for example, movement of the tympanic membrane is generally diminished or absent. The pneumatic otoscope may also be useful in distinguishing between a thin atrophic intact tympanic membrane adherent to the medial wall of the middle ear, which can be made to move, and a large perforation, which will not move. This procedure provides a simple method for determining tympanic membrane mobility and is of value in the recognition of certain middle ear disorders.

For adults: This is accomplished by retracting the pinna upwards and backwards. For children: This is accomplished by retracting the pinna horizontally backwards. 4. The otoscope should be held like a pencil, between the thumb and forefinger, with the ulnar aspect of the hand resting firmly but gently against the patient's cheek. You can conveniently hold the bulb of the pneumatic attachment in the palm of the same hand. With this method, if the patient turns or moves, the otoscope will move in unison with the patient's head. This will avoid possible injury to the ear canal or even the tympanic membrane. It is very important that the otoscope be held correctly, particularly when examining children. A sudden movement by the patient could cause the skin on the inside of the ear canal to be pierced by the end of the speculum. 5. Because of the limited field of vision through even the largest speculum, it may be necessary for you to adjust your line of sight and the position of the speculum to view completely the entire ear canal and all areas of the tympanic membrane. In this way you will obtain a composite view of the external canal and the tympanic membrane.


THE NOSE & THROAT Disturbances of the upper respiratory tract are among the most common of human afflictions and account for more days lost from school and work than many other illnesses. The rapid and accurate assessment of the nose and throat, anatomically the nasopharynx, the oropharynx, and the laryngopharynx, is, therefore, an essential aspect of the clinical examination. Observation of the nasal cavity may reveal polyps, malignancies or mucous membrane changes characteristic of allergic rhinitis. Perforations of the nasal septum are also easily detected as are bleeding points and foreign bodies. Indirect nasopharyngeal examination may be used in establishing such diagnoses as sinusitis, enlarged adenoids or nasopharyngeal malignancy. Problems such as air pollution and smoking have increased the incidence of laryngeal and nasopharyngeal disorders. The common symptom of hoarseness directs attention specifically to the vocal cords and calls for laryngeal examination, which, if done by a practiced clinician, can differentiate almost all cases of benign laryngeal disease such as laryngitis, polyps and nodules, from premalignant diseases such as leukoplakia and malignant growths, such as carcinoma. Any patient with a history of hoarseness lasting over six weeks should have his or her larynx examined to ensure that a malignancy is not present.

FINNOFF TRANSILLUMINATOR This instrument is particularly useful for the transillumination of the frontal and maxillary sinuses. Throat and n passages may also be illuminated with the Finnoff transilluminator. Conventional illuminators offer inadequate light and cause patient discomfort due to lamp heat. The transilluminator uses halogen illumination and fibre optics for cold intense light and optimal vision. THE INTRANASAL EXAMINATION Inspection, the most important tool in the physical examination of the nose, is facilitated by the use of specially designed instruments, such as a nasal illuminator, a nasopharyngeal mirror, a Finnoff transilluminator, and a nasal speculum. The examiner should start with the external nose, anterior nasal septum and then to the nasal vestibules. The contents of the interior nasal cavities should then be examined using a nasal speculum or nasal illuminator. In the normal nose only the cartilaginous nasal septum and the anterior ends of the middle and inferior turbinates are available for direct inspection by anterior rhinoscopy, whereas the nasopharynx can only be examined by means of a nasopharyngeal mirror or a nasopharyngoscope. The application of a topical decongestant spray to the nasal mucous membranes may be required to shrink the turbinates. This would allow better visualization of the depths of the nasal cavity.

Structural disorders within the nasal cavities can usually be seen by direct inspection. The nasal mucous membranes, usually respond by turning one of three colours: red, white or blue. Reddish in infection; whitish in allergy; and bluish in vasomotor problems. THE LARYNX & NASOPHARYNX ILLUMINATORS Both instruments are equipped with convex Wide-angle mirrors which give the examiner excellent visibility. They also feature dual illumination which illuminates the throat cavity allowing the examiner to position the mirror correctly while also illuminating the laryngeal/ nasopharyngeal areas simultaneously. The nasopharyngeal mirror is identical to the laryngeal mirror except that it is round and smaller. An anti-fog solution is available for maintaining a clear mirror surface. The metal sleeves and mirrors of both instruments can be sterilized by steam, ethylene oxide gas or germicidal solution methods. NASAL ILLUMINATOR The nasal cavity provides the examiner with a valuable access route to the otorhinolaryngology system. It is essential to have good light combined with a comfortable speculum in order to carry out such important diagnostic procedures as the examination of the anterior nasal cavities.


THE NASOPHARYNGEAL EXAMINATION For indirect examination of the nasopharynx (posterior rhinoscopy) use the nasopharynx illuminator. Of interest are the "vault" of the nasopharynx and eustachian tube openings, adenoid tissue, polyps and tumours. For successful examination of the nasopharynx it is recommended that you subdue the lighting in the examining room. Reassure the patient and ask him or her to breathe through the mouth. A particularly apprehensive patient may require sedation and in some patients a topical anaesthetic applied to the palate or pharynx may be required to dull an excessive gag reflex. Once the patient is prepared, the following steps will produce the best examination results: 1. Sit to one side (patient's left) or in front of the patient. 2. Hold the hand piece with the attached nasopharyngeal mirror in your right hand. Turn the light switch on to illuminate the fibre optic light source. 3. The mirror should be warmed or coated with an antifogging solution to prevent "misting:' 4. Depress the patient's tongue with a tongue blade. Ask the patient to breathe simultaneously through his nose and mouth. This should relax the soft palate. 5. Pass the mirror into the mouth along the surface of the tongue blade until it rests between the soft palate and the pharyngeal wall. Do not touch the tongue, pharynx or palate with the mirror. 6. Depress the mirror handle and rotate it from side to side so that you can view successive parts of the nasopharynx. If the space between the palate and the pharyngeal wall is too narrow for examination use a soft palate retractor. A topical anaesthetic will relieve any excess gagging that may occur. 7. Compare identical structures of each side of the nasopharynx. Any variations in colour and/or contour from one side to the other should alert the examiner to possible abnormalities.

Therefore, it is preferable that the patient sit in a straightback chair with hips resting against the back rest, trunk forward, head back, chin extended, mouth open and tongue extended. 3. Hold the hand piece with the attached laryngeal mirror in your right hand. Turn on the light switch to illuminate the fiber optic light source. 4. The mirror should be warmed or coated with an antifogging solution to prevent "misting:' 5. A gauze square wrapped around the patient's tongue makes holding the tongue easier. Hold it between your thumb and the middle finger of your left hand. Elevate the upper lip with your index finger. You may ask the patient to hold his own tongue. 6. Insert the mirror into the patient's mouth. Light passing through the light aperture aids in positioning the mirror so that it passes between the tonsils and elevates the soft palate. Encourage the patient to relax and to breathe deeply through his mouth. 7. Reflected light in the mirror will illuminate the base of the tongue and the laryngopharynx. Rotating the laryngeal mirror a minor degree illuminates the various anatomical structures so that you can examine them. 8. Compare identical structures of opposite sides of the larynx. Any variations in color, contour and motion from one side to the other should indicate possible abnormalities. 9. Examine the anatomy of the structures composing the base of the tongue and the laryngopharynx in routine order: base of the tongue, valeculla, epiglottis, each arytenoid cartilage, aryepiglottic folds, pyriform fossae and oesophageal area. 10. In order to evaluate the mobility of each vocal cord ask the patient to phonate the letter "a" and the letter "e:' This will cause the epiglottis to move forward and the vocal cords will come together during phonation. Examine first the posterior surface of the epiglottis and then examine the right and left false vocal cords, true vocal cords, anterior and posterior commissures.

8. Examine the following anatomical structures bilaterally in routine order: auditory tube orifice, torus tubaris, fossa of Rosenmuller, adenoids, the posterior ends of the turbinates and the posterior edge of the nasal septum. THE LARYNGEAL EXAMINATION For successful examination of the laryngopharynx it is recommended that you subdue the lighting in the examining room. Reassure the patient and ask him or her to breathe through the mouth. A particularly apprehensive patient may require sedation and in some patients a topical anaesthetic applied to the palate or pharynx may be required to dull an excessive gag reflex. Once the patient is prepared, the following steps will produce the best examination results: 1. Sit to one side (usually the patient's left) or in front of the patient. 2. The patient's posture is important to the examination.




INSPECTION As usual, take clothes off completely down to briefs. Make sure legs are exposed. HANDS FACE, including conjunctivae. SKIN-examine. AREOLAE-inspect. LYMPH NODES with all lymph nodes note size, consistency, tenderness if any, distribution, and whether nodes discrete or matted together. CERVICAL lymph nodes (LN‟s) superficial: cervical: (two vertical chains along ant. jug. & ext. jug. veins; two rings: a large ring from chin to occiput; a small ring around upper airway & gut tube; plus tonsillar tissue/Waldeyer ring) also check anterior & posterior triangles of the neck. deep: along entire length of internal jugular veins (deep to SCM)  supraclavicular nodes AXILLARY LN‟s (incl. epitrochlear) superficial: anterior/pectoral, posterior/subscapular, lateral, central, infraclavicular. deep: apical nodes  supraclavicular nodes



INSPECTION Anaemia, plethora, petechiae, eccymoses, bruises, skin infections. Know how to do Hess test in suspected thrombocytopenia. HANDS Pallor of palmar creases in anaemia, also koilonychia (in iron deficiency). FACE - pale conjunctivae in anaemia. MOUTH inspect tongue & throat for petechiae at junction of hard and soft palate in infectious mononucleosis throat infections in leukaemia, aplastic anaemia herpes simplex & moniliasis in immunocompromised patients Blood vessel engorgement in polycythaemia. SKIN infections in agranulocytosis, and immunocompromised patients. also herpes zoster in the latter situation. Petechiae in thrombocytopenia. Raynaud‟s phenomenon in some of the dysgammaglobulinaemias. AREOLAE Pale in anaemia LYMPH NODES Various forms of lymphoma and (lymphatic) leukaemia. Also secondary carcinoma, lymphadenitis.

INGUINAL LN‟s superficial: scattered horizontally just below inguinal ligament and vertically along termination of great saphenous vein. deep: along femoral vein  external iliac  common iliac  para-aortic nodes ABDOMEN Feel particularly for liver, spleen. consider pre- and paraaortic LN‟s (but these nodes only palpable if very large).

ABDOMEN Splenomegaly - in leukaemia; lymphoma; myeloproliferative & lymphoproliferative disorders. Also secondary to liver disease, infections, haemolytic states.




LEGS Examine for petechial spots, rashes bruises etc.

LEGS Petechial spots in anaphylactic purpura, and some of the hypergammaglobulinaemias. Leg ulcers. Bruising.

BONES AND JOINTS Look for bone tenderness. Examine joints.

BONES AND JOINTS Sternal tenderness may occur in conditions infiltrating bone marrow. Haemarthrosis in haemophilia.

OPTIC FUNDI - examine.

OPTIC FUNDI Changes in severe anaemia. Engorged veins with â&#x20AC;&#x17E;cattle truckingâ&#x20AC;&#x; in hyperviscosity syndromes. Infiltrates and haemorrhages in leukaemia.

GENERAL COMMENT This system includes not just formed blood elements (haematopoietic system), but but immunological function (lymphatic system), as well. Therefore assess immunological function both on history and examination at the same time. Also we include the reticulo-endothelial system here.

GENERAL COMMENT Recognise the lymphoproliferative disorders. Recognise immunological disorders including hypogammaglobulinaemias, and dys/ hypergammaglobulinaemias. Recognise infiltrative conditions such as amyloidosis, reticulo-endothelial system infiltration.






THYROID Know how to examine the thyroid gland. First look for uniform or irregular enlargement; also ask the patient to take a sip of water, hold it in their mouth, and swallow on command, a thyroid enlargement should move upwards. Palpate the thyroid gland bi-manually, first generally, then each lobe in turn which can be made more prominent by pushing the opposite lobe towards the midline. In addition, it helps to examine with hands placed fore and aft the sternocleidomastoid muscle. Also remember to examine the thyroid isthmus. Thyroid auscultation Retrosternal percussion Look for pressure symptoms in goitre.

THYROID Differentiate smooth thyroid enlargement of Graves‟ disease from nodular thyroid goitre. Recognise the signs of hyper-thyroidism including eye signs, tremor, restlessness, appetite increase, weight loss, proximal myopathy, sweating, tachycardia, warm hands, hyperdynamic circulation, thyroid buit; occasionally „thyroid apathy‟, pretibial myxoedema Be able to diagnose myxoedema clinically from examining face, eyebrows, thinning of hair, coarse skin, deep voice, slow pulse, reduced body temperature, weight gain, weather preference, menstrual change, mental slowing, delayed relaxation phase of tendon jerks. Recognise difficulty of differentiating thyroid cysts from solid tumours clinically. Recognise clinical characteristics of Hashimoto‟s disease; Riedel‟s thyroid disease (rare). Thyroid tenderness in sub-acute thyroiditis.

PITUITARY Examine skin, limbs, tongue, jaw, eyes, visual fields, optic fundi, hair distribution, gonads, blood pressure, urine, body build (height versus span).

PITUITARY Diagnose acromegaly on physical signs including visual fields, optic atrophy, spade-like hands, large feet, lantern jaw, macroglossia, hypertension, glycosuria. Diagnose other space-occupying lesions (headache, nausea, visual disturbances). Recognise syndrome of inappropriate ADH secretion. Diagnose pan-hypopituitism - i.e. pituitary dwarf in prepubertal disease. Loss of body hair, hypogonadism, amenorrhoea, change in libido and/or potency, change in hair distribution, galactorrhoea, in adult. Diabetes insipidus in posterior pituitary/hypothalamic lesion.

GONADS Examine testicular size, tenderness. Pelvic examination in the female. Secondary sex characteristics; recognise virilisation in the female which includes not just hirsuitism but deepening of the voice, temporal hair recession, development of male distribution of body hair, clitoral enlargement. (Loss of secondary sex characteristics occurs in adult hypogonadism e.g. from pituitary disease).

GONADS Recognise hypogonadism including that associated with Kleinfelter‟s syndrome Boys who have adequate growth hormone and continue to grow in the absence of puberty will develop a eunuchoid habitus with relatively long arms and legs (thus greater span than height). Female virilisation syndromes (ovarian and/or adrenal).

PARATHYROIDS Examine neck. Know how to look for signs of hypocalcaemia including Trousseau‟s sign, Chvostek‟s sign. Examine eyes, particularly towards the periphery of the cornea.

PARATHYROIDS Recognise hypoparathyroidism. Recognise hyperparathyroidism (including keratopathy near the corneo-scleral junction).





ADRENAL Examine body build, weight, skin, blood pressure, state of hydration/ECF volume, face, hair distribution, spine.

ADRENAL Addison‟s disease - pigmentation, reduced ECF volume with hypotension, lethargy. Cushing syndrome - bruising, thin skin, purple striae, centripetal obesity, buffalo hump over base of neck, glycosuria, virilisation (hirsuitism, clitoral enlargement, male distribution of body hair, deepened voice), hypertension, moon face, acne, osteoporosis. Phaeochromocytoma - intermittent hypertension, glycosuria if adrenaline-producing (only adrenal phaeos can produce adrenaline).

METABOLIC Skin, particularly below inner angles of eyes (xanthelasma), fundi, urine (glucose, ketones), abdomen, particularly liver spleen kidneys.

METABOLIC Diagnose electrolyte disturbances, hepatic failure, renal failure, metabolic acidosis, hyperlipidaemia (xanthelasma, tendon and skin xanthomata, particularly over bony prominences, lipaemia retinalis).

BREASTS Inspection, palpation with the flat of the hand, nipple discharge, axillary lymph nodes.

BREASTS Recognise carcinoma and other lumps.

PANCREAS i.e. Insulin Examine - CNS urine for glucose, ketones, protein (diabetes mellitus).

PANCREAS Hypoglycaemic attacks - pallor, sweating, tachycardia, confusion. Diabetic presentations - thirst, polyuria, vaginitis, visual change etc. Hyperglycaemic keto-acidosis - confusion, dehydration, Kussmaul‟s respiration. Hyperosmolar coma - dehydration, osmotic diuresis. Diabetic complications Eyes - cataracts, optic fundi. Peripheral (and autonomic) neuropathy. Vascular disease, both large and small.


GENETIC Turner‟s syndrome - short stature, etc. Kleinfelter‟s syndrome - hypogonadism, gynaecomastia, female body habitus. Down‟s Syndrome






GENITALIA Always examine genitalia (and lymph nodes) as part of the abdominal examination, and remember to percuss and palpate the bladder as well. Do rectal examination where indicated, examine both the prostate and seminal vesicles.

GENITALIA Herniae, epididymo - orchitis. Recognise urinary retention (bladder percussable/palpable or even visible above symphysis pubis). Recognise urinary incontinence, urethral, meatal obstruction.



GENERAL State of hydration - important to assess in renal disease. Differentiate between extracellular fluid loss (salt and water) and water loss (i.e. from both extracellular and intracellular compartments). The term â&#x20AC;&#x17E;dehydrationâ&#x20AC;&#x; should rightly be reserved for pure water loss, but is often loosely applied to cases of ECF loss (salt and water) as well. With total body water loss, the tongue is often dry (although interpretation of this is difficult in mouth breathers); also loss of tissue turgor (best assessed over bodily weight can be most helpful; also history. ECF loss. Salt and water depletion best assessed by history, daily weight, diminished venous pressure (may have to lie patient flat to see it), fall in blood pressure on standing, daily urinary output.

GENERAL Recognise various states of fluid loss particularly sodium and/or water loss. Also fluid overload. As with dehydration, ECF overload recognised by weight change and vascular parameters including JVP, as well as evidence of interstitial compartment expansion (dependent oedema). Pure water overload produces cellular over-hydration and clinically this is manifest mostly in the brain as irritability, confusion and eventually fitting; with severe degrees of water overload, plasma sodium falls (in this context recognise the syndrome of inappropriate ADH effect - SIADH). Recognise nephrotic syndrome; acute renal failure (prerenal, renal, post-renal). Also recognise signs of chronic impairment of renal function such as anaemia, fluid overload including pulmonary oedema (occasional patients with renal medullary involvement actually get salt loss); also pigmentation, peripheral neuropathy, hypertension, bruising (abnormal platelet function), hypocalcaemia (sometimes with tetany), renal osteodystrophy, signs of hyperkalaemia. Recognise acute glomerulonephritis, pyelonephritis, perinephric abscess.

URINE TESTING Inspection Colour - increased - decreased - abnormal Clear or cloudy

URINE TESTING Inspection - dark colour in dehydration, pale in diabetes insipidus. Blood (smoky appearance); urobilinogen (orange, pale-tea coloured). Yellow, often with olive-green appearance when (conjugated) bilirubin appears in the urine - e.g. obstructive jaundice. Absence of bile in the urine in haemolytic jaundice (unconjugated bilirubin is not filtered by glomerulus).




Inspection (contd.)

Inspection (contd). Pink urine with porphyrins, heavy concentration of urates, blood, phenolphthalein, beetroot ingestion. Cloudy urine due to phosphates (alkaline pH), urates (in acid or neutral pH, or in refrigerated urine), or suspended cellular elements.

Specific gravity. (multistix-SG)

Specific gravity Decreased in diabetes insipidus. Increased in diabetes mellitus, dehydration, and after IVP.Fixed (1.010) in renal failure.

Urinary pH. (multistix)

Urinary pH. Recognise range of variation in normal. Significance of pH in relation to acid/base balance. Importance of acidifying urine in patients with proteus infection.

Test for Protein (multistix)

Protein Degree of proteinuria (Dipstix are only semi-quantitative. Therefore if more than a trace, do 24 hour urine to quantitate). Recognise Bence-Jones protein (light chains) in myeloma (abnormal response to heating urine - may have to concentrate urine to detect).

Test for Glucose (multistix)

Glucose Diabetes mellitus. Also where low renal threshold for glucose.

Ketones - multistix adequate in most cases. Older tests such as Rothera rarely needed nowadays.

Ketones Degrees of ketonuria and their significance in relation to starvation, diabetic keto-acidosis. recognize that diabetic coma can occur without keto-acidosis (non-ketotic diabetic coma) particularly in the elderly

Bile constituents Simple tests for urobilinogen/bile in urine (Multistix).

Bile constituents Urobilinogen â&#x20AC;&#x201C; trace normally present in urine; excess in haemolytic anaemia, hepatocellular damage. Bilirubin â&#x20AC;&#x201C; not normally present in urine. Notr present in haemolytic jaundice either. Present in obstructive jaundice or hepatocellular damage (conjugated bilirubin).

Blood It is claimed that Multistix can differentiate between a trace of haemolysed blood (uniformly stained strip) and a trace of non-haemolysed blood (patchy staining of strip), although in practice this is not always easy.

Blood Differentiate between blood coming from the lower urinary tract (often admixed with urine) versus upper nephron (often red cell casts, also abnormally shaped cells recognized by phase contrast microscopy if glomerulus is damaged or inflamed).




Other constituents Can be detected by multistix

Other constituents dipstix can detect phenylketonuria and also salicylates in cases of suspected analgesic OD

Urine deposit macroscopic appearance. microscopic examination of centrifuged deposit. miscroscopy is of the utmost importance and you must know how to do it. examine for: red cells white cells epithelial cells casts: both granular & hyaline phase contrast microscopy to detect abnormally shaped cells

Urine deposit Macroscopic appearance â&#x20AC;&#x201C; note Microscopic appearance â&#x20AC;&#x201C; recognize different types of casts, abnormal red cells. Special use of phase contrast microscopy to determine the characteristic abnormallyshaped red cells in glomerular damage with the so-called glomerulonephritides.


Swellings (lumps & masses) A swelling is a common presenting feature. In reporting the discovery of a lump, a patient often makes an erroneous deduction that it has appeared suddenly because nothing had been noticed previously. Similarly physical examination may reveal a lump whose presence is unknown to the patient. An open mind must always be kept about the apparent duration of a lump or gross errors about its nature will be made. By systematic attention to detail it should be possible to determine the origin of a swelling if the examiner is acquainted with the anatomy of the region. The local findings should also give at least some indication of the pathological nature of the swelling - whether this is due to trauma, inflammation or neoplasm. In the first place, inspection may show the position, the approximate size and shape, and any unusual colour of the mass. By palpation, further information should be obtained about its position, size, and shape; tenderness may be elicited, the mobility, consistency, surface texture, and type of edge of the mass may be determined, and any enlargement of the regional lymph nodes can be detected. Other methods of examination, such as auscultation, are usually much less informative. The examination of a goitre (p. 79) provides a good example of the methods in practice. INSPECTION & PALPATION Position. The anatomical situation of a mass must be defined as accurately as possible. Frequently this will present little or no difficulty, as in the case of a swelling in the breast, in the thyroid, or in the parotid gland. Elsewhere, however, the precision with which a lump can be located will vary in spite of the most careful palpation, especially with some masses in the abdomen. In these circumstances, other features, such as its shape or mobility, will help to identify its anatomical origin. Size. The size of a swelling should always be measured. A diagram, indicating the dimensions, position and shape of the swelling should be recorded and dated (Fig. 3.2). In this way, significant changes, which may occur later, can be recognised. In contrast, vague statements about size, such as large, medium or small, or comparisons with fruit, eggs or vegetables, are inaccurate and misleading. Shape. Many swellings have characteristic shapes, as, for example, diffuse enlargement of the thyroid gland with its two lobes linked by the isthmus. The swollen parotid gland of mumps fills in the hollow between the posterior border of the mandible and the mastoid process, and often lifts up the ear and extends forward on to the cheek below the zygoma as the accessory parotid gland. The characteristic outline of a mass in the appropriate position should simplify the recognition of an enlarged spleen or liver, a distended bladder, or the fundus of the uterus in the later months of pregnancy. Even with these familiar examples, however, errors can arise, and some additional evidence may be required, such as the disappearance after catheterisation of a swelling when this was due to a full bladder. Colour & Temperature. The skin over acute inflammatory lesions near the surface is usually red and

this will be accompanied by a rise in temperature due to an increase in blood flow. A vascular skin tumour may range in colour from red to blue or purple according to the proportions of reduced haemoglobin present and the depth of the layer of skin through which it is seen. Other colour changes over swellings may occur, for example in haematomas the pigment from extravasated blood may produce the range of colours caused by various breakdown products of haemoglobin so familiar in a bruise. Melanin deposition may be responsible for brown pigmentation in the skin over swellings when there is any undue pressure from clothing and other causes. A brown or black colour is common in melanomas, though some are not pigmented. A xanthoma is a small skin nodule which may be identified by its yellow colour due to the lipids it contains. Tenderness. Inflammatory swellings are characterised by tenderness. While this sign must be deliberately sought, palpation should be particularly gentle whenever the patient complains of pain. Many large tumours, in contrast, are entirely free from pain or tenderness, partly because they carry no nerve supply and also because they may have developed in an area where tissue tension is low and where a mass can be accommodated without subjecting any structure to u~due stretching. Tumours eroding bone or growing into nerve roots and plexuses are capable of causing severe persistent pain of a most intractable type, and this is often worse at night. Movement. The mobility of a mass must be tested in order to determine whether it is part of, attached to, or free from adjacent structures, such as skin or bone. So far as the skin is concerned, this may be tested by attempting to pick up a fold of skin over the swelling and comparing this with the mobility of the skin over other structures in the vicinity. Fixation of the skin may be associated with a fine dimpling at the opening of the hair follicles resembling 'pigskin' or 'orange skin' when there is lymphatic obstruction. Such a change is most commonly due to malignant disease. Fixation to deeper structures such as bone or muscle will be recognised by attempting to move the swelling in different planes relative to the surrounding tissues. For example, with a tumour in the breast, the patient is asked to press the hand firmly on the hip of the affected side. The mobility of the mass may then be tested in relation to the contracted and immobilised pectoral muscle. Again it may be difficult to decide whether a mass is situated in the abdominal wall or within the abdominal cavity. This distinction is made by noting the effect of contraction of the rectus and other muscles on the accessibility of the swelling, as described on page 207. In the case of the thyroid, most goitres will move up and down on swallowing. Adherence to adjacent structures such as a blood vessel, a nerve or a viscus, may cause pulsation, paralysis, pain or obstructive symptoms. Pulsation of a lump will readily be appreciated if the palpating hand is kept still for a few moments. It is then necessary to determine whether this is the expansile pulsation of an aneurysm or a vascular tumour, or whether the movement is transmitted from an artery nearby. An impulse on coughing is characteristically felt in certain swellings within which a rise in pressure may occur


because their contents communicate with the thoracic or abdominal cavity. The commonest example is an inguinal hernia. Consistency. The consistency of a swelling may vary from soft and fluctuant through increasing degrees of firmness until this may be so striking as to merit the term 'stony hard'. Very hard swellings are usually malignant or calcified, or consist largely of dense fibrous tissue. Fluctuation indicates a fluid-containing swelling, such as an abscess or a cyst. Soft tumours such as lipomas may also show some degree of fluctuation. The sign is elicited by detecting with one finger the bulge created by compressing the swelling Suddenly with another finger placed at a distance. Fluctuation should be detectable in two planes before the sign is regarded as positive. Surface Texture. The surface of a swelling may vary widely from the uniformly smooth to the grossly irregular, as is commonly illustrated in enlargements of the thyroid gland and the liver. The surface of a simple goitre and of some primary toxic goitres is usually uniformly smooth, whereas other goitres, especially those of long standing, may be so irregular in outline that they are described as nodular. A similar variety of texture may be noted on palpation of the liver, ranging from the smooth surface usually found in right ventricular failure, through the fine irregularity of portal cirrhosis, to the gross degree of nodular change in some cases of metastatic tumour. However, a thick abdominal wall may make it impossible to appreciate these variations with confidence. Ulceration. Lesions which arise within the skin, such as squamous or basal cell carcinomas, or lesions which lie close to the skin, such as breast cancer or malignancy in axillary lymph nodes, may ulcerate. The character of the edge, the size and shape of the ulcer and the nature of its base should all be noted. Similar observations should be made of visible or palpable ulcers in the mouth or rectum. Margin. The edge or margin may be well or ill-defined, regular or irregular, sharp or rounded. The margins of enlarged organs such as the thyroid gland, liver, spleen or kidney can usually be defined more clearly than those of inflammatory or malignant masses. The indefinite margin of a mass is sometimes a valuable indication of an infiltrating malignant growth as opposed to the clearly defined edge of a localised benign tumour.

may be audible over the swelling. A murmur is commonly present over vascular goitres and, if it is sufficiently marked, a thrill may also be palpable. Systolic murmurs may also be heard over arterial aneurysms, while over the very rare swellings due to arteriovenous aneurysms there is a continuous murmur, often accompanied by a thrill, similar to the bruit of a persistent ductus arteriosus (p. 136). Fetal Heart Sounds. These may be audible over the pregnant uterus after the 30th week. Bowel Sounds. These may be heard over a hernia which contains intestine. Friction. This may sometimes be heard over an enlarged spleen or liver when fibrinous perisplenitis or perihepatitis is present. Transillumination. This is occasionally a useful test in distinguishing between a swelling composed of solid tissue and one consisting of transparent or semitransparent liquid which may be under such tension that fluctuation cannot be elicited. The sign is sought in darkened surroundings by pressing the lighted end of a torch into one side of the tumour. A cystic swelling will light up like a lantern if the fluid within it is translucent provided that the covering tissues are not too thick. The sign is useful in helping to distinguish a hydrocele from a solid tumour of the testis, though it must be borne in mind that a testicular tumour may lie within the hydrocele. Further Investigation. Radiographs may define a mass either directly or by the use of various contrast media and ultrasonography distinguishes between a solid and a cystic swelling. Biopsy is required if there is any suspicion of malignancy. CONCLUSION The examination of a swelling illustrates the value of a strictly methodical approach, making particular use of two of the basic procedures in physical examination, namely, inspection and palpation. The same principles are applied in defining the physical characteristics and in deducing the nature of any mass wherever it may be situated.

Associated Swellings. The nature of a lump can sometimes be inferred by identifying others with similar characteristics. Conditions in which multiple swellings occur include neurofibromatosis (Plate I), lipomatosis, metastases in the skin, lymph nodes in the lymphomas, and fibrocystic changes in the breast. The suspicion that a tumour is malignant should invariably lead to a thorough examination for evidence of involvement of the lymph nodes draining the area concerned. Percussion. This technique is of very limited value in the examination of a swelling, although occasionally it may be helpful in defining an abdominal mass (p. 212). Auscultation. Vascular Sounds. If the blood supply through a tumour is very large, a systolic murmur (bruit)






GENERAL Examine all joints, including neck, neck spine and other axial joints (costo-chondral, costo-vertebral, sternoclavicular, acromio-clavicular, sacro-iliac, symphysis pubis) as well as joints of the extremities. Examine each joint by inspection and palpation, and by putting the limb passively and actively through the full range of its various movements (be gentle!). Determine the degree of any deformity and, quite separately, the amount of active inflammation because both of these may cause pain and restriction of movement, and treatment is very different.

GENERAL Examine all joints to determine the pattern of small and large joint involvement because this varies greatly with different conditions and is very helpful in diagnosis.

INFLAMMATION Determine on examination by evidence of: swelling (including effusions), redness, tenderness, increased warmth, and reduction in passive range of movements. Evidence of acute inflammation on examination can be very subtle, so you should enquire about both general (malaise, lethargy, fever etc.) and local (night pain, rest pain, morning stiffness lasting more than 15 minutes) evidence of inflammation. With more inflammation, synovial thickening may occur, so examine carefully for this where appropriate.

INFLAMMATION Important to distinguish whether pain and limitation of movement due to inflammation or deformity, as the treatments are so different. Demonstrate effusions, especially in knee (patella tap, „bulge‟ sign). Distinguish synovitis from other forms of arthritis or joint inflammation, such as articular, bony or cartilaginous damage.

DEFORMITY Determine by degree, and look for the presence of joint subluxation/dislocation, as well as limitation of movement from fibrous or even bony ankylosis.

DEFORMITY Distinguished limitation of movement due to pain and/or voluntary muscular damage.

WASTING of muscles related to joint movement, due to disuse.

WASTING of muscles. May occur rapidly in any immobile limb.

FUNCTION Assess in relation to patient‟s daily activities (washing, bathing, eating, sitting down, lying down, walking housework, stairs, defaecation, etc.)

FUNCTION Observe the patient performing various tasks, preferably in their home situation.

ASSOCIATED FEATURES Examine joints for cysts, bursae. Examine related tendons for evidence of tendonitis, tenosynovitis, synovial fluid or thickening, nodules. Examine subcutaneous tissue (nodules)

ASSOCIATED PHENOMENA These help to differentiate different forms of arthritis. Joint signs - associated cysts, bursae, nodules (e.g. Baker‟s cyst of knee and Heberden‟s nodes in osteoarthritis). Tendon thickening, including nodules (rheumatoid arthritis); tendon inflammation in the spondyloarthropathies. Subcutaneous nodules, particularly over bony prominences, in rheumatoid arthritis; tophi in gout.



B. JOINTS - SIGNS (contd.)

ASSOCIATED FEATURES Examine skin for rash, vasculitis. Examine nails carefully. Examine eyes, including degree of lacrimation; examine sclerae, conjunctivae, iris and anterior chamber, particularly for any evidence of inflammation. Examine mouth, especially for ulceration. Examine genitalia, urine.

ASSOCIATED PHENOMENA Skin may show evidence of vasculitis related to either rheumatoid arthritis or systemic lupus erythematosis; also evidence of psoriasis. Keratoderma blephorrhagica in Reiter‟s syndrome. Anaphylactoid purpura (mostly lower limbs) in Henoch-Schonlein purpura. Purpuric skin pustules (target lesions) associated with gonococcal arthritis. Nails, vasculitis, psoriasis. Eyes - dry eyes in kerato-conjunctivitis sicca (Sjogren‟s syndrome). Conjunctivitis, iritis, uveitis, associated with various arthritides including ankylosing spondylitis, Reiter‟s syndrome, Behcet‟s disease. Mouth (mucosal) involvement including ulceration in Stevens-Johnson syndrome (severe erythema multiforme with associated joint inflammation), Reiter‟s syndrome, Behcet‟s disease. Gonnococcal pharyngitis. Genital involvement (e.g. balanitis) in Behcet‟s disease, Reiter‟s syndrome). Urethritis in Reiter‟s syndrome; gonnorrhoea. GENERAL COMMENT Be able to diagnose the main arthritides, namely rheumatoid arthritis, osteo-arthrosis, rheumatic fever, gout, infective arthritides (e.g. gonococcal). Also the less common including systemic lupus erythematosis, ankylosing spondylitis, Reiter‟s syndrome, the enteropathic arthopathies, psoriatic arthropathy, Behcet‟s disease, and reactive or post-inflammatory arthritides such as those following enteric infection (e.g. with salmonella, yersinia, campylobacter) and rubella. Be aware that any sudden flare-up in one joint in a patient with rheumatoid arthritis on steroids may be infective (aspirate if slightest doubt).



Have a systematic approach and stick to it:

Basic principles (for all joint examinations)


The order of an orthopaedic examination:

Skin changes (evidence of inflammation; bruising; abrasions; lacerations; discharging fistulae/sinuses)

1. 2. 3. 4.

INSPECT PALPATE MOVE (active before passive) SPECIAL CLINICAL TESTS (e.g. ligament stress testing) 5. IMAGING Regarding „specific inspection‟. Always compare both sides in limbs and consider bones & joints above and below the region to be examined. Examine from ALL directions so that you do not miss anything. In the ED and on the wards, it is probably safer (for the patient) to leave gait until spinal cord & limb function have been assessed neurologically (you do not want to have your patient fall over, or cause them unnecessary pain, discomfort or embarrassment). However in an ambulatory (outpatient or GP clinic) setting, gait may conveniently be examined first – as the patient is walking with you from the waiting room to your office.

Alignment of bones - is there any abnormal alignment of the affected region? (angular deformity, rotational deformity; apparent or real shortening) Wasting /atrophy of muscles Soft tissue swellings/masses - is there any swellings or masses ? (making sure to turn the patient over and examine from ALL sides & angles) PRINCIPLES OF ORTHOPAEDIC MANAGEMENT    

     

resuscitation pain relief (splinting; immobilizing; PC narcotic IV infusion for severe injuries) optimize patient physiology early anatomical reduction of fractures (correcting angular, rotational and length deformities) reduction and enlocation of subluxed/dislocated joints appropriate internal or external fixation (avoiding stress shields & stress risors) assess joints above and below the injury early active movement of the affected limb joints avoid passive movement/massage compression and distraction forces required for optimal bone healing and remodeling ensure adequate nutrition during rehabilitation



 




Flexion (50)

extension (60)

range (110)

saggital loss =

Lateral rotation (80) range



L axial loss =

Lateral flexion (45)


range (90)



% L

coronal loss =


Right C5 C6 C7 C8 T1

    

Left C5 C6 C7 C8 T1

    


C5/6 C7/8

 

C5/6 C7/8

 


C5 C6 C7 C8 T1

    

C5 C6 C7 C8 T1

    








Examination Look, feel, move: motor, reflexes, sensory, autonomic Work regionally: proximal to distal Expose: male to waist, female to slip bra straps to side Look


Horner‟s, axilla, signs of assoc injury asymmetry & muscle wasting asymmetry & muscle wasting

behind Feel & Move


1. Motor scapulothoracic glenohumeral

thoracohumeral elbow wrist finger

shrug retract protract flexion td abdn ext rotn int rotn lift off hand hipcough hand hipant push flexion extension flexion extension test

trapezius rhomb serr ant deltoid s‟spin i‟sp/teres m pec/subscap subscap lat dorsi pec M&m biceps triceps fcr&u ecrl&b, ecu ei 1st dors i‟oss apb

2. Reflexes

biceps jerk triceps jerk

3. Sensory

dermatomes C5-T2

4. Autonomic

“no sweaty hands” dryness & absence of sweating in the hand = T1 root lesion close to the canal

access n dors scap n long thx n axillary n supracap n suprascap n pec ns, sbscp n u&l subscap n th‟dorsal n l&m pec ns mus‟cut n radial n ant i‟oss, ulna radial radial ulna median

C5-6 C7-8 (C7 = middle finger)

Based on hand examination – use NH lists for protocol LOOK Screening examination for ROM Neck Shoulder

Elbow Wrist

(Pillow on patient's lap) Hand Volar

palms up

Little 

MOVE Screening examination for ROM Thumb(ROM & opposition) Index MiddleRing Little


Detailed examination of: Thumb DIP J Extension Active Passive

Index MiddleRing Little


Flexion Active

Stability Passive


FEEL Lumps

R Superficial Deep


 

Tenderness & Stability NEURO

Which nerve and what level? Motor Proximal

Median Ulna Radial


Sensory Distal APB 1st D IOss EI

Rad 3.5 Ulna 1.5 1st D web

Palm cut br Dorsal br

SPECIAL TESTS Grind CMC OA  Froments pref use of FPL vs AP  Allen's radial / ulnar artery  Intrinsics tightness  (passively hyperextend MCPJ & attempt to flex the PIPJ – intrinsic tightness = rubbery resistance which decreases with MCPJ flexion)



test shrug retract



resisted vertical push-up hand-on-hip and cough hand-on-hip and anterior push

muscle trapezius levator scapulae rhomboids serratus anterior



posterior cord


C5 C5/6/7

(of bell) thoraco-dorsal

pectoralis major & minor

lateral pectoral

lateral cord


medial pectoral

medial cord


posterior cord


posterior cord






upper & lower subscapular axillary

thumbs down abduction external rotation



upper trunk


infraspinatus teres minor

suprascapular axillary

upper trunk posterior cord

C5/6 C5/6

internal rotation

pectoralis major & minor

lateral pectoral

lateral cord


medial pectoral

medial cord


posterior cord


teres major

upper & lower subscapular lower subscapular

posterior cord





lateral cord





posterior cord



flexor carpi radialis

median lateral root ulnar radial - above elbow radial – posterior interosseous

lateral cord


medial cord posterior cord

C7/8 C6/7

posterior cord


medial cord


medial cord




long thoracic

origin roots c1-6 root c 5 behind roots c 5 / 6 / 7 behind

(winging) latissimus dorsi



nerve spinal accessory dorsal scapular

flexor carpi ulnaris extensor carpi radialis longus extensor carpi radialis brevis extensor carpi ulnaris

index extension

extensor indicis

index abduction thumb abduction

first dorsal interosseus

radial – posterior interosseous ulnar

abductor pollicus brevis

median – medial root



(= normal


Alignment shoulders Wasting quads Side Kyphosis Behind Skin scar, spbif, caulait Scoliosis Wasting FEEL

      balanced  mobile 



 square  tilted raised on R

MOVE Flexion (60)  range


extension (30) 

(90) 

saggital loss =

Rotation (30) range



R 

L  axial loss =

Lateral flexion (25)

R 

range (50)

coronal loss =

Paraspinal spasm

Simulated Rotation Axial loading

 

WALK On heels L4/5 motor On toes S1/2 motor


% L  %

 



(= normal


SIT Look Feel

Pelvic tilt

 N/A location of deformity  corrects  lower limb  continues  spinal



 N/A on flexion curve  less  postural / mobile  more  structural / rigid Right


Distraction Formal D- F > 40o


regional weak Reflexes

L3/4 S1/2



regional sens  PRONE

L2 L3 L4 L5 S1 

Tenderness Spondylolisthesis Hip Rotation Femoral stretch Pulses

 L3 L4 L5 S1 S2

        rw


L2 L3 L4 L5 S1 

       

L3/4 S1/2

 

     

 L3 L4 L5 S1 S2 rs 

     

    

  

  L2






LOOK Front Side Behind Skin

Skin Shape Positn Axilla Shape

C SPINE Look Feel Move FEEL Behind Side

scar pec wasting/SCJ/ACJ limb rotatn mass/effusn scar asymm/ACJ wasting/s'sp/delt

      

Alignment Tenderness ROM

   full  restrictn

Tenderness post s'sp/i'sp/spine/PJL lat acmn/ACJ/s'sp tendon ant GT/BG/LT s'cl/i'cl/clav/STCJ

MOVE Flexion 180o ER Abduction AB ER AD IR

Active  80o 180o



    Power

    

    

    R

painful arc Neer's Hawkin's


Speed's Yergason's

 


O'Brien's deep pain

AC joint

O'Brien's acj pain X body compressn

 


GH translation


apprehension relocation

 



 

jerk Inferior


Lig laxity



  

 




OUTLET SYNDROME provocation Adson's

HAND Neuro


  motor

Radial Ulnar Median Vascular colour  radial pulse 

temp 

cap return 






LOOK C spine Shoulder Front Behind Skin MOVE Flexion 140o Extension Supination Pronation

screening test ROM  screening test AB ER  Skin scar Shape flexor wasting Positn carrying angle (FFD!!!) scar Shape extensor wasting 

0o 90o 90o

FEEL Tenderness

Active    

 med

    Passive    

 lat

 ant

Power    



SPECIAL TESTS EPICONDYLITIS Medial resisted wrist flexion; flex elbow, supinate, extend elbow Lateral resisted wrist extension in pronation with elbow extended

 

INSTABILITY Varus shoulder full IR, forearm pronated Valgus supine Post - Lat / Pivot shift RADIO-CAPITELLAR STRESS ULNA NERVE Tinel's / subluxation HAND neuro vascular

      






LOOK Shoulder AB ER screening test Elbow FL / EX screening test

 

Pillow on patient's lap Wrist

Volar Dorsal Ulna Radial Axial

MOVE Flexion 60o Extension Radial devn Ulnar devn Pronation Supination

    

Active      

50o 15 o 50o 90o 90o

FEEL 1 Lumps 2

palms up palms down salute chop end on

Passive      


Symptomatic area radial dorsal ulnar volar


Power      

   

Routine examination sequence radial






Routine Examination

bone then soft tissue; relaxed then taught

Radial Area Scaphoid tubercle Radial styloid Snuff box APL / EPB 1st cpt Lister's / EPL 3rd cpt Special Tests Finklestein's Watson's Grind

    

de Quervain's scapholunate instability CMC OA

  

Dorsal Area include radial area examination if starting here S-L ligament between 3-4cpts  Lunate  ECRL + B 2nd cpt  EDC 4th cpt  L-T interval 4th ray  EDM 5th cpt  ECU 6th cpt  Ulnar Area ECU supination, pronation DRUJ Ulna head TFCC FCU & pisiform piso-triquetral instability Special Tests TFCC load Piano key Compression

ulnocarpal abutment DRUJ stability DRUJ arthritis

Volar Area Pisiform & FCU PT OA Hook x hamate # Flexors FDS/P, FPL, FCR Special Tests Allen's Phalen's Compression

radial / ulnar artery CTS CTS

       

     






LOOK Screening examination for ROM Neck Shoulder Elbow Wrist (Pillow on patient's lap) Hand Volar Dorsal Ulna Radial Axial

palms up palms down salute chop end on

    

MOVE Screening examination for ROM Thumb (ROM & opposition) Index MiddleRing Little Detailed examination of: Thumb MCP J Tenderness

PIP J Tenderness

DIP J Tenderness




Index MiddleRing Little Extension Active



Flexion Active



Extension Active



Flexion Active



Extension Active



Flexion Active







Superficial Deep


 

Sensation & Circulation Sensation Light touch


Circulation Colour


Capillary Return

Thumb Index Middle Ring Little NEURO

Which nerve and what level? Motor Proximal

Median Ulna Radial


Sensory Distal APB 1st D IOss EI

Rad 3.5 Ulna 1.5 1st D web

Palm cut br Dorsal br

SPECIAL TESTS Grind CMC OA  Froment‟s pref use of FPL vs AP  Allen's radial / ulnar artery  Intrinsic tightness  (passively hyperextend MCPJ & attempt to flex the PIPJ – intrinsic tightness = rubbery resistance which decreases with MCPJ flexion)







Alignment Wasting Weight distribution Side Knee extension Behind Alignment Spine Pelvis Wasting Trendelenberg WALK Gait

 Normal  Limp

         Short leg  T'berg  Antalgic

SUPINE Leg length Apparent  Equal  Short Thomas  None  FFD ROM0

 Complex


Flexion Rotation




External Internal Abduction Telescope Leg Length



  Equal

FOOT Neuro

 Short Sensory

cm  Above

 Below GT  Tibia


Tibial Peroneal Vascular Colour  Pulse

Temp  DP 

Cap return  PT





SUMMARY PFJ TFJ STAND Front Side Behind Skin

Skin scar Alignment Wasting quads Knee extension varicosity Alignment Spine Pelvis Foot Wasting calf

        


 Normal


 Full



SUPINE pathological if m > 150, f > 190

Rotational profile


Quad tone Tracking Crepitus Recrvtm plri Ps'cyst Baja / alta Q angle Tender Glide/grind Apprehn Tib torsn Fem antvn Lig laxity

Rotation in flexion Effusion Tenderness Quad mech Lateral Medial

Limp  Antalgic  Thrust  Other

 Partial              R


    


ROM Stress tests Abduction

0o 30 o 0o 30 o

 med cpt ligs + pcl  med cpt ligs Adduction  lat cpt ligs + pcl  lat cpt ligs Lachman  acl Pivot ext-flx  alri Ant draw 0, er, ir  0(amal) er(amri) ir(alri) Post draw  pcl + pol + arcuate dial  er300(p'lat) 30+900(+pcl) Instability  none straight  med lat ant post rotatory  AL AM PL ALPL AMAL Menisci McMurray's Med Lat

 

PRONE Swelling Apley's grind FOOT Neuro

  distractn  Sensory


Tibial Peroneal Vascular Colour  Pulse

Temp  DP 

Cap return  PT






STAND Shoe Wear Pattern Front Skin scar Alignment knee/ankle/foot Weight Distributn Wasting calf Side Knee extension Behind Wasting calf Alignment hindfoot Tib post too many toes heel varus on S/L toe raise Planus on toe raise Cavus

WALK Gait ankle subtalar SUPINE Hip Knee Feel

           n/a  corrects (mobile)  continues (rigid)  Normal

on heels on toes everted inverted rotation in flexion flexion / stability tenderness ankle subtalar arch / midfoot great / lesser toes

Limp           







d'flex 30o p'flex 45 o

 

 

 


inversn 45o eversn 30o

 

 

 

Midfoot s

upinatn pronatn

 

 

 

Great Toe

flexn extensn

 

 

 

Less'r Toes

flexn extensn

 

 

 

SPECIAL TESTS Lateral Ligament

anterior + posterior talofibular and calcaneofibular

Inversion Stress Test t-f + c-f ipsilateral tilt < contralateral tilt + 10o = normal  ipsilateral tilt > contralateral tilt + 10o = injured  Anterior Drawer Sign Medial Ligament

ant t-f

stable = normal  sublux = injured deltoid: superficial and deep

Eversion Stress Test

FOOT Neuro


stable = normal  excess = injured


Tibial Peroneal Vascular Colour  Pulse

Temp  DP 

Cap return  PT


EMERGENCY MEDICINE PROFESSIONAL DEVELOPMENT During undergraduate and early PG training every trainee doctor should: 

Acquire a fundamental knowledge of basic sciences as applied to emergency medicine and have the ability to assess and immediately treat common emergencies.

Develop existing clinical examination skills and apply them in clinical practice to develop differential diagnoses and provisional management plans for acute medical conditions and undifferentiated patients.

Acquire expertise in a range of commonly used emergency procedural skills, including basic life support.

Perform allocated tasks, learn to process serially so as to optimally manage time within the shift, and meet clinical deadlines.

Teach informally in the clinical setting and in specified circumstances in a more formal setting.

Develop an understanding and basic awareness of clinical management issues when applied to acute care situations.

Select and perform simple audit projects and under· stand the audit cycle to monitor care delivery and improve care quality.

Understand the principles of critical appraisal and research methodology and apply these to acute care situations.

Demonstrate the capacity to work in multi professional teams.

Learn to recognize his or her own limitations in the provision of emergency care.

EDUCATIONAL OUTCOMES - LEARNING OBJECTIVES These learning objectives are designed to allow easy modification to the local needs and are written so that objective measures of performance and competency can be designed to measure attainment of the learning objective. The Student should: 1. Acquire basic life support skills, including the diagnosis and treatment of shock and the related basic procedural skills; and demonstrate the basic application of these principles in real or simulated patient care scenarios. 2. Demonstrate the capacity to differentiate and treat common acute problems. 3. Provide a comprehensive assessment of the undifferentiated patient. 4. Demonstrate proficiency in basic life support skills and cardiopulmonary resuscitation (CPR). 5. Recognize and initiate first aid for airway obstruction. 6. Recognize and be prepared to intervene for all causes of shock in any age group. 7. Be able to provide rapid stabilization with intravenous access and fluid/blood administration. 8. Understand the principles of cerebral resuscitation in brain illness and injury. 9. Demonstrate proficiency in the use of an automatic external defibrillator (AED). 10. Understand the principles of wound care. 11. Demonstrate basic wound care techniques. 12. Understand the principles of trauma management. 13. Demonstrate basic trauma management skills, such as initial assessment using the ABC approach and full spine immobilization. 14. Demonstrate mastery of basic procedural skills, such as airway management and venous access. 15. Recognize life-threatening illness or injury, and apply basic principles of stabilization to the early management of these entities. 16. Demonstrate the capacity to prioritize attention to those patients with more urgent conditions. 17. Describe the importance of the ED as a key link between the general population and the health care system. 18. Understand the role of the situations that are unique to emergency medicine: acute critical illness, intoxicated patients, media, out-of-hospital personnel, death notification for sudden unexpected death, disaster, language barriers, environmental illness/ injury, injury prevention, assessment of complex and undifferentiated


patients, ability to synthesize multiple and often incomplete sources of information to develop a management plan.

1. Demonstrate endotracheal intubation


3. List contraindications for intubation

Undifferentiated patient presentation Time constrained decision making Environmental illness and injury Pre-hospital care Transition point between community and hospital Focused history and exam Prioritized differential diagnoses LEAD ROLE AREAS FOR EMERGENCY MEDICINE IN FOUNDATION TRAINING Acute illness Acute injury Disaster management Death notification Injury prevention Medical decision making Resource utilization Toxicology

2. List indications for intubation

4. Describe medications used for rapid sequence intubation 5. Describe the physiology of artificial ventilation Outcome measures At time of graduation, student will demonstrate the ability to: • manage an obstructed airway • manage a basic airway, and • perform an endotracheal intubation. This will be assessed by simulation on a mannequin or using direct observation of student skills by trained faculty during clinical situations.

EXAMPLE CURRICULUM FORMAT To assist educators in crafting a curriculum that fits local needs, an example is provided of a 4 year plan for a single learning objective. Educators may use this as a guide to construct individual-, national-, and institution-specific models for content delivery. This method is not intended to be prescriptive, but to provide a simple model for tailoring content to the unique educational models that exist throughout the world. Learning Objective # 5: Recognize and initiate first aid for airway obstruction Curriculum year 1 Readings - Basic life support manuals, basic first aid manuals [e.g., American Heart Association Advanced Life Support Manual, Dallas, TX USA or equivalent manuals from the local community.] Performance indicators: 1. Obtain basic cardiac life support (BCLS) certification 2. Demonstrate jaw thrust 3. Demonstrate bag valve mask ventilation 4. Demonstrate the ability to clear an obstructed airway Curriculum year 2 Readings - Pathophysiology of respiratory failure Curriculum year 3 and/or 4 Readings - Introduction to anaesthesia, Introduction to airway management Performance indicators:


UNDERGRADUATE EMERGENCY MEDICINE CURRICULUM CONTENT SKILLS CURRICULUM 1. Clinical care skills 1.1. History and examination 1.2. Documentation 1.3. Decision making 1.4. Time management 1.5. Safe prescribing 1.6. Continuity of care 1.7. Therapeutic interventions 2. Communication skills 2.1. With colleagues 2.2. With patients and caregivers 2.3. Breaking bad news 2.4. Working with a team 3. Maintaining good medical practice - life long learning 3.1. Audit and clinical outcomes 3.2. Critical appraisal 3.3. Information management 4. Professional behaviour and probity- professional attributes 4.1. Career & professional development 5. Ethics and Legal 5.1. DNAR and advanced directives 5.2. The competent adult 5.3. Informed consent 6. Education - developing learning for others 6.1. Basic educational information delivery 6.2. Assessment and appraisal 6.3. Feedback 7. Maintaining good clinical care - risk management 7.1. Medico-Legal issues 7.2. Confidentiality SPECIALTY SPECIFIC CURRICULUM 1: Generic Objectives for Resuscitation 1.1: Resuscitation - Airway 1.2: Cardiac Arrest / Peri-arrest 1.3: Shock - all varieties 1.4: Coma 2: Anaesthetics and Pain Relief - Pain Management 2.1: Local anaesthetic techniques 2.2: Safe conscious sedation 3: Wound Management 3.1: Basic wound debridement & closure 3.2: Identification & treatment of infected wounds 4: Generic Objectives for Trauma 4.1: major trauma 4.2: head injury 4.3: chest trauma 4.4: abdominal trauma 4.5: spinal injury 4.6: maxillo-facial trauma 4.7: burns 4.8: orthopaedic trauma

5.2: Lower limb and pelvis disorders 5.3: Spine and spinal cord conditions 6: Vascular Emergencies 6.1: Arterial limb threat 6.2: Deep Venous Thrombosis (DVT) 7: Abdominal Conditions 7.1: Undifferentiated abdominal pain 7.2: Haematemesis / melaena 7.3: Anal pain and rectal bleeding 7.4: Diverticulitis 7.5: Abdominal aortic aneurysm 8: Urology 8.1: Acute urinary retention or bladder obstruction 8.2: Nephrolithiasis and colic 9: Sexually Transmitted Diseases 9.1: Identification and initial treatment for endemic diseases 10: Eye Problems 10.1: Acute conjunctivitis - bacterial and viral 10.2: Acute vision loss 10.3: Acute eye trauma including globe rupture 11: Ear, nose and throat (ENT) Conditions 11.1: Epistaxis 11.2: Infections of the head and neck 12: Dental Emergencies 12.1: Dental abscess 12.2: Dental fracture 13: Gynaecology 13.1: Pelvic pain 13.2: Dysfunctional uterine bleeding 14: Obstetrics 14.1: Ectopic pregnancy 14.2: Uncomplicated emergency vaginal delivery 15: Cardiology 15.1: Basic electrocardiographic analysis 15.2: Recognition and initial treatment of acute myocardial infarction 15.3: Recognition and initial treatment of life threatening arrhythmia 16: Respiratory Medicine 16.1: Airway obstruction 16.2: Respiratory failure 16.3: Asthma and restrictive airway disease 16.4: Acute pneumothorax 16.5: Pulmonary embolism 17: Neurological Emergencies 17.1: Acute stroke 17.2: Spinal cord lesions 17.3: Peripheral neuropathies 17.4: Acute mental status change 17.5: Migraine 17.6: Meningitis 17.7: Vertigo

5: Generic Objectives for Musculoskeletal Conditions 5.1: Upper limb disorders


18: Hepatic Disorders 18.1: Acute hepatitis 18.2: Liver failure 18.3: Acute cholecystitis & cholangitis 19: Toxicology 19.1: Treatment of acute ingestions 19.2: Identification of basic toxidromes 20: Acid Base and Ventilatory Disorders 20.1: Identification of acid base disorders 20.2: Initial management of the mechanically ventilated patient 21: Fluid and Electrolytes 21.1: Basic principles of fluid administration 21.2: Dehydration 21.3: Hyperkalaemia 21.4: Hyponatraemia 22: Renal Disease 22.1: Acute renal failure 23: Diabetes and Endocrinology 23.1: Disorders of glucose metabolism 23.2: Thyroid disorders 24: Haematology 24.1: Anaemia 24.2: Disorders of red cell function 24.3: Disorders of clotting 25: Infectious Diseases and Sepsis 25.1: Endemic infectious diseases 25.2: Sepsis 25.3: Common infectious diseases or conditions (e.g. pneumonia) 25.4: Cellulitis and gangrene 26: Dermatology 26.1: Blistering and exfoliative diseases 26.2: Differential diagnosis of rash 26.3: Parasitic conditions & infestations

31: Oncology 31.1: Acute leukaemia 31.2: Neutropaenia and neutropaenic fever 31.3: Solid tumours 31.4: Complications of chemotherapeutic agents 32: Paediatrics 32.1: Basic management of paediatric airway 32.2: Basic paediatric resuscitation 32.3: Common infectious diseases of childhood 32.4: Fever in the first 6 months of life 32.5: Common injury patterns for normal children 33: Psychiatry 33.1: Acute psychosis 33.2: Mood disorders 33.3: Personality disorders 33.4: Acute suicidal and homicidal ideation 33.5: Substance abuse 34: Major Incident Management 34.1: Concepts and application of triage 34.2: Field to hospital communication and chain of command 35: Legal Aspects of Emergency Medicine 35.1: Refusal of care 35.2: Informed consent 35.3: Malpractice 36: Research 36.1: Formulating a research question 36.2: Review of the medical literature 36.3: Basic research design 36.4: Basic preparation of manuscripts and written publications 37: Management 37.1: Leading teams and giving orders 37.2: Basic concepts of debriefing and giving feedback 37.3: Time flow management

27: Rheumatology and Immunology 27.1: Crystal arthropathy 27.2: Arthritis 27.3: Immune disorders 27.4: Anaphylaxis 28: Child Protection & Children in Special Circumstances 28.1: Child abuse signs and symptoms 28.2: Legal rights of parents to refuse care 29: Neonatology 29.1: Neonatal resuscitation 29.2: Hyperbilirubinemia 29.3: Disorders of feeding 29.4: Neonatal fever 30: Environmental Emergencies 30.1: Hyperthermia 30.2: Hypothermia and frostbite 30.3: Envenomation & environmental toxin exposure


TRAUMA PRINCIPLES (Dr. A, B, C, D, E, F) Injuries account for approximately 16% of the global burden of disease (WHO, 1999) it is a Public Health Disease. Injury Statistics in Fiji ? The burden of disease due to injury is largely preventable. The DR - ABCDEF system of trauma management: Danger – to patient &/or doctor Response – from doctor  call from help & initiate assessment & resuscitation if required from patient  conscious state to verbal & physical stimuli (jaw thrust is an appropriate stimulus) Airway (jaw thrust +Cx-spine) Breathing (assess resp. rate, depth & symmetry + O2) Circulation (assess HR & BP; stop external bleeding; peripheral IV wide bore access plus saline infusion) Disability (head to toes assessment) Environment/Exposure (to metabolic insults) Fractures The ABCDEF system of trauma management gives a standardized systematic and rapid approach to emergency patients. Resuscitation forms part of this approach. The goal of ABCDEF is to assess, resuscitate, stabilize and optimize the patient. Variations in the ABCDEF system Rural vs. urban: geographic distance; transport issues; lack of tertiary trauma centres; difficulty retaining staff experienced in emergency medicine and nursing; poorly resourced hospitals (equipment, imaging, drugs) Medical vs. Surgical - Cx-spine, haemorrhage, fractures, thoracic/abdominal/pelvic trauma Paediatric trauma - different anatomy, smaller plasma volume, venous access and GCS, child abuse, neglect. LEARNING OBJECTIVES - AIRWAY ANATOMY OF THE AIRWAYS Airways allow air to flow from the external environment to the alveoli. Trachea is 10-12cm in length and divides into right and left main bronchi. The right main bronchus is wider, shorter and more vertical than the left (think aspiration and FB) 25 divisions between the trachea and the alveoli. Dr. ABCDEF SYSTEM IN EMERGENCY MEDICINE

RECOGNISING A COMPROMISED AIRWAY Look Agitation = hypoxia Decreased chest movement Paradoxical respirations Use of accessory muscles Listen Noisy breathing = partial Obstruction Snoring = tongue, palate, pharynx Stridor = larynx Hoarseness = larynx No noise = bad news! Feel Maxillofacial/laryngeal crepitus Tracheal deviation AIRWAY MANAGEMENT TECHNIQUES JAW-THRUST MANOEUVRE push angles of the mandible on each side, displacing the mandible forward. (Translocation of the TMJ). This pulls the tongue anteriorly via genioglossus muscles and opens the airway. This manoeuvre must be maintained (usually with your little finger) while utilizing the face mask of a bag-mask device. OROPHARYNGEAL AIRWAY Two main techniques: Depress the tongue and insert the airway posteriorly, taking care not to push the tongue backward. The oral airway is inserted upside down and then rotated 180 so the concavity is directed inferiorly over the tongue (different in children). NASOPHARYNGEAL AIRWAY Inserted in one nostril and passed gently into the posterior oropharynx. Should be well lubricated and inserted into the nostril that appears to be unobstructed. (ENDO-)TRACHEAL INTUBATION The insertion of a tube into the trachea either orally or nasally with a cuff inflated = definitive airway No cuff in children. Laryngeal mask airway is good, but not definitive Indications for intubation – the 5 P‟s Patency of a airway required (decreased LOC, epiglottitis) Protect the lungs from aspiration (absent protective reflexes, transport) PPV (hypoventilation, apnoea) Pulmonary toilet (unable to clear secretions) Pharmacology (provides route of administration of some drugs)

CAUSES OF AIRWAY OBSTRUCTION Lying supine (lax tongue falling back with gravity) Coma/CNS Aspiration/FB Maxillofacial trauma Neck trauma


SURGICAL AIRWAY Indications: Inability to intubate trachea Maxillofacial trauma Neck injury Methods Needle cricothyroidotomy with jet insufflation: cannula inserted through the cricothyroid membrane into trachea and connected to O2 at 15 L/min. Surgical cricothyroidotomy: endotracheal or tracheostomy tube following a skin incision through the cricothyroid membrane. SUMMARY Suspect airway compromise Protect Cx-spine Open airway (jaw thrust)and ventilate If in doubt  Definitive airway Urgency of need Clinical judgment and skill Achieve optimal oxygenation LEARNING OBJECTIVES - BREATHING The Anatomy of Breathing The Physiology of Breathing Principals in Respiratory Pathology The respiratory system contains an airflow conducting network (trachea, bronchi, bronchioles), a gas exchange organ (alveolus) and a ventilation pump (the respiratory muscles/thorax). Dysfunction in any component can cause respiratory failure. Principals in Respiratory Pathology Ventilation:Perfusion (V/Q) Mismatch Monitoring Breathing Clinical - is there a problem? LOOK LISTEN FEEL. Change in RR is best indicator - but often not done or done poorly - do it yourself! SaO2 is a rapid aid. Bloods e.g. Hb, WCC, ABG, D-dimer Spirometry - good to differentiate restrictive vs. obstructive lung disease. Imaging - good to exclude pneumothorax, infiltrates, fibrosis, effusions, consolidation Arterial Oxygen Pressure (PaO2) versus Oxygen Saturation (SaO2). PaO2 is the driving pressure of O2 into the blood proportional to that in the alveolus, and acts to keep O2 bound to Hb (not the absolute amount of O2 in blood). Normally 90-100mmHg. That is, 12-13.3 kPa SaO2 is the percentage of haemoglobin that has O2 bound, and is determined by the PaO2. If < 90% supplemental O2 is needed. Alveolar-arterial Gradient A-a = 713 x FiO2 - PaO2 - PaCO2/0.8 Calculates difference in PO2 between alveolus and blood. Should be normally < 15mmHg, or about 10 + 1/10 of the patient‟s age. Normally there is a small difference due to shunt via bronchial and thesbian veins.

Increased A-a gradient is due to; Diffusion defect e.g. fibrosing alveolitis Right to left shunts e.g asthma, COPD, obstructed airway, lung collapse V/Q mismatch e.g. PE, pulmonary arteritis SaO2 vs ABG vs A-a Gradient. SaO2 is non-invasive, accurate to 1-2% when above 60% saturation, but does not give a good indication of effectiveness of oxygenation. Also requires good peripheral perfusion. ABG can guide O2 therapy and indicate severity of respiratory failure. It considerers both acid-base disturbances and alterations in oxygenation. A-a gradient gives indication of gas-exchange function, or V/Q. ABG readout How to use all this information? Chest Tubes Drain air, exudates, or blood from pleural space. Good for correcting compressive lung collapse and V/Q mismatch. Life-saving in tension or large pneumohaemothorax. Oxygen Masks and O2 Delivery Low Flow - nasal prongs (0.5-4L/min) Medium flow - Hudson (6-10 L/min) High Flow - Venturi Mask, reservoir mask (nonrebreather) LEARNING OBJECTIVES - CIRCULATION Cardiac Physiology Recognition of Shock DEFINITION OF SHOCK Shock is a failure of the body (specifically the circulatory system) to provide adequate tissue perfusion. In shock, the tissues fail to receive adequate oxygen and nutrients. There are various types of shock. Low blood pressure is usual in shock, but one can be in shock with a normal BP. TYPES OF SHOCK Haemorrhagic Non-haemorrhagic - cardiogenic - anaphylactic - obstructive (e.g. tension pneumothorax) septic - neurogenic Class I Haemorrhage Class II Haemorrhage Class III Haemorrhage Class IV Haemorrhage Fluid Shifts Compounds intravascular loss Assessment and Management Recognise – ABCDE system in trauma assessment Stop the bleeding Replenish intravascular volume Restore organ perfusion


Stop the Bleeding Direct pressure Immobilise and splint Vitamin K? Other? Operation Management: Vascular Access 2 large-calibre, short, peripheral IV lines: Femoral Jugular Subclavian Intraosseous – gun, hand driven, drill Obtain bloods for cross-match Management: Fluid Therapy (Warmed) isotonic or hypertonic crystalloid solution e.g. lactated Ringer‟s (Hartmans), normal saline 0.9% Rapid fluid bolus: Adult: 2 litres (or 250 ml of hypertonic saline) Child: 20ml/kg 3 to 1 rule: replace each 1mL of blood loss with 3 mL of crystalloid Must balance the goal of organ perfusion with risk of rebleeding (due to increased BP) Continuously monitor response to ongoing therapy If require pRBC‟s (massive haemorrhage) match unit for unit with FFP Re-evaluate Organ Perfusion Monitor: Vital signs Urine output CNS status Skin perfusion Pulse oximetry Resuscitation Evaluation Summary of Management Early recognition of the shock state Oxygenate and ventilate Stop the bleeding Restore volume Continuous monitoring of response LEARNING OBJECTIVES - DISABILITY Disability (of the CNS) Assess early to avoid secondary brain injury. Can use AVPU (alert, responds to voice/pain, unresponsive) or GCS (score out of 15). Check Pupils. black, round, equal, react to light and size:<4mm and > 2mm) Give glucose/glucagon +/- insulin infusion if DM and abnorfmal BSL/altered mental status. Consider ETOH/drug overdose. Head and Spinal Injury Cranium is a fixed space. Signs of Head Injury Confusion, altered mental status, GCS, headache, N/V. Local signs of traumatic injury. CSF/blood leaking through nose/ear. Nerve palsies (esp. cranial nerves). Racoon eyes, Battle sign. Asymmetric pupils, Cushing's triad.

NOTE: Intracranial haemorrhage may include a “lucid interval” (no CT scans in small towns!) Spinal Injury Assume spinal injury with suspicious mechanism of injury or if intoxicated  semi-rigid C-spine collar is indicated. Look for sensory & motor changes, signs of focal tenderness, “step down” in spine, paraesthesiae, autonomic dysfunction, rectal tone. May result in neurogenic (haemodynamic) or spinal (paralysis and paraesthesia) shock. Management of Head Injury ABC takes priority - maintain MAP >90mmHg (thus cerebral blood flow), give O2, maintain PaCO2 <35mmHg. Give drugs to avoid seizure-induced injury? Determine if penetrating or blunt injury Frequent neurological exam/GCS, HEAD CT. If deteriorating, ventilate, ? Mannitol and hyperventilate to  cerebral oedema. Management of Spinal Injury Secure Cx-spine with collar or other. Caution during airway management, avoid head-tilt if possible. Log roll (4 assistants) - assess for “step down”, tenderness, PR tone, bruising. Use opportunity to check for chest and retroperitoneal trauma Cx-spine x-rays ± thoracolumbar Lateral, odontoid ±swimmers views. Neurosurgical consult or transfer to definitive care. LEARNING OBJECTIVES – ENVIRONMENT & EXPOSURE Environment/Exposure Aim to assess entire patient whilst avoiding hypothermia and maintaining dignity. but remove wet clothes immediately and avoid direct contact with cold metal trolleys and beds Assess for heat/cold/electrical/chemical injuries (e.g. burns). Thermal Injury Stop the burning - remove clothes, jewellery etc. Think inhalation injury, CO exposure. High risk of hypovolaemic shock with widespread burns. Risk of neurovascular compromise in circumferential burns. Partial thickness = blistering/erythema Full thickness = leathery skin Basic Thermal Injury Management Estimate burn TBSA.


4mL crystalloid/kg/% TBSA over 24hrs. 1/2 over first 8 hrs. Add extra for electrical, paediatric, TBSA > 80% and if other trauma present. CO poisoning Rx = 100% O2. Escharotomy. Tetanus booster Antibiotics. Chemical Burns Similar principals and effects to thermal burns. May also get toxicity from systemic absorption. Most are either acid (causes coagulation and hard eschar formation), or alkalis (causes deep liquefactive necrosis). Alkali worse, esp. eye. Injuries to Extremities Fractures Check neurovascular integrity, open or closed. Caution for compartment syndrome, get surgical consult. Also consider dislocations and ligament instability. Management Principals Immobilise, analgesia, irrigation, control bleeding. Imaging (x-ray, CT, U/S, etc) Antibiotics if open or otherwises suspicious Tetanus prophylaxis. Injuries to Extremities Soft tissue injuries Crush injury; compartment syndrome. Lacerations; consider underlying structures. Irrigate, achieve haemostasis and avoid adrenaline on digits/penis. Pain Relief and Fluids in the ED Types of Fluids - maintenance +/- replacement Oral, IMI, subcut or IV analgesia Nerve blocks Topical anaesthetics Intrathecal Inhalational analgesia Splinting Fluids Fluids maintenance or replacement? Maintenance Requirements 2500mls, 76mmol Na+, 50mmol K+, 100g dextrose. Normal saline = 0.9% NaCl Example of adult Maintenance Regime; 2500mL of 4% dextrose + 1/5 normal saline PLUS 50mmol KCl. Fluids maintenance or replacement? Replacement requirement - is patient dehydrated? Bleeding Fever GI (K+ requirement, loss of acid in vomitus) Third space e.g. bowel obstruction adds ≥ 2L Hartmann‟s to baseline requirement Large fluid losses may occur very slowly or very fast - without a good history, you will never know!

Fluids - blood Generally accepted that if minimal haemodynamic improvement after rapid infusion of 2 - 3L of crystalloid, blood is indicated. „Group and Hold‟ is often what is required of ED. Think of O-negative or O-positive if you are unable to cross-match in timely fashion Must observe patient for hypersensitivity and other reactions. Priority is to identify and stop bleeding. Over-aggressive fluid resuscitation prior to definitive treatment may be harmful. Aim for small boluses of fluid to maintain systolic BP of 80 - 90mmHg. Give FFP if a massive transfusion indicated. Fluids - cautions Caution against inducing acute pulmonary oedema in a person with CCF. Electrolyte abnormalities. Large volumes of NS may result in metabolic acidosis. Dilutional coagulopathy. Caution against hypothermia Some potential fluid regimes LEARNING OBJECTIVES - PAIN Pain Management in the ED May aim to; Eliminate cause Block local inflammatory responses Block transmission Modify central perception / processing Consider risk benefit Is pain affecting A, B, C or D? Will pain relief affect A, B, C, or D? Multimodal to  efficacy whilst  side-effects. Pain Management in the ED Anxiolysis is the reduction of apprehension without alterations in the level of consciousness e.g. reassurance, valium. Neurolepsis is quiescence, indifference to surroundings, and reduced motor activity. Agents used for this purpose include haloperidol and droperidol. Dissociation is characterized by amnesia, analgesia, sedation, and maintenance of muscle tone. Ketamine is the only commonly used dissociative agent. Sedation is controlled reduction of environmental awareness Pain Management in ED Start with simple analgesia PO. Paracetamol NSAIDs (e.g. ibuprofen, diclofenac) Regular doses rather than „PRN‟ Note contra-indications May go multimodal E.g. IMI, subcut, IV Basic Therapeutics Opiates


Not accurately predicted by weight Wide individual variation Dependent on magnitude of stimulus Potential for abuse Procedural Sedation Morphine or + reversible, analgesia Fentanyl - resp. depression, repeat dosages needed Ketamine+ analgesia, good for children, airway maintained emergence delirium, N/V !CI in HR/BP/ICP, RTI Midazolam+ safe, reversible, amnesia no analgesia, resp./CV depression Nitrous Oxide+ minimal resp./CV/CNS depression, rapid onset N/V, inadequate for +++pain !CI in gas distention. Proprofol+ rapid onset/recovery, no hangover no analgesia, transient apnoea, BP/HR, tremors Local Anaesthesia Can have ester (e.g. Procaine) or amide (e.g. Lidocaine) based LA. Can use subcut, IV or topical. Block voltage-gated Na+ channels of local area or supplying peripheral nerves. Can have additives (e.g. HCO3-), infiltrate into wound margin to minimize pain of infiltration (esp. in Qld) Toxicity CNS - excitatory and depressant e.g. confusion seizures. CVS - myocardial depression and dysrhythmias. Nerve Blocks Advantageous in ED setting as less total drug delivery, and often less painful e.g. hands, fingers, toes, leg. Must check neurovascular status prior to block, to avoid further injury. Onset of anaesthesia is slower than LA. SUMMARY “Dr. ABCDEF” Trauma/Reduced Conscious State/Coma Cardio/Respiratory Arrest: D - assess danger to patient & to Doc R - response from patient (verbal, jaw thrust) & from Doc --> call alert; seek help/assistance (no lone-rangers) A - airway: jaw thrust ? definitive airway + Cx spine immobilization; call anaesthetist if having problems B - breathing: chest moving appropriate rate, depth & symmetry ? assisted ventilation (bag/mask) + OXYGEN (15 L/min) C - circulation: is heart beating at appropriate rate & rhythm ? attach AED and follow commands … targeted CVS & fluid assessment, intravenous access via x2 large bore (>16 G) short, peripheral cannulae (or intraosseous); stop external bleeding (direct pressure, compression, elevation, splinting); consider internal bleeding in all body cavities (pelvic sling with „open book‟ #‟s) IDC

D - disability: secondary survey head to toes: scalp, skull, brain; entire vertebral column/spinal cord; viscera, vessels & other hollow tubes of: neck; thorax; abdomen; pelvis; limbs. E - exposure: to metabolic & other insults: Hypoxaemia/Anaemia Hypovolaemia Hypo/hyperglycaemia Hypo/hyperthermia Hypo/hyperkalaemia Tamponade --> pericardiocentesis; pericardial window Tension PneumoTx --> thoracocentesis needle; ICC insertion Toxins/poisons/drugs --> ? antidotes Thromboembolic: (pulmonary; coronary; mesenteric) ? thrombolytics „Thrombocytopaenia‟ ? transfuse whole blood, pRBC‟s; FFP; Vit K … F - fractures: (plain X-Ray/CT) • skull • spine • pelvis • limbs Cardiac Arrest, consider: definitive airway --> secure by endotracheal intubation • adrenaline 1mg/kg every 3 mins Antiarrhythmics: • amiodarone (300mg) • lignocaine (1-1.5mg/kg) • magnesium (5mmol) Electrolytes: • potassium 5mmol Buffer: Buffer for acidosis: • NaHCO, 1mmol/kg Asystole & Bradycardia: • atropine 1-3mg • external pacing Raised ICP prevent secondary brain damage via all of the above points plus double check: • oxygen (hyperventilation is contentious – but certainly avoid underventilating) • fluids & BP (as CBF=MAB-ICP) • glucose • bed in head-up position • prevent seizures (see below) Consider, under supervision, short-term use of: • mannitol ? dose • diuretics • dexamethazone 4mg qid dose • barbiturates (e.g.thiopentone, pentobarbitone) ? dose With seizures: • diazepam 2-10 mg per dose up to 0.5mg/kg bd-qid IV (IM or PR) – antidote is flumazenil Note: endotracheal drug administration may be used if IV access not obtained, but doses need to diluted with normal saline or sterile water.


Part IV - GENERAL PHYSICAL EXAMINATION ORDER OF MINIMUM ROUTINE The foregoing has concentrated on particular systems, and we now need to consider the order and minimum routine of the general examination beyond anyone particular system of interest. General inspection First observe patient standing and walking where relevant. Then patient stripped to pants, uncovered and lying with chest/neck at angle of about 45째. Stand at the end of bed and observe general demeanour, mood, skin, face, respiration (including symmetry), neck veins, any pulsation (normal or abnormal), abdomen distension, asymmetry etc. FULL PHYSICAL EXAMINATION hands check dorsal & palmar aspects of both hands wrists radial pulse (rate & rhythm) and respiratory rate arms blood pressure face eyes; ears; mouth; tongue; parotids; temperature neck carotids; JVP; trachea, lymph nodes breasts chest heart: inspection palpation, percussion; auscultation (also listen in neck and abdomen) axillary lymph nodes: palpate (bimanual examination may help to trap nodes) sit patient up, listen for aortic diastolic murmur, feel for sternal tenderness, then examine: (a) chest, posteriorly: observe, percuss and auscultate, particularly over apices, bases (b) lumbar-sacral area: oedema; tenderness (including percussion tenderness); limitation of movement (c) cervical lymph nodes/ thyroid gland: From in front (or behind if you prefer)

lie patient flat: then examine: (a) abdomen - remember to auscultate, especially for epigastric bruits (b) femoral pulses (including radio-femoral delay) (c) femoral and inguinal areas, including inguinal lymph nodes (d) external genitalia (e) popliteal/foot pulses (f) legs - colour, oedema, varicose veins, calf tenderness, rashes, wasting, abnormal movements prop patient up slightly and then examine the nervous/locomotor systems (a) higher cerebral function (b) cranial nerves and examine optic fundi (c) limbs: upper limbs first then lower. Compare both sides as you go along. Inspection and palpation first, (including joints), and examine at rest and during movement. Note any tenderness/ swelling/fasciculation/ wasting/ tremor / involuntary movements. Then tone, power, reflexes, co-ordination, sensation (touch, pinprick, vibration, position) ask patient to walk if not done already but only if the patient is safely able to do so. Examine particular areas after performing manoeuvres which precipitate symptoms, in appropriate cases (see also below) Make sure you have examined urine and taken temperature, and done rectal/pelvic examination where necessary Think your way through the history & examination At end of whole examination, pause and think of what more you should examine in the light of the history and findings so far. Particularly if the history is episodic, and episodes are precipitated by accessible factors, put the patient under the appropriate load and re-examine - e.g. the complaint of 'giddiness' on neck movements should be further examined by moving the patient's neck appropriately and observing for nystagmus; obscure shortness of breath on exertion should be further investigated by re-examining the patient (particularly the cardiovascular and respiratory systems) after exercise; a complaint of staggering should be examined by observing gait (obvious but easy to forget when you get caught up in the routine).




You must be able to do your routine examination efficiently, accurately and thoroughly. It must become like driving a car, i.e. sufficiently routine so that you are not too preoccupied with its performance to miss additional clues in the individual case, or to be thrown off the order of your routine by following them up.

At the end of Second Year – MSAT Clinicals

There are three aspects of the general examination which students tend to forget and should be thought about at the end of each examination. They are: temperature, urine examination and blood pressure. Make sure that you have determined all of these before leaving the bedside. Remember: 1. ask patient to remove all clothing except underpants/briefs/bra for initial inspection. 2. position patient correctly. 3. initial inspection from end of bed. 4. approach your patient as a person, get their confidence, don't hurt them. 5. approach each step first with an open, then with a more closed mind, i.e. pause at the end of each routine step and ask what special aspects you might like to do now in the light of clues from history and examination so far. 6. before you leave the patient, ask yourself whether you do have a complete anatomical, pathological, and functional diagnosis (clinical), and if not whether you might like to ask further questions, particularly about the aetiological background (e.g. 'risk-factors' for ischaemia heart disease) 7. if there are multiple symptoms/ signs remember the following in diagnosis: (a) try to see the condition first as one primary underlying problem with secondary symptoms / signs occurring elsewhere as a consequence (e.g. liver disease with secondary splenomegaly, gynaecomastia, ascites, parotid enlargement, spider naevi, testicular atrophy, jaundice etc.) (b) if you are having trouble seeing which (symptom) is cause and which is effect in synthesising your diagnosis, go back to the history and find out which came first in time, e.g. myocardial ischaemia and atrial fibrillation could be related either way around, so find out whether the patient noticed chest pain or palpitation first. (c) always be on the look out (especially unusual presentation of) reversible diagnoses. They are, after all, what matters.

There will be an assessment of your ability: (i) to carry out a routine examination efficiently. thoroughly and accurately. (ii) to recognise certain major common abnormalities; and (iii) comment sensibly on their meaning in physiological. anatomical. and general pathological terms. At the end of Third Year – MSAT Clinicals There will be an assessment of your ability: (i) to carry out a routine examination efficiently. thoroughly and accurately (ii) to recognise most major abnormalities; and (iii) comment sensibly on their meaning in physiological. anatomical. general & specific pathological terms. Fourth & Fifth Year Clinicals Check Faculty handbook for details


CLINICAL COMPETENCIES - SUMMARY CHECK LISTS CNS higher cortical functions (MMSE) cranial nerves basal nuclei cerebellum cervical spine lumbar/sacral spine PNS brachial plexus upper limbs lower limbs cauda equina systems CVS (incl. peripheral vascular & ECG) respiratory (incl. pulmonary FTâ&#x20AC;&#x;s) GIT (inc. herniae, male external genitalia, PR) hepato-biliary (incl. LFTâ&#x20AC;&#x;s) haemopoietic/lymphatic (incl. FBE) endocrine (& thyroid) renal (incl. urinalysis)

regions eyes ENT breast pregnant abdomen; uterus (& PV) cervical smear test (PAP) trauma primary survey (Airway; Breathing; Circulation) secondary survey (Disability, Exposure, Fractures) patient optimization (physiological/nutritional) wound assessment suturing orthopaedic examinations Cx spine L/S spine bones & joints of upper limb (shoulder, elbow, wrist, hand) tendons of upper limb (hand) bones & joints of lower limb (hip, knee, ankle, foot)


ASSESSMENT EXAMPLE – OSCE – MBBS YEAR 3 CASE INFORMATION FOR STUDENT You are asked to perform a targeted examination of the patient‟s cardiovascular system to demonstrate & explain the relevant signs to look for in congestive cardiac failure. You are not required to take any further history from this patient. You should begin this CVS examination starting from the patient‟s hands. Finish after auscultation of the heart Please give a running commentary with interpretation as you proceed.

COMMENTS FOR EXAMINERS The students are to perform a targeted examination of the cardiovascular system, specifically to confirm or exclude congestive cardiac failure. If they need a prompt then say (once only): “Would you like to read the question again?” The student is required to correctly demonstrate how each sign is elicited, interpret the information (supports or goes against the diagnosis) and explain why, before you award them the appropriate marks. Due to time constraints please stop them from taking the BP ... but ask them to explain what they might expect to find and why. Stop the student if the patient is experiencing any obvious pain or discomfort.

COMMENTS FOR THE ROLE PLAYING PATIENT In this station the student will be asked to examine your cardiovascular system, You are conscious, not in any pain and co-operative. Please follow any reasonable instructions given to you by the student. Please take off your shirt and lie back on the examination couch before the student enters the room. Indicate to the student or examiner if the examination is causing pain or significant discomfort.


Student No: ........................................... Example of an MB-3 SUMMATIVE OSCE/MSAT TARGETTED EXAMTN CVS MARKING GUIDE FOR EXAMINER





state of perfusion  expects cold & clammy ++




capillary return  expects increased filling time (+/- peripheral cyanosis)




pulse rate  expects tachycardia ++ (>100 b/min)




pulse rhythm  possibly irregularly irregular ++ (c/w AF)




respiratory rate  expects tachypnoea ++ (>22 breaths/min)










JVP height: (looks/confirms/measures/character) expects to be elevated >4 cm above sternal angle ++ (c/w CCF)




JVP character: mentions cannon „a‟ waves with type 3 complete heart block (possible cause of CCF) mentions giant „V‟ waves with tricuspid incompetence (as consequence of dilated CCF)




carotid arteries  student feels at cricoid cartilage, level C6, retracts SCM, palpates common carotid artery







hands (marks only given for relevant signs)


arms systolic BP: if they attempt give them 125/80  student may say possibly reduced in severe cases (<100 mmHg) face tongue & lips  looks for central cyanosis ++ (c/w CCF) neck

amplitude/volume  decreased ++ (c/w reduced CO) character/waveform  NAD (but mentions aortic valve dysfunction as possible cause of CCF)






position  displaced inferiorly and laterally +++ (c/w dilated „volume‟ overloaded left ventricle)




size  increased ++ >50 cent coin (c/w dilated „volume‟ overloaded left ventricle)




character  weak & diffuse ++ (c/w dilated „volume‟ overloaded left ventricle)




S1 & S2  both present, normal intensity (timed with carotid)




added sounds  S3 ++ (low pitched, mid diastolic „gallop rhythm c/w rapid diastolic filling into a dilated LV c/w CCF)




murmurs  listens between S1-S2 for mid systolic murmurs consistent with functional MI/TI secondary to dilated ventricles c/w CCF.




Global competency




apex beat (looks/feels for position, size, character)

heart sounds (due to time constraints, stop them after they have listened in one spot and ask for their findings and interpretation)



Examiner‟s Signature: ………………………………………………………………………….....................................................………


COMMENT ON APPROACH TO MSAT Clinical Exams Get on with things - examine each part, reach your conclusions and give your findings (precisely) as you go. Don't waste time. Don't talk about what you are going to do or about what you might do! Do each segment within each system, and give your findings and interpretation while you are continuing to proceed through the examination. Do not stop at any stage. For example In the CVS, give findings at each stage after completing your examination of the hands, the blood pressure, the neck (JVP), the heart (including auscultation of all areas), the lungs, the abdomen, the peripheral pulses, the optic fundi. By and large the examiners want to watch your examination performance in each segment, and are only interested in hearing your conclusions at the end of each stage, not in your speculations about what you might do! Examine the part correctly and efficiently, give your findings accurately and precisely and interpret them with decision. On management 1. First make sure diagnosis is correct, and that you have considered and excluded important reversible conditions (by investigational tests if necessary). 2. Problem list. Draw one up in complicated cases (often multiple problems in the elderly). 3. Define objectives of investigation and treatment: e.g. (a) (b) (c) (d) (e) (f)

are you looking for cure or palliation? investigation and treatment of functional manifestations. investigation and treatment of underlying pathology. investigation and treatment of underlying anatomical problem (e.g. coronary angiography and coronary artery bypass surgery, where indicated). investigation and treatment of underlying 'risk factors' for further recurrence (e.g. smoking and heart attack). primary preventative treatment. (e.g. hypertension treatment mainly for prevention of heart attack/ stroke. (Therefore treat other vascular 'risk factors' as well i.e. smoking, obesity etc.).

Conclusion The details of knowledge, clinical performance and diagnosis are now up to you. This book is meant merely to provide guidelines for allowing you to see the wood through the trees. Get on now and practise it.

PART VI â&#x20AC;&#x201C; CONCLUSIONS On history-taking 1. Did you use words the patient could not understand? 2. Was the patient's real problem concealed amongst your insignificant questions? 3. The best kind of history-taking is at the same time the best kind of psychotherapy.' (Ericson). On examination 1. Do not touch the patient at first - merely state what you see; this cultivates your powers of observation (after William OsIer). 2. The gentle touch of a good physical examination is at the same time an important means of reassurance and therefore healing. On diagnosis 1. When you hear hoof beats, think first of horses, not zebras. 2. 'Every psychoneurotic ultimately dies of organic disease.' 3. 'Never lose a holy curiosity.' (Einstein). 4. 'The great questions are those an intelligent child asks, and getting no answers stops asking ...' (George Wald). 5. 'Common sense is not common.' (Voltaire) On investigation 1. No patient was ever cured by a laboratory determination â&#x20AC;Ś or a radiograph. 2. The more questionable the indications for requesting a laboratory test, the greater the problems the answer will cause ... or ... Do a silly test and you get a silly answer. (Merskey's rule) On management 1. Littman's rule - the longer it takes for a condition to develop, the more time you should take to return the patient toward normal. 2. Life is not a drug-dependent state. 3. Always remember the old Egyptian proverb: 'Health is a crown on a well man's head, but noone can see it but a sick man'. 4. Exercise/Move or you die 5. The best (evidence-based) exercise is daily walking >20 min per session On information 1. 'To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.' (William Osler). 2

Textbooks of a previous generation were as large as the textbooks of today, but contained a different body of misinformation.


'Statistics are like a bikini. What they reveal is suggestive; what they conceal is vital ... (A. Koestler).

Finally, always remember Loeb's Laws of Medicine: (a) If what you are doing is working, keep doing it. (b) If what you are doing is not working, stop doing it. (c) If you don't know what to do, don't do anything. (d) Above all, never let a surgeon get your patient. 4.


Clinical Method