Candidate 137

Final FRCS

Centre:    Muscat

   Date:    November 2009

MY FRCS EXPERIENCES –Muscat- Nov 15- 18 ,2009. Dr. Sreelekha.S
( FRCS Ophthalmology Part B, Glasgow )

Day 1

Problem Solving Paper with my answers in short. ( I was exempted from MCQ )

1- A 6 month old baby girl is brought to you by her parents complaining that her left upper eyelid is drooping. On examination the infant appears to have bilateral ptosis, more marked on the left, and objects to having the right eye occluded. The baby seems to be otherwise well, although the mother was diagnosed with multiple sclerosis 2 yrs earlier.
What are the possible diagnoses with this patient and how would you investigate and manage the case?

This 6 month old healthy baby girl with bilateral ptosis more marked on the left side with possible developing amblyopia in LE will be most probably having simple congenital ptosis . However other conditions such as Marcus Gunn Jaw winking , Blepharophimosis and Malignant conditions such as metastatic neuroblastoma (but more rapid onset and associated proptosis with ecchymosis ) to be excluded. History of Multiple sclerosis in the mother may not have direct relationship with the ptosis as demyelination is unlikely in infancy. However maternal steroid intake during pregnancy may cause malformations such as Optic nerve hypoplasia. History- of onset and duration of ptosis, family history, Basic ptosis evaluation, Hirschberg reflex, cover /uncover, observe for jaw winking when baby is sucking at the milk bottle, cycloplegic refraction and fundoscopy, rule out organic cause for Amblyopia. No special investigations needed for simple congenital ptosis. However referral to Paediatrician for a systemic work up and an Anaesthesia work up for fitness for GA. Consultation with Paediatric Ophthalmologist for management of Ptosis. Best option would be temporary Frontalis suture sling suspension to clear the visual axis and refractive correction with occlusion treatment for amblyopia. Definitive procedure such as Levator resection as needed when a formal assessment of ptosis is possible by Preschool age of 4-5 years. Neuroimaging ( CT/MRI orbits and brain ) is required if there is associated neurological deficits ,developmental delay or Optic nerve hypoplasia/ Optic atrophy.

2- A 35 yr old lady presents to casualty with a 2- day history of severe pain in her right eye which has kept her awake at night. On examination the eye is grossly injected and there is a small corneal ulcer just at the limbus. Acuities are 6/12 right and 6\6 left. She also has a history of rheumatoid arthritis. What is the differential diagnosis and how would you manage the case?

This adult female with history of Rheumatoid arthritis has presented with acute painful R red eye with peripheral corneal ulcer. Her ocular problem is most likely related to her systemic disease – Peripheral ulcerative keratitis in association with Rheumatoid arthritis. However infective microbial keratitis should be ruled out urgently by Smears and C&S studies. Occasionally problem may be unrelated . Other causes of Peripheral ulcerative keratitis to be ruled out by history and clinical evaluation ( Blepharitis, trichiasis, Rosasea keratitis, idiopathic Mooren’s ). I will admit the patient and treat for corneal ulcer and urgently consult with Rheumatologist for management of systemic disease which will require systemic steroids and immunosuppressive therapy. History of onset ,any precipitating factors such as trauma or contact lens use, previous episodes in the same or fellow eye including treatment ,medical history of systemic treatment for rheumatoid arthritis and any drug allergies. Examination BE- evidence of dry eyes, lid abnormalities, episcleritis, scleritis, PUK, fundus for retinal vasculitis. Investigations-CBC, ESR, Autoimmune markers( RA factor, ANA, anti ds DNA, c-ANCA ), Infection screen before starting immunosuppressives ( VDRL,FTA Abs, Chest XRay, Mantoux ). Management- Systemic immunosuppressive therapy by Rheumatologist . Ocular management in consultation with cornea specialist - Exclude infection( smear for gram stain and koh, C&S), Topical steroids/ Cyclosporine under prophylactic antibiotic cover, lubricants, cycloplegic, collagenase inhibitor acetyl cysteine, control of IOP, watch out for impending perforation which may need cyanoacrylate tissue glue with BandageContact Lens .Perforation may require emergency lamellar keratoplasty or tectonic patch graft. Long term follow up for dry eyes, recurrence, scleritis , secondary glaucoma, complicated cataract, complications of systemic treatment ( chloroquine maculopathy, steroid induced glaucoma and cataract ).

3- A 75 year old retired accountant gives a 6 –month history of recurrent severe headaches and for the last few weeks has also been aware of episodes of transient loss of vision on the right side. His acuities remain at 6/6 bilaterally and he is a lifelong smoker with mild respiratory disease. How would you further investigate and manage this patient?

This elderly male who is a chronic smoker with recurrent episodes of headache for the past 6 months has presented with recent episodes of transient obscurations of vision in RE with normal vision in BE. The most probable cause for his symptoms is carotid atherosclerosis of right side with embolic Transient ischemic attacks and amaurosis fugax as smoking is a risk factor for atherosclerosis.
Other causes to be excluded include Emboli from the heart ,Giant cell arteritis, , Papilloedema, Lung cancer with metastasis. History of onset and duration of symptoms, nature of headache ,changes with posture or diurnal variation ( worse in the morning on waking up and clears during the day in papilloedema ), any associated nausea or vomiting, photopsiae/flashes, diplopia, scotoma/field defect, ocular/periocular pain ( ocular ischemic syndrome or GCA ) Other symptoms such as scalp tenderness, jaw claudication, proximal muscle weakness, night sweats and recent weight loss suggestive of giant cell arteritis. Past medical history of cough or haemoptysis( lung cancer ), hypertension, diabetes , cardiovascular disease, hyperlipidaemia, sedentary life style. Examination-Vision, colour vision, visual fields , pupils for RAPD, ocular motility, Anterior segment –any evidence of ocular ischaemic syndrome,fundus for papilloedema, retinal emboli, hypoperfusion retinopathy( venous dilation, new vessels , midperipheral retinal dot haemorrhages and microneurysms ). Systemic examination- In collaboration with cardiovascular physician and Neurophysician- Pulse for any irregularity, BP, Palpation of carotids for a weak ipsilateral pulsation ( carotid stenosis ) and of the superficial temporal arteries for thickening, nodularity ,tenderness and weak or absent pulsations ( arteritis ). Auscultation for carotid bruit and cardiac murmers, neurological evaluation to exclude focal neurological deficit such as hemipareisis or hemi sensory defects .Investigations- Blood-Exclude GCA by ESR, CRP and Platelet counts. CBC, Fasting blood glucose and Lipids, U&E, Coagulation profile. ECG, Chest X Ray( for lung cancer and cardiomegaly ), Carotid duplex Ultrasonography, Echo cardiography, CT /MRI of brain with contrast to evaluate the severity of cerebral ischaemia, old infarcts and to rule out space occupying lesions including metastasis if papilloedema. Management- For carotid atherosclerosis –A multidisciplinary team approach in conjunction with Physician , Cardiologist and Neurologist .Admission for full evaluation and optimization of therapy aimed at decreasing the risk of morbidity and mortality from stroke by preventing its recurrence.( General measures addressing associated risk factors, specific therapy- Antiplatelets, Anticoagulants if not controlled by antiplatelets alone, Carotid endarterectomy for significant carotid stenosis of more than 70% with recurrent TIAs on optimal medical therapy)
If clinical features of GCA-Immediately start systemic steroids ( IV Methyl prednisolone and oral prednisolone ) in consultation with Physician and arrangement for temporal artery biopsy within a week of starting steroids .Long term follow up for recurrence , steroid therapy and complications.
If Papilloedema with Space occupying lesion- Referral to Neuro surgeon. Consult with Specialist Oncologist if lung primary with suspected brain secondaries.

( A word of advise to future candidates in problem solving . A variety of almost all possible scenarios –around 50 in number-are available from the previous candidate experiences in the Chua site. It is good to make your own answer plans to these cases and go through your answers 2-3 days before the theory paper so that at the exam an answer plan immediately comes to your mind . A guidance to write these answers can be obtained by joining Prof Muthusamy’s university ( mvupgo ) and FRCOphth yahoo group online file site. Many candidates find the time to be less and find it difficult to complete the answers. On receiving the questions spend the first 10-15 minutes reading through all questions and making an answer plan for each in your mind. Then proceed with writing. Time the answers giving 30 minutes for completing each. Spend the last 15-30 minutes in reading through your answers for minor additions or modifications )

Day 3 VIVA.

Station 1- General Medicine and Neurology

Examiner 1

Q.A picture on the laptop showing localized bulbar conjunctival congestion near the inferonasal limbus in a middle aged female, to comment on the picture and possible diagnosis.
A. I gave a differential diagnosis of local pathology ( Trichiasis , Blepharitis, ), Episcleritis, Scleritis.
Q.Why it cannot be conjunctivitis ? A: because in conjunctivitis diffuse congestion.
Q. How do you confirm that it is Scleritis ? A; From history, nature of pain ( pain on ocular movts, globe tenderness, radiation of pain, may wake the patient from sleep ), Confirm the level of congestion on the slit lamp, Ask for H/O collagen vascular disease.
Q.What collagen vascular D/S, A: The most common association is Rheumatoid arthritis. Other conditions-Wegeners Granulomatosis, SLE, Polyarteriti s Nodosa.
Q. What are the manifestations of Wegeners Granulomatosis ? A: Orbit( Proptosis, usually eccentric ), lids and lacrimal( Dacryoadenitis, Dacryocystitis, NLD obstruction with epiphora ), Keratoconjunctivitis sicca, Peripheral ulcerative keratitis, Episcleritis, Scleritis, Posterior segment-Retinal vasculitis, Optic neuritis, Ophthalmoplegia due to 3,4,6 CN involvement.
Q. How will you confirm WG ? A: Autoimmune marker C ANCA, ESR.
Q.Is there a role for biopsy? A: Yes, when diagnosis is in doubt. WG shows necrotizing granulomatous vasculitis .
Q. How will you manage this case if wageners? A. I will consult the Physician as this patient needs systemic steroids and immunosuppressive agents especially cyclophosphamide.


Examiner 2


Q. You have done a cataract surgery on an elderly female who is a known case of nephritis. In the evening you got a call from the ward that the patient vomited blood. What features will help you to determine that it is a major bleed.? A: The quantity of blood in the vomitus, the no: of times vomited, patient’s general condition, sweating , rapid thready pulse, hypotension, altered sensorium.
Q The patient has all these. What do you call that condition? A: The patient is in a state of circulatory shock.
Q.How will you manage her? First of all I will ensure adequate airway, O2 inhalation by face mask, 2 wide bore IV cannula and start crystalloid 0.9% normal saline fast.
Q. Any other crystalloid you know of ? A: Yes. Ringer lactate.
Q.Other than crystalloid what else can you use? A: Colloids.
Q.What are the colloids you know of ? A: Plasma expanders.. ( The examiner reminded me of blood transfusion )
Q.Causes of Upper GI bleed A: Peptic Ulcer –Gastritis, Drugs-NSAID,Steroids
Q What are NSAID?A: Non steroidal anti-inflammatory agents such as Diclofenac, Ibuprofen…
Q. Any infection which can cause peptic ulcer? A: Yes. Helicobacter Pylori.( The examiner was pleased )
Q. Any other causes for bleeding? Yes, Liver disease with Cirrhosis eg Chronic Alcoholism can cause haematemesis by decrease in coagulation factors synthesized by liver and rupture of eosophageal varices . Q. Cause for the varices ? I was thinking when the examiner mentioned portal hypertension.
Q. You started blood transfusion for this patient? What complications you expect? A: Transfusion reactions, fluid overload ( The examiner was pleased and said “ yes , fluid overload can occur particularly in this patient with renal failure )Q: So what precautions will you take for that? A: Pretreatment with IV Frusemide before starting transfusion, slow transfusion, use of packed cells instead of whole blood.Q What is the significance of packed cells? A: Only less volume need to be infused, so less risk of overload.
Q The patient developed reaction during blood transfusion. What are the manifestations? A: Chills and rigour, generalized itching and hives, may progress on to more severe anaphylaxis with facial oedema ( periorbital and perioral ), oedema of tongue and larynx with wheeze progressing on to stridor, cyanosis, coma.Q How will you manage ? A: I will stop the transfusion, Adrenaline,Hydrocortisone…… Bell Rang.

Station 2 Ophthalmic Surgery and Pathology.

Examiner 1

Q To read a visual field ( Humphreys )A: After reading the field I gave a diagnosis of enlarged blind spot or a Seidel’s scotoma communicating with the blind spot.I was Asked about conditions causing enlargement of blind spot and what a Seidel’s scotoma is ?
QWhat is glaucoma? A: Gave the definition as An optic neuropathy with characteristic optic disc changes and visual field defects the most common risk factor being raised IOP.Q Is it due to Raised IOP? A : Raised IOP is only one of the risk factors. Other factors such as optic nerve head perfusion .
Q Why it is Optic neuropathy? Is it inflammatory or degenerative? What is “ pathy “ A: Pathy means disease without specifying the causative factor? It can be multifactorial.
Q A patient has all the features of open angle glaucoma. How will you manage? A: First of all I will evaluate to rule out secondary causes such as pseudoexfoliation , pigment or inflammatory. Do gonioscopy to evaluate the status of the angle, base line IOP and visual fields. Management can be medical, laser or surgical. Initially starting with medical therapy….
Q: Is there any situation where you will initially manage surgically a case of POAG? A: Yes, in advanced glaucoma where medications maynot adequately preserve the optic nervehead and visual fields, a very high initial IOP which is unlikely to be controlled by medications alone, or a non-compliant patient who is not available for followup.
Q. Trabeculectomy and conjunctival flap which you prefer ? Why ? ( Fornix based , easy dissection with less risk of button holing and good exposure of limbus ), complications of Trabeculectomy ( Intraoperative, postoperative ), Management of these complications, Artificial drainage devices, types , Indications for their use.


Examiner 2

Q.Endophthalmitis causative organisms A: I gave the common spectrum of organisms for Post operative, Post traumatic and Endogenous Endophthalmitis. Asked about endogenous endophthalmitis types ( Bacterial and fungal ) and risk factors.
Q. Evaluation of corneal ulcer- Specifically collection of material for smears for gram staining and KOH, Technique of Gram staining ( Just remember Mother Violet Goes After Child – Primary stain Methyl Violet, application of Gram’s Iodine, decolourisation with organic solvent Acetone and counter stain with Carbol Fuschin ), G+ve organisms resist decolorisation and retain the primary stain violet, G-ve organisms are decolorized by acetone and take up the counter stain appearing red. how to classify bacteria by Gram staining.( Gram positive Vs Gram Negative , Cocci (, (eg Streptococcus and Staphylococcus by arrangement) Vs Bacilli
Q; What is Retinoblastoma? A: I started talking about everything I knew of retinoblastoma from definition, genetics, inheritance, symptoms and signs as there was no interruption from the examiner in between. Finally I was asked about management but the bell rang.


Station 3 Ophthalmic Medicine.

Examiner 1


Q; A Picture of Punctate epithelial erosion stained with fluorescein viewed in cobalt blue light. Differential diagnosis based on location ( Superior, interpalpebral, inferior, diffuse )
Q. Dry eyes and management in stages , types of lubricant eyedrops/gel and their components ,differences between them, punctual occlusion, Mucolytic Acetyl cysteine, Role of topical cyclosporine and its concentration ,uses
Q. Picture of B/L everted upperlid with congested palpebral conjunctiva Diagnosis and management- A; Floppy eyelid syndrome, exposure during sleep with papillary hypertrophy and chronic inflammation and keratinisation. Topical lubricants, definitive surgical treatment by Lid tightening procedures such as lateral canthal sling/ lateral tarsal strip and horizontal lid shortening by full thickness pentagon excision of lid.
Q. The same patient picture of Oxygen tubes in place near the nostrils, Diagnosis ? A: Obstructive Sleep apnoea syndrome , obese individual, increased risk of floppy eyelids in such individuals.

Examiner 2

Q.Fundus photograph diagnosis and management- A; Angioid streaks, systemic evaluation for associations such as connective tissue disorders (pseudo xanthoma elasticum, Erlers danlos,) Pagets disease , Haemoglobinopathies, Evaluation of baseline visual acuity and Amsler grid and follow up with Amsler grid at home , to report if any visual distortions, avoid trauma to the eye and contact sports.
Q Cause of visual loss in this case A: Direct involvement of fovea by a streak or Sub retinal choroidal neovascular membrane with bleed , choroidal rupture which may involve the fovea following relatively trivial trauma .
Q.Picture in same case showing extensive deep retinal haemorrhages and grayish membrane at the macula. Diagnosis A: SRNVM with bleeding.
Q.A patient known case treated as Normal tension glaucoma for long time now with vision bare light perception in RE. A fundus picture of the eye was shown to comment upon. A: Fundus picture showing uniformely pale disc with cup:disc 0.3, pallor more than cupping, pale NRR without thinning, vessels centrally placed and appearing normal, mild peripapillary pigmentary changes, background retina appears normal.Picture unlikely to be due to glaucoma. I would like to exclude other causes such as anterior ischaemic optic neuropathy, previous episode of circulatory disturbance such as severe blood loss or major surgery, history of cardiovascular disease, peripheral vascular disease or migraine.
Q. The patient does not have any of these .How would you proceed? A: Vision, pupil for RAPD, visual fields.
Q. This is his visual field . So what would you do? A; Field showing supero- temporal defect obeying the vertical midline. I will order a CT scan orbits and brain to rule out compressive optic neuropathy and chiasmal compression. The bell rang.

Day 4- Clinics ( There were a lack of adequate number of cases as my turn was towards the end of the day and most of the patients had already left )

Case 1

Proptosis RE Eccentric ( down and in ) in an elderly male – Discussion regarding possible causes( Thyroid, lacrimal ,orbital inflammatory disease , granulomatous such as Wegeners.

Case 2

Ocular motility in the same case – I asked permission to start with cover-uncover test . The patient could not see my fixation target with RE and was not able to take up fixation. I commented upon probable poor vision in RE and needs further evaluation of vision, colour vision, visual fields , pupil for RAPD and fundus for optic disc oedema or atrophy. I continued with ocular motility which revealed gross restriction of all ocular movts especially elevation and abduction in RE. Asked about evaluation.-CT scan of orbits for space occupying lesion in superolateral orbit/bone erosion /calcification

Case 3

Pupil examination in an elderly female- Revealed RAPD LE, discussion regarding possible etiologies ( Optic atrophy, retinal pathology). Slitlamp 90 D in the same patient revealed optic atrophy.

Case 4

Indirect Ophthalmoscopy of RE in a young adult male- Localised chorioretinal degeneration with pigmentation seen nasal to the disc .Rest of the retina and macula normal. Discussion regarding possible aetiology and management ( Toxoplasma, trauma with choroidal rupture, sectoral RP)
The same case to examine in Slit lamp with 90 D- Discussion about the level of pigmentation, and how to distinguish .

Case 5

Elderly female B/L Slitlamp examination- RE- Meibomitis with few oil capped gland orifices, herberts pits with corneal opacification near superior limbus, few endothelial guttae, pseudoexfoliation, pupil dilated, lens grade 2 nuclear sclerosis( I asked whether I can evert the upperlid to look for tarsal scarring and also to perform fundus examination by 90D but examiner refused both ). LE- Similar changes but more extensive with extension of corneal opacities to involve visual axis and also extensive endothelial guttae. Discussion of management of cataract and corneal opacity.

Case 6

Elderly male B/L Slitlamp anterior segment- RE- Lid margin thickening and scarring with blepharitis, extensive corneal degeneration with patchy scattered areas of dense opacification and stromal thinning and scarring, few endothelial pigments, iris atrophy, pseudoexfoliation, immature cataract. LE- Blepharitis, PKP graft in place, peripheral totally opaque host cornea with mild vascularisation, clear PKP graft, suture track opacities, no endothelial precipitates or AC reaction, only few pigments on the endothelium, extensive iris atrophy and dilated pupil, pseudoexfoliation, pseudophakia with pigments on the IOL, Posterior capsular circular opening possibly of YAG capsulotomy. Possible cause for the graft? Whether it is degeneration or a dystrophy? I replied that it is degeneration considering the local pathology ( blepharitis and scarring ) and the asymmetric patchy nature of the corneal opacities in the other eye.


More candidates' experience