I am Dr. Tariq Farooq Babar working in the Department
of Ophthalmology, PGMI, Hayatabad Medical Complex, Peshawar. I am
presenting my experience how I passed FRCS Glasgow Exam.
I studied the following books for this Exam:-
a. J.J. Kanski A—Z
b. Wills Eye Manual (Just two topics – treatment of ACG & Multiple
c. Wills Eye series atlases of Ophthalmology – a seven volume set –
easy to revise within hours before viva.
d. Short Oxford of Ophthalmology,] studied twice and then make my own
notes from it.
f. American Academy of Ophthalmology Series- I have studied them once
no need to waste time. But if you are also preparing for MCQs – then
you need to study
Medical Ophthalmology volume of American Academy of Ophthalmology
g. Chua Web site (www.mrcophth.com)- a gold mine for FRCS students
various sections of Exam
Whats important in it:-
- Past experience of candidates - must go through it – at least twice
- How to read CT scan / MRI, FFA
- Systemic diseases related to Ophthalmology.
- Important topics in pathology & how to read pathology slides.
h. Short Oxford book of Medicine
Candidates only prepare last 70 pages of emergency medicine.
- But it’s better to prepare all important medical topics and read
i. The Massachusetts Eye and Ear infirmary review Manual for
edition. Rama D Jager, Jeffrey C Lamkin (a goldmine for MCQ portion of
FRCS Part 2 Exam).
j. Rapid interpretation of EKGs by Dale Dubin (only from page 334 to
363). This book gives review of ECGs – understanding of which is must
for emergency medicine section of viva.
My advice to candidates is that there are four sections in the
practicals – anterior segment, posterior, segment Oculoplasty& Orbit
and Neuro- ophthalmology and Strabismus. You have to pass each segment
individually. One segment marks can’t be compensated by the other
segment. If you are weak in one segment don’t take Exam- why to waste
Rs. 5 lacks / attempt. The Examiners are interested in findings but
not in diagnosis as will be clear from my experience. See as many
cases as possible – practice makes ones perfect. Regarding oral viva-
practice with your friend so that your speaking power develops. The
Examiners are interested in findings. If you miss the findings the
remaining theoretical details are irreverent. For practicals – the
ideal set up is at Al Shifa Trust Eye Hospital, Rawalpindi where
Ophthalmology is divided into multiple segments like:-
a. Oculoplasty& Orbit
c. Pediatric Ophthalmology
f. Refraction or Optometry
The only missing component is Neuro- ophthalmology, which is to some
extent compensated by very well developed Oculoplasty / Orbit and
I am thankful to the staff of Al-Shifa Hospital which I visited thrice
to four times / week for three months from Peshawar to have an
experience of various sub-specialities of Ophthalmology. My special
thanks to Dr. NadeemQureshi& Dr. Sara (Vitreo-Retina) Dr. Shama Khan
(Cornea) and Dr. Tayyab Afghani (Oculoplasty& Orbit)
Majority of time I was alone in this Journey but occasionally I was
accompanied by Dr. Jawad (from Lady Reading Hospital, Peshawar) Dr.
Inayat (from Shifa Hospital Islamabad and Dr. Imran (from WahCantt)
I went to Glasgow along with my friend Dr. Jawad on 30thMay, 2014. My
practicals were on 3rd June while Dr. Jawad’s on 4thJune, 2014 at
Calodian University. Orals were scheduled on 5th June and 6th June,
2014 respectively at RCPSG, St. Vincent’s street. During these three
days we revised important topics together.
3rd June, 2014 – (Practical Exam)
The day was reserved for my practical Exam. Our Hotel was situated
about 2 km away from Exam place. We went for walk in rain because a
taxi driver refused to go as for him the place was very near and
We were five candidates in the group. The practicals started fifteen
A. Anterior Segment
My first station was anterior segment. I was welcomed by two young
Indian Examiners. After using hand sanitizer was asked to examine the
i. I saw an old lady in her 60—70 years at Slit lamp. From distance
the patient was blinking excessively. One of the Examiners asked me
what’s your differential diagnosis?
I said two differential diagnoses.
Ok what are they?
a).Essential blepharospasm or
Then the Examiner asked me to proceed?
I said “Can I start with slit lamp Examination (SLE)”
Then I started SLE and gave him running commentary of my findings.
Lids and conjunctiva were within normal limits. In the right eye there
was punctal plug. Corneas showed filamentary Keratopathy Rt. > Lt.
Marginal tear strip was absent. Anterior chamber was quiet. Examiners
stopped me and said whats your diagnosis? I said filamentary
keratopathy due to dry eyes.
One of the Examiners said “What are the causes of filamentary
I said the causes may be:-
- Keratoconjunctvitissicca (KCS)
- Essential blepharospasm
- Contact lens wearers
The examiner said “Give me diagnose in this case”
I said “KCS”.
He said “what is the main factor deficient in KCS – lipid. mucus or
I said “aqueous layer deficiency” Then the examiner said that’s’ fine
and took me to another room to show me their second case.
ii. My 2nd case was another female patient of about 70 years. The
examiners said just examine the anterior segment of both eyes. I said
I started my examination from the lids, conjunctiva and sclera which
were normal. When I saw (Rt.) cornea I thought its lattice dystrophy.
But my joy was very short lived as the lesions in the cornea were at
the level of epithelium and not stroma and were unilateral. There were
criss cross lines at the periphery of the right cornea at epithelium
level which I couldn’t fit it in any disorder. They said OK. What else
you find in the corneas?
I re-examined the cornea in further detail. To my surprise both the
endothelium showed small blackish spots Rt. > Lt. The examiners said
whats on endothelium?
I said I will give you two diagnoses?
The examiners said “OK”.
1. Posterior polymorphous dystrophy &
2. Fuchs’ endothelial dystrophy.
The examiners said what’s your impression?
I said “Can I see the patient again?
The examiners said proceed.
The lesions in the endothelium were more localized. There were no band
like lesions or vesicles in the Rt. Eye as seen in posterior
polymorphous dystrophy and the lattice like lesions were purely
unilateral. The Lt. Eye was normal. The examiners said give one
diagnosis? I said corneal guttata due to Fuch’s endothelial dystrophy”
They said “Great” What about epithelial lesion? I said I have never
seen such a lesion in my life They said “OK” Can you give differential
diagnosis. I said my first diagnosis is corneal verticillata due to
Fabry’s disease or amiodarone induced. But it is not because in that
case they are central greyish, bilaterall and arranged in a whorled
My 2nd diagnosis is ghost vessels as seen in interstitial Keratitis
due to congenital or acquired syphilis or Cogan syndrome. But they are
never arranged in a criss- cross pattern as in this case. Then he
acquired the pathogenesis of these ghost vessel which I elaborated to
“There is primary inflammation of corneal stroma without involvement
of endothelium / descement’s membrane and epithelium. Invasion of
cornea by blood vessels and fibroblasts. The blood vessels leak,
deposition of blood in corneal stroma, blood re-absorb, leaving ghost
vessels in cornea”
My 3rd diagnosis is prominent corneal nerves. But they never arrange
in a criss cross fashion.
I told them that they do not fit in either dystrophy or degeneration.
After the Exam I consulted my atlases but couldn’t find such a lesion.
It may be remnant of anterior stromal puncture for recurrent corneal
erosion although I have never seen such a procedure in my life.
B. Neuro-ophthalmology and strabismus.
I was greeted at the station by an Indian and a British examiner.
i. My 1st case was a squint. I was asked to look at the patient and do
relevent tests. My initial observation revealed Rt. Esotropia. I said
“ I will do cover test and extra-ocular movements”. The examiner said
proceed. I demanded on occluder and a fixation target. To my surprise
they were not available. Luckily I had brought my own instruments to
the examination hall. When I told them “Can I use my instruments”.
They were delighted. The message is clear always bring your own
instruments to exam hall. Don’t trust college, I started the
examination by doing cover test. On inspection I said there is no AHP’,
proptosis or enophthalmeos or ptosis. There is Rt. Esotropia, about
15—20o which increases to 30o after removing glasses. On covering Lt.
Eye the Rt eye goes out and took fixation. On uncovering the Lt. eye,
the eye had deviated inward but immediate took fixation. I said its
basically Rt. Esotropia and fixating eye is the Lt. one and with good
Extra-ocular movements were full with no I00A or DVD or Duane
retraction syndrome synodrome. Then one of the examiners handed over
the patient’s glasses and said comments on these glasses. I put a
cross on a piece of paper and move the glasses along with it. There
was against movement. I said “Its hyperopic glasses”. The examiners
said “OK, anything else”. I said “yes there is a prism in it. They
were delighted. The examiner then said, “why it is mainly central and
what is the name of the prism. I kept quiet and then said, “Probably
for centralization of the image”. But I forget to tell them the name
of the prism which was “fresnel prism”.
The bell then rang and the examiners then took me to another room to
show me their second case.
ii. My 2nd case was an elderly female in her 70’s. Again the examiners
asked me to observe and then do relevant tests. Inspection revealed
Lt. ptosis. I said I will do cover test, extra-ocular movements and
ptosis measurements. They said “Proceed”.
I started my examination with a cover test Observation revealed Lt.
side ptosis with exotropia On covering Rt. Eye , the Lt. eye failed to
take up fixation. On uncovering the Rt. Eye there was no deviation.
Extraocular movements revealed limitation of abduction in Rt eye and
total Ophthalmoplegia in the Lt eye. there was moderate ptosis with
good levator function on Lt. side. The Examiner smiled and said “whats
your differential diagnosis? I said “its some type of ophthalmoplegia.
They said “Yes you are right”, how you proceed I said in practical
life I will take history from patient to get clues. Give me just one
clue. The examiners said OK. Patient has heart block. I said the
patient has asymmetrical ophthalmolplegia and ptosis. The examiners
said” you are right but he is a confirmed case of CPEO. Then he asked
me the features of CPEO and how you investigate and treat?
I said usually bilateral symmetrical ophthamolplegia with ptosis
rarely asymmetrical usually no diplopia but if asymmetrical then may
have. Systemically can have heart block, cerebellar ataxia, deafness,
diabetes and failure to thrive. Investigations include skin biopsy for
ragged muscle fibers, ECG for cardiac conduction defects and
peripheral blood for mitochondrial DNA analysis. Treatment is usually
a. CPEO alone
b. CPEO plus (Kearns Sayre syndrome) because it is mitochondrial
cytopathy with mitochondrial DNA deletions).
c. MELAS syndrome
d. Oculopharyngeal dystrophy
After this the bell rang and I went to the third segment i.e.
oculoplasty and orbit which is my favourite sub speciality .
C). Oculoplasty and orbit
The examiners greeted me and took me to their first case to examine
with a torch.
(i) My first case was bilateral lower lid involutionalectropion with
punctal eversion. The examiners said demonstrate us all signs of
involutionalectropion? I demonstrated to them.
- Punctual Eversion which were positive
- Horizontal lid laxity
- Medical canthal tendon laxity
- Lateral canthal tendon laxity- which was absent
The examiners said, How you manage. I said I have a number of options.
They said, “Can you describe to us these options. I said, “OK”. I
narrated to them steps of following procedures.
• Retro punctual cautery
• Tarsoconjunctival wedge excision
• Lazy-T procedure
• KuhntZsymanuski procedure
• Lateral tarsal sling
They were speechless when they listened my discussion.
ii. My second case was again an eyelid case. A 70 year male with
redundant skin and no other abnormality. I said the patient has
bilateral dermatochalasis. They said OK would you like to examine the
patient again? I realized I have missed some thing. Probably ptosis. I
re-examine the patient and to my expectation turned out be bilateral 1
mm aponeurotic ptosis with lipodermoid cyst. When I narrated these
findings to the examiners they were delighted. They said “Brilliant”
How you manage? I said will discuss the issue with the patient because
it is mild dermotochalasis and aponeurotic ptosis - one option is
conservative and the other surgical. Surgical options include
blepharoplasty with levator resection.
The examiners said, “Have you ever done this procedure in your life? I
said, “Yes They said “ Can you give us the steps of this procedure? I
said, “yes”. The examiners said “proceed” I gave them a detailed
description of the procedure. They became astonished. One of the
examiner said, what you want to do with lipodermoid” I said I am not
offering surgery for this” They said “why” I said Surgery will create
more problems like dry eyes, motility problems, irregular ocular
surface and damage to palpebral lobe of lacrimal gland. The examiners
said “OK” Then they enquired from me functions of different parts of
lachrymal gland. I initially become puzzled but then recover to give
them a detailed answer.
The examiners were literally bowled by my answers and seemed very
satisfied and impressed. I said any more cases? They said “No” it’s
enough. The bell rang and I went for posterior segment cases.
D. Posterior segment
i. The examiners welcomed me and guide me towards my first case in
I started examining the case with slit lamp and gave them a running
commentary. I said, Sir, would you like to come as both pupils are
severely miosed and difficult to comment on fundus. The examiners
said, “ Don’t worry, just gave us your findings. I said, “Ok”. Both
anterior segment shows coloboma of iris, lenticular colobomas. They
said, Ok what’s in fundus? I tried again to see through the pin point
pupils and luckily got the findings. I said colobomas of choroid above
the optic disc as well as involvement of the discs. They said anything
else? I said, “No” The examiners seemed satisfied with my answer. They
enquired from me differences between colobomas and staphylomas and
iris coloboma and traumatic iris rupture which I answered them.
ii. My second case in posterior segment was again an un-dilated pupil.
I took my 78 D lens to
examine the fundi. One of the examiner stopped me and said, “Take my
90 D lens and examine
fundus as 90 D lens is best for seeing fundi in constricted pupil. I
said “OK” but cursed the examiner in my mind that why on earth they
failed to dilate the pupil. Any how I started examining fundi. I said
the patient has bilateral nucleosclerosis, the discs appears pale, but
the vessels are normal looking. There are scars of PRPC in both eyes
involving macula. I said my impression is that the patient is diabetic
and underwent PRPC for his proliferative DR. The examiners didn’t
agree to my answer. They said would you like to re-examine fundi and
comment on vasculature and vessels. I said, “OK” I re-examined fundi
and said that the vasculature is in normal limits and there is no
attenuation, there are old photocoagulation scars but no bone spicules.
The examiners said, “Whats your final diagnosis”? I said, “Diabetes
Mellitis” but the examiners thought that the patient had Retinitis
pigmentosa. The examiners said, “How you proceed? I said, “well ask
patient whether he is suffering from diabetes or laser therapy in eyes
in the past. The examiners then enquired from the patient the patient
said that he is diabetic and had laser in eyes in the past. The
examiners were stunned and clean bowled. They were speechless. I was
delighted and in high spirits as I have conquered the whole world. The
examiners were convinced that their so called bone spicules were
actually old photo coagulation scars and pale discs were due to
extensive PRPC and not waxy pallor of the disc due to retinitis
pigmentosa. They apologize from me because of their failure to dilate
the pupil and to make correct diagnosis. The examiners acquired from
me differences between photocoagulation scars and bone spicules and
the treatment of diabetic macular oedema which was my favourite topic.
The bell rang and I was satisfied with my performance.
A. Ophthalmic pathology and surgery.
The table viva was due on 5thJune, 2014 at RCOPSG. The viva started
half hour late. There were two examiners at each segment - usually one
Indian and the other English.
(i) Corneal ulcer with hypopyon
The examiner greeted me and asked me to let us know if you need
something. One of the examiner started viva by showing me a slide of
corneal ulcer with hypopyon. I narrated my findings and said that it’s
corneal ulcer with hypopyon. The examiner said”. How you investigate,
I said with
2. Swab for culture and sensitivity for bacteria and fungi.
The examiner said how you take swab for culture and sensitivity, I
explained the whole method Then he enquired from me different media
for culture and sensitivity.
ii. Corneal laceration with iris in wound.
I narrated him the findings. The examiners said,”How you manage. “I
said” “I will start with a
• History – asking about history of trauma,blunt or penetrating + IOFB
• Investigations – for culture and sensitivity
As AC was shallow I said during surgery reformation of AC, separation
of iris from wound with viscoelastic,
If corneal laceration small 2mm—cyano acrylate glue, will work
If wound large ( more than 2 mm)- tectonic or therapeutic Keratoplasty
will be required
iii. Corneal graft failure
The examiner showed me his third slide. I said, the picture shows full
thickness keratoplasty with separate 10/0 nylon suture. The graft was
central and thick but there were no KPs. I said in practicel life I
will examine the patient on slit lamp for anterior chamber reaction to
differentiate between graft rejection and failure. He said, “whats
your impression”? I said corneal graft failure. Then the examiner
enquired from me complications of full thickness keratoplasty,
differences between graft failure and rejection and treatment of both
The second examiner showed me his first slide. I said, “there is
extensive rubeosisiridis. He said “OK” Anything else”? Suddenly it
clicked that I have missed some obvious finding. When I saw it again I
said, “ I am sorry, there is also ectropionuveae. The examiner was
stunned with my findings. He then enquired from me pathogenesis of
ectropionuveae and causes of rubeosisiridis. I said, I will like to
check IOP for neovascular glaucoma and B-Scan for posterior segment
evaluation. The discussion went into stages and treatment options for
NVG. I said”. Different options depending upon cause, complications
and visual potential in the eye. It may include:
• PRPC for CRVO
• Trabeculectomy with Inj. MMC
• Anterior trabeculectomy
• Glaucoma shunts
• Retro bulbar alcohol
ii. Flat anterior chamber
My second slide was flat anterior chamber. The examiner said, “ How
much flat”? I said, “grade 3,”. In the 1st grade there is peripheral
angle touch, grade 2 - there is central iris touch to endothelium and
in grade 3 there is central corneal touch. No details were visible. I
said, “ it seems post trabeculectomy flatness of AC. He then enquired
from me causes of shallow AC and their management. I divided the
causes into- shallow AC – with low IOP and shallow AC- with high IOP.
I said, I will check IOP, pupil block and fundoscopy for choroidal
detachment and hypotonic maculopathy. The discussion went into shallow
AC with high IOP like pupil block and malignant glaucoma. The examiner
said”. How you treat malignant glaucoma. I divided the management
• Medical therapy with mydriatics and IV mannitol
• Laser therapy with Nd YAG laser and cyclodiode
• Surgical therapy with pars planavitrectomy
The examiner even told me that you are right as this patient does had
iii. Chemical injury
My 3rdslide was anterior segment showing lacerations / burns of lid,
conjunctiva and cornea. The cornea showed epithelial defects and
inferior half of limbal ischemia. I said” It’s chemical or sodium
bicarbonate injury. The examiner then enquired from me management plan
for chemical injury.
I gave him the Roper Hall Classification of chemical injury into
various stages and correspondingly its management which included:-
• Lubricants, cycloplegics
• Topical steroids
• Ascorbicacid- topical / systemic
• Lysis of developing symblepharon
• AMT, limbal stem cell transplantation
• Kerato prosthesis
(iv) Endogenous Endophthalmitis
My fourth slide was that of a clear cornea with hypopyon and occluded
pupil. I gave him differential diagnosis of hypopyon without
involvement of cornea. The examiner said, “Elaborate” I said, “OK”.
• Hypopyon Uveitis e.g. Ankylosing spondylitis, Behcet disease, spill
over from posterior
segment- like vitritis, intermediate uveitis, choroiditis, retinitis
• Hypopyon with endophthalmitis.
The examiner said, ‘OK” what will be your diagnosis if the patient
give history of catheterization in the last 2 weeks. I said
“endogenous endophthalmitis”. The examiner smiled and said”. How you
manage such a case? I said “, will examine the patient in detail,
which may include:-
History – for catheterization sore throat, pneumonia, fever, sub acute
bacterial endocarditis etc.
Examination – Ocularly & systemically
Investigations - vitreous tap, blood culture, urine culture, ECG,
Ocular – Intensive antibiotics and steroids from all routes - topical,
systemic, intravitreal, subconjunctival
Systemic - Treatment of cause e.g. sub acute bacterial endocarditis,
As the discussion was going on the bell rang and the examiners shake
hands with me and said “good bye” with smile on their faces. I was
sure that they must have given me maximum marks as no single question
2. General medicine and emergency medicine related to Ophthalmology
I was greeted by the examiners.
The examiner showed me a fundus photograph. I started describing the
photograph – and said that the optic disc shows secondary optic
atrophy as the disc is pale, raised and irregular margins. I enquired
from the examiner “Sir, can I ask you one question? He said, “Yes” I
said, What’s the age of this patient”? he said, 7’0 years”. I said
“Then it’s AlON- the examiner was literally yorked with my answer and
he said” Great, how you manage? I said, “there are two types
The examiner said, “How you manage arteritis AION. I elaborated on
both systemic and ocular features of giant cell arteritis like jaw
claudication, fever, polymyalgia rheumatica, anterior or posterior
Ischemic optic neuropathy, CRAO, BRAO, Ophthalmic artery occlusion
etc. Investigations include ESR, platelets count and temporal artery
biopsy. The examiner interrupted and said, “ What’s if biopsy comes
out negative”? I said, “we have to keep in mind the phenomenon of skip
lesions. He said “ what will you do then”? I said “ I will then take
biopsy from the other side. What if that biopsy is also negative’? I
said if the suspicion of GCA is high negative biopsy does not rule out
GCA. The examiner was amazed by my answer. He then said, “How you
manage GCA? I said, “with systemic steroids. The examiner then said, “
How you give systemic steroids” I said, “ I will first take history of
hypertension, Diabetes, peptic ulcer. I will start therapy with IV
methylprednisolone 1g / day for 3 days, then oral prednisone 1—2 mg /
kg / day. After 3 days then oral dose is, reduced to 60 mg and then 50
mg each for one week. The daily dose then reduced by 5 mg weekly until
10 mg is reached. The examiner said “ what factors govern tapering of
steroids”? I said, patient’s clinical features, ESR and C-reactive
protein. The examiner was question less.
(ii). 6 D myope with vitreous hemorrhage
The examiner said, “ Suppose a 6 D myope presents to you with vitreous
hemorrhage, how you manage”? I elaborated all causes of vitreous
hemorrhage especially in a high myope - from a retinal tear or PVD or
CNV or RD.
I said,” I will examine the patient with slit lamp and indirect
ophthalmoscope. If there is no view I will do B- Scan to rule out R/D.
So if the retina is flat I will admit the patient for periodic review.
If the vitreous hemorrhage is absorbing, I will observe the patient.
If not absorbing or B- Scan shows retinal detachment, I will go for
PPV. The examiner said “How long you will wait for the vitreous
hemorrhage to absorb? I said there are two schools of thought-
depending on experience. Some surgeons go for early vitrectomy and
other wait for 4—6 weeks before going in. The examiner said “What will
you do? I said, “ I will wait for at least 4—6 weeks for PPV. The
examiner said “ Do youi know late vitrectomy can increase the risk of
RD. I said “Yes, but I have seen all complications of PPV including
corneal erosions, re-detachment and endophthalmitis. It is not an
innocent surgery. The examiner said, “ what if patient turned out to
be your mother-in-law? I said “ yes” I will wait at least for one
month before intervening. The examiner laughed and smiled at my reply.
(iii). 16 D myope with cataract
As there was some time the 1st examiner gave me another scenario— “A
16 D myope with a cataract. How you manage”? I replied, “ We can
handle this case at three levels.
Preoperatively –Biometry with IOL Master.
Assessment of eye for retinal tears, RD and predisposing factors.
Avoid peribulbaranaesthesia and give topical anaestheisa to prevent
globe penetration in case of posterior staphyloma.
Operatively – Phaco is the safest procedure. As AC is very deep one
should be very careful during sculpting. There is increased risk of PC
rupture because of stressed posterior capsule and chopping seems to be
a safe technique as compared to divide and conqueror. Hydrophilic
acrylic IOL seems to a best choice.
My answer was still incomplete but the bell rang and I was through to
the second examiner.
(i). Myocardial infarction.The 2ndexaminer was a middle age English
lady asking questions in emergency medicine. She gave me a scenario
and said that there is an elderly lady for phaco surgery tomorrow. In
the evening a sister phoned you that the lady has developed
indigestion. The examiner gave me her ECG and wanted my opinion. I
said”, No problem, whether you want me to give detailed account of
this ECG or just positive findings. The examiner said, “ Give me just
positive findings. I said, “OK”. There were typical signs of ST
Segment and T waves’ elevation in chest leads. I said, “ The patient
has myocardial infarction. The examiner said”, You mean her
indigestion is due to myocardial infarction. I said “Yes”. Hearing
this she become delighted. “Is this acute or chronic MI”? I re-examine
the ECG but failed to answer. She said”, It’s ok probably it’s too
much for an ophthalmologist to answer. Later on I came to know that T
wave inversion signifies chronic MI. The examiner then asked one how
would you handle this case? I said that I will follow good medical
practice guidelines. The examiner said what are they? I said that in
such scenario I will postpone phaco surgery for 6 months and will
refer the patient for cardiologist’s opinion. She said. How will you
convince the patient that surgery is not safe for her at this stage? I
said I will reassure the patient about two facts. There is a high risk
for fatal arrhythmias after infarction if surgery is carried out
within 6 months of MI and acute MI requires emergency treatment in
form of injections like streptokinase, O2, Aspirin and others very
early, which is only possible if phaco surgery is postponed.
She said, “Great we will now move to 2nd scenario. I said OK”.
ii. Drug induced hemoptysis and shock. My 2nd scenario was an elderly
lady admitted in eye ward for some eye problem suddenly present with
hemoptysis.She has osteoarthritis. The examiner said, The patient has
thready pulse and BP of 100 systolic, what will you do? I said, The
cause of bleeding may be gastric or duodenal ulcer, gastritis, Mallory
Weis syndrome, bleeding from portal hypertension due to cirrhosis
liver and drug induced gastropathy. I will follow the ABCDE guidelines
which includes clear airways, chest movements and respiratory rate and
maintenance of two wide-bored I/V lines as the patient is in shock I
will raise foot end of the patient and will give I/V dextrose saline
one to two liters fast to revive her circulation. If there is severe
hemoptysis. I will take blood for cross- matching and ABO
compatibility. The examiner said”, Anything else you want to do? I
said, Yes, I will call for gastroenterologist to do endoscopy for the
patient. She said “what do you think is the cause of hemoptysis”? I
said, It may be peptic ulcer or drug- induced because the patient may
have taken some NSAID for her osteoarthritis. The examiner said,
iii. The examiner said as there is some time we will take a 3rd
scenario. I said. “OK” She said that there is an elderly patient with
initial abduction limitation but suddenly developed medial rectus
limitation. Give me one diagnosis? I said, “Myasthenia Gravis” She
said, It could be. The bell rang. The examiners seems very impressed
with my performance and said good bye to me.
(3). Ophthalmic medicine
(i) Choroidal mass (melanoma)
My 1st slide was that of a fundus photograph with a large choroidal
mass invading vitreous. I gave my findings and said that it’s
choroidal melanoma. The examiner was delighted over such a quick
response and said, “Can you give the differential diagnosis”. I said
the differentials include choroidal nevus, choroidal detachment,
choroidalhemangioma etc. But only one differential diagnosis in this
case. The examiner then enquired from me clinical features,
investigations and treatment options for such a lesion. The discussion
then went into complications of charged particle irradiation such as
protons including cataract, papillopathy,maculopathy,loss of lashes,
eyelid de-pigmentation and keratitis.
(ii) Thyroid related orbitopathy
The examiner said suppose a patient comes with bilateral proptosis,
how you manage such a case? What comes into your mind? I said Thyroid
Related Ophthalmopathy. He then enquired from me all ocular and
systemic features of TRO, its investigations and its treatment options
• Systemic steroids
• Radioactive iodine
• Orbital decompression
(iii) Conjunctival nodule
The examiner showed me a slide of a conjunctivalthicking / nodule. I
said, it may be sclertis or episcleritis or phyctenolosis. The viva
then went into features and treatment of scleritis with options like
systemic steroids and immuno modulator therapy.
(iv) Fourth slide
The examiner then showed me a fundus photograph. On first look I
couldn’t find any pathology. Luckily the bell rang & I moved to the
i. Kerato conjunctivitis sicca. My first slide was that of an
irregular corneal surface with filaments. The examiner said”, give me
most important cause? I said, kerato conjunctivitis sicca due to dry
eyes. The discussion went into investigations like BUT, Shirmer test,
fluorescein stain, Rose bengal dye and treatment with lubricants,
collagen plugs and mucolytic agents like acetyl cysteine 5 % drops for
The examiner said, “A patient has presented to you with easy
fatigability. I said, “Its Myasthenia Gravis”. The examiner was
interested in the clinical signs and investigations of Myasthenia
Gravis which I elaborated indetail.
iii. Marcus Gunn Jaw Winking ptosis
The examiner said a mother has brought a 5 months old child with
droopy left eyelid. she says that when my child takes milk there is
retraction of left eyelid. What’s your diagnosis? I said, “It’s Marcus
Gunn Jaw Winking Ptosis”. He said, how you manage such a case? I said
that in MGJWP there is anomalous connection between levatoraponeurosis
and medial pterygoid muscle and is usually unilated. I said there are
a number of treatment options depending on grade of wink amount of
ptosis and associated syndromes.
In mild winking- we have just to do levater resection ignoring
In moderate to severe winking-Bilateral. levatordisinsertion followed
by brow suspension with fascia lata or any other suspension material
(preferred procedure to have a symmetrical result).
Unilateral levatordisinsertion followed by brow suspension.
Unilateral levatordisinsertion followed by frontalis flap.
The examiner said, Have you done frontalis flap procedure in your
life? I said “Yes”. He then enquired from me the steps of frontals
(iv). Angioid streaks. As there was some time the examiner took the
same fundus photograph which I couldn’t diagnose with the 1st
examiner. When I saw the same fundus photograph, I thought that the
examiner has clean bowled me because I knew nothing about the slide.
Then suddenly I pick up the diagnosis and started describing the
findings. There were subtle grey or dark red linear lesions radiating
from the disk. I said, “Sir, the photograph shows angioid streaks. The
examiner was literally stunned when he heard my diagnosis as it was
missed by all previous candidates. He then enquired from me about the
pathogenesis of angioid streaks (cracks like dehiscences in the
Bruch’s membrane) causes (PEPSI- Idiopathic, sickle cell disease,
Pagets disease, Ehlers Danlos syndrome pseudoxanthomaelasticum,
acromegaly and Marfan syndrome), and complications (streak involving
fovea and SRNVM and choroidal rupture).
As the discussion was going on the bell rang and the game was over.
The examiners were so impressed that they shake hands with me and said
After the exam I was hopeful that I will pass the FRCS Exam but I was
unsure about my anterior segment viva. On 18thJune, 2014 my friend
called me that result is out. When I gave my roll number he
congratulated me on my success. This was the happiest day of my life.
Any ophthalmologist interested in getting tips of passing any portion
of FRCS Glasgow Ophthalmology Exam my services are available. Just
e-mail me at email@example.com
I will be glad to help.
Dr. Tariq Farooq Babar