MY FRCS EXPERIENCES –Muscat- Nov 15- 18 ,2009. Dr.
( FRCS Ophthalmology Part B, Glasgow )
Problem Solving Paper with my answers in short. ( I was exempted from
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 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
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
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.
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
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
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.
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
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.
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.
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
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.
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 )
Proptosis RE Eccentric ( down and in ) in an elderly
male – Discussion regarding possible causes( Thyroid, lacrimal
,orbital inflammatory disease , granulomatous such as Wegeners.
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
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.
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 .
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.
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.