Foreword
1
Dr. A.K. Grover President, Ocular Trauma Society of India It is a great pleasure to write the foreword for the “handbook” on ocular trauma by Dr. Gopal Pillai, the current secretary of Cochin Ophthalmic Club. Ophthalmic trauma is estimated to be responsible for 1.6 million cases of blindness in the world with 23 million cases of low vision and 19 million with monocular blindness. A book on the subject that highlights the diagnostic, therapeutic and preventive aspects is therefore of great importance and most welcome. Prof. Gopal Pillai, head of the department of ophthalmology at the prestigious Amrita Institute of Medical Science, Kochi, has brought his immense experience as an eminent teacher, academician, clinician and surgeon to the fore in the Handbook. This is reflected in the superb choice of the authors and the subjects that cover the entire gamut of ophthalmic trauma. The subjects include classification of ocular trauma, pathophysiology, blunt trauma and open globe trauma. Clinical evaluation, diagnostic modalities and the legal aspects have received special attention. An atlas of ophthalmic trauma, adds to the value. I have had the privilege to know Prof Gopal Pillai for over two decades and have always appreciated his unlimited initiative, ability and enthusiasm. This book reflects those qualities well. The excellent choice of subjects and the well written text makes the book extremely useful both for the residents and the clinicians. The release of the Handbook on the ‘World Trauma Day” makes it particularly timely. Dr. A.K. Grover MD, MNAMS, FRCS, FICO, FAICO PRESIDENT, OCULAR TRAUMA SOCIETY OF INDIA PAST PRESIDENT, ALL INDIA OPHTHALMOLOGICAL SOCIETY (AIOS) ASIA PACIFIC SOCIETY OF OCULOPLASTIC AND RECONSTRUCTIVE SURGERY (APSOPRS) OCULOPLASTICS ASSOCIATION OF INDIA (OPAI) CHAIRMAN, DEPARTEMENT OF OPHTHALMOLOGY SIR GANGA RAM HOSPITAL & VISION EYE CENTRES, NEW DELHI.
Presidential Message: Asia Pacific Ophthalmic Trauma Society
2
Padmashri Dr. S. Natarajan President Asia Pacific Ophthalmic Trauma Society It’s a great pleasure to be writing this message for the Handbook of Ocular Trauma brought out by Cochin Ophthalmic Club by its enthusiastic secretary, Dr Gopal S Pillai, A renowned Vitreo-retinal surgeon. World trauma day is observed each year on October 17th to remember the basic theme- Prevention is better than cure. Preventing trauma by employing and adopting safety processes and adhering to those methods. Most of trauma, when we look at it could have been prevented. Many people who lose eyes in trauma had been careless or retrospectively, they all think, this would never have occurred if they had adopted a bit more safety precautions. I have been involved in management of ocular and ophthalmic trauma cases over past almost Four decades and the most important factors in the prognosis of trauma is its severity, time to intervention and expertise. As the key person who was involved as key VR surgeon in management of ocular and ophthalmic injuries of Jammu and Kashmir, I would want to say that expertise in management of ocular and ophthalmic trauma is a vital element in achieving success in extreme Trauma. Such Handbooks will act as ready references and many budding Ophthalmologists can get new points from these easily readable handbooks, as many large textbooks are so difficult to read and assimilate. Asia Pacific Ophthalmic trauma society offers advocacy, Pearls for prevention of ophthalmic trauma and Management. I wish Dr Gopal S Pillai and Cochin Ophthalmic Club all the best. PadmaShri Prof. Dr.S. Natarajan, President, Asia Pacific Ophthalmic Trauma Society www.APOTS.org
2
Presidential Message KSOS
3
Dr. Babu Krishnakumar Hon. President Kerala Society of Ophthalmic Surgeons
World Trauma Day. Trauma remains one of the maladies of humankind irrespective of changing centuries. Modalities of injuries have transformed through ages like, falling from a tree to falling from a building or animal attacks to vehicle accidents. From the necessity of keeping vigilance, World Trauma Day is observed on 17th of October every year. The day highlight the increasing rate of accidents and injuries causing death and disability across the world and the need to prevent them. Every year 5 million people die all over the world. Trauma is an injury to the body. It may be from Road accidents, Fires, Chemical Injury, Burns, Falls or Acts of Violence. Injuries produce disability that may be temporary or permanent affecting productivity.
Eyes are prone to trauma widely as indicated by statistical annotations that every year 55 million eyes are injured to varying severity. 750000 people are hospitalized related to trauma every year. Open Globe Injuries amounts to 200000. 1.6 million goes blind from injuries, 2.3 million left to bilateral low vision and 19 million affected with unilateral blindness or low vision. Severity of eye injuries are marked as 1. Potentially blinding bilateral injuries, 2. Open globe injuries, 3. Endophthalmitis, 4. Enucleation and 5. Defined Visual impairment.
Our role in checking trauma as ophthalmologists are in two ways. First is preventive and Protective and second is management aiming at salvaging maximum vision.
3
Presidential Message KSOS
4
Preventive aspect aims at making the public aware of the proneness to injury from workstations ranging from home, schools, roads to factories. We can conduct eye camps detailinging to them with the help of projecting slide shows, videos etc. Distribution of leaflets denoting types of accidents, methods to prevent it, necessary first aids and also about nearest ophthalmologists to be consulted with. Messages and interviews in media are extremely helpful in reaching the targeted groups. Demonstrate in your speech on various eye protective devises and how helpful they are in preventing injuries to eyes.
Manage the eye injury as an emergency with at most care and dedication. Identify the severity of injury and if facilities are not adequate with you don’t hesitate to refer to a higher Centre. Assure the patient and alleviate his anxiety while attending the affected and disclose the nature of severity to the close relatives. Withholding the nature of severity and not briefing properly may land you in unnecessary troubles. Proper care in time and judiciously will help the traumatized eye see the world happily.
Dr. Babu Krishnakumar Hon. President Kerala Society Of Ophthalmic Surgeons
4
Presidential Message - COC
5
Dr. S.J. Saikumar President, Cochin Ophthalmic Club As all of us are aware, October 17th th is celebrated all over the world as World Trauma day. Trauma day is usually observed to make people around aware about the safety precautions to be taken to prevent trauma. Eye injuries are a major cause of vision loss and morbidity. Hence this handbook on Ocular Trauma. We have tried to cover all the aspects of ocular trauma. Added to it is an Atlas with interesting images related to Eye trauma. I am sure this will be a collector’s item for all Ophthalmologists. I thank my Secretary, Dr Gopal S Pillai for his efforts in releasing this book. I also thank all the contributors for this book.
Dr. S.J. Saikumar Medical Superintendent and Head of Cataract and Glaucoma Services Giridhar Eye Institute Cochin 682020 President, Cochin Ophthalmic Club Vice President, Kerala Society of Ophthalmic Surgeons Chief Organizing Secretary, AIOC 2023
5
From The Editor’s Desk
Dr. Gopal S. Pillai Editor Dear friends, Trauma is a very accidental occurrence and completely change the fate of a person. Trauma may be due to road accidents, fires, burns, falls, and even violence. Road Traffic Accident (RTA) is the most common cause of ocular and other trauma and many injuries may lead to temporary or permanent visual disability. In India alone, it is estimated that one million people die and 20 million are hospitalized every year due to injuries. The burden of disease due to trauma is increasing at an alarming rate. Eye trauma constitutes 7% of all bodily injuries and 10%–15% of all eye diseases. Globally, there are approximately 1.6 million people who are blind from eye injuries, 2.3 million are bilaterally visually impaired, and 1.9 million have unilateral visual loss. Ocular trauma affects the national productivity on account of younger population being mainly involved in road accidents. Therefore, we should all take the required precautions in order to prevent any injuries. Treated in time and effectively, we can often prevent the permeant effects of ocular trauma and almost always, the thin line between excellent care and ordinary care can be a few minutes of good clinical examination and early intervention. This small book is a very humble attempt by the Cochin Ophthalmic Club to plug the gap between patient reporting and rapid effective treatment. I need to apologise that this is not a complete book in the subject and a best, it will guide you as a pocket companion in times of dire difficulty. However, we have made all attempt to make it extremely readable and useful.
6
From The Editor’s Desk I am thankful to all authors, who have spared no efforts in bringing out this book in the blink of an eye and I am sure that the effort will be taken with both hands by our fraternity. Sincerely hope that this will be a small, but firm step in the better management of ocular trauma patients. Finally, I would also like to thank all my colleagues in Cochin Ophthalmic Club and my post graduate students as well as post graduates from other institutes who have helped us in our quest to make this handbook, with a special mention to Dr. Yashovardhan Siwach who compiled all the data and images submitted and gave it a final finish overnight. Thanks, and regards
Dr Gopal S. Pillai MD DNB FRCS, Professor and HOD Ophthalmology, Amrita Institute, Kochi Secretary Cochin Ophthalmic Club Editor
7
INDEX S. No. a. b. c. d. e. f. 1. 2.
3.
Topic Foreword Message from the APOTS President Message from the KSOS President Message from the COC President From the Editor’s Desk Index Overview and classification of ocular Trauma Pathophysiology of Blunt trauma
7
Author Dr. A. K. Grover Padmashri Dr. S Natarajan Dr. Babu Krishnakumar Dr. S. J. Saikumar Dr. Gopal S. Pillai Dr. Rizana Mohamed
Page No. 1 2 3- 4 5 6- 7 8 9- 13
Dr. Natasha Radhakrishnan Dr. Lisa Maria George Dr. Divya Balakrishnan
14- 19
Dr. Gopal S. Pillai
25- 28
Dr. Sujitra H. Dr. CK Anusha Dr. Mariyan Pauly Dr. Remya S Dr. Vinay Pillai Dr. Sugaranjni G Dr. Anil Radhakrishnan
29- 36
5.
Pathophysiology of Penetrating trauma Clinical Evaluation of a patient with ocular trauma Acute Eyelid trauma and repair
6.
Late management of lid trauma
7.
Corneal trauma and laceration
8.
Scleral Tear and occult globe rupture and laceration
9.
Traumatic Hyphema
Dr. Karthika Mohandas
51- 58
10.
Traumatic Lens Injuries
59- 68
11.
Glaucoma following Ocular trauma
12.
Traumatic uveitis
13. 14. 15.
Retinal manifestations of blunt trauma Penetrating retinal trauma Retained intraocular foreign body.
16.
Traumatic Optic neuropathy
Dr. Saikumar SJ Dr. Sruthi R Dr. Manoj Prathapan Dr. Praveena Shyam Dr. Reesha KR Dr. Arunlal JS Dr. Rahul Menon Dr. Praveen Murali Dr. Remya Mareen Poulose Dr. Thomas Cherian Dr. Rehna Rasheed Dr. Kannisha Shah
17.
Ultrasound in trauma
120- 124
18.
CT and MRI Imaging in ocular trauma
19.
Trauma Atlas
Dr. Gopal Pillai Dr. Yashovardhan Siwach Dr. Rajesh Kannan Dr. Niya Joy Dr. Rehna Rasheed Dr. CK Anusha
4.
20- 24
37- 41 42- 45 46- 50
69- 77 78- 81 82- 84 85- 93 94- 102
103- 119
125- 128 129- 146
8
Handbook Of Ocular Trauma
Dr. Gopal S. Pillai Secretary Cochin Ophthalmic Club Editor
Dr. Babu Krishnakumar Hon. President Kerala Society of Ophthalmic Surgeons
Dr. S.J. Saikumar President, Cochin Ophthalmic Club
Dr. Anil Radhakrishnan Cornea and Refractive Surgeon Amrita Institute of Medical Sciences
Dr, Karthika Mohandas Consultant, Dr. Tony Fernandez Eye Hospital
Dr. Arunlal J.S. LF Angamaly
Dr. Divya Balakrishnan Senior consultant, Vitreo-Retina Services Giridhar Eye Hospital
Dr. Lisa Maria George MS Junior Resident, Amrita Institute of Medical Sciences
Dr. Manoj Prathapan Associate Professor Amrita Institute of Medical Sciences
Dr. CK Anusha MS Junior Resident, Amrita Institute of Medical Sciences
Dr. Kannisha Shah MS Junior Resident, Amrita Institute of Medical Sciences
Dr. Mariyan Pauly Senior Consultant & Head, Oculoplasty Giridhar eye Institute, Ernakulam
Handbook Of Ocular Trauma
Dr. Praveen Murali Dr. Natasha Radhakrishnan Dr. NIya K Joy Senior Consultant M.S.,D.O., DNB, MRCophth MS Junior Resident, Professor, Amrita Institute Amrita Institute of Medical Sciences Vitreo-Retina Surgery Eye Foundation Hospital of Medical Scienes
Dr. Rahul R. Menon Dr. Rajesh Kannan Senior consultant, Professor, Radiology Vitreo-Retina Surgery Chaitanya Hospital, Ernakulam Amrita Institute of Medical Sciences
Dr. Praveena Shyam MS Junior Resident, Amrita Institute of Medical Sciences
DR. Reesha K R Senior Consultant Uveitis LF Hospital, Angamaly
Dr. Rehna Rasheed Assistant Professor Amrita Institute of Medical Sciences
Dr. Remya Mareen Paulose Consultant VR Surgeon LF Hospital, Angamaly
Dr. Remya S.
Dr. Sugaranjini G Cornea Fellow Giridhar Eye Hospital
Dr. Rizana V Mohammed MS, FICO, MRCSEd
Dr. Sujithra H. Associate Professor Amrita Institute of Medical sciences
Dr. Vinay S Pillai HOD and Senior Consultant Cornea and Refractive surgery
Dr. Shruthi R.
Dr. Thomas Cherian Cheif of VR Surgeon LF Hospital, Angamaly
Dr. Yashovardhan Siwach MS Junior Resident, Amrita Institute of Medical Sciences
Trauma Overview Ocular Trauma: Overview & Classification Dr. Rizana V Mohammed MS, FICO, MRCSEd
Ocular trauma is an important cause of blindness in both developing and developed countries. This becomes particularly significant when it affects children who constitute approximately 30 % of total affected, because of the actual number of years they have to live blind. Though not a disease per se, this can be considered so because, this has got well established natural history, risk factors, prevention, classification and treatment methodologies. It is interesting to note that certain aspects of ocular trauma remain consistent over years: Bimodal age distribution-the first one in late adolescence to early adulthood, the second one in elderly population. Male predominance-because of comparatively more involvement of males in outdoor activities. Causes poor vision especially in poor socio-economic strata probably because of less access to specialised health care. Eye trauma constitutes 7% of all bodily injuries and 10%–15% of all eye diseases.[1] WHO reports that globally, there are approximately 1.6 million people who are blind from eye injuries, 2.3 million are bilaterally visually impaired, and 1.9 million have unilateral visual loss.[2],[3] It has been estimated that 90% of all ocular injuries are preventable. [4] Classification: Based on nature, ocular traumas can be broadly classified as Mechanical Injuries • Open Globe • Closed Globe Chemical Injuries • Acid • Alkali Thermal Injuries • Heat 9
Trauma Overview • Cold Radiation • Ionising radiations • Ultraviolet rays • Laser Burns Miscellaneous
Eye Injury Is a full thickness eyewall defect present?
NO
YES
Closed Globe
Open Globe
Is a partial thickness eyewall defect present?
Was the injuring object blunt or sharp?
NO
Contusion
YES Lamellar laceration
Blunt
Sharp
Rupture
Laceration
Same entry and exit wound
Retained Foreign body
Penetration
IOFB
Different entry and exit wouns
Perforation
10
Trauma Overview Birmingham Eye Trauma Society (BETTS) Classification of Ocular Trauma was introduced in 1996 by Kuhn et al to provide a clear definition of all injury types. It is widely accepted all over the world and is unambiguous, consistent and simple. [5] The term Eyewall is used to denote sclera and cornea. It is to be noted that all real world injuries do not fall strictly into one of the described categories. Such injuries are broadly termed as mixed mechanism injuries. How to prognosticate? The usual questions that physicians encounter are “Will I go blind ? ” or “Will I get my vision back?” Poor presenting visual acuity, RAPD, Retinal detachment, presence of large sclera lacerations are poor prognostic indicators for final visual outcome. Ocular Trauma Score[6] Allows physician to estimate probability of visual acuity recovery. Six variables which affect the visual prognosis are assigned a raw score, the sum of which is broken into five categories. How to use OTS system? Assign an initial raw score based on the presenting visual acuity (VA) – see A in Table 1. From this initial raw score, subtract points for each of the factors B to F in Table 1. Once the raw score sum has been calculated, find the relevant category in Table 2 and find the corresponding OTS score. For each OTS score, Table 2 gives the estimated probability of each follow-up visual acuity category.
11
Trauma Overview
Limitations of OTS: Does not consider facial and adnexal injuries which may have a bearing on visual prognosis. Does not include other associated injuries like chemical, thermal, electric etc which can affect visual outcome. Does not have a provision to consider imaging reports like Ultrasound B scan, CT, MRI etc. It must be remembered that OTS is just an arbitrary estimate to prognosticate visual acuity recovery and a guideline to make informed treatment decisions. While discussing the prognosis, individual case scenario must be thoroughly 12
Trauma Overview studied and counselling must be based on clinical experience and most importantly common sense. The patient’s emotional status must be valued and he must be involved in decision making processes. For traumatic cases, visual recovery is a long process which may need multiple interventions in multiple settings. This must be clearly explained to the affected before taking up for reconstructive surgeries. References: 1. Acar U, Tok OY, Acar DE, Burcu A, Ornek F. A new ocular trauma score in pediatric penetrating eye injuries. Eye (Lond) 2011;25:370-4. 2. Négrel AD, Thylefors B. The global impact of eye injuries. Ophthalmic Epidemiol 1998;5:143-69. 3. Pizzarello LD. Ocular trauma: Time for action. Ophthalmic Epidemiol 1998;5:115-6. 4. Hutton WL, Fuller DG. Factors influencing final visual results in severely injured eyes. Am J Ophthalmol 1984;97:715-22. 5. Kuhn F, Morris R, Witherspoon CD. Birmingham Eye Trauma Terminology (BETT): Terminology and classification of mechanical eye injuries Ophthalmol Clin N Am. 2002;15:139–43 6. Kuhn F, Maisiak R, Mann L . The ocular trauma score (OTS). Ophthalmol Clin North Am 2002; 15: 163–165.
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Blunt Trauma Pathophysiology of Blunt Trauma. Dr. Natasha Radhakrishnan M.S.,D.O., DNB, MRCophth Professor, Amrita Institute of Medical Sciences Kochi
Dr. Lisa Maria George MS Junior resident, Amrita Institute of Medical Sciences Kochi
Blunt trauma is the most common type of injury in both adults and children. Blunt trauma affects all the structures starting from anterior segment to optic nerve. In this chapter we will discuss the pathophysiology of blunt trauma. The most common causes of blunt trauma are shuttle cock injuries, football injuries, champagne corks and tennis balls. Apart from the acute effects in the eye produced by the injury blunt trauma is known to have guarded prognosis due to long term effects of the trauma. Pathophysiology: The mechanism of damage to the eye in blunt trauma is the result of anteroposterior compression of the eye ball with simultaneous expansion along the equator which causes transient and severe increase in IOP. This results in the posterior displacement of lens – iris diaphragm which in turn transmits mechanical shock waves on to the retina. The fluids of the eye cannot be compressed. They expand following a trauma which completely disrupts the normal architecture of ocular tissue. Following a closed globe injury the ocular structures that are anterior to equator which have a circumferential orientation are
14
Blunt Trauma damaged.
This
results
in
the
seven
rings
of
trauma.
Figure 1- Transmission of force from anterior blunt injury to the posterior segment.
The Seven Rings of trauma are: 1. 2. 3. 4. 5. 6. 7.
Iris sphincter tear Iridodialysis Cyclodialysis Angle Recession Trabecular Meshwork Tear Zonular dialysis, Subluxation of lens Retinal dialysis, Tears
1. Iris Sphincter tear: -The sphincter pupillae supplied by parasympathetic nervous system is the involuntary muscle that aids miosis. It is seen at pupillary margin and is 0.75mm wide. Radial sphincter tears at the pupillary margin of iris occurs due to the stretching and this causes traumatic mydriasis. 2. Iridodialysis: - D shaped pupil is seen when there is separation of iris root and ciliary body which is also called iridodialysis. Damage to pigment layer of iris characteristically occur at the root of iris and such lesions are best seen with retro illumination. Circumferential synechiae can block the flow of aqueous from exiting posterior chamber causing increased pressure and distend the iris forward called iris bombe. Iris Prolapse, uveal tissue prolapse, iritis, Iridodialysis, tears of 15
Blunt Trauma the pupillary margins causing sectorial or focal defect are common complications. Both mydriasis and miosis can be seen. Permanent traumatic mydriasis can be one of the complications of blunt trauma. Miotic iris can be seen as a consequence of iris inflammation. 3. Angle recession: - Anterior ciliary body trauma can be seen in gonioscopy as angle recession where there is longitudinal tear of ciliary body separating circular fibres from longitudinal fibres. On gonioscopy posterior to scleral spur, posterior displacement of iris root and widened ciliary body band can be appreciated. There is damage to trabecular meshwork which can lead to glaucoma later on. Angle recession also contributes to development of glaucoma. Angle recession is the most common finding after contusion. Acute injury shows brown coloured, broad angle recess, glistening white scleral spur and depression in overlying trabecular meshwork. Gradually peripheral anterior synechiae is seen at the border of recession or anywhere in the angle and damaged iris processes. Foreign body in angle must be looked for diligently. Gonioscopy is contraindicated in the setting of ruptured globe as it can cause extrusion of intraocular contents. 4. Cyclodialysis: - results in cyclodialysis cleft and exposes the internal scleral wall. The early common complication is hypotony due to free passage of aqueous from anterior chamber to the suprachoroidal space. Long term sequelae is ocular hypertension once the cyclodialysis cleft closes with resistance to aqueous outflow. 5. Trabecular meshwork: - Tear of trabecular meshwork or flap at the point of rupture may occur in blunt trauma. 6. Zonular dialysis: - Subluxation or dislocation of crystalline lens can be seen in zonular dialysis. Phacodonesis is caused due to zonular dialysis. Vossius ring of iris pigment on anterior lens capsule may be see due to impression of posterior iris on lens produced by concussive force driving iris posteriorly onto the lens. Traumatic cataract which can be seen as total cataract where no clear lens matter is seen between the capsule and nucleus, membranous cataract where a membrane of varying density is formed due to fusion of capsule and organized matter, white soft fluffy cataract consisting of loose cortical matter along with ruptured lens capsule and rosette cataract. 7. Retinal dialysis/tears: - Disinsertion of the retina at the ora serrata is called Retinal dialysis. Most common site is inferotemporal quadrant but superonasal dialysis is pathognomonic of trauma.Tobacco dust also called Schafers sign is the visualization of pigment granules from RPE in anterior chamber which is pathognomonic of a retinal break. 16
Blunt Trauma Other Clinical features with their pathophysiology
Figure 2. Ruptured globe after blunt trauma. Note total hyphema, lid swelling, and distortion of globe.
Anterior segment and ocular adnexa The medial wall and floor are the most common orbital fractures involved. A fracture of the medial orbital wall occurs with break in the paper-thin lamina papyracea, which separates the orbit from the ethmoidal sinus. There could be damage to the lacrimal system. An orbital blowout fracture refers to a fracture of the orbital floor without involvement of the inferior orbital rim. Posteromedial floor near the infraorbital groove is the weakest part of the bony orbit.
Figure 3. Left orbital floor fracture on a coronal CT scan. 17
Blunt Trauma Mechanical strabismus is seen when a fractured bone, springing back tethers the prolapsed tissue. Enophthalmos is seen when there is Prolapse of orbital fat and Extraocular muscles, herniation of them into maxillary sinus, proptosis. Eyelids has loose areolar tissue and blood collects in this space leading to ecchymosis. Mechanical ptosis may be seen due to lid edema. Subconjunctival hemorrhage is one of the common findings in blunt trauma. A bullous subconjunctival hemorrhage indicates possibility of scleral involvement. Corneal abrasions and epithelial defects can occur. Corneal edema can result from endothelial dysfunction and high IOP. Formation of Descemet’s folds represent corneal endothelial damage. Hyphema is caused by shearing forces from the injury that tears the vessels over iris, ciliary body, Trabecular meshwork. Vitreous and Retina: Vitreous involvement presents with symptoms of floaters and flashes. Detachment of the vitreous base leads to retinal tears. Avulsion of vitreous base is pathognomonic feature of previous ocular trauma. Vitreous can be seen prolapsing into the anterior chamber. Vitreous hemorrhage is caused due to the rupture of fine retinal blood vessels due to compression and blood enters the vitreous cavity through internal limiting membrane. Vitreous cells with special interest for WBCs should be checked as it could be indicator of traumatic endophthalmitis. Retinal pathologies include abnormalities like Berlin’s edema, retinal tears. Berlin’s edema is caused due to damage to the retinal pigment epithelium and photoreceptor cell loss and thinning of the outer nuclear and outer plexiform layers. As retina is not an elastic structure it takes the full effect of shock waves caused due to blunt injury and posterior displacement of lens – iris diaphragm which result in injury to various layers. Restoration of photoreceptors outer segments begins at 1 week and takes over 2 months for complete recovery. Normal fundus appearance is restored within 1 week and later pigmentary changes can be seen depending on severity of injury. Retinal tears with the superonasal and inferotemporal quadrants being most commonly involved sites for tears is the other complication in blunt trauma. Choroidal ruptures are indirect ruptures and the common site is in the posterior pole away from the point of impact. Vitreous Hemorrhage can obscure the view of these tears. They appear as crescent shaped and are found concentric to the optic disc. Foveal involvement can result in visual loss.
18
Blunt Trauma Optic nerve: The nerve head appear normal initially, but the pupillary examination can help detect optic nerve injury. A hidden optic nerve injury is easily picked up in simple pupillary examination. Abnormal pupil shape, Abnormal pupil reflexes in case of damage to optic nerve, Relative Afferent pupillary defect must be looked for. Sudden elevation in intraocular pressure during blunt trauma results in rupture of lamina cribrosa and avulsion of optic nerve. The factors responsible for this injury are forceful rotation and forward displacement of the globe. References: Ocular trauma : acute evaluation, cataract, glaucoma – aao.org Blunt Force trauma – Simon LV, Lopez RA, King KC. August 11, 2021 Anterior Segment consequences of blunt ocular injury YM CANAVAN and DB ARCHER, British journal Ophthalmology, 1982 Albert and Jakobiecs Principles and Practice of Ophthalmology – Third edition
19
Penetrating Trauma Pathophysiology of Penetrating trauma. Dr. Divya Balakrishnan Senior consultant, Vitreo-Retina Services Giridhar Eye Hospital
A penetrating ocular injury is a full thickness tear of the globe with a sharp object with a single entry wound and no exit wound by the Bermingham Eye Trauma Terminology (BETT) definition.[1] It may or may not be associated with an intraocular foreign body (IOFB). If more than one entry wounds are present, then it should be with multiple objects. It can occur either by a sharp object or by a high velocity object like bullets or metal piece. Penetrating injuries are usually associated with intraocular foreign body embedded in the eye. The common materials are wood, metals and stone. The incidence of penetrating eye injury is around 3.1- 4/1000, 000 population.[2] Penetrating trauma accounts for 27 to 80% of the cases of ocular trauma in literature review.
[2, 3]
Etiology of penetrating injury: The various causes of penetrating trauma were occupational injuries, falls, sports injuries, road traffic accidents, blast injuries and fire work injuries. The usual modes of injuries were with sharp objects like stick, pencil, pen, arrow, needle, glass, stone and metal pieces. The common settings where injury occurred varied 20
Penetrating Trauma from workplace to household in different studies. This difference in observation indicates the difference in etiology, time period and location in various studies. The reported incidence of penetrating trauma at workplace was 45.8%. [3] A study by Fujikawa et al had shown that common causes of injury in males were workrelated, while it was fall in females and the mean ages were 51.3 ± 18.1 years for the work-related trauma and 61.1 ± 8.8 years for the falls. [4] The common professional groups involved with increased ocular injuries were those involved in farming, manufacturing, welding, mining, plumbing, electrical works, carpentry, carving stones or breaking and chiseling rocks. The modes of ocular trauma varied in different age groups. In geriatric age group, the common causes of ocular trauma were found to be fall, wood strike and knife touch. [5] Various studies reported that penetrating injuries account for 15 -50% of eye injuries in geriatric age. [5, 6] Males were found to be more affected in most of the studies except one where both were equally affected. [7, 8] Study by Zamani M et al found that zone 1 injuries were more, while others reported zone II and III injuries were more in elderly. [5, 8] The final visual outcome was found to be worse in this age group.[8] A majority of them had a previous history of intraocular of intraocular surgery. Ocular injury in children occur more in preschool children (2-7 years).[9, 10] A study by Pereira RM et al reported that most of the injuries in children occurred at home(74.4%) and preschool children (2-6 years) were commonly affected. [10] Children in this age group have lack of co-ordination, inability to escape from danger and curious mind to explore which exposes them to dangers. But a study by Prakash et al from India reported ocular trauma to be more prevalent in the age group from 11- 15 years. Children are usually injured with pencil, pen, arrow and needles. Most of the children get injured while at school, home or street. 21
Penetrating Trauma Mechanism of injury: The extend and type of damage depends on the size, composition and velocity of the object at the time of impact. A high velocity object can cause damage to the tissues due to the kinetic energy. The energy transfer by a sharp object in a small area causes tissue penetration causing a single entry wound. A sharp object can cause conjunctival laceration, corneal lacerations, traumatic cataract, vitreous hemorrhage, retinal breaks and retinal detachment. The presence of subconjunctival hemorrhage with pigments indicates an underlying injury. Cornel injuries were more common in penetrating injuries. The presence of subconjunctival hemorrhage with pigments indicates an underlying injury. The presence of iris hole indicates a high chance of IOFB. In cases with high suspicion of IOFB, the inferior angle at 6 O’clock in anterior chamber and inferior pars plana region should be carefully examined for IOFB. Most of the penetrating injuries happen in the inferior part of globe as many of them have strong Bells and the eye ball moves up when encounter any obstacle. The effects of penetrating trauma occur due to the direct mechanical injury at the site, introduction of infection leading to endophthalmitis and late complications like sympathetic ophthalmia and phthisis bulbi. Prognostic factors: Zone III injuries, wound size larger than 5 mm, co-existing ocular damage like expulsion of crystalline lens, retinal detachment (RD) and vitreous hemorrhage were found to be poor prognostic factors.[3]Ocular trauma score (OTS) was found to be an accurate predictive tool for final visual acuity.
[11]
Ho et al reported that
presenting visual acuity, mechanism of injury and retinal detachment were the
22
Penetrating Trauma prognostic factors. Penetrating injuries and IOFBs did very well compared to globe rupture in their study.[12]
A detailed history about the circumstances and mode of injury is extremely important while dealing with ocular trauma as it gives a clue to the possible type of ocular injury. Penetrating injury while chiseling or hammering increases the chances of intraocular foreign body (IOFB). Type and mode of eye injury is important to decide on the management and prognosis. References: 1.
Kuhn, F., et al., A standardized classification of ocular trauma. Ophthalmology, 1996. 103(2): p. 240-3.
2.
Chang, Y.S., et al., Major ocular trauma in Taiwan: 2002-2004 versus 2012-2014. Sci Rep, 2018. 8(1): p. 7081.
3.
Islam, M.S., A.H. Golam Quddus, and A.R. Foroushani, Pattern of ocular injuries in Bangladesh and its surgical management at hospital setting: A retrospective study. J Pak Med Assoc, 2019. 69(Suppl 1)(1): p. S17-S20.
4.
Fujikawa, A., et al., Visual outcomes and prognostic factors in open-globe injuries. BMC Ophthalmol, 2018. 18(1): p. 138.
5.
Zamani, M., et al., Open globe injuries in geriatric population in Iran: characteristics and outcomes. Int J Ophthalmol, 2021. 14(8): p. 1237-1240.
6.
Kavoussi, S.C., et al., Characteristics and outcomes of fall-related open-globe injuries in pseudophakic patients. Clin Ophthalmol, 2015. 9: p. 403-8.
7.
Yuksel, H., et al., Etiology and prognosis of penetrating eye injuries in geriatric patients in the Southeastern region of Anatolia Turkey. Ulus Travma Acil Cerrahi Derg, 2014. 20(4): p. 253-7.
8.
Andreoli, M.T. and C.M. Andreoli, Geriatric traumatic open globe injuries. Ophthalmology, 2011. 118(1): p. 156-9.
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Penetrating Trauma 9.
El-Sebaity, D.M., et al., Pediatric eye injuries in upper Egypt. Clin Ophthalmol, 2011. 5: p. 1417-23.
10.
Pereira, R.M., et al., Epidemiology of Ocular Trauma in a Pediatric Referral Unit, Sao Paulo, Brazil. Indian Pediatr, 2021. 58(6): p. 589-590.
11.
Shrestha, S.M., et al., Factors affecting final functional outcomes in open-globe injuries and use of ocular trauma score as a predictive tool in Nepalese population. BMC Ophthalmol, 2021. 21(1): p. 69.
12.
Ho, H., et al., Prognostic factors and epidemiology of adult open globe injuries from Western Sydney: a twelve-year review. BMC Ophthalmol, 2021. 21(1): p. 173.
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Trauma Evaluation Evaluation of a Patient with Ocular Trauma. Dr. Gopal S Pillai MD DNB FRCS Professor and HOD, Ophthalmology Amrita institute of Medical Sciences, Kochi
General Considerations: Most cases of ocular trauma present in an emergency situation and may be part of a multi-region trauma including head injury, maxillofacial as well as more severe life-threatening injuries. Hence the evaluation of ocular trauma in such a situation should be fast, triaging as well as directed to find out the severity of eye injury as also risk to life. Airway, breathing and circulation should be evaluated in the first 10-20 seconds in such an acute presentation. A rapid systemic survey of mental status, chest and abdomen as well as a skeletal survey is often needed. In cases where the patient presents late, we will have ample time to ask for a clear history and lead of events and properly evaluate the patient in full detail. Always think that the initial evaluation will always be subject to legal evaluations on a later date so that documentations are very important. Let children stay with their parents to avoid tension. Even if injury is serious, avoid giving that indication at the beginning, either by what you say to patients, what you say to other staff members, or through your facial expressions. Treat patients with courtesy, even if the cause of their injury is as the result of a fight. Give oral analgesics as needed. History taking: An accurate and well documented history, with exact nature of injury as well as the actual objects will go a long way in ascertaining the pathophysiology of injury and its impact. Many times, there are pressure situations for patients who may give false histories. It is important that we correlate the history to the clinical examination findings to see that the connection to the trauma and its effect be established. Address these questions to the patient: 1. What was the eye condition before the trauma in terms of vision and surgeries done? 2. When did trauma occur? 3. What was the exact nature of the trauma? 25
Trauma Evaluation 4. What were the actual materials involved in trauma? 5. What was done for the trauma? 6. Spectacles/ Contact Lens? 7. Loss of consciousness? 8. What are the systemic diseases that he has? 9. Any other area of trauma? 10. Current situations in terms of vision and symptoms
Examination of the ocular trauma eye: It is always advisable to do the ocular examination as soon as possible after trauma as edema may set in fast and further evaluation may become more difficult. It should be fast, complete and well documented for further legal procedure. External inspection: Inspection in a diffuse illumination can give a lot of insight regarding the outer part of the eye including the orbit, lids and adnexa. Edema, blood, laceration, foreign bodies, enophthalmos or exophthalmos and position of eye can be easily found out by inspection. If there is lid involvement, canaliculi need to be evaluated carefully. Palpation: With feeling the orbital margins and looking for any cracks or foreign bodies, we can easily assess that area. Crepitus, air, subcutaneous foreign bodies and fractures can be made out. Visual acuity: Vision is a very important decision maker in management of most cases and is an important document in legal point of view. Snellen’s, ETDRS, Reduced Snellen’s or near vision charts can be used at the bedside first before the patient can be taken up for a detailed evaluation. Even if we are examining a patient where proper facilities for vision evaluation are not there, we have to document approximate vision and the method with which we reached that vision. Visual Fields: Confrontation visual fields can be a very rapid method to find out gross defects which may occur in massive intraocular hemorrhage, retinal detachment or optic nerve problems.
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Trauma Evaluation Pupils: One of the most important examinations to find out if there is significant involvement of the intraocular structures affecting the visual pathway. Size of the pupil and comparison with the other eye gives us information about the local trauma as well as brain status. Shape of the pupil will give us information about local trauma effects Pupillary reaction will give us information regarding the afferent visual pathway Intraocular pressure: Even a digital IOP evaluation can help us determine whether there is a rupture of the globe, as much as possible try to document an IOP and if not possible, can measure it digitally. In retinal detachment, choroidal detachment, ciliary body injury or phthisis bulbi, we may have reduction of IOP. Traumatic glaucomas can cause high IOP. Ocular movements: Both ductions and versions will help us determine if there is any problems with the muscles or entrapments, cranial nerve injuries or mechanical problems. Slit lamp Examination: After the initial triage, a later more detailed exam of the affected eye with slit lamp will help us look at the finer aspects of trauma and will improve our understanding about the pathophysiology and thus the prognosis of the traumatic eye. We should spend enough time to look at: Lids and lid margins for any laceration, edema, foreign bodies, canalicular area. Conjunctiva: - both bulbar and palpebral conjunctiva for lacerations or foreign body. Sclera to be carefully scanned for any rupture, entry wound or inflammation. Cornea is easily visible and any foreign body, trauma and laceration can be picked up easily. Anterior chamber for regularity, hyphema, hypopion or any other abnormality. Angle of the eye may need evaluation after 2 weeks after the acute trauma as recessions can be picked up, the gap of two weeks is to prevent recurrence of hyphema. Lens can get injured by blunt or penetrating trauma.
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Trauma Evaluation Iris will get involved if there is perforation and iris prolapse or change in pupillary shape may be noticed. Retrolental area to look for blood or cells. Retinal examination: Usually, we can use a slit lamp bio-microscopy with 90 D lens for the posterior pole evaluation. Retinal periphery can be looked at with indirect ophthalmoscope. Indentation indirect ophthalmoscopy is usually reserved for 2 weeks after the trauma to prevent manipulation or recurrent hyphema. Ocular Imaging: X-ray, Ultrasonography, CT, MDCT or MRI may be utilized judiciously as the clinician feels fit. If there is any evidence of RIOFB, all possible methods should be employed to find out where it is localized. Moreover, it will give excellent information regarding posterior structures which we find difficult to see with slit lamp or retinal examination. Photo documentation: As much as possible, try to photo document the ocular trauma from various angles and save in the file. These files may be helpful later. What you need for trauma evaluation at your centre:
Visual acuity chart Torch Cotton buds Lid speculum Eye shield (plastic/metallic) Local anaesthetic drops Antiseptic, e.g. iodine solution Tetanus toxoid Analgesics Irrigating fluid Topical anaesthetic drops Gloves for examination Additional (in an ideal scenario) Slit lamp Tonometer Magnifying loupe Direct ophthalmoscope Eye pads Fluorescein strips Litmus paper Cycloplegic drops Topical and systemic antibiotics 28
Eyelid Trauma- Acute Acute Eyelid Trauma and Repair Dr. Sujithra H Associate Professor, Oculoplasty Amrita Institute of Medical Sciences Kochi
Dr. C.K.Anusha MS Junior Resident, Amrita Institute of Medical Sciences Kochi
Introduction: Eyelids provide mechanical protection to the eyeball. Normal blinking action helps in even distribution of tear film over the ocular surface. Any damage to the lid causes anatomical disruption of the ocular surface thereby compromising its functionality. Injuries to the lids may also be associated with trauma to the head and neck region. It is mandatory to rule out cervical spine injury and provide stabilization if necessary. If adnexal injury is significant, intravenous antibiotics should be administered. Tetanus toxoid 0.5 ml should be administered if the patient has not had taken it in the last 5 years. Proper analgesia should be provided. Precise repair of the eyelid laceration is important so as to obtain good cosmetic and functional outcomes. Evaluation: A carefully gathered history about the mode and type of injury is of utmost importance. Mechanism of injury can indicate depth of the wound and the possibility of presence of a foreign body. Decrease in vision suggests injury to the optic nerve or globe. Diplopia, hypesthesia and painful eye movements could indicate an orbital fracture. Pain on jaw movement also suggests bony trauma. A history of previous ocular abnormalities, systemic medications and known allergies has to be taken. As surgeries are usually under general anesthesia, recent food or liquid intake (including alcohol) should be noted. Examination: - It is done under 4 steps:
Ocular examination. Soft tissue adnexal examination. Orbital evaluation. Examination of the face.
Ocular examination: Conscious patient: - Visual acuity, pupillary response, slit lamp examination, IOP and detailed fundus examination should be performed. 29
Eyelid Trauma- Acute Unconscious patients: - Maximum possible examination should be performed. For some cases examination under anesthesia is necessary, because trying to manipulate the lids can cause further injury to the globe. Adnexal examination: While examining adnexa lid position, levator function, extent and depth of laceration, involvement of canaliculus and lid margins are to be noted. Specific signs of canalicular injury include laceration medial to punctum and lateral punctal displacement. Orbital evaluation: Orbital evaluation includes the following: Extraocular muscle movements, range of motion and diplopia in all gazes. Hypo-aesthesia of cheek, side of nose, upper lip and gum. Palpation of bony orbital rims for evidence of fractures. Imaging: - CT/ MRI should be done for evaluating suspicion of intraocular foreign body, optic nerve status (entrapment/ strut fractures/ other injuries). If a metallic foreign body is suspected MRI is contraindicated. Photographing and complete documentation of all the findings is crucial. Examination of face for other injuries should be done. Wound care and basic principles: A wound should be closed as early as possible unless indicated otherwise. In patients with concurrent systemic illness, hemodynamic instability, ethanol intoxication, life threatening injuries or dog bite, wound repair can be delayed. An open globe should be treated prior to repair of the soft tissue. If immediate wound repair cannot be performed, one can safely wait 24 to 48 hours without an increase in the complication rate or poor long-term outcome, until then tissues should be repositioned into their anatomic position as closely as possible. Careful tissue saving debridement with thorough wound exploration and removal of all foreign bodies if any has to be performed. Pre-operative radiographic mapping of foreign bodies may be of great help.
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Eyelid Trauma- Acute Next step is to re-establish the integrity of 5 basic components of the eyelids:
Anterior lamellae – skin and orbicularis Posterior lamellae – tarsus and conjunctiva Canthal tendons Upper and lower canaliculi Levator complex
Often, mere retraction of the wound margins may appear as tissue loss, which should be properly assessed and taken care of while operating. Fat prolapse through the lacerated wound is indicative of deep injury involving orbital septum. Under such conditions exploration of the wound for deeper injuries or foreign bodies should be looked for. Septum should not be incorporated in any repair of the lids as it can lead to marked lid retraction and lagophthalmos. Lid lacerations can be broadly divided into: Lacerations involving eye lid margin Lacerations not involving the eyelid margin Lacerations involving canaliculi Lacerations with tissue loss Lacerations due to animal bite Surgical aspects: 1. Lacerations involving eyelid margin. Step 1. (figure 1A): Non absorbable 6-0 silk is used to approximate eyelid margin. 2 or 3 sutures are made at eyelid margin passing through lash line, gray line and meibomian gland plane. Sutures are tied and left long. Step 2. (figure 1B): Absorbable 6-0 vicryl is used to close the orbicularis muscle and tarsal plate. The tarsal sutures should not extend through the conjunctival surface avoiding corneal epithelial damage. Step 3. (figure 1C): non absorbable 6-0 silk is used to close the skin. Tails of the margin sutures are brought down and tied along with the skin sutures to prevent corneal epithelial disruption. Accurate suture placement with adequate suture tension has to be ensured so as to obtain good cosmetic and functional outcome. Eyelid margin closure should result in a moderate eversion of the well- approximated wound edges. Anterior skin sutures are removed at 5th post operative day and lid margin sutures are removed at 10-14 days. 31
Eyelid Trauma- Acute
Figure 1: Steps during the repair of eyelid laceration involving lid margin.
Figure 2: Pre and post operative picture of eyelid laceration involving lid margin.
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Eyelid Trauma- Acute 2. Lacerations not involving eyelid margin. Superficial wounds with minimal involvement of orbicularis muscle can be managed by suturing the skin alone with non absorbable 6-0 silk. Orbital fat prolapse in an upper eyelid wound indicates that there is violation of orbital septum and possibility of injury to levator muscle or its aponeurosis. Careful repair of the levator muscle or its aponeurosis must be done to avoid ptosis. Orbital septum lacerations should not be sutured. Meticulous closure of orbicularis muscle with 6-0 vicryl and skin with 6-0 silk should be done. 3. Lacerations involving canaliculi. Canalicular involvement should be suspected when there is laceration medial to the punctum with lateral displacement. Step 1: Anesthetize the medial canthus with 1% to 2% lidocaine and epinephrine. Step 2: Punctum is dilated with punctum dilator following which probing is done to locate the lateral cut end. Medial cut end can be identified by direct visualization under microscope. If it is not visible then the medial cut end can be identified by the egress of fluid while irrigating fluorescein stained saline through the opposite normal punctum. Step 3: A mono-canalicular stent is passed through the punctum, lateral cut end and the medial cut end. Step 4: Peri-canalicular tissue is sutured using absorbable 6-0 vicryl. Step 5: repair of eyelid wound should be done in layers.
Figure 3: pre and post operative picture of eye lid laceration involving medial canalicus.
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Eyelid Trauma- Acute 4. Lacerations with tissue loss If the defect is too large to be closed directly, transposition or advancement skin flaps may be used. Anterior lamellar upper eyelid defects are best repaired with full thickness skin graft from the contralateral upper eyelid. For lower eyelid defects preauricular or postauricular skin graft may be used. For reconstruction of full thickness eye lid defect either the anterior or the posterior lamella is reconstructed with graft and the other layer with pedicle flap with blood supply. A graft placed on graft has high failure rate. Tarso-conjuctval grafts are good substitutes for posterior lamellar eyeid defects. Conjunctival defect can be repaired with buccal mucosal graft.. Hard palate composite graft can also be used for posterior lamellar defect in lower eyelid. Cutler-Beard procedure may be done to reconstruct full thickness central eyelid defect. For reconstruction of large defects in upper eyelid, lower eyelid switch flap or medial forehead flap with tarsoconjunctival graft may be used. Large defect in lower eyelid can be reconstructed with tarsoconjunctival graft with skin flap ( Hughes procedure), or Tarsoconjunctival flap from upper eyelid and skin graft, or composite graft with cheek advancement flap( Mustarde flap).
Figure 4: Tarso-conjunctival graft - Upper lid
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Eyelid Trauma- Acute
A B C Figure 5: A: Cutler-Beard procedure B: switch flap C: medial forehead flap
Figure 6: Tarso-conjunctival graft - lower lid.
A
Figure 7 A: Tarso-conjunctival flap,
B
B: Mustarde flap
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Eyelid Trauma- Acute
Figure 8: Pre and post operative picture of upper eye lid avulsion injury lid with full thickness lower lid laceration involving lid margin.
Animal bites: Tetanus and rabies protocols should be observed. Wound should be thoroughly and extensively washed with soap and water. Povidone iodine or antiseptic with anti-viral activity should be applied. Eyes, that are exposed should be thoroughly rinsed with water. Systemic antibiotics should be given. Large and deep wounds are best treated by daily dressing followed by secondary suturing. In some cases where suturing cannot be avoided, wound should be thoroughly cleaned and infiltrated with immune globulin. We should wait for few hours to allow diffusion of immunoglobulins into the tissue layers. Minimal suturing is done to oppose the wound margins.
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Eyelid Trauma Late repair in lid trauma. Dr. Mariyan Pauly Senior Consultant & Head, Oculoplasty Giridhar eye Institute, Ernakulam
Dr. Remya S. Giridhar Eye Institute, Ernakulam
Introduction: - In lid tears, proper primary repair should be done to minimise sequalae. If late repair is done ideally should wait for 3-9 months for the inflammation to subside. Adequate measures should be taken to minimise infection and scarring. It is not uncommon in extensive traumatic eyelid repair to require secondary surgery. Till the secondary surgery temporary measures – tarsorhaphy /skin graft can be done. Anti scar Treatment: - The following measures can be done as after primary repair to prevent scars: Avoid direct sunlight Start scar massage after suture removal Scar reducing creams Silicone gel sheet (Fig-1)
Figure 1: Sequelae of lid tear repair are: Notching with trichiasis Lagophthalmos Ectropion/Entropion Canalicular block Canthal malpositions Ptosis
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Eyelid Trauma
Figure. 2A
Figure. 2B Fig. -2 A & B: -Notching with trichiasis occurs when the lid margin is not aligned correctly . It can be managed by wedge resction. Lagopthalmos Occurs from unrecognised tissue loss, scarring or incorporation of septum into the superficial wound. Prevention is the key, but once occurred it can be corrected by vertical lid lengthening, lengthening of skin and muscle with skin graft. Ectropion occurs from anterior lamellar deficiency. Mild ectropion can be corrected with anti-scar treatment. if refractory it can be managed with scar revision with Z plasty or skin graft.
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Eyelid Trauma
Fig. 3A 2 months RTA
Fig. 3B Post scar treatment.
Fig. 3C FTSG
Fig. 3D 1 month post FTSG
Z plasty-Single/multiple is used for localised scar • Each Z increases the length of wound by 30 % & redirects it by relaxing the area under tension.
Figure 4.
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Eyelid Trauma Traumatic Ptosis :
Figure. 5 Occurs due to: Lid oedema Lid avulsion Assoscaited with fractures of roof with foreign bodies Post-contusional ptosis Cicatricial ptosis Neurogenic ptosis Post-surgical ptosis Management: - Wait for 6- 12 months for spontaneous improvement. If not improving can have ptosis correction based on the action of levator muscle. Lacrimal Drainage Obstruction
Managed with DCR +/-Intubation. Late repair of canaliculus with trephination and minimonoka can be done Bicanalicular Block managed with CDCR Botulinum toxin is another option.
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Eyelid Trauma Eyelash And Eyebrow Loss : Options are: Artificial eye lashes. Eyelash transplantation. Follicular isolation technique with de-epithelialization for eyebrow and eyelash reconstruction can be used. Eyelash Transplantation Using Leg Hair by Follicular Unit Extraction is another method of management. Conclusion: Simple to Complex undertaking. Proper knowledge of anatomy is important in proper management. Multiple surgeries maybe needed. Excellent results is got in majority of cases.
Final aim is: Preservation of vision. Restoration of eyelid structure and function to near normal as possible. Achievement of adequate cosmesis.
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Cornea Corneal Trauma and Lacerations Dr. Vinay S Pillai HOD & Senior Consultant Cornea & Refractive Surgery, Giridhar Eye Institute, Kochi, Kerala
Dr. Sugaranjini G Cornea and Refractive Surgery Fellow Giridhar Eye Institute, Kochi, Kerala
Introduction: - Cornea being the most anterior structure of eye, is particularly vulnerable to damage in ocular trauma. Opacification of cornea due to corneal injuries adds to existing burden of preventable blindness. A sound knowledge of trauma management will enable ophthalmologist to promptly treat these injuries better and minimise structural and visual sequelae. The most common causes of eye injuries include road traffic accidents, domestic trauma and occupational accidents. Risk factors include male gender, younger age, high activity professionals (e. g., police personnel), low education, contact sports, and failure to use safety equipments. Intial ophthalmic evaluation in crucial and one must adhere to an universal grading system for better communications between proffesionals, for prognostications and management purposes of ocular trauma. Ocular Trauma Classification System (OTS)(1) developed in 1997 is ideal for the same. Vision at the time of presentation and the presence or absence of afferent pupillary defect are the most important prognostic factors in OTS. Open globe injuries of cornea include penetrating eye injuries, perforating injuries, intraocular foreign bodies and corneal rupture where as closed globe injuries without full thickness wound to cornea include contusion and lamellar corneal laceration. A Detailed Slit lamp evaluation is imperative to assess the extent of wound and status of other ocular structures. Systemic antibiotic prophylaxis should be started at the earliest and tetanus prophylaxis must be enquired upon. Open globe corneal injuries: Penetrating injuries less than 2mm in length and those which are self sealed with good wound approximation and minimal to nil gape can be given a trial of bandage contact lens or tissue adhesive under topical broad spectrum antibiotics, cycloplegics and hypotensive medicines. These patient must be followed up closely to watch for wound healing and signs of infections.They must also refrain from any strenuous activities and use eye shield or goggles for 42
Cornea protection. In case of persistent non sealing or gaping of wound margins, a surgical closure of the wound is warranted. Non self sealing , large corneal tears needs surgical suturing at the earliest to reduce risk of endophthalmitis, expulsive hemorrhage and tissue necrosis. Goals of surgical closure include obtaining a water tight wound closure, tissue preservation, restoration of normal structural integrity, to improve final visual outcome and to reduce complications. Wound must be carefully explored prior to closure to remove foreign body if any. Surgical plan on the technique to be employed and approach to the wound must be formulated beforehand . This helps to reduce surgery time and increases the comfort of the patient . Open globe injuries of cornea are better sutured under general anaesthesia as retro / peribulbar anaesthesia often lead to increase in intraocular pressure with expulsion of intraocular contents. Meticulous care must be taken while draping the patient to avoid the extrusion of intraocular contents . Prolapsed and incacerated tissue must be released first from the wound as they may hinder wound sealing. Prolapsed tissue which in necrosis and beyond 24-48 hours of prolapse must be excised at tissue plane and reposition is avoided as far as possible to prevent post operative infection. Monofilament , suture with low tissue reactivity is preferred such as nylon or polypropylene. Corneal sutures must be 90% deep in the stroma and of equal depth on both sides of the wound. Full-thickness sutures can be indentified by pin point leak from suture entry and exit point . They act as a conduit for microbial invasion. Suture passes should be approximately 1.5 to 2.0 mm in total length, and equally spaced on either side of the wound. It is important to incorporate healthy , non-macerated, edema free tissue in every bite or else the suture may tear through the tissue on tying. On being tied , the suture creates two traingular compression zone on either side of the wound which abut at the wound margin and approximate it. Incomplete overlap of compression zones results in persistent gaping and wound leak. Anatomy and orientation of the wound must be studied prior to initiation of closure . Perpendicular parts of wound are closed first followed by oblique parts of the wound. Initially, temporary sutures are placed to ensure watertight closure of wound. These sutures are then replaced by astigamtically neutral sutures at the end. Rowsey – Hays technique(2) of corneal suturing must be adhered to with long, tight sutures in the corneal periphery to cause flattening and shorter, minimally compressive sutures in corneal center to induce central steepening. Distance between two sutures must be equal to the legth of the suture bite. So peripheral longer sutures are more distantly placed compared to closely spaced short central sutures to overlap compression zones. Suture bites through visual axis must be avoided and all suture knots must be buried away from visual axis. 43
Cornea Perpendicular wounds are best approximated if the entry point and exit point of suture are equidistant from the wound on either side . Overide of tissue must be avoided and can be minimised by placing sutures which enter and exit the wound at equal depth. However in oblique wounds , entry and exit point of the suture on the posterior aspect of cornea must be equidistant rather than the points on the anterior portion of cornea to ensure approximation. In zigzag tears, the linear aspects of the wound can be sutured with interrupted sutures and the apex of the wound usually self seal or sutured with a mattress suture(3) if not. In stellate lacerations, as in zig-zag lacerations, the staright arms of the incision are first approximated with the stellate portion being dealt with at the end. Purse string suturing technique is helpful in such wounds by either Eisner method(4) involving a partial thickness incision between the arms of the laceration or by Akkin method(5) without partial thickness incisions. Rarely penetrating keratoplasty may be needed at time of preliminary closure . Surgeon must notify the eye banks in such scenarios for corneal tissue. Closed globe injuries: Corneal abrasions and lamellar tears are the most common closed globe corneal injuries presenting to the emergency. They are caused by trauma with fingernails, contact lens wear, paper cuts amongst many.Though extremely painful, most corneal abrasions heal rapidly without scarring within 48 -72 hours . Patients are advised to avoid head bath till full epithelisation of the wound and to maintain hand hygiene while instilling medications. Bandage contact lens can be of aid to alleiviate pain . Overnight patching with antibiotic and cycloplegic can hasten the healing process. Topical antibiotic along with lubricants for a period of 7 days is apt . Corneal foreign bodies consititute a majority of patients presenting with redness pain. Simple stains can help identify foreigh body hidden to the naked eye . Long standing foreign body may be associated with corneal infection and traumatic uveitis . Removal of foreign body under topical anesthesia using a 26 gauge needle or cotton bud followed by topical antiobitic medication along with lubricant should suffice in most cases. Cycloplegic may be added in case of traumatic uveitis . Conclusion: Post trauma patient require follow up for long term for inadvertent complications such as iris damage needing secondary reconstruction or cosmetic contact lens if associated with glare, cataract formation, post operative endophthalmitis, persistent wound leak, tissue necrosis, glaucoma, retinal detachment, irregular astigmatism and amblyopia. It must be borne in mind that an ideal initial surgical repair cutbacks the need for future reconstructions thus saving both time and cost for the patient. 44
Cornea Reference: 1. Pieramici DJ, Sternberg P, Jr., Aaberg TM, Sr., et al. A system for classifying mechanical injuries of the eye (globe). The Ocular Trauma Classi cation Group. Am J Ophthalmol 1997;123:820–831. 2.Rowsey JJ, Hays JC. Refractive reconstruction for acute eye injuries. Ophthalmic Surg 1984;15:569–574. 3. Brightbill FS. Corneal surgery: theory, technique and tissue, 3rd ed. St. Louis: Mosby, 1999:xxii, 942 s. 4.Eisner G. Eye surgery: an introduction to operative technique, 2nd, fully rev. and expanded ed. Berlin Hei- delberg New York: Springer, 1990:xiv, 317 p. 5. Akkin C, Kayikcioglu O, Erakgun T. A novel suture technique in stellate corneal lacerations. Ophthalmic Surg Lasers 2001;32:436–437.
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Sclera Scleral Tear and Occult Globe Rupture. Dr. Anil Radhakrishnan Cornea and Refractive Surgeon Amrita Institute of Medical Sciences, Kochi
The visual outcome of severe ocular trauma has improved significantly in the last two to three decades. A variety of reasons viz. advances in microsurgical instrumentation, suture materials, viscoelastics, vitrectomy capability both for the anterior segment surgeon and vitreoretinal surgeon, intravitreal antibiotic prophylaxis, better vitreous substitutes, better vitrectomy systems with excellent illumination, better understanding of corneal irregularities, more targeted corneal replacements, better contact lens materials are all responsible. However, a good primary repair is essential for any future intervention, whether surgical or otherwise. The salient points in the primary management of scleral injury are listed below. In emergency room Stabilising the patient - Securing the airway and circulation takes precedence in an emergency room, especially in the setting of polytrauma, as in a road traffic accident. Once stabilised, however an open eye should be given preference over fractures or open wounds. Portable slit lamp can be immensely useful, especially when multiple mobility restricting injuries are present. Bedside assessment of visual acuity and IOP should be done in such a scenario. An eye shield must be provided after instilling antibiotic drops [preferably, preservative free]. Eye ointments are better avoided in an open eye. Tetanus prophylaxis – Though in a clean wound Tetanus toxoid should suffice, in a dirty or contaminated wound Tetanus Immunoglobulin [TIG] 250 IU should be given in addition to thorough wound cleaning. Intravenous antibiotics – A combination of Cefazolin or Vancomycin [ 500mg - 1 gm 8th hourly] and Ceftazidime/ Ceftriaxone [1 gm 8th hourly] is 46
Sclera administered for adequate [ both gram positive and gram negative] antibiotic cover. In large corneoscleral tears or when uveal prolapse is obvious, it’s better to avoid further injury to the ocular structures by inserting a speculum, especially in children. Detailed evaluation can be done under the comfort of general anaesthesia. Clinical evaluation: The clinical findings suggestive of scleral laceration, when not apparent are [1] visual acuity of light perception or less [2] soft eye ball [ IOP < 5 mm Hg] [3] both shallow or blood filled anterior chamber [4] media opacity preventing view of fundus [5] intense periocular haemorrhage. However, normal or even slightly high IOP is possible as the scleral defect may be closed by clot or orbital tissue.
Fig 1 – Large corneoscleral tear with globe collapse resultant enophthalmos, severe chemosis and uveal prolapse Occult scleral rupture / globe rupture is a traumatic dehiscence of sclera at or posterior to rectus muscle insertions without a visible defect, which typically occurs in blunt trauma. It should be suspected when the anterior chamber [AC] is abnormally deep with a posteriorly retracted iris. The other ancilliary findings are [1] extensive chemosis, often haemorrhagic [2] presence of vitreous bleed and [3] hypotony. Its prompt detection is important to prevent damage to the eye and to initiate surgical repair. The deep AC is due to loss of vitreous volume form the scleral defect. However, extensive vitreous bleed may prevent deepening of AC.
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Sclera The common sites of scleral perforation are [1] at the limbus [2] area of rectus muscle insertions and [3] concentric to optic disc. In blunt trauma, multiple scleral tears can occur, often in a concentric fashion, due to equatorial expansion of the globe.
Fig 2 - Occult scleral rupture with deep AC, severe chemosis, presence of anterior vitreous bleed
Investigations / Imaging:B-scan ultrasonography – Extreme care is required while performing contact Bscan ultrasonography in ocular trauma, with copious amount of gel. It can reveal posterior segment pathologies like lens dislocation, vitreous and choroidal bleed, ciliochoroidal detachment, retinal detachment etc. The findings suggestive of scleral rupture are presence of scleral folds, distortion or shortening of globe and rarely presence of fluid between sclera and orbital fat. In the presence of extensive scleral laceration or globe rupture, multidimensional computerised tomography [MD-CT] may be preferred. However, Magnetic Resonance Imaging [MRI], though better for soft tissue delineation can potentially damage the ocular structures if there is an intraocular metallic foreign body and hence better avoided.
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Sclera Surgical repair The intention of primary repair is to have an intact globe and to prevent complications / infection, so that restoration of anatomical and functional integrity as much as possible can be planned later. Anaesthesia - General anaesthesia is preferred, as peribulbar or retrobulbar injection can potentially extrude intraocular contents if ocular injury is extensive. If local anaesthesia is to be given, a small retrobulbar block with a good facial block is preferred. Exposure - Lid sutures [with 4.0 silk] maybe preferred instead of speculum in large lacerations, to avoid pressure on the globe. Suture material - As in corneal lacerations ,10.0/9.0 monofilament nylon [ ethilon] is the preferred suture material in view of its high tensile strength. However, 8.0 nylon/vicryl can also be used. A cutting needle, preferably a spatulated one is better used to minimise tissue resistance while passing the needle. For the same reason, a round bodied needle is better avoided. Suturing - is done at 80 – 90% depth with approximately equal bites in both sides. Full thickness suturing is to be avoided to prevent retinal / uveal tissue incarceration in the wound. In places with obvious uveal prolapse, macerated uveal tissue is abcissed and wound margins are apposed tightly after reposition of uveal tissue. In corneo-scleral lacerations, a tight suture with long bites is placed at the limbus first, as it provides a stable landmark. The scleral part is then tackled first. The scleral defect may be closed by zipping it up from limbus backwards. In a small well visualised scleral tear, localised peritomy may suffice. However, in large ones, 360 degrees peritomy with relaxing incisions at 3 and 9’0 clock is required. If the scleral tear is extending beyond the rectus muscle insertions, multiple button holes in Tenon’s fascia are made near rectus muscle insertions, muscles hooked and then inspected. Retraction of Tenon’s capsule and direct visualisation as far as possible is done. If scleral rupture passes underneath muscle insertion, the recti may be disinserted and reattached after repair of scleral wound. However, forceful rotation of the globe should be avoided in very posterior ruptures to prevent deformation of globe and extrusion of ocular contents. Automated vitrectomy is done to remove prolapsed vitreous. After ensuring water tight closure of sclera and cornea, Tenon’s capsule and later conjunctiva is closed with 8.0 vicryl sutures. Intracameral / intravitreal antibiotic injection is given to reduce the chances of endophthalmitis. 49
Sclera Immediate postoperative care – Intensive topical steroids, antibiotics and cycloplegics are administered in the early postoperative period in addition to systemic antibiotics. Systemic steroids [ Prednisolone 1 mg/kg] is also added, once infection is ruled out. Primary Pars Plana Vitrectomy may be done one to two weeks after primary repair for dense vitreous haemorrhage, dislocated lens, retinal detachment or retinal incarceration in wound. Conclusion – Visual outcome after ocular trauma is dependent on a variety of risk factors and variables. However, a badly done primary repair can often cause irretrievable visual loss while a well performed primary repair can often be the first firm step towards visual recovery.
References: 1] Beatty RF, Beatty RL. The repair of corneal and scleral lacerations. Semin Ophthalmol. 1994 Sep;9(3):165-76. 2] Chronopoulos A, Ong JM, Thumann G, Schutz JS. Occult globe rupture: diagnostic and treatment challenge. Surv Ophthalmol. 2018 Sep-Oct;63(5):694699. 3] J S Berestka, S Navon. Repairing corneoscleral lacerations. J Cataract Refract Surg.1994 Jul;20(13)80190-3.
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Hyphema TRAUMATIC HYPHEMA Dr. Karthika Mohandas Consultant, Dr. Tony Fernandez Eye Hospital
Hyphema (blood in the anterior chamber) can occur after blunt or lacerating trauma, or after intraocular surgery. Hyphema can occur spontaneously in conditions such as rubeosis iridis (e.g., associated with diabetic retinopathy, central retinal vein occlusion, carotid occlusive disease, or chronic retinal detachment), vascular tufts at the pupillary margin, juvenile xanthogranuloma, iris melanoma, myotonic dystrophy, keratouveitis (e.g., herpes zoster), leukemia, hemophilia, thrombocytopenia, or Von Willebrand disease. Hyphema also occurs in association with the use of substances that alter platelet or thrombin function (e.g., ethanol, aspirin, warfarin). Blunt trauma is the most common cause of a hyphema. Compressive force to the globe can result in injury to the iris, ciliary body, trabecular meshwork, and their associated vasculature. The shearing forces from the injury can tear these vessels and result in the accumulation of red blood cells within the anterior chamber. Even small amounts of blood within the anterior chamber can lead to complications such as glaucoma, corneal blood staining, and secondary hemorrhage; thus, proper management of this condition is crucial to prevent loss of vision
EPIDEMIOLOGY OF TRAUMATIC HYPHEMA: The annual incidence of traumatic hyphema has been estimated at 17 injuries per 100,000 populations, with majority being male patients (80%). The peak incidence is ages between 10-20 years. Projectile injuries usually through ball related sports tend to account for a greater proportion of hyphema-related injuries among children than adults, and blows to the eye (most commonly assaults) tend to account for a greater proportion of hyphema-related injuries among adults. In children without a history of trauma, if there is no evidence of a predisposing ocular or systemic disease or medication, then the possibility of child abuse should be considered.
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Hyphema PATHOPHYSIOLOGY: Blunt injury is associated with antero-posterior compression of the globe and simultaneous equatorial globe expansion. Equatorial expansion induces stress on anterior chamber angle structures, which may lead to rupture of iris stromal and/or ciliary body vessels with subsequent hemorrhage. Lacerating injury can also be associated with direct damage to blood vessels and hypotony, both of which can precipitate hyphema. Hyphema after intraocular surgery can be due to granulation tissue in the wound margin or due to damaged uveal vessels (e.g., from surgical trauma or from intraocular lensinduced uveal trauma. Secondary hemorrhage, also termed rebleeding, may be due to clot lysis and retraction from traumatized vessels. Secondary hemorrhage occurs in 0-60% cases depending on the extent of the initial hemorrhage, the treatment, and the series of patients being reported. Most secondary hemorrhages occur from two to five days after the initial injury, and nearly all occur before the seventh day. The pathogenesis of rebleeding is not known. It may be related to fibrinolysis and retraction of clots or to bleeding of fragile new capillaries
HISTORY AND EXAMINATION: Most patients present with a history of trauma and decreased vision or pain in the eye. When a person presents with a hyphema, it is imperative to ask a detailed history and perform a complete eye examination. History should include questions related to the possibility of an intraocular foreign body, changes in vision, photophobia, eye pain, nausea, vomiting, and any history of bleeding diathesis, especially sickle cell disease or trait. Complete ophthalmological examination should include intraocular pressure measurement and dilated funduscopic assessment. A ruptured globe must be ruled out. A ruptured globe might not be readily apparent, particularly if there is significant subconjunctival hemorrhage. Signs of occult rupture in the setting of a traumatic hyphema include poor vision, low intraocular pressure, an abnormally deep anterior chamber, and pupillary distortion. If trauma-induced, the patient should also be evaluated for acute
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Hyphema orbital compartment syndrome. Signs of orbital compartment syndrome include proptosis, decreased visual acuity, and a relative afferent pupillary defect Once these are ruled out detailed evaluation includes inspection of the lids, lashes, lacrimal apparatus, and cornea. Fluorescein staining of cornea is done to assess for corneal abrasion. Direct and consensual pupillary responses are evaluated and check for relative afferent pupillary defect. Visual acuity, confrontational visual fields, and extra-ocular muscles should be examined as well. Findings typical in the setting of hyphema include decreased visual acuity, photophobia, anisocoria, and the visual findings of blood in the anterior chamber. After an open globe injury has been ruled out, intraocular pressure is measured. Visual acuity typically worsens with the supine position and the symptoms may improve with the elevation of the head due to the layering of blood below the visual axis. Decreased visual acuity is a result of the refractory changes induced by the blood in the anterior chamber. Anisocoria results from tears to the iris sphincter muscles, which may cause either miosis or mydriasis of the affected eye. Approximately 1 month after injury, careful gonioscopy should be performed to evaluate for potential bleeding sites and to examine for the presence of angle recession. A dilated retinal examination with scleral depression should also be performed at 1 month to rule out retinal pathology. . Vision, hyphema status, intraocular pressure, and evaluation for corneal blood staining should be determined every day for the first 4 days after the initial injury.
GRADING OF HYPHEMA: Grade 0 or microhyphema occurs with scattered RBCs in the anterior chamber that do not layer out. Grade I hyphema has less than 33% anterior chamber filling. Grade II has 33% to 50% filling. Grade III has greater than 50%, but less than total filling of the anterior chamber. Grade IV has 100% anterior chamber filling.
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Hyphema
INVESTIGATIONS: Bleeding time, hemoglobin electrophoresis, platelet count, prothrombin time, partial thromboplastin time, liver function, and blood urea nitrogen and creatinine may be tested, depending on the patient’s history, on the ocular examination, and on what treatment will be initiated Computerized tomography (CT) of the orbit should be utilized in patients with a concern for an open globe, an intraocular foreign body, or a suspected orbital fracture. Ultrasound of the orbit may be beneficial to evaluate for lens dislocation, intraocular foreign body, retinal detachment, and posterior vitreous haemorrhage. Ultrasound to be performed only after open globe injury is ruled out. COMPLICATIONS: Aside from associated injuries, the major complications of traumatic hyphema are glaucoma and blood staining of the cornea. Acutely, the IOP may be elevated due to the following: occlusion of the trabecular meshwork by clot, inflammatory cells, or erythrocytic debris; or pupillary block secondary to a collar button-shaped clot involving both the anterior and posterior chambers. 54
Hyphema The intraocular pressure varies unpredictably with the size of the hyphema. Secondary hemorrhage is often associated with increased intraocular pressure. The incidence of late-onset glaucoma in eyes with a history of traumatic hyphema ranges from 0–20%. Glaucoma developing days to years after the inciting injury can arise from damage to the trabecular meshwork (often associated with angle recession), descemetization and fibrosis of the trabecular meshwork, or peripheral anterior synechia formation leading to secondary angle closure glaucoma. The incidence of angle recession after eye trauma ranges from 20–94%. a. Ghost-cell glaucoma, caused by dehemoglobinized erythrocyte diffusion from the vitreous cavity into the anterior chamber weeks to months after a vitreous hemorrhage, can be associated with a khaki-colored hyphema and is another cause of late onset intraocular pressure elevation after trauma. The incidence of traumatic hyphema-associated corneal bloodstaining varies from 2–11%. Among patients with total hyphema, however, the incidence is substantially higher, ranging from 33– 100%. 2 Corneal bloodstaining can cause decreased visual acuity after hyphema resolution and can cause deprivation amblyopia in infants and children. Corneal bloodstaining tends to occur in the setting of larger hyphemas, re-bleeding, prolonged clot duration, sustained increased intraocular pressure, and corneal endothelial cell dysfunction. Other complications include optic atrophy (as a result of raised IOP or optic nerve contusion), secondary hemorrhage, accommodation impairment etc. MANAGEMENT MEDICAL MANAGEMENT: Bed rest- encourage limited activity. The head of the bed should be elevated upto 30 degree to encourage the hyphema to gravitate to the inferior angle and away from the visual axis. Eye shield- to be worn at all times, including nighttime, until the hyphema clears. Aspirin and alcohol inhibit platelet aggregation and should be avoided. Topical cycloplegics- dilates the pupil and helps to relax the ciliary body, thereby decreasing inflammation and improving the patient’s comfort. Topical steroids- to decrease the inflammation and to improve the patient’s comfort. Also decrease the risk of re-bleeding.
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Hyphema Topical steroids may limit healing if there are associated corneal abrasions. The development of cataracts or glaucoma from prolonged steroid use can cause unwanted complications. Anti fibrinolytic agents- aid in clot stabilization. Aminocaproic acid and tranexamic acid are examples of antifibrinolytic agents. They inhibits the conversion of plasminogen to plasmin, which therefore decreases the amount of plasmin available for the fibrinolysis. Tranexamic acid is more potent than aminocaproic acid and has fewer side effects NEWER MODALITIES: Tissue plasminogen activator is a newer modality that may serve as an adjuvant to known therapies. Transcorneal oxygen therapy has also been tried in those with hyphema and sickle cell trait SURGICAL MANAGEMENT: In approximately 5 % of patients, failure of medical therapy necessitates surgical intervention. The indications for surgery are said to be:
uncontrolled glaucoma early blood staining of the cornea large or total hyphemas of more than nine days' duration detection of a site of active bleeding.
The simplest procedure is paracentesis or the release of blood through a small limbal incision. If this is unsuccessful, Manual irrigation and aspiration of the blood is a common technique that is considered. This technique is relatively easy. Using an irrigation aspiration cannula a washout of suspending debris may occur through a one- or two-cornea incision approach. Evacuation of the hyphema sometimes requires the use of vitrectomy instrumentation, owing to clot retention.33 Care should be taken not to damage the corneal endothelium, lens capsule, or iris during the procedure MANAGEMENT OF COMPLICATIONS:If corneal blood staining is noted, the clot should be evacuated, and care should be taken to control the intraocular pressure. Clearing may take several months 56
Hyphema to years and usually starts first at the peripheral cornea. Penetrating keratoplasty should be considered in children who have significant corneal changes and who are in the amblyopic age range Management of glaucoma: The treatment of elevated pressure is chiefly medical. Topical beta-adrenergic antagonists are usually the first line of therapy. Topical -adrenergic agonists, topical and oral carbonic anhydrase inhibitors may be used. Owing to the increase in the inflammatory response, miotics should not be used. Prostaglandin analogs may also cause an inflammatory response, and hence used with caution. Special consideration should be given to those with sickle cell disease or trait. If sustained lowering of the intraocular pressure is not achieved, consider surgical therapy Surgical anterior chamber washout is indicated to prevent optic atrophy if the IOP averages greater than 60 mm Hg for 2 days, or greater than 35 mm Hg for 7 days. PROGNOSIS: The larger the hyphemas, the worser the prognosis. Small hyphemas usually disappear within four or five days. Those that occupy half or more of the anterior chamber (grade II or III) are more likely to be associated with delayed clearing, glaucoma, blood staining, rebleeding, and poor visual results. The chance of recovering visual acuity of 20150 or better is 75-90% with grade I hyphemas ; 65 - 70% with grade II ;and 25-50% with grade III. The most common cause for vision impairment is corneal staining of the visual axis, which underscores the worsening prognosis for higher grade hyphemas. Preservation of vision following hyphema can be achieved with appropriate diagnosis and management of hyphema and its complications. REFERENCES: Sankar, Prithvi S.; Chen, Teresa C.; Grosskreutz, Cynthia L.; Pasquale, Louis R. (2002). Traumatic Hyphema. International Ophthalmology Clinics, 42(3), 57– 68. doi:10.1097/00004397-200207000-00008 Wilson, Fred M. (1980). Traumatic Hyphema. Ophthalmology, 87(9), 910– 919. doi:10.1016/S0161-6420(80)35144-0
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Hyphema William Walton; Stanley Von Hagen; Ruben Grigorian; Marco Zarbin (2002). Management of Traumatic Hyphema. , 47(4), 0– 334. doi:10.1016/s0039-6257(02)00317-x Kennedy RH, Brubaker RF. Traumatic hyphema in a defined population. Am J Ophthalmol. 1988 Aug 15;106(2):123-30 Little BC, Aylward GW. The medical management of traumatic hyphaema: a survey of opinion among ophthalmologists in the UK. J R Soc Med. 1993 Aug;86(8):458-9.
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Lens Traumatic Lens Injuries. Dr. S J Saikumar Medical Superintendent and Head of Cataract and Glaucoma Services Giridhar Eye Institute, Kochi
Dr. Sruthi R Giridhar Eye Institute, Kochi
Lens injury is very common in trauma involving the eye. Injury to the lens alone is usually having better prognosis compared to the trauma to other structures of the eye. But associated injuries can cause bad visual prognosis in those eyes. Both blunt trauma and penetrating trauma can cause injury to the crystalline lens. The patient should be examined carefully and managed properly to provide the most favourable outcome. Various changes that are occurring in the lens following trauma and their management are described below. Vossius ring: A circular ring of pigment resulted from blunt trauma that forms a complete or incomplete ring on the anterior capsule of lens. It usually has the same size as the contracted pupil. It is due to the coup injury causing impression of iris over the lens capsule. Minute sub capsular opacities may be seen after resorption of the pigment.
Concussion cataract (traumatic cataract in closed globe injury) Pathogenesis: Blunt trauma can cause lens injuries either by coup or by contrecoup mechanisms. The resulting shockwave and equatorial expansion of the globe leads to injury to anterior and posterior structures of the lens.
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Lens The cataract formation in blunt trauma is mainly due to two factors. One is the mechanical effect of injury to the lens fibres. Second is the entry of aqueous into the lens due to disruption of the lens capsule or impairment of capsular semi-permeability. Capsular tears can be in the anterior capsule, in the equatorial region or in the posterior capsule. The tears may not be visible in many cases especially if it is small and peripheral. In these cases, if the entrance of aqueous is stopped after sometime, then the lens opacity may remain stationary. But, if the capsular tear remains open then the lens opacification may progress to involve the entire lens. The typical appearance of concussion cataract is rosette- shaped cataract. It typically occurs in the posterior cortex, sometimes in the anterior cortex or both. In this cataract, the fluid accumulation delineates the star shaped arrangement of cortical sutures and feathery lines of opacity outlining the lens fibres radiates from them. A rosette may disappear, progress or remain stationary. A late rosette- shaped cataract may develop in the posterior cortex 1 or 2 years after a concussion. It is smaller and more compact than the early type and its sutural extensions are short. Signs and symptoms: Defective vision, glare and mono ocular diplopia are the usual complaints. Some may develop cataract immediately after the trauma while in others the cataract may take years to develop. Some cataracts will remain localised while others will develop a total cataract. The typical traumatic cataract is star shaped, called the rosette cataract. On slit lamp examination, the integrity of the anterior and posterior capsule should be noted. Any lens induced intraocular inflammation should be noted and the lens stability should be assessed. Trauma to the other ocular structures should be assessed. A B-scan may be needed if there is no view of the posterior segment. CT orbit may be needed if there is high suspicion of a penetrating injury or intra ocular foreign body. Cataract in open globe injuries: Penetrating trauma or intraocular foreign bodies (IOFBs) can lacerate the anterior lens capsule, leading to focal cortical changes, or rapid lens 60
Lens opacification. If the wound in the capsule is small, the entry of aqueous causes a localised cloudiness and opacifies in the form of feathery lines in the posterior cortex leading to the formation of rosette-shaped cataract. They usually progresses into a total cataract. If the lens fibres are damaged, it opacifies rapidly and flocculent grey masses protrude through the opening in the capsule, sometimes filling the whole anterior chamber. A cataract of this type will cause severe iridocyclitis and secondary glaucoma. Treatment of traumatic cataract: When a diagnosis of traumatic lens injury is made, the decision regarding whether primary cataract extraction is needed or the lens can be removed as a secondary procedure is debatable. The advantages and disadvantages of primary lens extraction are given below. Advantages: Eliminates the source of inflammation resulting from lens particles floating in the AC* or vitreous Eliminates one potential source of IOP elevation Allows visualization of the posterior segment Allows early visual rehabilitation of the patient, which is crucial in the amblyopic age Establishing a clear visual axis in patients less likely to return for followup May allow single (rather than repeated) surgical intervention If there is vitreous hemorrhage along with lens damage, the “vitreouslens admixture” is a risk factor for the development of proliferative vireo retinopathy (PVR). Disadvantages: Lens may not have been truly cataractous Cataract might not have become visually significant Surgery in itself is a source of inflammation Surgeon commonly inexperienced Operating room not always prepared for primary lens removal In general, primary cataract removal is recommended if the lens is fragmentized, swollen or causing papillary block. 61
Lens Technique of surgery:Cataract surgery in the setting of trauma primarily depends on the presence of injury to the posterior capsule and the vitreous prolapse. If the posterior capsule is intact and there is no vitreous prolapsed, phacoemulsification/ECCE alone is sufficient. If the condition of posterior capsule is questionable, without any vitreous prolapse, careful phacoemulsification/ECCE can be done and in case vitreous is found intra-operatively, vitrectomy can be done. If there is a large posterior capsular tear without any vitreous prolapsed, vitrectomy should be done. If there is vitreous prolapsed, irrespective of the condition of the posterior capsule, vitrectomy should be done. The obvious advantage of using the vitrectomy probe for cataract extraction is that whether or not vitreous is encountered, no traction is exerted at the vitreous base, eliminating the risk of an iatrogenic retinal break. The second question is whether should the IOL implantation be concurrent with cataract removal or be done as a secondary procedure. Advantages of primary IOL implantation: In a child in the amblyopic age, it is always better to implant the IOL along with lens extraction in order to prevent amblyopia. The chance of synechiae formation which can lead to closing of the bag by the time of secondary implantation can be prevented. It is more convenient to the patient and less expensive Disadvantages of primary IOL implantation: It may be difficult to determine the IOL power prior to the surgery. There is a chance for inflammatory debris settling on the IOL which may require a second procedure Conditions in which primary IOL implantation is usually not usually recommended: Children <1 year Severe inflammation/endophthalmitis is present Significant corneal damage 62
Lens Risk of AC rebleeding Significant iris loss Inadequate capsular support for the remaining capsule Posterior segment cannot be visualised Serious posterior segment injury Increased risk of PVR It is preferable to use a PCIOL and place it in the bag if the posterior capsule is intact. If there is injury to the posterior capsule, sulcus-placed IOLs, iris-fixated, ACIOLs or scleral fixated IOLs are the options. If aniridia is also present, a specially designed black-diaphragm IOL is used to counter the effects of iris loss. Subluxation and Dislocation of the lens: Closed globe injuries as well as open globe injuries can cause zonular dehiscence or displacement ofthe crystalline lens. Partial change in lens position is called subluxation when the lens remains in the papillary space( Figure 1) and total change in lens position is called luxation (dislocation) when the lens is lying outside the hyaloids fossa, free- floating in the vitreous, in the anterior chamber or on the retina (Figure 2). Luxation also includes extrusion of the lens from the eye.
Figure 1: Interotemporal subluxation of lens
Figure 2: Posterior dislocation of cataractous lens
Pathogenesis: In blunt trauma, zonular dehiscence is caused due to the sudden expansion of the globe at the equatorial region followed by sudden compression of the globe. Partial damage to the zonules (at least 25%) causes lens subluxation and complete loss of zonules cause lens dislocation.If a mild injury causes lens 63
Lens subluxation, then any systemic conditions or ocular conditions associated with weak zonules should be considered. Signs and symptoms: Symptoms of lens subluxation/ dislocation depend on the degree of zonular injury and lens displacement. If there is only mild subluxation, patient may not experience any defective vision. Lenticular astigmatism can be present if there is significant tilt in the lens position. A dislocated lens causes significant disturbance of vision. If the subluxated lens edge crosses the pupil, uniocular diplopia can be present. Subluxation may produce variation in the anterior chamber depth, where it is deeper in the part unsupported by the lens. The edge of lens may be seen in the papillary area. Phacodonesis can be present. A dislocated lens, if clear is seen with some difficulty but, if it turns into a yellow mass, it is spotted easily. Lens becomes more globular due to its freedom from the tension of the zonules and looks like a globule of oil in the anterior chamber. Lens in the anterior chamber causes spasm of the papillary sphincter as it passes through the pupil. If the anteriorly dislocated lens is allowed to be in that position for a long time, iridocyclitis or secondary glaucoma can be resulted. Dislocation of lens causes iridodonesis and IOP can be elevated. Sometimes lens can be extruded out, sometimes seen subconjunctival. This occurs usually in the setting of globe rupture. Management of subluxated lens: Management depends mainly on the patient’s symptoms if the IOP is normal.No intervention is necessary if the complaints areminimal. Conservative treatment such as a contact lens may be attempted. In a child in the amblyopic age, early surgery is needed if there is significant subluxation. This is to achieve early visual rehabilitation. If there is a significant subluxation in any patient with diplopia, astigmatism, defective vision, then surgery is necessary. Surgery is also recommended if cataract is present.
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Lens Lens extraction via a small incision phacoemulsification and PCIOL implantation should be attempted in every case if possible.Incision should be placed away from area of zonular weakness to help reduce stress on the existing zonules during phacoemulsification.Surgeon should work through the smallest incision possible. This will minimize fluid egress through the incision and prevent anterior chamber collapse. A large amount of highly retentive viscoelastic is placed over the area of zonular dialysis to help tamponade the vitreous and to maintain a deep non collapsing AC. The capsulorhexis is started in an area remote from the dialysis to help utilize the counter acting forces of the remaining healthy zonules. A second instrument is used for counter traction or to push the lens into view if it is significantly decentred under the iris.A rhexis of 5.5 mm – 6mm will facilitate all manipulations of the nucleus. Hydro dissection should be performed carefully yet thoroughly to maximally free the nucleus thereby decreasing zonular stress while manipulating the nucleus. A soft nucleus can be completely prolapsed into the anterior chamber to simplify removal and virtually eliminate all zonular stress.Phacoemulsification should be performed using low vacuum and aspiration settings in order to keep the bottle height at a minimum.Divide and or chop technique are preferred in eyes with zonular weakness. This technique minimises zonular stress during phacoemulsification. Manually aspirate with a 24/ 27 G cannula striping cortex in a tangential manner instead of radially to limit stress on zonules. In cases of moderate zonular loss or dysfunction in more than 3 clock hour range, some form of augmented capsule support will likely be needed.Flexible capsular hooks are placed through limbal stab incisions can be used to hook the capsulorhexis edge and support the bag. Capsule hooks support the bag by its equator, not the capsule margin, thereby keeping the bag distended and also reducing the likelihood of aspiration of the bag equator as the lens material is evacuated. CTR (capsular tension ring) s are indicated in cases of mild, diffuse zonular weakness or small, localized zonular dialysis (generally less than 4 clock hours). If there is more than 4 clock hours of damage or if the lens is moderately to severely displaced, a fixation device is required either Cionni Ring or Ahmed capsule tension segment.
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Lens Early placement of CTR can also cause stress on the zonules. If early placement is necessary, we can consider a Henderson CTR or a CTS (capsular tension segment) to allow for greater ease of aspiration of cortex. In the setting of an anterior or posterior capsular tear, which are contraindications to the use of a CTR or MCTR (modified CTR), a CTS can be used. In cases of generalized zonular weakness and dehicense 270 degrees or more, cataract extraction followed by scleral fixation of PCIOL /anterior chamber IOL implantation/iris claw IOL is a safer option for the longterm stability of the IOL. Management of lens dislocation: Dislocated lens causes corneal edema, inflammation, IOP elevation, vitreous hemorrhage, CME andretinal detachment. The rate and severity of complications increase if the lens is ruptured or fragmented. In the case of an anteriorly dislocated lens, lens removal can be done either by pars plana route or through a scleral tunnel, both approaches need a complete pars plana vitrectomy to be on the safer side. For removal of posterior dislocated crystalline lens, a completevitrectomy is first performed to remove vitreous traction from the lens.Subsequently, the lens is lifted off the retina with the help of suction fromthe vitrector, or a needle, with or without the use of perfluorocarbonliquid (PFO) to float the lens off the retina.The lens is thenremoved from the eye by phacofragmentation in the anterior vitreouscavity, away from the retina. The timing of vitrectomyis still controversial, as someauthors found no differencewhether the interventionwas early or delayed. Most authors, foundmuch lower rates of complications and a significantlybetter outcome if the intervention was performed duringthe first week. Complications following lens injuries: Most common complication following lens injury is rise in IOP which leads to glaucoma. Rise in IOP can occur due to different mechanisms.
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Lens 1) Macroscopic lens particles released in to the anterior chamber following capsular rupture causing aqueous outflow obstruction- lens induced glaucoma 2) Lens particles released into the anterior chamber causing severe granulomatous inflammation – phacoanaphylactic glaucoma (keratic precipitates and severe anterior chamber inflammation will be present). 3) Lens dislocated into the anterior chamber causes pupillary block and angle closure glaucoma 4) Vitreous in anterior chamber due to the displaced lens causes IOP rise Foreign bodies in the lens: A foreign body can pass into or through the lens via iris or pupil. If it is passed through the iris, a hole in the iris can be seen in slitlamp examination, which shows redglow on retro illumination. A foreign body can be spotted in the lens on examination. An inert IOFB embedded in a lens with no cataract may be observed. If a cataract is present, the lens may be removed during primary or secondary repair. If the lens is removed, IOL placement should be deferred when vitreoretinal damage is suspected or when endophthalmitis is present or at high risk of developing. TRAUMA IN PSEUDOPHAKIC PATIENTS: Subluxation and dislocation of intra ocular lens: Blunt trauma can cause subluxation, dislocation ( Figure 3) or extrusion of the intra ocular lens (IOL). In cases of malposition not affecting the visual acuity, surgical intervention is not needed. Surgery is indicated in cases ofvisual impairment, glaucoma, IOL dislocation into the vitreous cavity, cystoid macular edema, and retinal detachment.
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Lens
Figure 3: Anterior dislocation of intra ocular lens Treatment: In case of subluxation, repositioning of the IOL, suturing one or both haptics to the iris or suture fixation of haptics to the sclera can be tried. In case of intravitreallydislocated IOLs, it is recommended to remove the IOL. But it can also be retained and suture fixated in the sulcus. After a complete vitrectomy, the IOL is brought anteriorly using intravitreal forceps or PFCL. A limbal extraction incision is made and the IOL is taken out through the incision.
Wound dehiscence: Wound dehiscence can occur in any patient who had undergone intraocular surgery and it should be ruled out in a pseudophakic patient after ocular trauma. The risk decreases with a longer interval fromsurgery to trauma as the integrity of the woundstrengthens.The risk is higher with longer incisions and ECCE and SICS wounds are at higher risk. It needs a primary repair of the globe. References: 1)Kaufman SC, Lazzaro DR. Textbook of Ocular Trauma. Springer International Publishing AG;2017. 2)Kuhn F., 2010. Traumatic cataract: what, when, how. 3)Weber CH, Cionni RJ. All about capsular tension rings. Current opinion in ophthalmology. 2015 Jan 1;26(1):10-5. 68
Lens 4)Hoffman RS, Snyder ME, Devgan U, Allen QB, Yeoh R, Braga-Mele R, ASCRS Cataract Clinical Committee. Management of the subluxated crystalline lens. Journal of Cataract & Refractive Surgery. 2013 Dec 1;39(12):1904-15. 5)Salehi-Had H, Turalba A. Management of Traumatic Crystalline lens subluxation and dislocation. International ophthalmology clinics. 2010 Jan 1;50(1):167-79.
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Trauma Sequalae Glaucoma following Ocular Trauma. Dr. Manoj Prathapan MS, FAEH Glaucoma Associate Professor Amrita Institute of Medical Sciences, Kochi
Dr. Praveena Shyam MS, Junior Resident Amrita Institute of Medical Sciences, Kochi
Ocular trauma is not an uncommon presentation in an emergency room or ophthalmology clinic. Usually, the clinical profile is that of a young males who sustained an injury to the eye following a sporting/ road traffic accident/ occupational hazard. Gender preponderance to male sex is well established from literature, through hospital and general population based studies[1,2]. Ocular trauma may be prevented in predisposed individuals by using appropriate protection gears, but in most other instances it comes as a surprise. With careful examination and management, the ocular morbidity and blindness from this can be prevented or treated. One of the causes for preventable blindness associated with trauma in glaucoma. Traumarelated incidence of glaucoma is especially higher among the younger age group. A study by SihotaRN et al. showed an incidence of 36% in patients under the age of 30 years and only 1.3% among patients over 30 years of age[3]. Glaucoma diagnosis may be overlooked because of the lack of symptoms. As the signs and symptoms of associated ocular injuries are more glaring to the observer; unless a meticulous examination is done including a IOP measurement, glaucoma may be missed. Another reason for misdiagnosis is the frequent late presentation of glaucoma especially in angle recession glaucoma. Unless the patient is advised for regular follow up, many late onset glaucoma may be identified only once visual disability is noted by the patient. By this time it may be too late and irreversible damage might have already occurred to optic disc. Traumatic glaucomas represent a very heterogeneous group of entities with multiple pathomechanisms for elevated IOP. Therefore it becomes important to have a thorough understanding of the various clinical signs symptoms and pathogenesis of traumatic glaucoma as early identification and management is the key to prevent elevated IOP related permanent vision loss. The mechanism and management of various types of traumatic glaucoma are discussed in the following sections.
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Trauma Sequalae Glaucoma associated with BLUNT TRAUMA: Data from an epidemiological study on ocular trauma done by Vats S et al. in 500 families in an urban slum in New Delhi revealed a prevalence of 2.4% with blunt trauma being the most common mode of injury(41.7%). The most common mechanism of damage to ocular structures is the direct transfer of vector forces leading to ischemia and necrosis of the tissue. Another mechanism is due to the change in the shape of the globe resulting in secondary shearing forces leading to the tear of intraocular tissues at their roots.’
Figure 1 showing the mechanism of injury to ocular structure due to anteroposterior compression following trauma. Anteroposterior compression leads to equatorial elongation of the globe and posterior displacement of the iris lens diaphragm. This leads to shearing forces at the attachments leading to tear. Early post-trauma period: Immediately following a contusion there will be a drop in Intraocular pressures (IOP). Ocular hypotony following blunt trauma can be persistent or transient. It can be due to : ● Cyclodialysis (increased uveoscleral outflow) ● Direct neurovascular dysfunction leading to ischemic necrosis of ciliary body (decreased aqueous production) Ciliary body damage is the most common reason for transient hypotony whereas cyclodialysis and ciliary body necrosis leads to persistent hypotony
Figure 2 : Detachment of ciliary body from scleral spur (black arrow, left), Anterior segment OCT showing cyclodialysis cleft(white arrow, right) 70
Trauma Sequalae The most common causes for early onset elevation in IOP following contusion injuries are traumatic iritis, hyphaema, trabecular meshwork disruption, choroidal haemorrhage, uveal effusion, aqueous misdirection syndrome, steroid-induced and acute pupillary block glaucoma associated with lens anterior dislocation or lens subluxation. These early onset secondary ocular hypertension are mostly transient and appropriate medical management would suffice in most cases. With time the IOP returns to normal levels and it may be possible to stop the AGMs in almost all cases. Timely intervention and monitoring is the key to successful management of these glaucomas. Special situations like pupillary block glaucoma may need to be addressed differently. Traumatic iritis contributes to 20% of the total incidence of iritis[5]. It occurs due to disruption of the blood-aqueous barrier that causes a rise in IOP secondary to trabeculitis or obstruction of the trabecular meshwork by inflammatory cells. Most of the cases of iritis are self-limiting but a few will require short term therapy with topical corticosteroids and cycloplegics. The use of corticosteroids can cause steroid-induced ocular hypertension and subsequent optic neuropathy if not monitored regularly. Prostaglandins are usually avoided during the acute phase as they can exacerbate the inflammation. Hyphaema results from disruption of the vascular network of the ciliary body and iris (major arterial circle). This occurs secondary to the anteroposterior compression of the globe during the impact. The accumulated blood along with fibrin and other inflammatory debris obstructs the trabecular meshwork causing an elevation in IOP. Figure 3: Eightball hyphaema (left) with black coloured blood in AC (similar to number 8 ball in billiards) suggestive of impaired aqueous outflow and decreased oxygen concentration. Total hyphaema (right) with bright coloured blood completely filling the AC A 6-month cohort study by the United States Eye Injury Registry found a two times higher risk of developing glaucoma in patients with hyphaema (Odds ratio = 2.23)[6]. Most patients are usually managed medically with topical aqueous suppressants like beta-blockers or alphaadrenergic agonists. The indications for surgical AC washout in a case of hyphaema include: Uncontrolled glaucoma 100% persistent hyphaema called eight ball hyphema 71
Trauma Sequalae Early corneal endothelial staining More than 50% hyphema persisting for >14 days Eyes with active rebleeding Trabecular meshwork injury: Full or partial thickness tears of the trabecular meshwork lead to decreased aqueous outflow. Non Pupillary Bock Glaucoma: Choroidal Hemorrhage, Uveal effusion and Aqueous misdirection are causes of secondary non-pupillary block angle-closure glaucoma with an underlying posterior push mechanism contributing to outflow obstruction. Aqueous misdirection syndrome is characterised by the presence of closed angles with a uniformly shallow anterior chamber (Figure 4). There is no role for YAG PI in these cases. The main stay of management is pars plana vitrectomy with strong cycloplegics like atropine as adjuvants.
Figure 4 showing the mechanism of aqueous misdirection(left) with an accumulation of aqueous in the anterior vitreous which pushes the iris-lens diaphragm anteriorly. The right image shows a uniformly shallow AC with iridocorneal touch in spite of a patent inferior PI. Pupillary Block Glaucoma: Contusion injuries can also cause either anterior dislocation of lens or IOL into AC or posterior dislocation with vitreous prolapse into the anterior chamber(AC). This results in a pupillary block with iris bombe formation. Shallow AC in this case can be differentiated by the presence of a shallow peripheral and relatively normal central AC depth along with a convex iris configuration. This pupillary block mechanism should be differentiated from nonpupillary block angle closure glaucoma mentioned earlier as the management is entirely different. The angle-closure attack is initially aborted with topical and systemic aqueous suppressants and then the pupillary block is relieved with laser peripheral iridotomy or surgical iridotomy. More definitive approach targeting the inciting cause like removal of dislocated lens may be warranted on a case to case basis. 72
Trauma Sequalae
Figure 4 showing anterior dislocation of the lens with pupillary block Delayed-onset Glaucoma Angle recession glaucoma is the most common long term sequalae of blunt trauma. Though the injury may have been unilateral sometimes glaucoma can be seen in both eyes with the eye affected by angle recession having greater amount of glaucomatous disc damage. Angle recession is not an indicator of glaucoma but an indicator of significant trauma to the eye. Nearly 60% of the eyes with concussion injuries and 60-100% of eyes with hyphaema have an angle recession[7,8]. Angle recession is a tear between the longitudinal and circular muscles of the ciliary body. It can also cause rupture of the blood vessels of the ciliary body and at the root of the iris. This explains the correlation between hyphaema and angle recession. Angle recession is not directly causing an elevation in IOP but eventual scarring and fibrosis of the trabecular meshwork and schlemm’s canal increase the trabecular meshwork resistance. Therefore, the risk of angles recession glaucoma increases in an eye with predisposed trabecular meshwork damage. So this warrants the need for periodic evaluation. It is usually said that an angle recession of more than 180 degrees increases the risk of developing glaucoma in later years. The patients can present one year after the trauma or it can be as late as 10 years. Eyes with more than 270 degrees of recession presents much earlier than the eye with a lesser degree of angle involvement.
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Figure 6. Gonioscopy showing broad irregular ciliary body band suggestive of angle recession Lens associated glaucoma The intraocular lens can cause early or delayed onset glaucoma by either an open-angle mechanism as in phacolytic glaucoma, lens particle glaucoma and phacoanaphylactic glaucoma or by an angle-closure mechanism secondary to lens subluxation or phacomorphic glaucoma. Phacolytic, phaco anaphylactic and lens particle glaucoma usually occur following leakage of lens matter into AC due to trauma which initiates an inflammatory reaction. These lens particles along with the inflammatory cells obstruct the trabecular meshwork thus increasing the outflow resistance. Phacolytic glaucoma is common with mature or hypermature cataracts and the definitive management is the removal of the lens. Phacoanaphylactic glaucoma may take days (1-14 days) to stimulate granulomatous uveitis whereas the phacolytic glaucoma occurs latter ranging from days to years after the inciting trauma. Ruptured lens capsule releasing lens particles into AC causing clogging of trabecular meshwork. These uveitic reactions are managed medically with topical corticosteroid and cycloplegics but the definitive management is lens extraction. Subluxation of the lens following trauma occurs due to zonular weakness or dehiscence. Patients usually present with decreased visual acuity or diplopia or features of acute IOP elevation. Pupillary block is due to anterior subluxation of lens iris diaphragm or due to vitreous prolapse through dehiscent zonules. In phacomorphic glaucoma, the pupillary block is secondary to an acute increase in the lens thickness due to traumatic cataract formation. Cataract surgery is the mainstay of treatment in these cases, though a temporary YAG PI may work in some cases till a definitive treatment like cataract surgery is done.
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Figure 7 showing phacomorphic glaucoma with shallow AC(left) and anterior lens subluxation(right) Ghost cell or Hemosiderotic or hemolytic Glaucoma are the open-angle mechanisms of glaucoma following posterior segment hemorrhage. Ghost cells are rigid non-flexible erythrocytes of altered shape and consistency which clogs the trabecular meshwork and deranges the conventional aqueous outflow pathway. Hemosiderotic and hemolytic are very rare forms of traumatic glaucoma
Figure 8 showing all the 7 rings of trauma Glaucoma associated with OPEN GLOBE INJURIES: Penetrating injury to the eye can occur due to blunt force, sharp lacerations or missiles. Blunt force-induced open globe injuries are very common among post-SICS cataract surgery patients. They can have wound dehiscence with IOL expulsion. Intraocular pressure usually 75
Trauma Sequalae falls in the immediate post-trauma period due to the presence of a penetrating wound with the aqueous leak. Following surgical wound repair they develop high IOP secondary to inflammation and intraocular tissue changes following penetrating trauma Common mechanisms of elevation in IOP following open globe injuries are acute anterior uveitis, hyphaema, peripheral anterior synechiae due to aqueous loss and resultant flat AC, epithelial downgrowth or by retained intraocular foreign bodies like those with iron causes siderotic glaucoma and copper deposits causes chalcosis with secondary tissue damage Apart from the normal findings in an ocular trauma like hyphaema, iridodialysis, traumatic cataract, asymmetric AC depth, iridodonesis or phacodonesis we have to also look for clinical features like: - Lacerations or foreign body entry - Self-sealed lacerations - Foreign bodies like glass, hair, metallic splinters The primary management in penetrating trauma is the surgical exploration and FB removal if present, debride necrotic iris tissue and meticulous closure of the lacerated wound to prevent intraocular infections. AC should be formed intraoperatively to prevent flat AC. Gonioscopy in Traumatic Glaucoma: Gonioscopic findings are the tell-tale evidences in all types of glaucoma. It guides an ophthalmologist in deciding the optimal and accurate management plan required to control the disease progression. Similarly, trauma induced changes in the anterior chamber angle and trabecular meshwork are more evident after a careful gonioscopic examination. However, gonioscopy is usually avoided in the early post-traumatic period to prevent the dislodging of blood clot and a subsequent increase in hyphema. Moreover, corneal oedema and hyphema masks the angle structures and an early gonioscopy on day 1 or day 2 does not necessarily change the initial management plan as well. Ideally, gonioscopy can be done 1 month following the trauma to look for the following features : - Cyclodialysis cleft (white/ black /grey area posterior to scleral spur with posterior displacement of iris root and ciliary body band) - Angle recession (widening of ciliary body band with posterior displacement of the root of iris) - Trabecular meshwork flap hinged at scleral spur (in TM tears) - Torn iris processes - Blood in schelmm’s canal - Goniohyphema - Foreign bodies lodged in the angle 76
Trauma Sequalae References: 1.
Charles O, Ericson O, Olakunle T, Bukola O, Chidi O, olumuyiwa A. Pattern of ocular injuries in Owo, Nigeria.J Ophthalmic Vis Res. 2011; 6(2): 114–118. Pmid:22454720
2.
Tejas D, Chinmayi V, Suhani D, Shiv M. Pattern of ocular injury in pediatric population in western India. NHL Journal of Medical Sciences. 2013; 2(2):37–40.
3.
Sihota R, Sood NN, Agarwal HC. Traumatic glaucoma. Acta Ophthalmol Scand. 1995;73(3):252-254. doi:10.1111/j.16000420.1995.tb00279.x
4.
Vats S, Murthy GV, Chandra M, Gupta SK, Vashist P, Gogoi M. Epidemiological study of ocular trauma in an urban slum population in Delhi, India. Indian J Ophthalmol. 2008;56(4):313-316. doi:10.4103/0301-4738.41413
5.
AAO, Basic and Clinical Science Course. Section 8: External Disease and Cornea, 2013-2014.
6.
Girkin CA, McGwin G Jr, Long C, et al. Glaucoma after ocular contusion: a cohort study of the United States Eye Injury Registry. J Glaucoma. 2005;14(6):470-473.
7.
Herschler J. Trabecular damage due to blunt anterior segment injury and its relationship to traumatic glaucoma. Trans Am Acad Ophthalmol Otolaryngol .1977;83:239.
8.
Blanton FM. Anterior chamber angle recession and secondary glaucoma: a study of the after effects of traumatic hyphemas. Arch Ophthalmol. 1964;72:39–44.
9.
Ocular trauma principles and practices - By Ferenc Kuhn
10. Shields textbook of glaucoma - sixth edition
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Trauma Sequalae TRAUMATIC UVEITIS Dr. Reesha K.R. Senior consultant Uveitis & ocular inflammation Little Flower Hospital and Research Centre Angamaly
Dr. Arunlal J.S. LF Hospital and Research Centre Angamaly
Definition: Traumatic uveitis refers to the inflammation of the uvea following trauma. Introduction: Although traumatic uveitis is generally considered less complicated and tend to have better visual outcomes than endogenous forms of uveitis, it can be associated with a significant disease burden and challenging management, especially because it disproportionately affects younger patients. Etiology: Blunt contusion, penetrating and perforating wounds, chemical exposure, electrical and radiation injury and certain intraocular metallic foreign bodies (e.g., iron, lead, copper) that are toxic are the most important cause of traumatic uveitis. Epidemiology1: Blunt trauma is said to be the most important cause of traumatic uveitis. Iritis accounts for 90% of uveitis. Traumatic iritis accounts for 20% of iritis. There is no racial predilection. Young men are affected more often than women because of occupational exposure and life-style differences. Pathogenesis: The pathophysiology of traumatic uveitis is incompletely understood. Trauma results in compromise of the blood - ocular barriers from mechanical injury to the vascular endothelium, non-pigmented ciliary epithelium, and retinal pigment epithelium. Serum proteins and leukocytes gain access to the eye, resulting in flare, fibrin formation, and the presence of inflammatory cells. Injured tissues release arachidonic acid and, in the presence of cyclooxygenase, form 78
Trauma Sequalae prostaglandins and thromboxane. Leukotrienes and hydroperoxyeicosatetraenoic acids (HPETES) are generated from arachidonic acid via the lipoxygenase pathway. These arachidonic acid metabolites further promote an inflammatory response and recruit white blood cells to the site of injury for the repair process. Intraocular foreign bodies such as glass, gold, silver, and plastic are well tolerated in the eye. If retained, these materials rarely incite inflammation. Iron, copper, zinc, and lead, however, are toxic and can promote further injury and often chronic or severe inflammation. Clinical Presentation2: Traumatic iritis is one of the most frequent findings after contusive ocular trauma. Symptoms are similar to other forms of iritis and include pain, photophobia, and mildly decreased vision. The intraocular pressure (IOP) is often lower in the injured eye due to ciliary body dysfunction, although elevated IOP due to trabecular meshwork damage or inflammatory cells blocking the outflow can occur. The classic slit lamp finding is anterior chamber cells and flare. Traumatic iritis is often seen in conjunction with traumatic mydriasis and spasm of accommodation. Hyphema and vitreous hemorrhage may be present. The angle structures may be damaged with angle recession or cyclodialysis. A Vossius pigment ring is often noted on the anterior lens capsule from impact with the pigmented iris epithelium. Retinal commotio, retinal tears, choroidal detachments, and ruptures may be noted in severe blunt trauma. Intraocular foreign bodies may be noted on bio-microscopic or dilated fundus examination. General physical examination often supports the diagnosis through other signs of trauma such as facial bruising, burns, localized swelling, or lacerations. Diagnosis: -
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Trauma Sequalae The diagnosis is made on clinical grounds in most cases. The history, physical examination, and ocular examination support the diagnosis. Traumatic iritis typically presents with unilateral ocular involvement in the context of recent history of blunt ocular trauma. Photophobia, pain, and blurred vision are the symptoms most frequently elicited. Although symptoms can arise rapidly following severe injuries, the presentation is often delayed 3–4 days following a mild contusive injury. As mentioned above, the IOP can be quite variable although relative hypotony compared to the uninvolved eye is most frequently encountered. Diagnosis of traumatic iritis requires visualization of anterior chamber cells and flare. These findings are best seen under high magnification with a short, narrow slit beam placed tangentially at maximum intensity. Prominent perilimbal injection is often seen and is referred to as a ciliary flush. Ultrasonography and radiologic studies should be performed when the presence of a retained intraocular foreign body is suspected. Differential Diagnosis Bacterial or fungal endophthalmitis, which may result from perforating or penetrating injuries and from contaminated intraocular foreign bodies. Histopathologically, chronic inflammatory cells are demonstrated infiltrating the ciliary body. Treatment3: The first goals in treating uveitis associated with nonsurgical trauma are removing the noxious stimuli and assisting with tissue repair. To achieve these goals the clinician may rinse chemical material from the cul de-sac, repair a laceration, or remove a foreign body. In most injuries such as contusion, penetrating wounds, and electrical or radiation burns, the tissue damage is completed by the time of the ophthalmic examination. Post traumatic inflammation can be treated with topical non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroid preparations. Mydriasis and cycloplegia help prevent synechiae formation and control ocular pain. The treatment of choice for traumatic iritis is cycloplegia (atropine 1% two to four times daily) in combination with a steroid drop (prednisolone acetate 1% four times daily). Treatment is typically necessary for only a short time (1–2 weeks), although a more persistent and exuberant cellular reaction has been described. Systemic or regional corticosteroids may be required in severe trauma or to assist in control of retinal edema, or choroidal effusions. Prophylactic, broad-spectrum topical and oral antibiotics can also be prescribed as and when required.
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Trauma Sequalae References: 1. Augsburger JJ, Corrêa ZM. Chapter 19. Ophthalmic Trauma. In: RiordanEva P, Cunningham, Jr. ET, eds. Vaughan &amp; Asbury's General Ophthalmology. 18th ed. New York, NY: McGraw-Hill; 2011:371-382. 2. Ramstead C, Ng M, Rudnisky CJ. Ocular injuries associated with Airsoft guns: a case series. Canadian Journal of Ophthalmology. 2008. 43(5):584587. 3. Trobe JD. The Physician’s Guide to Eye Care. San Francisco, CA: American Academy of Ophthalmology; 2006:50-51.
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Retina Retinal Manifestations in Blunt Trauma. Dr. Rahul R. Menon Senior consultant, Vitreo-Retina Surgery Chaitanya Hospital, Ernakulam
Retina is a layer of neural tissue lining the back part of the eye. Light from outside is focussed on the retina which converts into electrical signal and sends it across to the brain for visual recognition. It is an extremely thin layer tissue measuring around 200 to 250 micron (for scale 1 micron is about one thousandth part of a millimetre). So any trauma to the eye can cause a great deal of damage to this delicate structure. Blunt trauma to the eye occurs due to sudden force applied on the eye from an impact. Common causes of blunt trauma include falls, impact from punch or car accident or sports. The damage to retina in such cases might be due to direct transmission of the shockwave or mechanical deformation due to the trauma. The various retinal sequelae to blunt trauma are 1. Commotio retinae: This occurs immediately after the trauma and you may experience blurry vision. This is retinal damage caused by the shockwave generated by the trauma. This may be at the site of damage (coup) and sometimes away from the actual site of trauma (countercoup). When it affects the macula it’s called as Berlins edema .This can be diagnosed by an ophthalmologist with a dilated fundus examination. This condition usually does not require any treatment and most patient completely recover in a few days. However if the damage is extensive complete recovery may not be possible. 2. Choroidal rupture: Choroid is a layer of tissue behind the retina which supplies blood and nutrient to the outer part of retina. The rapid compression and decompression can lead to 82
Retina rupture of this choroid. This generally results in bleeding in the space beneath the retina. Depending on the location it can cause severe visual impairment. If the location of bleeding is in the macular region (central part of retina responsible for fine vision) the visual impairment is very severe and in such cases vision can be sometimes be regained by displacing the blood by surgical intervention. The choroidal rupture per se does not change over time. Also individual with choroidal rupture need regular follow up as they can develop complications such as Choroidal neovascular membrane. 3. Retinal tears: Retinal tears can be secondary to blunt trauma and usually occurs in the periphery. Retinal dialysis is a type of break which is associated with blunt trauma. Traumatic retinal breaks have high chances of progressing to retinal detachment (separation of the retina from the underlying supporting tissue). Retinal tears leading to retinal detachment require an emergency surgery to restore vision. And if not treated may lead to blindness. These retinal breaks can be treated by a non-surgical approach with lasers if diagnosed earlier. Hence a dilated fundus examination at the earliest is very essential. These retinal tears if present near retinal blood vessels might also cause bleeding inside the eye called as vitreous haemorrhage. These require serial follow ups and sometimes surgery is required to remove this blood to restore vision.
4. Macular hole: Macula is the central part of retina responsible for fineness and acuity of vision. Trauma can cause formation of a hole in the centre of macula called as macular hole. It may occur immediately after the trauma or can present after few weeks. Though there is a chance of spontaneous closure of these holes in case it is small, most require surgery for closure. Improvement of vision in such cases depends on the presence of other co-existing tissue damage.
5. Chorioretinitis sclopeteria: It is a closed globe injury where there is rupture of the choroid and retina together due to the force of a high velocity projectile passing very close to the 83
Retina eye. The visual recovery depends on the location and the extent of damage. The treatment has to be individually tapered and may either be observation or surgery.
6. Traumatic optic Neuropathy: Optic nerve is a bundle of nerve fibres taking the visual signals from retina to brain. Blunt trauma depending on severity can cause simple contusion of these nerve fibres to as blinding conditions such as complete avulsion of the nerve from the eye. Medical management has been tried with little success. In short the old dictum Prevention is better than cure holds true in cases of retinal injuries due to blunt trauma. While injuries to the eye can be minimised by using protective eyewear, all injuries are not preventable. Consulting an ophthalmologist at the earliest can prevent permanent loss of vision in the event of traumatic injury.
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Retina Penetrating Retinal Trauma. Dr. Praveen Murali Senior Consultant, Vitreo-retina surgery Eye Foundation Hospital, Ernakulam
INTRODUCTION: Ocular trauma is an important cause of preventable morbidity worldwide, and is a major cause of unilateral visual loss in developing countries. Violation of the globe integrity, also known as a ruptured globe is an ocular emergency and prompt recognition and management is prudent. Non-detection of serious eye injury has potential to jeopardise a potentially treatable sight-threatening condition in addition to the medico-legal problems for the healthcare workers involved (1,2)
TERMINOLOGY: Penetrating injury Injury which penetrates into the eye but not through and through - meaning there is no exit wound. Perforating injuries have both entrance and exit wounds. Typically, to constitute one of these injuries, a full-thickness rupture of the cornea and/or sclera must be present. Retained foreign object Is technically a penetrating injury, but grouped separately because of different clinical implications Perforating injury: Entrance and exit wounds and both wounds caused by the same agent
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Retina
Epidemiology: - Incidence varies from region to region. - Worldwide, approximately 1.6 million people are blind from eye injuries, 2.3 million with bilateral visual impairment and 19 million with unilateral vision loss (3,4). Most commonly occurs in the age group of 18-45 years (50%) followed by people above 46 years (27%). 23% occur in children and youths aged 0–18 years. - More common in males, ratio ranging from 3:1 to 7.4:1. (3,4) - Injuries occurred commonly in working place mostly caused are by sharp objects. Other causes include road traffic accidents, sports, gunshot, fireworks, hammering on metal, fall from height and explosions (5) Worldwide, approximately 1.6 million people are blind from eye injuries, 2.3 million with bilateral visual impairment and 19 million with unilateral vision loss. Nearly 50% of all reported eye injuries occur in people aged 18 to 45 years. In addition, 25% occur in children and youths aged 0–18 years and 27% occur in people aged 46 years and older. Across all age groups, men are more frequently exposed to ocular trauma with male to female ratio ranging from 3.1 to 7.4:1. The majority of the injuries sustained occur in working place or home, and significant proportions of these injuries are preven table by taking appropriate safety measures. Few other places more prone to injuries are—streets, sports, farms, schools and public buildings. e major causes of ocular trauma are blunt objects. Other causes are sharp objects, 86
Retina road traffic accidents, sports, gunshot, fireworks, hammering on metal, fall from height and explosion. In India, incidence of penetrating injury is higher in rural areas with annual incidence of 9.75 severe eye injuries per 1000 adults. In 65% cases, domestic accidents were responsible for causing injury. Eye injuries account for approximately 8% to 14% of total injuries in children and are the most common type requiring hospitalization (up to 40% of cases). Blunt trauma was found to be more common than penetrating trauma (6) GROSS ANATOMY A working knowledge of the basic ocular anatomy is useful. The eyeball has three layers 1.
2. 3.
The outermost layer is the fibrous coat, responsible for maintaining the shape of eye and supporting the inner two coats, i.e. choroid and retina, which are under positive pressure (the intraocular pressure) The vascular coat consists of iris, ciliary body and choroid The nervous coat, i.e. retina
For the normal functioning of eyes, the below given are important: a. Integrity of fibrous coat, nervous (retina) coat and good perfusion from the middle coat (vascular coat). b. Integrity/transparency of the various refractive media, i.e. cornea, lens and vitreous. c. The visual pathways, i.e. the optic nerve, optic chiasma, optic tract, lateral geniculate body, optic radiations and occipital cortex. d. Normal intraocular pressure, which may be compromised in severe trauma Mechanism of penetrating injury: Objects likely to cause penetrating ocular injuries include hammer and chisel, glass pieces, knives, thorns, darts, nails and pencils. Perforating injuries causes more damage to eyeball with poorer visual prognosis as compared to penetrating injury. The more posterior the injury, the more difficult to manage with a poorer visual prognosis. Small penetrating injuries of the cornea may self seal with little visual morbidity, especially if they are off the visual axis. It may involve the 87
Retina anterior capsule of the lens and cause a localized or more commonly a diffuse lenticular opacity. As part of the protective reflex, the eye rotates upwards as it closes (Bell’s phenomenon) and penetrating injuries are often situated inferiorly in the sclera. Thus, majority of the scleral and corneo-scleral wounds involve underlying structures, and prolapsed iris or choroid need to be replaced or removed prior to closure of the wound. Posterior wounds involve the retina, and the development of vitreo-retinal traction and scarring in the period after the injury are important factors in the development of complex retinal detachments. Another type of injury that needs mention is the intraocular foreign body (IOFB) with penetrating injuries which will be discussed as another chapter as it itself is a huge topic
OCULAR TRAUMA SCORE (OTS) : The OTS uses a limited number of variables (readily determined at the time of the initial evaluation) and basic mathematics. It has a predictive accuracy approximately 80% regarding the final functional outcome. It is recommended that the OTS be at hand (for e.g., in the form of a wall chart) wherever patients with eye injuries are treated. The OTS range from 1 (most severe injury and worst prognosis at 6 months follow-up) to 5 (least severe injury and least poor prognosis at 6 months).
MANAGEMENT: The course of events and final outcome following ocular trauma is also important from medicolegal purposes—litigation against the accused, insurance claims, workers’ compensation issues and even cases of medical negligence. Thus, the consequences are legal, social and economic. Resident doctors or emergency medical officers with little or no training in ophthalmology are often involved in the recognition, initial documentation and management of ocular trauma. In these situations, the lack of clear instructions and guidance to support decision making has been a key challenge, which also has been compounded by the inconsistent terminologies and classification used to describe ocular injuries. A standardized algorithm is mandatory for proper evaluation of ocular trauma and accurate conveying of information 88
Retina Sometimes, an ophthalmologist may be requested by the police or the court to examine victims with ocular injury and to give expert evidence. In such situations, the victims may be seen several weeks or months after the assault or the cause for the litigation, while the original injuries have changed with time due to healing, repair and remodeling. In these cases, it is imperative that the initial medical report issued/prepared by the doctor who first saw the case should be documented properly. If documentation is not properly done at the first instance, it may lead to failure of proving the alleged issue by the victim in the court of law leading to miscarriage of justice. Consequently, because of the complexity of the context, the forensic approach should show more diligence, accuracy and responsibility. It requires a detailed eye examination, including an accurate documentation of lesions and appropriate investigations to support the diagnosis
REMEDIES AND IMMEDIATE MANAGEMENT: History taking very important to 1. To identify cause of trauma and risk of retained IOFB 2. Possible size of object 3. Risk of intra-ocular penetration 4. Possible organic injury 5. Risk of unwitnessed fall (elderly patient), needs medical work up On examination: Document visual acuity of both eyes and relative afferent papillary defect (RAPD) if present. Careful examination should be performed with adequate analgesia (use preservative free topical anaesthetic agent or consider systemic analgesia) - Wear gloves and manipulate lids gently without exerting pressure on globe - Do not try to remove foreign bodies: risk of extruding contents - Do not instil antiseptic agents - Use preservative free dilating agents for fundoscopy
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Retina ∙ Look for: - Peri-orbital swelling, orbital fracture - Through-and-through eyelid wounds - Chemosis/sub-conjunctival haemorrhage may be an indicator of occult injury - Limited eye movements - Full thickness corneal (perform Seidel test with 2% fluorescein for cases where penetration is in doubt) or scleral laceration (uveal tissue visible) - Anterior chamber- depth disparity (compare to other eye), deep or shallow, hyphaema - Intra-ocular pressure disparity if no obvious signs of injury - Iris- Iridodialysis, Iris transillumination defects
prolapsed,
peaked
pupil
towards
wound,
- Careful gonioscopy for IOFB hidden in angle - Lens: Lens subluxation or dislocation. Focal cataract may indicate the presence of an IOFB - Vitreous haemorrhage may indicate posterior trauma and /or IOFB - Choroidal rupture - Commotio retinae or retinal haemorrhages - Retinal breaks and/or detachment
ACUTE MANAGEMENT: ∙ Continuous monitoring of ABCDE and keep nil by mouth ∙ Place eye shield ∙ Adequate intravenous pain management with anti-emetic to avoid vomiting ∙ Administer IV fluids and systemic antibiotics as appropriate ∙ Confirm tetanus status and administer prophylaxis if required ∙ Admit, bed-rest, advice to avoid valsalva ∙ Determine necessary imaging: CT brain and orbits if suspected IOFB and cannot visualise anterior and posterior segments. 90
Retina ∙ Avoid B scan if perforation or globe rupture suspected as may extrude intraocular contents and contaminate wound further. Perform under senior supervision if necessary.
REFERAL: Refer the patient urgently to a facility that has the following: ●
An ophthalmic surgeon who is equipped for pars plana vitrectomy
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Imaging facilities: orbital X-ray and ultrasound, and CT scan. MRI is contraindicated until you have excluded the possibility of a metallic IOFB
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An operating theatre where urgent removal of IOFB, intravitreal antibiotic injection and surgical repair can be done.
Gently explain to the patient that multiple operations may be required and that visual prognosis is uncertain, but taking up the referral as quickly as possible will give them the best chance. Send the patient with a comprehensive referral note and alert the surgeon. Post ED management The main aims of ophthalmic care are to preserve vision wherever possible, restore normal anatomy and prevent future complications. Surgery is not always indicated but primary repair is usually attempted to close the wounds even if the eye has very little or no visual potential. An intact eye is much better cosmetically. The alternative is evisceration or enucleation. SPECIALITY CLINIC INVOLVEMENT: CLINIC
Involve if
Cornea
∙ History of corneal transplant or corneal diagnosis impacting on management plan ∙ Associated microbial keratitis
Glaucoma
Recalcitrant increased intra-ocular pressure during admission ∙ Severe hypotony due to suspected cyclodialysis cleft ∙ Patients with previous filtering surgery/drainage device directly involved in the injury
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Retina Neuroophthalmolo gy
Traumatic optic neuropathy
Orbit
Orbital fracture with diplopia or globe displacement ∙ Significant retrobulbar haemorrhage with potential visual loss ∙ Complicated lid lacerations involving levator and canalicular system ∙ Severe ocular trauma where evisceration/enucleation may be required ∙ Compartment syndrome ∙ Orbital foreign body ∙ Optic canal fracture with potential need for decompression
Vitreo retina ∙ presence of an IOFB in the posterior segment ∙ if the Perforation extends behind the muscle insertion ∙ after primary repair, if there is posterior segment involvement, e.g. RD . endophthalmitis
SUMMARY: Penetrating injuries are rare but important. Prompt and accurate detection improves outcome. Hopefully this has provided a structure to enable targeted story taking, effective examination, appropriate investigation and accurate referral
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Retina REFERENCE: 1. Thylefors B. Epidemiological patterns of ocular trauma. Aust N Z J Ophthalmol. 1992;20:95–8. 2. Negrel AD, Thylefors B. The global impact of eye injuries. Ophthalmic Epidemiol. 1998;5:143–69 3. Gothwal VK, Adolph S, Jalali S, Naduvilath TJ. Demography and prognostic factors of ocular injuries in South India. Aust N Z J Ophthalmol. 1999;27:318–25 4. Ilsar M, Chirambo M, Belkin M. Ocular injuries in Malawi. Br J Ophthalmol. 1982;66:145–8. 5. Olurin O. Eye injuries in Nigeria. Am J Ophthalmol. 1971;72:159–66 6. Ocular Surgery News Asia Pacific Edition, October 2010.
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R.I.O.F.B Retained Intraocular Foreign Body Dr. Thomas Cherian, MS, FLVPEI Chief of Vitreo-Retina services Little Flower Hospital and Research Center, Angamaly, Kerala
Dr. Remya Mareen Paulose DNB, FLVPEI, FICO, FAICO Consultant VR Surgeon Little Flower Hospital and Research Center, Angamaly
Introduction: Foreign objects that penetrate the eyeball and become lodged inside are called intraocular foreign bodies (IOFB). They are present in up to 16- 41 percent of all open globe injuries. [1-3] Retained IOFB represent true emergency as improper diagnosis or delay in management can lead to sight threatening complications by endophthalmitis, retinal detachment and metallosis. Hence RIOFB needs to be meticulously worked up and managed. Retained intraocular foreign bodies most commonly result from occupational activities and predominantly involve males in 3rd to 4th decade.[4] The visual prognosis depends on the zone of injury, type and size of foreign body and the subsequent complications. Increased awareness about eye protection, improved surgical techniques, and advancements in bioengineering are responsible for an improved outcome in injuries with IOFB. Pathophysiology: The final resting place as well as the damage caused by an IOFB depend on several factors, including the size, shape, and composition of the object as well as the momentum of the object at time of impact. [5] Inert substances such as glass, stone, and plastic are better tolerated than metals such as copper or iron. Metallic and magnetic objects are the most common IOFBs. Organic material such as vegetable matter or cilia are highly contaminated , hence cause severe tissue reaction and are associated with a significant risk of endophthalmitis. The extent of injury varies depending on the size of the object and the mechanism of entry. Foreign bodies entering the sclera usually cause more 94
R.I.O.F.B damage than those entering the cornea. IOFBs traversing the lens are less likely to cause major retinal damage; conversely, a smaller wound size usually means deeper penetration. High-speed, small FB will cause a small linear laceration that is less damaging than blunt trauma. However, large irregular IOFBs can cause significant initial damage. A foreign body entering the eye can cause damage to the ocular tissues either by direct impact (as shown in Fig.1), or infective/ chemical as well as inflammatory interaction on the ocular tissues.
Fig 1. A- Fundus imaging reveals a large macular tear caused by a direct highvelocity impact. B- Note the large visible metallic IOFB on the inferonasal retina. An IOFB can be associated with penetrating or perforating injury and can involve the anterior chamber (Fig. 2), crystalline lens, posterior chamber, and even the orbit if a posterior exit wound is present. The location of IOFB is an important factor determining the visual prognosis. Posteior segment foreign bodies are generally associated with poorer visual prognosis than anterior segment foreign bodies. Evaluation of a patient with IOFB : It is important to consider all open-globe injuries to have an IOFB until proven otherwise, especially in patients with a history of drilling, hammering, and grinding.[6] In case of doubt, it is advisable to err on the side of an IOFB presence. There are certain key findings in history and clinical examination which help the physician to raise suspicion regarding presence of IOFB. (summarized in table. 1) The most common medicolegal issue against the ophthalmologist in a trauma case is a missed foreign body. Hence it is imperative to note that the vision may be unaffected initially and the patient may be unaware of any object entering/ striking the eye. 95
R.I.O.F.B History
Clinical examination
Occupation- Drilling, Hammering Blast injury Lack of protective eye wear Time elapsed after injury
Corneal wound/ opacity Self-sealed corneal tear Localized lenticular opacity Iris hole Iris heterochromia
Table 1. Key features in history taking and clinical examination that should raise suspicion of a retained IOFB. History taking: A detailed history is very important in IOFB injuries to ascertain the type or material of the foreign body and mechanism of injury. In addition, unilaterality or bilaterality should be determined as well as extraocular injuries to appropriately manage the patient. Blast injuries usually cause bilateral ocular damage with multiple foreign bodies. Patients might be asymptomatic or often report a sensation of something entering the eye with no obvious external changes and the incident may be dismissed initially. Other patients may notice decreased vision, a foreign body sensation, redness, tearing, flashes or floaters. Still others might be asymptomatic but on exam an small entry wound is found. Clinical Examination: A complete examination of both eyes is necessary, including the visual acuity. A corneal entry wound and a localised lenticular opacity/ hole in the iris provide clue towards the path of IOFB. Careful slit lamp evaluation is extremely useful in detailing all anterior segment pathologies. Fundus evaluation with indirect ophthalmoscopy should be done through a dilated pupil which may allow direct visualization of the IOFB. Generally, gonioscopy and scleral depression are not recommended unless the entry wound has been surgically closed.
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Fig 2- Evident foreign body entry sites- Scleral entry (2a) and corneal entry with protruding IOFB(2b). Fig 2c Localised corneal scar with corresponding iris hole and traumatic cataract provide clue towards the trajectory of IOFB. Investigations: Computerized Tomography scan (CT)- Non contrast computed tomography is currently considered the “gold standard” for the detection, localization of both metallic foreign bodies. A CT scan with axial and coronal views with thin slices (<1.5 mm) is highly sensitive (~95%) for the detection and localization of an IOFB and rules out the presence of a metallic foreign body.[7] In a patient with acute trauma, a CT scan offers several advantages in the form of no manipulation with an open globe, minimal co-operation required from the patient. In addition to detecting and accurately localizing the foreign body, CT also helps to find out the composition by comparing with the radiodensity of bone and thus helps in surgical planning. CT scan on the other hand may not be beneficial in detecting smaller foreign bodies < 0.7 mm or a wooden FB.
Fig 3. CT scan orbit of a case of penetrating iron nail. Lateral view (3c) provides more information on the depth of penetration which is further well delineated with 3dimensional reconstruction images as in fig 3d.
X- ray Orbits- Although less sensitive than CT scan, X ray should be done in all high velocity injuries with a suspicion of IOFB as a part of screening. It can detect 97
R.I.O.F.B radiopaque FBs (metal and stone) in majority of cases. However X rays have 60% false negative rate among all cases of foreign bodies. [8] Ocular Ultrasonography- USG B scan of the eye is done only after the repair of scleral or corneal perforation. It can detect a radiopaque or radiolucent foreign body. In B scan each foreign body is characterised by the high reflective nature persisting on low gain and acoustic shadowing. In addition, it can also pick up concurrent pathologies like vitreous haemorrhage, posterior globe perforation, retinal detachment and endophthalmitis. Use of a B-scan has several advantages, including its high resolution (0.01 to 0.1 mm), quick generation of multiple crosssections, and low cost, making it one of the most commonly used tests, but it must be performed extremely carefully in eyes with open-globe injury because the pressure of the probe on the eye poses a risk of contamination or extrusion of globe material. [8,9]
Fig 4. Ultrasound B scan showing high spike vitreous echo with posterior acoustic shadowing. MRI scan- MRI is not routinely used to detect intraocular foreign bodies, despite its greater sensitivity and soft tissue resolution, but may be useful for detecting radiolucent foreign bodies. It [11] It may be considered in suspicious cases after ruling out a metallic foreign body with CT scan. It is usually indicated for the detection of small wooden or plastic foreign bodies not picked up on conventional CT scan. Preoperative prognostic factors: Poor prognostic factors Poor visual acuity at presentation Presence of relative afferent pupillary defect Delay in presentation Posterior location and large size of foreign body Multiple foreign bodies 98
R.I.O.F.B Associated damage to other ocular structures like lens, retina, choroid etc Presence of infection Management of IOFB: Initial treatment Treatment of the injured eye with an IOFB includes protection of the globe with a shield, not a patch, avoiding any pressure over the globe. Tetanus status should be determined and updated as needed. The surrounding area should be cleaned and small pieces of foreign bodies around the eye should be removed, especially in cases of explosives. A delay in management can increase the risk for infection. Broad-spectrum intravenous antibiotic prophylaxis should be started. Counselling After the presence of IOFB is confirmed, the management plan should be discussed with the patient and family. Patients with better presenting vision are more likely to have better visual outcome. Nevertheless, even in patients with good presenting vision need to be counselled on the unpredictable final vision due to potential vision threatening sequelae (eg. Retinal detachment or endophthalmitis) Timing of surgery The timing of intervention is primarily determined by whether the risk of endophthalmitis is high. If the risk is high, immediate (emergency) surgery, for intraocular foreign body (IOFB) removal as well as vitrectomy if the IOFB is in the posterior segment, is indicated.[12] In most other cases, the surgeon has the option of deferring intervention for a few days to reduce the risk of intraoperative haemorrhage. The wound, however, should be closed as soon as possible. Surgical management: Closure of entry wound The first and foremost step in any open globe injury is the closure of the entry site. While corneal wounds are easily identified, a conjunctival peritomy will be requires to identify and repair the full extent of the scleral wound. Anterior chamber foreign body If the lens is not involved, the pupil should not be dilated or constricted by miotics to prevent any further injury to the lens. Removal of the IOFB is not 99
R.I.O.F.B recommended through the original entry wound. The foreign body should be removed through a surgical incision depending on the location and size of the foreign body. Usually a shelved incision that is the size of the IOFB is created either in clear cornea or sclera. Viscoelastics should be used to reduce the risk of iatrogenic damage to the corneal endothelium and the lens. Posterior segment IOFB: Pars plana approach is the preferred procedure in posterior segment IOFB cases. The standard 3 port set up is used. Sclerotomy incision should avoid the area of the entry wound to prevent further damage to intraocular tissues if any incarceration is suspected. The first goal of the vitrectomy is to remove any adhesions of the IOFB, to avoid any pull on the retina. Once the foreign body is free from all the adhesions, it can be removed with forceps or a magnet. Before removing the foreign body, peripheral examination of the retina and removal of the peripheral vitreous should be performed to avoid any traction while removing the foreign body through the sclerotomy. If the IOFB is larger than the sclerotomy site, enlargement of the sclerotomy in a circumferential direction may be necessary. A very large IOFB is best managed through a limbal incision after a lensectomy.
Fig 5- Step wise approach in a case of posterior segment IOFB with traumatic cataract. 5a- Lensectomy done. Note that the anterior capsular rim is kept intact for future intraocular lens implantation. 5b- Removing all vitreous adhesions form the IOFB with the vitrectomy cutter. 5c- Endolaser done all around the retinal impact site. 5d- Engaging the foreign body with suction cannula. 5e- IOFB 100
R.I.O.F.B brought in to the anterior chamber. 5f- Meticulous removal of IOFB with the help of forceps through a self- sealing corneoscleral tunnel incision. Intraocular antibiotics: Use of intravitreal antibiotics should be considered in contaminated cases. For endophthalmitis prophylaxis, intravitreal vancomycin (1.0mg/0.1ml) and ceftazidime (2.25mg/0.1ml) is given. In cases of penicillin allergy, intravitreal amikacin (0.4mg/0.1ml) may be given instead of ceftazidime. If fungal infection is suspected, intravitreal amphotericin or voriconazole is indicated. Complications: Early Endophthalmitis Retinal detachment Optic neuropathy
Complications of IOFB Late Proliferative vitreoretinopathy Sympathetic ophthalmia Siderosis & Chalcosis
Table 3- Complications of IOFB Conclusion: Accurate and timely determination of an intraocular foreign body is important in all cases of open-globe injuries. The type of foreign body, mechanism of trauma, and time between trauma and patient presentation at a health facility are very important factors in the prognosis, given the potential for good visual recovery with an adequate surgical treatment. Understanding the limits in the detection of each type of foreign body and the respective imaging modality that is used, as well as the characteristics of the different intraocular foreign bodies, is of utmost importance to optimize the management of patients with ocular trauma. References: 1.
2.
3.
S. Yeh, M. H. Colyer, and E. D. Weichel, “Current trends in the management of intraocular foreign bodies,” Current Opinion in Ophthalmology, vol. 19, no. 3, pp. 225–233, 2008. Y. Zhang, M. Zhang, C. Jiang, and H. Y. Qiu, “Intraocular foreign bodies in China: clinical characteristics, prognostic factors, and visual outcomes in 1421 eyes,” American Journal of Ophthalmology, vol. 152, no. 1, pp. 66–73, 2011. C. C. H. Liu, J. M. K. Tong, P. S. H. Li, and K. K. W. Li, “Epidemiology and clinical outcome of intraocular foreign bodies in Hong Kong: a 13101
R.I.O.F.B 4. 5. 6.
7.
8. 9. 10.
11.
12.
year review,” International Ophthalmology, vol. 37, no. 1, pp. 55–61, 2017. Behrens-Baumann W, Praetorius G. Intraocular foreign bodies. 297 consecutive cases. Ophthalmologica. 1989; 198: 848. Potts AM, Distler JA. Shape factor in the penetration of intraocular foreign bodies. Am J Ophthalmol. 1986. 100:183-187. Williams DF, Mieler WF, Abrams GW, Lewis H. Results and prognostic factors in penetrating ocular injuries with retained intraocular foreign bodies. Ophthalmology. 1988;95(7):911-916. Patel SN, Langer PD, Zarbin MA, Bhagat N. Diagnostic value of clinical examination and radiographic imaging in identification of intraocular foreign bodies in open globe injury. Eur J Ophthalmol. 2012 Mar-Apr;22(2):259-68 Bryden FM et.al Real Time Ultrasound in Assessment of IOFB Eye 1990; 4: 727-31. Lit ES, Young LH. Anterior and posterior segment intraocular foreign bodies. Int Ophthalmol Clin. 2002 Summer;42(3):107-20. Zacks DN, Hart L, Young LH. Ultrasonography in the traumatized eye: intraocular foreign body versus artifact. Int Ophthalmol Clin. 2002 Summer;42(3):121-8. Ahmed Y, Schimel AM, Pathengay A, Colyer MH, Flynn HW Jr. Endophthalmitis following open-globe injuries. Eye (Lond). 2012 Feb;26(2):212-7. Kuhn F, Morris R, Witherspoon CD. Intraocular foreign body (posterior segment). In: Masters Techniques in Ophthalmic Surgery. Baltimore: Williams and Wilkins;. 1995:1201-1212.
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Optic Nerve TRAUMATIC OPTIC NEUROPATHY Dr. Rehna Rasheed Dr. Kannisha Shah MS, DO, FRCO London Junior resident MS Assistant Professor Amrita Institute of Medical Sciences, Kochi Amrita Institute of Medical Sciences, Kochi
Anatomy: The visual pathway begins with the retina and the optic nerve (ON). It continues posteriorly as the of the optic chiasma, optic tracts, lateral geniculate nucleus (LGN), optic radiations and visual cortex. Frontal eye fields present in Brodmann area 8 also contributes to vision. (1-4) The retina consists of 500,000 to 1.2 million ganglion cells. The axons of these ganglion cells converge to form the optic nerve at the optic disc. (1,4) The optic nerve is the only tract in the central nervous system (CNS) which leaves the cranial cavity and can be examined clinically. (2) The ON can be divided into 4 parts:
Fig. 1 – Parts of the optic nerve – 1) Intraocular ON , 2) Intraorbital ON, 3) Intracanalicular ON and 4) Intracranial ON
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Optic Nerve 1) Intraocular portion - It is 1 mm in length and extends from the surface of the optic disc to the posterior aspect of the sclera. The bundles of axons eventually exit from the eyeball via the orifices of the lamina cribrosa, which represents the sclera in this area. It receives its blood supply from the anastomotic circle of Zinn formed by the short posterior ciliary arteries. (5) 2) Intraorbital Portion- It is 25 to 30 mm in length. It continues backwards and medially from the posterior aspect of the eye towards the optic canal in the sphenoid at the apex of the orbit.(1,2) The central retinal vessels traverses the subarachnoid space and are more vulnerable to raised intracranial pressure.(2) This portion of the ON has a slight S-shaped bend, which allows free ocular movement without stretching the nerve. (1, 2) Near the orbital apex, the ON is surrounded by the tendinous annulus of Zinn, arising from the rectus muscles.(2, 4)The anterior segment of the optic nerve, i.e. between the optic nerve head (ONH) and the site of entry of the central retinal artery into the nerve is supplied by (i) A Peripheral Centripetal Vascular System formed by multiple pial branches from the peripapillary choroid, circle of Haller and Zinn, central retinal artery, ophthalmic artery and other orbital arteries and (ii) An Axial Centrifugal Vascular System formed by branches of the central retinal artery. The posterior Segment is primarily supplied by the peripheral centripetal vascular system formed by the pial vascular plexus, supplied by small collateral arteries which arise directly from the ophthalmic artery or from other orbital arteries.(5) 3) Intracanalicular Portion-It is 4 to 10 mm long. It passes through the optic canal, present within the lesser wing of sphenoid, along with the ophthalmic artery and the post-ganglionic sympathetic nerves. (2) The ON is surrounded by the three meningeal sheaths. This portion of the optic nerve is fixed since the dural sheath covering it fuses with the periorbita lining the optic canal. The cerebrospinal fluid fills the subarachnoid space here, which is continuous with the intracranial subarachnoid space. Medially, the intracanalicular portion of the ON is separated from the sphenoidal and posterior ethmoidal air sinuses by a thin layer of bone. This portion is also supplied by branches from the pial plexus which in turn receives its supply from the ophthalmic artery. (6) 4) Intracranial Portion – After the ON leaves the cranial end of the optic canal, it passes medially, backwards and slightly upwards within the subarachnoid space of the middle cranial fossa and it terminates at the optic chiasma at the floor of the fourth ventricle. (1,2) Superiorly it is 104
Optic Nerve related to the olfactory tract, the gyrus rectus and the anterior cerebral artery and laterally to the interiorly carotid artery. (6) The intracranial part of the ON is also supplied by the pial plexus, however here the plexus receives its blood supply from branches from the superior hypophyseal artery, the internal carotid, the anterior cerebral artery and small recurrent branches from the ophthalmic artery (6)
Fig.2 : Shows the course and blood supply of the ON
Fig.3 : Arterial supply of the ON
Venous drainage of the optic nerve: The venous drainage of the ONH is mainly by the central retinal vein. The orbital portion is drained by the peripheral pial plexus and by the central retinal vein in its distal portion. The intracranial part is drained by the pial plexus which drains into the anterior cerebral and basal veins. (5)
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Fig. 4 : Venous Drainage of the ON
Epidemiology: Traumatic optic neuropathy (TON) is a devastating sequelae of blunt or penetrating trauma to the head which can lead to loss of visual function. A history of fall, motor vehicle accidents and assault are commonly elicited. Other causes include stab and gunshot wounds or during endoscopic sinus surgeries. The incidence of TON is between 0.7 – 2.5% (7-10). Males, the early 30s, are more commonly (80%) reported to have TON when compared to females. (11,12) There is a significant association between head injury and TON, as all patients with TON have head injuries. (12) Similar to adults, common etiologies of TON in the paediatric age group includes a history of fall or motor vehicle accident. (13)
Site, Mechanism and Pathophysiology of Injury: TON can be classified based on (14,15) A) Site of Injury: - ONH - Intraorbital portion - Intracanalicular portion - Intracranial portion B) Mode of Injury:
- Direct injury - Indirect Injury 106
Optic Nerve Direct injury: Direct trauma to the ON by a projectile or sharp object penetrating the orbit or due to anatomical disruption of the optic nerve with direct involvement of the optic nerve in the form of mechanical contusion or concussion, or by laceration of the ON by an orbital fracture fragment or by partial or complete ON avulsion. On the other hand, indirect TON occurs as a result of blunt head trauma causing transmission of forces to the ON via the oculofacial tissues and skeleton from a distant site. These forces tend to concentrate around the region of the optic canal. Indirect TON has a higher prevalence than direct TON. TON is seen in 0.5% to 5% in patients with closed head injury and in 2.5% of patients with midfacial fractures. (16,17) Intracanalicular segment of the optic nerve is most susceptible site of TON.This is because this segment of the ON is fixed as the dural sheath is adherent to the surrounding periosteum.(18,19) Also the canal itself is a closed bony structure, that restricts expansion due to edema or haemorrhage. The intraorbital portion however is usually spared due to the buffering effect of the surrounding fat and extraocular muscles and also because of its lax structure. The intracranial segment is spared not only because it is surrounded by the brain and skull but also due to the fact that maximum shearing forces are absorbed by intracanalicular segment. (20) A study using holographic interferometry on human skulls showed that damage to the frontal region leads to the deformation of the ipsilateral orbital roof, causing damage to the optic nerve and its supporting vasculature, especially upon the entry of the ON in the optic canal. (21) A study on trauma modelling in a virtual head and orbit suggested that even low intensity trauma to the frontal region, when transmitted to the optic foramen, can lead to indirect TON. This finding supports the theory that indirect TON is occurs more commonly secondary to a facial injury, when compared to trauma to the skull. (22) The pathophysiology of indirect injury leading to TON can be caterogorized into primary or secondary mechanism. (15,23,24) Primary mechanism: - Trauma to the head can lead to an immediate mechanical shearing of the ganglion cell axons of the optic nerve. Damage to the ON microcirculation lead to ischemia and contusion necrosis. Secondary mechanism: 107
Optic Nerve - Optic nerve swelling, which occurs from mechanical trauma or vascular ischemia, within the confines of the limited space in the optic canal, further compromises the blood supply to the retinal ganglion cells, leading to apoptosis of the already injured as well as the surrounding intact neurons.
Diagnosis: A)
Clinical Evaluation (25 ,26, 27) TON is a clinical diagnosis supported with a history of direct or indirect trauma to the head. A detailed history is to be taken regarding trauma. In situations where the patient is unconscious or in case of children, careful history can be taken from the witnesses or bystanders. Examination should include 1) unilateral or bilateral involvement, 2) ocular injuries, 3) visual acuity (VA), 4) colour vision, 5) extraocular muscles, 6) visual field examination, 7) pupil examination for relative afferent pupillary defect (RAPD), 8) Fundus examination. Patients with TON tend to have variable degrees of decrease in visual acuity, ranging from normal to no perception of light, defective colour vision, visual field defects and RAPD. In unconscious or disoriented patients, sometimes RAPD may be the only finding suggestive of TON. Also, in patients with mild TON, RAPD may be the only clinical finding before overt optic disc atrophy sets in. However, in cases with bilateral TON, RAPD may not be elicited. Fundus examination is also of utmost importance to rule out any other pre-existing cause of decrease of vision like retinopathy, maculopathy or optic neuropathy and also to look for any associated posterior segment pathologies related to trauma like pre-retinal haemorrhage, vitreous haemorrhage, retinal detachment, Berlin’s edema etc. In majority of the cases, posterior aspect of the ON is involved. Hence on clinical examination, ONH appears normal. In situations where the ON is damaged anterior to the entry of the central retinal vessels, ONH edema and retinal haemorrhages will be present. However, irrespective of the appearance of optic disc at the time of injury, optic atrophy tends to set in approximately six weeks after initial trauma. (28)
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Fig. 5 : Fundus picture of a 23 year old male with left eye TON 6 weeks later B)
Investigations: All patients who have sustained head or craniofacial trauma along with features of ON damage should undergo neuroimaging, especially when therapeutic interventions are being considered or when there is progressive visual impairment. CT scan In cases of trauma, high resolution CT with 1mm cuts is preferred. It is considered to be the better imaging modality to detect any optic canal fractures, orbital wall fractures or to look for the presence of haematoma in the orbit. It is also helpful in differentiating between direct and indirect TON as well as to plan any surgical intervention, if required. It has been found that the presence of posterior orbital wall fractures in patients with indirect TON has a poorer prognosis when compared to indirect TON with anterior orbital fractures. Hence CT scan can be used for prognostication (28 ,29,30).
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Fig.6: Axial cut of a CT scan showing a right sided optic strut fracture in a patient with Right sided TON
Fig.7: Coronal section of a CT scan showing a right sided orbital roof fracture at the orbital apex
Fig.8: Coronal section of a CT scan in right TON showing a right sided displaced fracture of the orbital roof fracture impinging onto the medial rectus.
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Magnetic Resonance Imaging Imaging with MRI is useful in evaluating the ON and to detect any haematoma within the ON sheath.(29) It is of utmost importance to rule out the presence of a metallic foreign body before taking up for MRI. A study conducted by Bodanapally et al., showed that indirect TON could be diagnosed based on optic nerve hyperintensity on diffusionweighted imaging (31). In another study, the diffusion tensor imaging technique showed fractional anisotropy reduction only by the second week in the damaged eye which continued to be visible after one month which suggest that CT scan is superior in the early phases post trauma.(32) Visual Evoked Potential (VEP) VEP can be of value in cases where pupillary responses are not reliable and in bilateral TON. It has been found that better responses to VEP have a better visual recovery as compared to those who do not.(33,34,35) A few studies have showed that pattern reversal and flash VEP can be helpful for determining the rate of visual recovery. A VEP amplitude of 50% in the affected eye will have a better vision recovery when compared to those patients with an absent VEP.(35-37). Optical Coherence Tomography(OCT) OCT scanning are being used to show retinal nerve fibre layer (RNFL) thinning in patients with TON. Performing an OCT scan can be difficult at initial presentation, it is valuable for the long- term follow up of ON injury. (38,39,40) Ultrasound Doppler Sonography This investigation can be used to evaluate the hemodynamic status of the central retinal artery (CRA). It has been found that the peak systolic velocity, end-diastolic velocity and the time-average mean velocity were reduced in TON.(41)
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Optic Nerve Visual Field (VF) Examination Visual field examination should be undertaken for all patients with TON. TON does not present with a particular visual field defect. They may present with either an arcuate, central or hemianopic field defects.(29)The baseline VF of these patients are usually severely depressed compared to normal subjects. But a baseline VF is useful for follow up to see any improvement in the VF.
Management: Medical Treatment The main medical treatment for TON is corticosteroids. The use of corticosteroids for TON was rationalized based on the neuroprotective effects due to their antioxidant properties.(42) The use of high-dose corticosteroids for TON was derived from the National Acute Spinal Cord Injury Study (NASCIS)(43). The NASCIS 2 was a multicenter clinical trial that evaluated patients with acute spinal cord injury treated with either a placebo, methylprednisolone, or naloxone. The study showed that methylprednisolone when started within 8 hours of injury was associated with a significant improvement in both motor and sensory function as compared to patients treated with a placebo. The findings of the NASCIS trials significantly influenced clinical practice in TON and led to an increased use of steroids in treating TON. The International Optic Nerve Trauma Study (IONTS)(44) was a large comparative study that analyzed 133 cases of indirect TON treated with either corticosteroids, surgical decompression of the optic nerve, and observation. However, following adjustment for baseline visual acuity (VA), no significant differences were found between the three groups. Neither the dose nor the timing was associated with a higher probability of visual recovery. In a placebo-controlled clinical trial, 31 eyes of 31 patients were divided into two management groups. Sixteen eyes received 250 mg intravenous methylprednisolone 6 hourly for 3 days, followed by oral administration of 1 mg/kg prednisolone for 14 days. The other 15 eyes received a placebo(45). This study confirmed previous understanding that there is no difference in VA improvement between steroids and placebo in the treatment of TON. 112
Optic Nerve In a pilot study in 2011, 7 cases with indirect TON received daily intravenous injections of 10,000 IU erythropoietin (EPO) for three days. They were compared to eight patients who received no specific treatment(46).The final VA was found to be significantly higher in the EPO group, suggesting a safer and more efficient treatment for patients with TON. In another case series, 18 eyes of 18 indirect TON patients received 20,000 IU EPO daily injections for three consecutive days(47). This study also reported a significant improvement in VA in patients with recent indirect TON, treated with EPO. In the Traumatic Optic Neuropathy Treatment Trial (TONTT), 120 patients underwent treatment with EPO, methylprednisolone, or observation(48). Although colour vision was reported to improve in the EPO group, no significant difference in improvement of VA was found between the three groups. Corticosteroids and EPO are not without complications. Corticosteroid Randomization after Significant Head Injury (CRASH) study was terminated prematurely due to the increased rate of death in the high-dose corticosteroid group (49). The Optic Neuritis Treatment Trial also had reported two cases of acute psychosis and acute pancreatitis in the steroid treatment group, both resolving without any sequelae(50). Transient hypotension has been reported in studies with EPO, which can be dangerous for patients having multiple trauma and unstable medical conditions(47) . Surgical Treatment: Decompression of the ON by releasing the edema, hematoma, or compression caused by fractured bone segments on the optic nerve is the rationale behind surgical therapy in TON. Surgical therapy is indicated in the presence of bone segments or hematoma compressing the nerve at the time of initial presentation and poor response to initial medical treatment, Some reports suggested that surgery should be performed within 2 or 3 days of the trauma (51, 52). However, according to a recent meta-analysis, more than half of the patients treated surgically even after seven days had an improvement in vision which was comparable with the early treatment group who underwent surgery within three days (53).
The three main approaches for ON decompression include medial transorbital and external ethmoidectomy, transcranial surgery, and endoscopic transnasal approach. The advantage of the transorbital and transcranial approaches are 113
Optic Nerve their superior surgical view and wide ON decompression, although at the expense of cosmesis. Transnasal approaches, on the other hand, do not have much cosmetic concerns, but they provide relatively less decompression of the optic nerve which may limit surgical outcomes. A modification to surgical decompression of the optic nerve has been proposed where the classic transcranial approach, the supraorbital approach may be performed through extradural unroofing of the optic canal via an endoscope(51,52) . In the endonasal approach, total circumference decompression of the ON through a combined transorbital and transnasal approach is underway(53). Prognosis: Direct and indirect TON have different prognoses. Direct TON causes severe, permanent visual impairment with minimal probability of visual recovery(28), while visual recovery can occur in 40–60% of cases with indirect TON even with conservative management. Baseline VA is found to be a significant predictor of the final outcome (19, 25,54). It has also been reported that visual recovery and final VA may also be lower in patients with loss of consciousness, lack of visual recovery after 48 hours, absence of visual evoked responses, presence of blood within the posterior ethmoid cells, age over 40 years, optic canal fracture, and intraconal hematoma and hematoma along the optic nerve (19, 26, 36, 54)
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Optic Nerve following traumatic optic neuropathy,” Arquivos brasileiros de oftalmologia, vol. 72, no. 5, pp. 622–625, 2009. 39) K. Mohan, H. Kecova, E. Hernandez-Merino, R. H. Kardon, and M. M. Harper, “Retinal ganglion cell damage in an experimental rodent model of blast-mediated traumatic brain injury,” Investigative Opthalmology & Visual Science, vol. 54, no. 5, pp. 3440–3450, 2013. 40) B. C. Chauhan, K. T. Stevens, J. M. Levesque et al., “Longitudinal in vivo imaging of retinal ganglion cells and retinal thickness changes following optic nerve injury in mice,” PLoSOne, vol. 7, no. 6, Article ID e40352, 2012. 41) S. Wei, H.-z. Wang, W.-x. Song, W.-l. Yang, W.-y. LI, and N.-l. Wang, “Axonal loss and blood flow disturbances in the natural course of indirect traumatic optic neuropathy,” Chinese Medical Journal, vol. 126, no. 7, pp. 1292–1297, 2013. 42) E. D. Hall, “The neuroprotective pharmacology of methylprednisolone,” Journal of Neurosurgery, vol. 76, no. 1, pp. 13–22, 1992. 43) M. B. Bracken, M. J. Shepard, W. F. Collins et al., “A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury,” New England Journal of Medicine, vol. 322, no. 20, pp. 1405–1411, 1990. 44) Levin LA, Beck RW, Joseph MP, Seiff S, Kraker R. The treatment of traumatic optic neuropathy — the International Optic Nerve Trauma Study. Ophthalmology. 1999;106:1268–1277. 45) M. Entezari, Z. Rajavi, N. Sedighi, N. Daftarian, and M. Sanagoo, “High-dose intravenous methylprednisolone in recent traumatic optic neuropathy; a randomized double-masked placebo-controlled clinical trial,” Graefe’s Archive for Clinical and Experimental Ophthalmology, vol. 245, no. 9, pp. 1267–1271, 2007. 46) M. B. Kashkouli, F. Pakdel, M. S. Sanjari et al., “Erythropoietin: a novel treatment for traumatic optic neuropathy—a pilot study,” Graefe’s Archive for Clinical and Experimental Ophthalmology, vol. 249, no. 5, pp. 731–736, 2011. 118
Optic Nerve 47) M. Entezari, M. Esmaeili, and M. Yaseri, “A pilot study of the effect of intravenous erythropoetin on improvement of visual function in patients with recent indirect traumatic optic neuropathy,” Graefe’s Archive for Clinical and Experimental Ophthalmology, vol. 252, no. 8, pp. 1309–1313, 2014. 48) M. B. Kashkouli, S. Yousefi, M. Nojomi et al., “Traumatic optic neuropathy treatment trial (TONTT): open label, phase 3, multicenter, semi-experimental trial,” Graefe’s Archive for Clinical and Experimental Ophthalmology, vol. 256, no. 1, pp. 209–218, 2018. 49) C. T. Collaborators, “Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury—outcomes at 6 months,” The Lancet, vol. 365, no. 9475, pp. 1957–1959, 2005. 50) R. W. Beck, P. A. Cleary, M. M. Anderson Jr. et al., “A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis,” New England Journal of Medicine, vol. 326, no. 9, pp. 581–588, 1992. 51) E. Emanuelli, M. Bignami, E. Digilio, S. Fusetti, T. Volo, and P. Castelnuovo, “Post-traumatic optic neuropathy: our surgical and medical protocol,” European Archives of Oto-Rhino-Laryngology, vol. 272, no. 11, pp. 3301–3309, 2015. 52) T.-M. Wohlrab, S. Maas, and J. P. De Carpentier, “Surgical decompression in traumatic optic neuropathy,” Acta Ophthalmologica Scandinavica, vol. 80, no. 3, pp. 287–293, 2002. 53) S. S. Dhaliwal, L. J. Sowerby, and B. W. Rotenberg, “Timing of endoscopic surgical decompression in traumatic optic neuropathy: a systematic review of the literature,” International Forum of Allergy & Rhinology, Wiley, Hoboken, NJ, USA, 2016. 54) P. I. Chou, A. A. Sadun, Y. C. Chen, W. Y. Su, S. Z. Lin, and C. C. Lee, “Clinical experiences in the management of traumatic optic neuropathy,” Neuro-Ophthalmology, vol. 16, no. 6, pp. 325–336, 1996.
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B-Scan USG Ultrasonography in Ocular Trauma Dr. Gopal S Pillai MD DNB FRCS, Professor and HOD Ophthalmology, Amrita Institute of Medical Sciences, Kochi
Dr. Yashovardhan Siwach MBBS (MS) Junior Resident, Amrita Institute of Medical Sciences, Kochi
Ko
35
YEAR
OLD
PATIENT
WITH
BLUNT TRAUMA PRESENTING WITH SUDDEN LOSS OF VISION REVEALS
MILD
TO
. USG
MODERATE
INTERNAL SPIKES SUGGESTIVE OF VITREOUS WITHOUT
HAEMORRHAGE
PVD
75 YEAR OLD PATIENT WITH BLUNT TRAUMA-USG TAKEN 2 MONTHS LATER REVEALS MILD-MODERATE INTERNAL SPIKES IN THE VITREOUS CAVITY
WITH
A
CLEAR
SPACE
BETWEEN RETINA & THE POSTERIOR
MARGIN SUGGESTIVE OF VITREOUS HAEMORRHAGE WITH PVD
60 YEAR OLD DIABETIC PATIENT WITH BLUNT TRAUMA AND SUDDEN LOSS OF VISION-
USG
REVEALS
MILD
TO
MODERATE INTERNAL SPIKES IN THE VITREOUS CAVITY J UST IN FRONT OF RETINA WITH A CLEAR SPACE BEHIND THE LENS SUGGESTIVE OF PRERETINAL HAEMORRHAGE
120
B-Scan USG
68
YEAR OLD DIABETIC PATIENT
WITH BLUNT TRAUMA WITH LOSS OF VISION-USG- MILD TO MODERATE INTERNAL SPIKES BEHIND A VERY THICK MEMBRANE ATTACHED TO RETINA-
THE
HEMORRHAGE
RETROHYALOID
DD
IS SUBRETINAL
HEMORRHAGE
25
YEAR OLD WITH CRICKET BALL
INJURY WITH SUDDEN LOSS OF VISION-
USG
SHOWS LOW AMPLITUDE SPIKES
IN THE MID VITREOUS
ASSOCIATED
WITH A MEMBRANE WHICH IS BULGED
OUT AND HAVING MODERATE TO HIGH AMPLITUDE
SPIKES
WITHIN
IT-
SUBRETINAL HEMORRHAGE
60 YEAR OLD PATIENT WITH BLUNT TRAUMA TO THE EYE PRESENTING WITH FLOATERS
– VERY THIN LOW
AMPLITUDE SPIKE WHICH FLOATS AROUND
ON
DYNAMIC
ULTRASOUND- SUGGESTIVE OF PVD
121
B-Scan USG 25
YEAR OLD BOY HAVING A FISH
ROD INJURY WITH COMPLICATED CATARACT HAVING COMPLETE LOSS
3 INJURY. USG OF VISION
WEEKS AFTER THE SHOWS THICK HIGH
REFLECTIVE MEMBRANE ATTACHED TO THE DISC- RETINAL DETACHMENT
55
YEAR
OLD
PERFORATION VISION
WITH
WITH
WAS
CORNEAL LOW
IOP.
INACCURATE
PROJECTION. USG SHOWS
DOME
SHAPED MEMBRANES WITHIN THE
VITREOUS CAVITY NOT EXTENDING BEYOND
THE
POSTERIOR
POLE-
CHOROIDAL DETACHMENT
35
YEAR OLD PATIENT AFTER A
LACERATED SCLERAL PERFORATION REPAIR WITH NO PL VISION. USG
SHOWS LOW REFLECTIVE POINT LIKE SPIKES
SCATTERED
IN
THE
VITREOUS ALONG WITH A THICK HYPERREFLECTIVE
MEMBRANE
SUGGESTIVE OF ENDOPHTHALMITIS
WITH RETINAL DETACHMENT
122
B-Scan USG
35 YEAR OLD PATIENT WITH BLUNT INJURY WITH
CORNEO SCLERAL
PERFORATION REPAIRED- THE NON CATARACTOUS LENS CAN BE SEEN DISLOCATED INTO THE VITREOUS ON USG
40 YEAR OLD WITH SUDDEN BURST OF MACHINE PARTS ON HIS FACE COMING WITH LOSS OF VISION. SCLERAL PERFORATION AND A HIGH REFLECTIVE SPIKE RIOFB SEEN JUST ANTERIOR TO THE RETINA WITH SHADOWING
50
YEAR OLD WITH HISTORY OF
SCLERAL PERFORATION REPAIRED
2
YEARS BACK WITH LOSS OF VISION OVER
1
YEAR. ON USG, THICK
MEMBRANE SEEN IN THE VITREOUS ATTACHED TO THE DISC SHOWING RETINAL
DETACHMENT
POSTERIOR PVR
123
WITH
B-Scan USG
60
YEAR OLD WITH HISTORY OF
CORNEO
SCLERAL
PERFORATION
REPAIRED 6 YEARS BACK WITH LOSS
OF VISION FROM THEN. ON USG, THICK MEMBRANE SEEN IN THE VITREOUS ATTACHED TO THE DISC SHOWING RETINAL DETACHMENT WITH CLOSED FUNNEL
35
YEAR OLD HIGH MYOPE WITH
BLUNT
INJURY
TO THE
EYE
6
MONTHS BACK, NOW COMPLAINTS OF SUDDEN LOSS OF VISION- USG SHOWS
RETINAL
DETACHMENT
INFERIORLY WITH FREE FLOATING MEMBRANE
WITH
HIGH
AFTERMOVEMENTS SUGGESTIVE OF GIANT RETINAL TEAR
25
YEAR OLD MAN BROUGHT INTO
THE CASUALTY AFTER A ROAD TRAFFIC INJURY
ACCIDENT AND
CONSCIOUSNESS.
WITH
HEAD
LOSS
OF
USG
SHOWS
DISCONTINUITY OF THE POSTERIOR LAYERS OF THE SCLERA INDICATING SCLERAL RUPTURE
124
Imaging In Trauma CT and MRI in Trauma Dr. Rajesh Kannan Professor, Radiology Amrita Institute of Medical Sciences, Kochi
Dr. Niya K. Joy Junior Resident Amrita Institute of Medical Sciences, Kochi
66 year old male with history of fall from height .Sagittal and coronal MRI : Right globe shows reduced volume and buckled scleral outline with discontinuity in right superolateral aspect.
55 year old male with history of fall from height..CT brain & orbit axial & sagittal sections showing thickened posterosuperior sclera of left eyeball suggestive of scleral contusion
125
Imaging In Trauma
66 year old female with h/o accidental trauma of left eye with iron rod.Axial section & sagittal section showing displacement of lens into vitreous with partial collapse of left eyeball.
44 year old male presented with alleged history of RTA .VRT image showing comminuted fracture of roof of right orbit,fracture of inferior wall & lateral wall & medial walls of both orbit.
126
Imaging In Trauma
43 year old male with alleged history of RTA .CT brain & orbit axial section showing completely collapsed globe on left side
35 year old patient with history of RTA .Coronal section showing fracture floor of left orbit with herniation of retrobulbar fat & inferior rectus muscle into maxillary sinus 127
Imaging In Trauma
Axial section of MRI showing left optic Nerve Avulsion post Perforating globe injury
CT scan axial section showing intraocular metallic foreign body in the right eye
128
ATLAS Lid Laceration :
Pre Op. Post Op. Right eye full thickness lower lid laceration involving lid margin.
Left eye lower lid laceration involving lower canaliculus.
129
ATLAS
Left lower lid laceration with involvement of lower canaliculus [pre op and post op ]
Upper eye lid avulsion injury lid with full thickness lower lid laceration involving lid margin [pre op and post op ]
130
ATLAS
Right eye upper and lower lid laceration involving lower lid margin and lower canaliculus [pre op and post op ]
131
ATLAS
Full thickness left upperlid laceration involving lid margin with conjunctival laceration
Full thickness lower lid laceration involving lid margin and canaliculus
Full thickness lower lid laceration involving lid margin 132
ATLAS CORNEAL TRAUMA:
Penetrating corneal injury with a wooden piece.
Penetrating corneal injury from a metal piece.
Stellate Corneal Tear
133
ATLAS
Full thickness corneal injury with a pen. Slit lamp examination showing full thickness involvement.
Full Thickness Corneal Tear.
134
ATLAS
Full thickness corneal injury with shallow anterior chamber.
Full thickness corneal tear with iris prolapse.
135
ATLAS Chemical injuries:
Grade 2 chemical injury with epithelial defect and limbal ischemia
Corneal burn in a child with Incense Stick.
136
ATLAS
Bullous sub conjunctival hemorrhage with SICS wound gape and uveal prolapse in a case of blunt trauma
Iris spinchter tear and lens subluxation
137
ATLAS Traumatic lens dislocation
Lens dislocation into the anterior chamber of the eye in a case of blunt trauma
IRIS TRAUMA
Traumatic iridodialysis after blunt eye trauma
138
ATLAS
Closed globe injury with traumatic aniridia
SCLERAL INJURY
Penetrating Scleral wound with metallic foreign body
139
ATLAS
scleral laceration with uveal prolapse in a case of trauma with scooter handle
GLOBE RUPTURE
Right eye globe rupture in a boy with full thickness laceration involving the limbus
140
ATLAS
Left eye globe rupture with uveal prolapse.
Posterior Globe rupture with shallow AC, hyphema and soft eyeball
141
ATLAS
Open globe injury with hammering nail penetrating injury
grade -4 zone 1
Full thickness laceration of upper and lower lids involving the margins and canaliculi.
142
ATLAS
Open globe injury with a repaired corneal tear. The glass foreign body at the exit wound was missed during primary repair.
143
ATLAS POSTERIOR SEGMENT
Intra ocular foreign body with inferior retinal detachment
Fundus left eye shows vitreous haemorrhage in a case of closed globe injury 144
ATLAS
Fundus picture of Right eye posterior pole shows Optic nerve avulsion
Fundus picture of left eye with choroidal rupture temporal to the fovea. 145
ATLAS
Fundus picture of Right eye with choroidal rupture nasal to the fovea.
Closed globe injury with Chorioretinitis Sclopetaria
146
ATLAS
Commotio retinea in a case of closed globe injury.
Penetrating injury with endophthalmitis
147
NOTES
147
147
NOTES
148
148