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Fundamental OSCE Guide in
Ophthalmology
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Fundamental OSCE Guide in
Ophthalmology
Val PHUA
MBBS, MMed (Ophth)
Singapore National Eye Centre, Singapore
Wei Yan NG
MBBS, MMed (Ophth), FRCOphth
Singapore National Eye Centre, Singapore
Li Lian FOO
MD, MMed (Ophth), FRCOphth
Singapore National Eye Centre, Singapore
Tien Yin WONG
MBBS, MMed (Ophth), MPH, PhD, FRCS (Ed), FRANZCO, FAMS
Singapore National Eye Centre, Singapore
Published by
World Scientific Publishing Co. Pte. Ltd.
5 Toh Tuck Link, Singapore 596224
USA office: 27 Warren Street, Suite 401-402, Hackensack, NJ 07601
UK office: 57 Shelton Street, Covent Garden, London WC2H 9HE
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FUNDAMENTAL OSCE GUIDE IN OPHTHALMOLOGY
Copyright © 2019 by World Scientific Publishing Co. Pte. Ltd.
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ISBN 978-981-3279-93-3
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Printed in Singapore
CONTENTS
About the Authors
List of Contributors
Chapter 1
Cornea
Chapter 2
Glaucoma
Chapter 3
Retina
Chapter 4
Uveitis
Chapter 5
Neuro-Ophthalmology
Chapter 6
Oculoplastics
Chapter 7
Paediatrics
Chapter 8
Imaging
Index
ABOUT THE AUTHORS
Wong Tien Yin is currently Provost’s Chair Professor of Ophthalmology and Medical Director at
the Singapore National Eye Center, Duke-NUS Medical School, National University of Singapore.
Prof. Wong has served previously as the Singapore Eye Research Institute (SERI) Executive Director
(2009–2013), and is currently the Chairman of SERI’s Board. Prior to these roles, Prof. Wong
was Head of the Department of Ophthalmology National University of Singapore, and Chair of
Department of Ophthalmology, Royal Victorian Eye and Ear Hospital, the University of Melbourne,
Australia. Prof. Wong has published more than 1000 peer-reviewed papers, given more than 300
invited named, plenary, and symposium lectures globally, and is a two times recipient of the Singapore
Translational Researcher Award (2008 and 2014), the highest award for the most senior clinicianscientists in Singapore. Prof. Wong serves on Editorial Boards of Investigative Ophthalmology and
Visual Sciences, JAMA-Ophthalmology, Diabetes Care, Ophthalmologica, and the Journal of
Hypertension. He was previously the Executive Editor of the American Journal of Ophthalmology. He
is a Board member of the National Medical Research Council, a Council member of the Asia Pacific
Academy of Ophthalmology and President of the College of Ophthalmologists in Singapore. For his
service, Prof. Wong has been recognized nationally and internationally with numerous awards, such as
the National Clinician Scientist Award and the President’s Science Award, two of the highest
awards in Singapore. He is a recipient of the 2013 Eisenhower Fellowship from the USA.
Val Phua (MBBS, MMed (Ophth)) graduated from the National University of Singapore in 2011 and
attained his MMed (Ophth) in 2017. Dr. Phua has presented at multiple local and international
ophthalmology conferences, including the National Ophthalmology Resident’s Research Day,
Malaysia-Singapore Joint Ophthalmic Congress (MSJOC), Asia–Pacific Academy of
Ophthalmology (APAO) Congress, and the Association for Research in Vision and Ophthalmology
(ARVO) annual meeting. He has published in several peer reviewed journals, including Investigative
Ophthalmology and Visual Sciences (IOVS), American Journal of Ophthalmology (AJO), British
Medical Journal (BMJ), Open Quality and BMJ Simulation & Technology Enhanced Learning. He is
currently a senior resident at the Singapore National Eye Centre (SNEC) and is often involved in
teaching of medical students doing their ophthalmology posting and junior ophthalmology residents.
Ng Wei Yan has attained Primary MMed (Ophth) in 2012, Part 1 FRCOphth in 2013, The Royal
College of Ophthalmologists Refraction Certificate in 2014, and Final MMed (Ophth) in 2016.
Since July 2017, he has been appointed as the Chief Registrar, Singapore National Eye Centre. Other
experiences he has include Deputy Lead Resident, Singapore National Eye Centre from February to
June 2016, and Lead Resident, Singapore National Eye Centre from July to December 2016.
Dr. Ng has been awarded the NUS Dean’s List in 2005, NUS Dean’s Dinner from 2005 to
2009, Inspiring Resident Educator Award 2017, and the RISE Award — Quality Improvement
Project Award 2017.
Foo Li Lian (MD, FRCOphth, MMed (Ophth), BEng (1st class honors)), graduated from National
University of Singapore in 2008 with Bachelor in Engineering (Chemical) — BEng (1st Class
Honors). In 2012, she was awarded Doctor of Medicine — MD, by Duke-NUS Graduate Medical
School. Her ophthalmology specialization, Fellow Royal College of Ophthalmologist (FRCOphth),
and Master of Medicine in Ophthalmology (MMed (Ophth)) were achieved in 2016 and 2017,
respectively.
She was awarded NUS Awards for Study Abroad (Exchange Awards) in 2006, Dean’s List in
2006, Young Investigator Award (Clinical) in Singapore General Hospital 19th Annual Scientific
Meeting in 2011, and the Singapore Society of Ophthalmologists Award for Best Oral Presentation,
Runner-Up in 2013.
Dr. Foo has also presented in several conferences, including Paper Presentation at National
Ophthalmology Residents’ Research Day in 2013, SGH Annual Scientific Meeting, and ARVO
Annual Meeting in 2011.
Dr. Foo is currently a senior resident at Singapore National Eye Centre.
LIST OF CONTRIBUTORS
We would like to express our heartfelt gratitude to the following prominent leaders and mentors in
Ophthalmology for making this book possible by dedicating their valuable time and resources. Their
contributions are sincerely appreciated and gratefully acknowledged.
Prof. Dan Milea
MD, PhD
Assoc. Prof. Ian Yeo
MMed(Ophth), FRCS(Ed), FRCSG, FAMS
Adj. Assoc. Prof. Quah Boon Long
MMed(Ophth), FRCS(Ed) FAMS
Dr. Anshu Arundhati
MMed(Ophth), FRCS(Ed)
Adj. Assoc. Prof. Seah Lay Leng
MBBS, FRCS(Ed), FRCOphth, FAMS
Dr. Jocelyn Chua Leng Leng
MMed(Ophth), FRCS(Ed)
Dr. Loo Jing Liang
MMed(Ophth), FRCS(Ed), FAMS
Dr. Ranjana Mathur
MMed(Ophth), FRCS(Ed)
Dr. Ong Hon Shing
MBBS, FRCOphth
Dr. Sonal Farzavandi
FRCS(Ed)
Dr. Yong Kai Ling
MMed(Ophth), FAMS
Mr. Mohan Ram
(Senior Ophthalmic Imaging Specialist)
Mr. Kasi Sandhanam
(Senior Ophthalmic Imaging Specialist)
CORNEA
1.
A 24-year-old contact lens wearer comes in with a two-day history of eye pain.
Figure 1.1
Q
1.1 What else do you want to know about in the history?
• Blurring of vision
• Contact lens history
• Contact with soil or contaminated water
• Immunosuppression: diabetes, human immunodeficiency virus, steroids, chemotherapy onset
• Progression
• Previous treatment
• Pain
• Trauma
Q
1.2 What are the signs?
• Conjunctiva: injected
• Corneal ulcer/infiltrate involving the visual axis
• Central epithelial defect
• Hypopyon
Q
1.3 What are your differential diagnoses?
• Contact lens-related infective keratitis
• Exposure infective keratitis/neurotrophic infective keratitis
Q
1.4 How do you manage the above patient?
• Admit the patient
• Perform a corneal scrape and send for microscopy and cultures
• Intensive topical antibiotic treatment: gentamicin 14 mg/ml hourly, cephazolin 50 mg/ml hourly
through the night
• Systemic antibiotic treatment if the infiltrate is near the limbus (oral ciprofloxacin 500 mg twice
a day for a week)
Q
1.5 What do you send the corneal scrapings for?
• Gram stain
• Blood agar
• Chocolate agar
• Thioglycate
• Brain heart infusion broth (BHIB)
• Sabouraud dextrose
• Others
⚬ Suspicious for fungal infection: giemsa stain, methenamine silver stain
Q
1.6 What are the complications of a corneal ulcer?
• Acute: thinning of the cornea resulting in corneal perforation leading to endophthalmitis
• Long-term: scar, astigmatism, blindness
2.
A 20-year-old man, a contact lens wearer, comes in with a I five-day history of eye
redness and pain.
Figure 1.2
Q
2.1 What are the signs?
• Conjunctiva: injected
• Cornea: surrounding stromal haze, radial keratoneuritis (yellow arrow)
Q
2.2 What is your diagnosis?
• Acanthamoeba keratitis
Q
2.3 What do you send the corneal scrapings for?
• Microscopy: calcofluor white/acridine orange stain (double-walled cysts)
• Culture: non-nutrient agar with Escherichia coli overlay
Q
2.4 How do you treat it?
• Biguanides: polyhexamethylene biguanide (PHMB), chlorhexidine
• Diamidines: propamidine, hexamidine
• Treatment is prolonged and requires a combination of biguanides and diamidines
3.
A 45-year-old diabetic patient comes in with a one-week history of right-eye redness
and blurring of vision.
Figure 1.3
Q
3.1 What are the signs?
• Conjunctiva: injected
• Cornea
⚬ Large corneal infiltrate inferior to the visual axis, involving the limbus
⚬ Edges of the infiltrates are feathery with presence of satellite lesions (yellow arrow)
Q
3.2 What is your diagnosis?
• Fungal keratitis
Q
3.3 What further test will you do?
• Scrape and send for fungal microscopy and culture
Q
3.4 How do you treat it?
• Topical: amphotericin B (yeast), natamycin (filamentous fungi)
• Consider intrastromal and/or systemic anti-fungals due to poor ocular penetration of topical antifungal eyedrops
4.
A 40-year-old lady comes in with a three-day history of eye discomfort.
Figure 1.4
Q
4.1 What are the signs?
• Large paracentral dendritic lesion with terminal bulbs, minimal stromal haze
Q
4.2 What is your diagnosis?
• Herpes simplex keratitis
Q
4.3 What are some potential complications?
• Anterior uveitis
• Acute retinal necrosis (ARN)
• Progressive outer retinal necrosis (PORN)
• Uveitic glaucoma
Q
4.4 How do you manage the above patient?
• Avoid steroids
• Epithelial keratitis: topical aciclovir ointment 5 times/day
5.
A 50-year-old man comes in with a three-day history of skin rash over the face.
Figure 1.5
Q
5.1 What are the signs?
• Injected conjunctiva
• Right upper eyelid erythema and oedema
• Vesicular rash over the right face in the distribution of the V1 dermatome, respecting the vertical
midline
Q
5.2 What is your diagnosis?
• Right herpes zoster ophthalmicus
Q
5.3 What is Hutchinson’s sign?
• Hutchinson’s sign describes the involvement of tip of the nose in the context of herpes
zoster ophthalmicus
• Ophthalmic branch of the trigeminal nerve (V1) has three main branches:
⚬ Lacrimal
⚬ Frontal
⚬ Nasociliary: supplies ethmoid sinus, skin to tip of nose, iris, cornea, ciliary muscle
• Positive sign indicates an increased risk of ocular involvement in herpes zoster ophthalmicus
Q
5.4 What are the complications of herpes zoster ophthalmicus?
• Lid scarring: Lagophthalmos, cicatricial entropion/ectropion, trichiasis, distichiasis
• Anterior segment:
⚬ Conjunctival scarring
⚬ Cornea: neurotrophic keratitis, exposure keratitis, scarring, glaucoma
⚬ Anterior chamber: anterior uveitis, iris atrophy, glaucoma
• Posterior segment:
⚬ Vitritis, retinitis, cystoid macular oedema, choroiditis
• Neurological: orbital apex syndrome, cranial nerve palsy
6.
A 40-year-old gentleman comes in with eye discomfort of sudden onset.
Figure 1.6
Q
6.1 What are the signs?
• Sharply demarcated, bread crumb-like deposits with clear intervening spaces
• Lesions involving central cornea and spares the periphery
Q
6.2 What is the diagnosis?
• Granular dystrophy
Q
6.3 What other sign would you like to look out for in your examination?
• Epithelial defect by staining with fluorescein
Q
6.4 What is the treatment?
• Lubricants
• Refractive correction
• Treat acute recurrent cornea abrasion episodes
• Corneal graft if significant corneal scarring develops resulting in poor visual acuity
7.
A 45-year-old man comes in with eye discomfort of sudden onset.
Figure 1.7
Q
7.1 What are the signs?
• Linear rope-like lines with clear intervening spaces
• Lesions involving central cornea and spares the periphery
Q
7.2 What is your diagnosis?
• Lattice dystrophy
Q
7.3 What other signs would you look out for in your examination?
• Epithelial defect by staining with fluorescein
• Systemic associations: dry/lax skin, pendulous ears, bilateral facial nerve palsies
Q
7.4 What is the treatment?
• Lubricants
• Refractive correction
• Treat acute recurrent cornea abrasion episodes
• Corneal graft when significant corneal scarring develops resulting in poor visual acuity
8.
A 45-year-old lady comes in with blurring of vision that worsens in the morning.
Figure 1.8
Q
8.1 What are the signs?
• Central guttata (excrescences of Descemet’s membrane) involving visual axis
• Resembling a ‘beaten metal appearance’
• Pigment deposition on the endothelium
Q
8.2 What is the slit lamp technique demonstrated above?
• Specular reflection
Q
8.3 What is your diagnosis?
• Fuch’s endothelial dystrophy (FED)
Q
8.4 What test will you perform?
• Specular microscopy: endothelial cell count
• Corneal pachymetry
Q
8.5 What are the concerns in this patient?
• Corneal decompensation which can be exacerbated by any intraocular lasers or surgeries
• Glaucoma
9.
A 20-year-old man comes in with a two-month history of painless progressive
blurring of vision.
Figure 1.9 A-B
Q
9.1 What are the signs?
• Conical apical protrusion
• Paracentral stromal thinning
• Vogt’s striae
Q
9.2 What is your diagnosis?
• Keratoconus (KC)
Q
9.3 What other signs do you want to elicit?
• Apical scars
• Direct ophthalmoscope (oil droplet sign)
• Fleischer ring using the cobalt blue filter
• Munson’s sign
• Placido disc (Distortion of the concentric rings due to irregular astigmatism)
• Prominent corneal nerves
• Rizutti’s sign
• Retinoscope (scissoring reflex)
Q
9.4 What are the associations?
• Ocular: vernal keratoconjunctivitis (VKC), retinitis pigmentosa (RP), contact lens use,
Leber’s congenital amaurosis
• Systemic: Atopic dermatitis, Marfan’s syndrome, Down’s syndrome
Q
9.5 What tests will you do?
• Corneal topography/tomography scan: orbscan/pentacam
Q
9.6 What are the treatment options available?
• Conservative
⚬ Advise not to rub eye
⚬ Use spectacles
⚬ Use rigid gas-permeable contact lens
• Progressive keratoconus
⚬ Collagen cross-linking: stabilise curvature and prevent further steepening of corneal stroma
• Severe keratoconus or presence of central corneal scar affecting the vision
⚬ Corneal transplant: penetrating keratoplasty (PK) or deep anterior lamellar keratoplasty
(DALK)
10.
A 50-year-old lady comes in with a history of chronic glaucoma; she is worried
about an increasing whitish lesion in the eye.
Figure 1.10
Q
10.1 What are the signs?
• Inter-palpebral horizontal band of calcific plaque involving the visual axis, extending from
limbus to limbus
• ‘Swiss cheese’-like appearance
Q
10.2 What is your diagnosis?
• Band keratopathy (calcium deposits in Bowman’s layer)
Q
10.3 What are the causes of band keratopathy?
• Systemic
⚬ Hypercalcaemia: hyperparathyroidism, Paget’s disease, sarcoidosis, bone metastases,
multiple myeloma
⚬ Hyperphosphatemia: renal failure
• Ocular
⚬ Silicon oil
⚬ Chronic inflammation, e.g. chronic uveitis, juvenile idiopathic arthritis, interstitial keratitis
⚬ Phthisis bulbi
Q
10.4 What are the treatment options?
• Use of lubricants
• Scraping off with forceps or blade
• Chelation with ethylenediaminetetraacetic acid (EDTA 3%)
11.
A 50-year-old man comes in with a fleshy growth that has been on the eye for the
past few years.
Figure 1.11
Q
11.1 What are the signs?
• Fibrovascular conjunctival lesion within the palpebral fissure extending onto the corneal surface,
involving the visual axis
• Triangular-shaped, fleshy lesions with the apex extending onto the cornea associated with
vascular straightening
Q
11.2 What is your diagnosis?
• Double-headed pterygium
Q
11.3 What sign would suggest chronicity?
• Stocker’s line (iron deposition adjacent to pterygium)
Q
11.4 What are the potential complications?
• Induced astigmatism (flattening of cornea)
• Inflammation
• Obscuration of visual axis
• Scarring
Q
11.5 What are your differential diagnoses?
• Conjunctival Intraepithelial neoplasia (CIN)
• Pannus
• Symblepharon secondary to chemical, thermal or mechanical injury
Q
11.6 What is the treatment?
• Pterygium excision with conjunctival autograft
12.
A 50-year-old man comes in with a three-day history of pain, blurring of vision and
redness of the eye. He underwent a corneal graft surgery three months ago.
Figure 1.12
Q
12.1 What are the signs?
• Corneal graft
• Graft is hazy
• Corneal interrupted suture tract scars
• Keratic precipitates
• Khodadoust line (endothelial rejection line) involving visual axis (black arrow)
Q
12.2 What is your diagnosis?
• Graft endothelial rejection
Q
12.3 What other signs do you want to look out for?
• Anterior chamber activity
• Cornea vascularisation
• Peripheral anterior synaechiae
• Raised intraocular pressure
Q
12.4 What are the types of graft rejection?
• Epithelial
• Subepithelial
• Stromal
• Endothelial
Q
12.5 What are the risk factors of rejection?
• Corneal vascularisation
• Exposed sutures
• Large/eccentric/repeat grafts
• Glaucoma
• Ocular inflammation
• Ocular surface abnormalities (entropion, ectropion)
• Peripheral anterior synechiae
• Young patient
13. A 35-year-old man complains of double vision in the left eye.
Figure 1.13
Q
13.1 What are the signs?
• Superotemporal dislocation of the lens
• Visible zonules inferonasally
Q
13.2 What are the causes?
• Primary
⚬ Idiopathic
⚬ Familial ectopia lentis
⚬ Ectopic lentis et pupillae
• Secondary
⚬ Systemic
▪ Connective tissue disorders: Marfan’s syndrome, Ehlers-Danlos syndrome, WeillMarchesani syndrome, Stickler syndrome
â–ª Metabolic: homocystinuria, sulphite oxidase deficiency
⚬ Ocular
â–ª Developmental disorders: megalocornea, buphthalmos, aniridia
â–ª Non-developmental disorders: trauma, uveitis, pseudoexfoliation, hypermature cataracts,
anterior uveal tumours
Q
13.3 What are the potential complications?
• Cataract
• Diplopia
• Dislocated lens
• Lens-induced glaucoma
• Optical distortion
Q
13.4 What are the treatment options?
• Spectacles
• Lens extraction
Q
13.5 What are the options for intraocular lens placement?
• In the bag with capsular bag stabilisation devices
• Sulcus with capsular bag stabilisation devices
• Iris fixated
• Scleral fixated
• Anterior chamber
14.
A 50-year-old presents with eye pain and redness. He underwent an uncomplicated
cataract surgery four days ago.
Figure 1.14
Q
14.1 What are the signs?
• Chemosis
• Hazy cornea
• Hypopyon
• Injected conjunctiva
• Pseudophakia
Q
14.2 What are your differential diagnoses?
• Postoperative endophthalmitis
• Reactivation of uveitis
• Retained lens fragments
• Toxic anterior segment syndrome
Q
14.3 What are the causes of a hypopyon?
• Infective:
⚬ Endophthalmitis (endogenous and exogenous)
⚬ Syphilis
⚬ Tuberculosis
• Inflammatory:
⚬ HLA B-27
⚬ Behcet’s disease
• Masquerade:
⚬ Lymphoma
⚬ Leukaemia
Q
14.4 What are the treatment options?
• Vitreous tap for microscopy and cultures
• Intravitreal antibiotics: intravitreal vancomycin (1 mg/0.1 ml), ceftazidime (2.25 mg/0.1 mL)
• Topical intensive hourly cephazolin/gentamicin
• Systemic antibiotics (ciprofloxacin)
• Trans-pars plana vitrectomy
15. A 25-year-old man comes in with discomfort in both eyes.
Figure 1.15 A–B
Q
15.1 What are the signs?
• Bilateral injected eyes
• Mild chemosis
Q
15.2 What are your differential diagnoses for red eyes?
• Conjunctival lymphoma
• Conjunctivitis
• Blepharitis
• Episcleritis
• Scleritis
• Anterior uveitis
• Conjunctival lymphoma
• Acute angle closure glaucoma
Q
15.3 Which test helps differentiate episcleritis from scleritis?
• Phenylephrine 10% drops
GLAUCOMA
1.
A 60-year-old lady complains of poor vision, making it difficult for her to drive.
Figure 2.1
Q
1.1 What are the signs?
• Large optic cup (cup-to-disc ratio of 0.9 or more)
• Notching of superior rim, severe retinal nerve fibre thinning
Q
1.2 What are other signs suggestive of glaucoma?
• Optic disc cupping ≥ 0.7
• Asymmetry of optic cup (difference of cup-to-disc ratio of 0.2 or more)
• Does not obey the ISNT rule (normal discs have the thickest rim inferior > superior > nasal >
temporal)
• Progressive enlargement of optic cup
• Focal signs: notching, drance haemorrhage, peripapillary atrophy
• Baring/nasalisation/bayoneting of disc vessels
Q
1.3 What other examination and investigations will you perform?
Examination:
• Intraocular pressure
• Gonioscopy
Investigations:
• Central corneal thickness (CCT)
• Phasing, stereo-disc photographs
• Structural tests
⚬ Optical coherence tomography (OCT) of the retinal nerve fibre layer
• Functional tests (Perimetry)
⚬ Humphrey visual field (HVF)
⚬ Goldmann visual field (GVF)
Q
1.4 How can the intraocular pressure be measured?
• Contact:
⚬ Goldman applanation tonometer (GAT) [gold standard]
⚬ Tonopen
• Non-contact:
⚬ Air puff tonometer
Q
1.5 What are the visual field defects in glaucoma?
• Arcuate defect/double arcuate
• Paracentral defect
• Nasal step/temporal wedge, central vision only (tunnel vision)
2.
A 40-year-old lady comes in with sudden painful red eye associated with nausea,
vomiting and headache.
Figure 2.2
Q
2.1 What are the signs?
• Hazy cornea
• Injected conjunctiva
• Mid-dilated pupil
• Nuclear sclerotic cataract
• Shallow anterior chamber
Q
2.2 What is your diagnosis?
• Acute primary angle closure (APAC)
Q
2.3 What are your differential diagnoses?
• Phacomorphic glaucoma
• Subluxated lens
Q
2.4 What are the treatment options?
• Medical management
⚬ Intravenous acetazolamide (diamox) 500 mg
⚬ Topical medications: beta-blockers (e.g. timolol), alpha-2 agonist (e.g. alphagan), prostaglandin
analogues (e.g. latanoprost), carbonic anhydrase inhibitors (e.g. brinzolamide)
⚬ Topical miotics (e.g. pilocarpine)
⚬ Topical steroids (e.g. prednisolone acetate)
⚬ Consider repeat intravenous diamox or intravenous mannitol if the intraocular pressure is still
high after the above measures
• Once the intraocular pressure has decreased and cornea clarity improves, perform laser
peripheral iridotomy (LPI) using sequential argon-YAG laser
• Surgical management:
⚬ Lens extraction
Q
2.5 How is angle closure classified?
• Angle closure (AC) is characterised by the extent of iridotrabecular contact (ITC):
⚬ Primary angle closure suspect (PACS): at least 180° ITC, normal intraocular pressure,
absence of peripheral anterior synechiae
⚬ Primary angle closure (PAC): at least 180° ITC, evidence of raised intraocular pressure or
peripheral anterior synechiae
⚬ Primary angle closure glaucoma (PACG): at least 180° ITC with glaucomatous optic
neuropathy
3.
A 50-year-old poorly controlled diabetic comes in with a two-week history of
painful red eyes.
Figure 2.3
Q
3.1 What are the signs?
• Rubeosis iridis (vessels 360° around the iris)
• Cornea is clear
• Cataract
• Pupil is mid-dilated
Q
3.2 What other examination would you perform?
• Measure intraocular pressure
• Perform gonioscopy to look for neovascularisation of the angles, peripheral anterior synechiae
• Perform dilated fundus examination to look for aetiology
• Examine the fellow eye
Q
3.3 What is your diagnosis?
• Neovascular glaucoma (NVG)
Q
3.4 What are the causes?
• Ischaemic central retinal vein occlusion (CRVO)
• Ocular ischaemic syndrome
• Proliferative diabetic retinopathy (PDR)
Q
3.5 What are the treatment options?
• Systemic:
⚬ Co-manage with the internist to optimise the cardiovascular risk factors: hypertension,
hyperlipidaemia, diabetes
• Ocular:
⚬ Acute setting:
â–ª Lower the intraocular pressure using topical and systemic intraocular pressure-lowering
medications
â–ª Treat underlying ischaemia: pan-retinal photocoagulation (PRP) if cornea clarity permits
⚬ Good visual potential: control intraocular pressure, consider early glaucoma filtration or tube
surgery
⚬ Poor visual potential:
â–ª Absence of pain: conservative management
â–ª Presence of ocular pain and high intraocular pressure: trans-scleral cyclophotocoagulation
(TCP)
4.
A 45-year-old man comes in for routine eye screening.
Figure 2.4
Q
4.1 What is the sign seen?
• Krukenberg’s spindle
Q
4.2 What other signs would you expect to see on examination?
• Deep anterior chamber
• Heavily pigmented trabecular meshwork in all four quadrants on gonioscopy
• Increased cup-to-disc ratio of the optic nerve
• Mid-peripheral iris atrophy (trans-illumination defects)
• Posterior bowing of the iris
• Raised intraocular pressure
Q
4.3 What is your diagnosis?
• Pigment dispersion syndrome
Q
4.4 What are the treatment options?
• Anti-glaucoma medications
• Laser trabeculoplasty
• Trabeculectomy
5.
A 70-year-old man with a history of aortic aneurysm comes in for a routine eye
examination.
Figure 2.5
Q
5.1 What are the signs?
• Hoarfrost ring on the anterior lens capsule (black arrow)
• Pseudoexfoliative material at the pupillary margin (red arrow)
• Iris atrophy at pupil margin
Q
5.2 What other signs would you expect to see on examination?
• Increased cup-to-disc ratio
• Lens subluxation
• Poorly dilating pupil
• Phacodonesis
• Raised intraocular pressure
• Sampolesi’s line (pigmentation anterior to Schwalbe’s line on gonioscopy)
Q
5.3 What is your diagnosis?
• Pseudoexfoliation (PXF) syndrome
Q
5.4 What are patients with pseudoexfoliation prone to?
• High intraocular pressure
• Poor pupil dilation (small pupils)
• Zonulysis
6.
A 20-year-old badminton player comes into the emergency room after getting hit in
the eye by a shuttlecock.
Figure 2.6
Q
6.1 What is the abnormality?
• Gross hyphema less than one-third of the anterior chamber volume
Q
6.2 What is your diagnosis?
• Traumatic hyphema
Q
6.3 What are the possible causes?
• Trauma
• Spontaneous
⚬ Vascular abnormalities (rubeosis iridis bleed)
⚬ Tumours
⚬ Clotting disorders (sickle cell anaemia, anticoagulant treatment, blood dyscrasias)
Q
6.4 What are the potential complications?
• Re-bleeding (usually at about day 5)
• Increased intraocular pressure
• Corneal blood staining
Q
6.5 What are the treatment options?
• Conservative
⚬ Avoid antiplatelets or anticoagulants
⚬ Close monitoring for complications (re-bleeding, raised intraocular pressure, corneal blood
staining)
⚬ Complete rest in bed
⚬ Posture 45 degrees head up
• Topical steroids, cycloplegics, anti-glaucoma medications (if intraocular pressure is elevated)
• Surgical:
⚬ Anterior chamber washout
⚬ Surgical clot removal
7.
A 40-year-old patient had glaucoma surgery done two weeks ago.
Figure 2.7
Q
7.1 What are the signs?
• Avascular bleb
• Injected conjunctiva
• Pus-filled bleb
Q
7.2 What are the signs to look out for?
• Anterior chamber: cells, flare and hypopyon
• Posterior chamber: vitritis
• Positive Siedel’s test for bleb leak
Q
7.3 What is your diagnosis?
• Blebitis
Q
7.4 What investigations will you do?
• Conjunctival swab for microscopy and cultures
• B-scan if fundal view is poor
Q
7.5 What are the treatment options?
• Fortified topical antibiotics
• Subsequent surgical bleb revision in the presence of bleb leak
Q
7.6 What are the risk factors?
• Diabetes mellitus, systemic immunosuppression
• Inferior location of the bleb
• Meibomian gland disease
• Nasolacrimal duct obstruction
• Thin, cystic, avascular, leaking bleb
8.
A 60-year-old man comes in with advanced glaucoma.
Figure 2.8
Q
8.1 What do you see?
• Clear cornea
• Glaucoma drainage device at 11 o’clock position extending to pupil margin
• Patent surgical iridectomy (black arrow)
• Pseudophakia
Q
8.2 What are the indications for a glaucoma drainage device?
• Previous failed trabeculectomy
• Glaucomas which have a high risk of trabeculectomy failure: uveitic, neovascular, traumatic,
congenital
Q
8.3 What are the potential complications?
• Base plate: encapsulation, diplopia (interference with extraocular movements)
• Excessive drainage: hypotony
• Tube blockage: high intraocular pressure
• Tube cornea touch: corneal decompensation
• Tube exposure/extrusion: endophthalmitis
9.
Glaucoma investigation.
Figure 2.9
Q
9.1 What is this investigation?
• Humphrey visual field
Q
9.2 What do you see?
• Superior arcuate defect in the left eye
Q
9.3 Name one other visual field test?
• Goldmann visual field
Q
9.4 What are the indications for performing a visual field test?
• Diagnosis of
⚬ Glaucoma
⚬ Malingering patients
⚬ Optic neuropathy unexplained visual loss
• Follow-up of
⚬ Glaucoma: assess progression over time
⚬ Optic neuropathy
RETINA
1.
A 45-year-old man comes in with sudden onset painless blurring of vision.
Figure 3.1
Q
1.1 What are the signs?
• Superior retinal detachment extending inferiorly, macula-off
• Superior nasal U-tear at 1 o’clock
Q
1.2 What is your diagnosis?
• Rhegmatogenous retinal detachment
Q
1.3 What are the risk factors?
• Connective tissue disease
• Lattice degeneration
• Myopia
Q
1.4 What are the other types of retinal detachment?
• Exudative retinal detachment
• Tractional retinal detachment
Q
1.5 What are the principles of retinal detachment surgery?
• Find all retinal breaks
• Seal all retinal breaks
• Drain subretinal fluid (SRF) if necessary
• Relieve all vitreoretinal traction
Q
1.6 What are Lincoff’s rules?
A set of rules that aids in the determination of location of retinal breaks in primary rhematogenous
retinal detachment
2.
A 40-year-old man comes in with sudden onset of floaters in the left eye.
Figure 3.2
Q
2.1 What are the signs?
• Horseshoe tear
• Surrounding subretinal fluid
Q
2.2 What is your diagnosis?
• Horseshoe retinal tear
Q
2.3 What are the types of retinal breaks?
• Hole:
⚬ Atrophic
⚬ Operculated
• Tear: U tear/horseshoe tear/flap tear
Q
2.4 What is the treatment?
• Laser retinopexy (3–5 rows of confluent burns around the tear)
3.
A 40-year-old came in for routine eye screening.
Figure 3.3
Q
3.1 What are the signs?
• Well-defined areas of retinal thinning
• Circumferentially orientated hyperpigmentation with white lines
Q
3.2 What is your diagnosis?
• Lattice degeneration
Q
3.3 What are the potential complications?
• Atrophic holes
• Horseshoe tears
• Retinal detachment
4.
A 45-year-old lawyer comes in with a six-month history of painless blurring of
vision.
Figure 3.4
Q
4.1 What are the signs?
• Round punched-out defect at the fovea measuring 1-disc diameter
Q
4.2 What is the diagnosis?
• Full thickness macular hole (FTMH)
Q
4.3 What are your differential diagnoses?
• Central retinal artery occlusion
• Lamellar hole
• Pseudohole
Q
4.4 What test will you perform?
• Watzke Allan test
• Optical coherence tomography (OCT)
Q
4.5 What is the prognosis?
• Guarded: Large hole, long duration
5.
A 65-year-old man comes in with a two-month history of painless blurring of vision.
Figure 3.5
Q
5.1 What are the signs?
• Large subretinal haemorrhage measuring 3-disc diameters in size centred around the fovea
• Surrounding subretinal fluid and hard exudates and drusen
Q
5.2 What is your diagnosis?
• Exudative age-related macular degeneration (AMD)
Q
5.3 What are your differential diagnoses?
• Myopic choroidal neovascularisation (CNV)
• Polypoidal choroidal vasculopathy (PCV)
• Traumatic choroidal neovascularisation (CNV)
Q
5.4 What are the risk factors?
• Advanced age
• Smoking
• Obesity
• Large, soft, confluent drusen
• Fellow eye history of age-related macular degeneration (AMD)
• Hyperpigmentation of retinal pigment epithelium (RPE)
Q
5.5 How is it classified?
• Non-exudative AMD
• Exudative AMD
Q
5.6 What investigations will you perform?
• Fundus photography
• Optical coherence tomography (OCT)
• Fundus fluorescein angiogram (FFA)
• Indocyanine green (ICG)
Q
5.7 What are the treatment options?
• Focal laser for extra-foveal lesions
• Intravitreal anti-vascular endothelial growth factor (Anti-VEGF) injections
• Combined intravitreal Anti-VEGF and Photodynamic therapy (PDT) for PCV lesions
6.
A 45-year-old poorly controlled diabetic comes in with a four-day history of
painless blurring of vision.
Figure 3.6
Q
6.1 What are the signs?
• Neovascularisation at the disc (NVD)
• Neovascularisation elsewhere (NVE)
• Pre-retinal haemorrhage superiorly and inferiorly
• Scattered dot and blot haemorrhages
• Cotton wool spots
Q
6.2 What is your diagnosis?
• Proliferative diabetic retinopathy
Q
6.3 How is this disease classified?
• Non-proliferative retinopathy (NPDR):
⚬ Mild NPDR
⚬ Moderate NPDR
⚬ Severe NPDR (Any one of the 4:2:1 Rule)
▪ Blot haemorrhages in four quadrants ≥ standard photograph 2A
▪ Venous beading in two quadrants ≥ standard photograph 6A
▪ Intraretinal microvascular abnormalities in one quadrant ≥ standard photograph 8A
▪ Very severe: ≥ two of the 4:2:1 Rule
• Proliferative diabetic retinopathy (PDR)
Q
6.4 What is clinically significant macular oedema (CSME)?
• Retinal thickening within 500 microns from fovea
• Hard exudates within 500 microns from fovea associated with adjacent retinal thickening
• Retinal thickening greater than 1500 microns in size, any part of which lies within 1500 microns
from fovea
Q
6.5 How is diabetic macula oedema (DME) classified?
• Centre-involving
• Non-centre-involving
Q
6.6 What are the treatment options?
• Systemic: Co-manage with the internist to optimise cardiovascular risk factors
• Ocular:
⚬ Lasers
â–ª Pan-retinal photocoagulation (PRP)
â–ª Focal laser
⚬ Intravitreal injection
â–ª Anti-vascular endothelial growth factors (Anti-VEGF)
â–ª Steroids
Q
6.7 What are the potential complications?
• Neovascular glaucoma
• Tractional retinal detachment
• Vitreous haemorrhage
7.
A 60-year-old man comes in with sudden onset painless blurring of vision.
Figure 3.7
Q
7.1 What are the signs?
• Attenuated retinal arterioles
• Oedematous pale retina with a cherry red spot
Q
7.2 What is your diagnosis?
• Central retinal artery occlusion (CRAO)
Q
7.3 What else will you examine?
• Auscultate carotids for bruit
• Check pulse for atrial fibrillation
Q
7.4 What are the causes of retinal artery occlusion?
• Systemic:
⚬ Carotid emboli
â–ª Cholesterol emboli
â–ª Fibrino-platelet emboli
â–ª Calcific emboli
⚬ Cardiac emboli
â–ª Thrombus
â–ª Calcific
â–ª Bacterial
⚬ Coagulation disorders
⚬ Vasculitis
â–ª Giant cell arteritis (GCA)
â–ª Systemic lupus erythematosus (SLE), polyarteritis nodosa (PAN)
• Ocular:
⚬ Atherosclerosis of carotid and retinal artery
⚬ Raised intraocular pressure
â–ª Retrobulbar haemorrhage
â–ª Orbital tumour
â–ª Orbital inflammatory disease
Q
7.5 What is the prognosis?
• Poor
8.
A 64-year-old lady comes in with a two-day history of painless blurring of vision.
Figure 3.8
Q
8.1 What are the signs?
• Dilated tortuous veins
• Flame-shaped and blot haemorrhages associated with cotton wool spots in all four quadrants of
the retina
• Hyperemic swollen disc
• Look for macular oedema
Q
8.2 What is the diagnosis?
• Central retinal vein occlusion (CRVO)
Q
8.3 What are your differential diagnoses?
• Diabetic retinopathy
• Radiation retinopathy
Q
8.4 What are the risk factors?
• Systemic:
⚬ Older age, diabetes mellitus, hypertension, smoking
⚬ Blood dyscrasias: factor V leiden, protein C/S deficiency, anti-phospholipid syndrome
⚬ Hyperviscosity states: leukaemia, myeloma
⚬ Oral contraceptive use
• Ocular:
⚬ Glaucoma
⚬ Vasculitis: Bechet’s, sarcoidosis
⚬ External compression: tumours, thyroid eye disease
Q
8.5 What are the complications?
• Cystoid macula oedema
• Macular ischaemia
• Neovascular glaucoma
Q
8.6 What investigations will you perform?
• Optical coherence tomography (OCT)
• Fundus fluorescein angiography (FFA)
Q
8.7 What are the treatment options?
• Optimise cardiovascular risk factors
• Intravitreal:
⚬ Anti-vascular endothelial growth factors (Anti-VEGF)
⚬ Steroids
• Pan-retinal photocoagulation (PRP)
9.
A 25-year-old banker comes in with a three-day history of painless blurring of
vision.
Figure 3.9
Q
9.1 What are the signs?
• Neurosensory detachment involving the macula, more than 6-disc diameters in size
Q
9.2 What is your diagnosis?
• Central serous chorioretinopathy (CSCR)
Q
9.3 What are the risk factors?
• Steroid use or use of traditional Chinese medicine
• Young age
• Male
• Stress
• Type A personality
• Pregnancy
• Cushing’s disease
Q
9.4 What investigations will you perform?
• Optical coherence tomography: quantify amount of subretinal fluid
• Fundus fluorescein angiography: ink blot or smoke-stack appearance
Q
9.5 What are the treatment options?
• Conservative: stop offending agents, reduce stress
⚬ 80% will improve in six months
• Focal laser for extrafoveal lesions
• Photodynamic therapy (PDT) (subfoveal/juxtafoveal lesions)
10. A 40-year-old comes in with longstanding painless blurring of vision.
Figure 3.10
Q
10.1 What are the signs?
• Tessellated fundus
• Tilted disc
• Peripapillary atrophy
• Chorioretinal atrophic changes over the macula
• Examine for:
⚬ Subretinal haemorrhage, lacquer crack, staphyloma
⚬ Examine the peripheral retina for lattice degeneration, retinal tears and retinal detachments
Q
10.2 What is your diagnosis?
• Pathological myopic degeneration
Q
10.3 What are the associations?
• Systemic:
⚬ Down’s syndrome
⚬ Ehlers-Danlos syndrome
⚬ Marfan’s syndrome
• Ocular:
⚬ Albinism
⚬ Congenital glaucoma
⚬ Congenital stationary night blindness
⚬ Retinopathy of prematurity
Q
10.4 What are the potential complications?
• Amblyopia
• Anisometropia
• Retina: retinal tears, retinal detachment
• Macula: Myopic choroidal neovascularisation (CNV), macular hole, macular degeneration
11. A 30-year-old man complains of poor vision at night.
Figure 3.11
Q
11.1 What are the signs?
• Bony spicule pigmentation
• Waxy disc pallor
• Arteriolar attenuation
• Atrophic degeneration of macula (Bull’s eye maculopathy)
Q
11.2 What is your diagnosis?
• Retinitis pigmentosa (RP)
Q
11.3 What are your differential diagnoses?
• Infective: syphillis, rubella, measles
• Inflammation: chronic uveitis
• Vascular: central retinal artery occlusion, ocular ischaemic syndrome
• Trauma: old retinal detachment
• Scar: pan-retinal photocoagulation, trauma
• Neoplastic: carcinoma-associated retinopathy (CAR), paraneoplastic
• Medications: chloroquine, phenothiazine
Q
11.4 What investigations will you perform?
• Electroretinogram (ERG)
• Goldman visual field
• Screen family members
Q
11.5 What are the causes of Bull’s eye maculopathy?
• Congenital:
⚬ Cone dystrophy
⚬ Cone rod dystrophy
⚬ Rod cone dystrophy
⚬ Stargardt disease
• Acquired:
⚬ Hydroxychloroquine/Chloroquine
⚬ Tamoxifen
⚬ Chlorfazimine
Q
11.6 What investigations will you perform?
• Amsler chart
• Auto-fluorescence
• Electroretinogram (ERG)
• Visual field
12. A child with pale skin comes in with longstanding poor vision.
Figure 3.12A
Figure 3.12B
Q
12.1 What are the signs?
• Hypopigmented/diaphanous iris with retroillumination defects
• Hypopigmented fundus with visible choroidal vessels
• Foveal hypoplasia
• Optic nerve hypoplasia
Q
12.2 What is your diagnosis?
• Oculocutaneous albinism
Q
12.3 What are the systemic associations?
• Hermansky-Pudlak syndrome
• Chediak-Higashi syndrome
Q
12.4 What would you expect the vision to be? Support your answer with one
expected clinical finding.
• Poor vision with the presence of sensory nystagmus
13.
A 50-year-old man comes in with a three-month history of blurred vision in the left
eye associated with distortion.
Figure 3.13
Q
13.1 What are the signs?
• Large elevated, pigmented endophytic choroidal lesion at the inferonasal region, obscuring the
optic disc.
• Subretinal fluid
• Surface lipofuscin (orange pigments)
Q
13.2 What is your diagnosis?
• Choroidal melanoma
Q
13.3 What is your differential diagnosis?
• Metastatic lesion: breast and lung
Q
13.4 What investigations will you perform?
• Ultrasound scan
• Fundus fluorescein angiography
• Magnetic resonance imaging of the brain and orbit: extraocular extension
• Systemic examination/imaging: exclude metastasis to and from the choroid
Q
13.5 What are the treatment options?
• Systemic: chemotherapy
• Ocular:
⚬ Focal laser
⚬ Infrared lasers: transpupillary thermotherapy
⚬ Radiotherapy
⚬ Enucleation
⚬ Orbital exenteration
14.
A 50-year-old man with a history of pheochromocytoma comes in for a routine eye
check.
Figure 3.14
Q
14.1 What are the signs?
• Well-defined lesion with dilated feeder and drainage vessels
Q
14.2 What is your diagnosis?
• Capillary haemangioma
Q
14.3 What are the potential complications?
• Exudative retinal detachment
• Vitreous haemorrhage
Q
14.4 What are the associations?
• Cerebellar haemangioma
• Pancreatic carcinoma
• Pheochromocytoma
• Renal cell carcinoma
• Von Hippel Lindau syndrome
Q
14.5 What are the treatment options?
• Conservative
• Focal laser
• Photodynamic therapy (PDT)
• Cryotherapy
• Vitrectomy if vitreous haemorrhage/tractional retinal detachment/epiretinal membrane
15.
A 60-year-old man with poorly controlled hypertension comes in with a two-week
history of painless blurring of vision.
Figure 3.15
Q
15.1 What are the signs?
• Localised dilation of the second-order inferotemporal retinal arteriole
• Surrounding oedema
• Subretinal, intra-retinal and pre-retinal bleeding, involving the macular (tri-layer bleed)
Q
15.2 What is your diagnosis?
• Macroaneurysm
Q
15.3 What are the treatment options?
• Conservative: monitor closely for progression
• Focal laser
16. Retinal differential diagnoses.
Figure 3.16
Q
16.1 What is the arrow pointing at?
• Roth’s spot: retinal haemorrhages with a fibrin thrombus occluding the vessel
Q
16.2 What are the causes?
• Blood disorders:
⚬ Anaemia, leukaemia, scurvy
• Infective:
⚬ AIDs retinopathy, candida retinopathy
⚬ Infective endocarditis, sepsis
• Vasculitis:
⚬ Systemic vasculitis (e.g. systemic lupus)
17. Retinal differential diagnoses.
Figure 3.17
Q
17.1 What do you see?
• Multiple cotton wool spots
Q
17.2 What are the causes?
• Embolic
⚬ Carotid/cardiac emboli
• Drugs
⚬ Interferon retinopathy
• Ischaemic
⚬ Diabetic retinopathy, hypertension, radiation, retinal vein occlusion
• Inflammation/infection
⚬ Giant cell arthritis (GCA)
⚬ HIV retinopathy, cat-scratch disease
⚬ Systemic lupus erythematosus, polyarthritis nodosa
• Neoplastic
⚬ Lymphoma, leukaemia
18. Retinal differential diagnoses.
Figure 3.18
Q
18.1 What do you see?
• Vitreous haemorrhage
Q
18.2 What are the causes?
• Rupture of normal vessels
⚬ Retinal tear, retinal detachment, posterior vitreous detachment (PVD)
⚬ Trauma
• Abnormal vessels
⚬ Macroaneurysm, choroidal neovascularisation, polypoidal choroidal vasculopathy
⚬ Proliferative diabetic retinopathy, ischaemic retinal vein occlusion
⚬ Retinopathy of prematurity, retinal telangiectasia
• Others
⚬ Bleeding diathesis, valsalva
19. Retinal differential diagnoses.
Figure 3.19
Q
19.1 What do you see?
• Cystoid macular oedema and subretinal fluid
Q
19.2 What imaging modality is this?
• Optical coherence tomography scan
Q
19.3 What are the causes?
• Vascular
⚬ Diabetic macular oedema (DME), retinal vein occlusion, choroidal neovascularisation
• Inflammation/infection
⚬ Uveitis, endophthalmitis
• Surgery
⚬ Irvine-Gass (post-cataract surgery)
⚬ Post vitrectomy
⚬ Laser photocoagulation
• Drugs
⚬ Prostaglandin analogues
⚬ Epinephrine eyedrops
• Tractional
⚬ Vitreomacular traction
⚬ Epiretinal membrane
• Others
⚬ Retinitis pigmentosa, X-linked retinoschisis
UVEITIS
1.
A 40-year-old lady comes in with a one-month history of blurring of vision.
Figure 4.1
Q
1.1 What are the signs?
• Extensive fluffy yellow patch of retinitis extending from and along the inferior temporal vascular
arcade towards the posterior pole, involving the macula
• Surrounding intraretina haemorrhage, resembling a ‘cheese and ketchup’ appearance
• Vasculitis
Q
1.2 What is your diagnosis?
• Cytomegalovirus retinitis
Q
1.3 What are your differential diagnoses?
• Bacterial: syphilis, tuberculosis
• Viral: acute retinal necrosis (ARN), progressive outer retinal necrosis (PORN)
• Parasitic: toxoplasmosis
• Autoimmune: Behcet’s disease, sarcoidosis
Q
1.4 What investigations will you perform?
• Blood
⚬ Infective screening:
— Complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein
(CRP)
— Cytomegalovirus serology: DNA polymerase chain reaction (PCR)
— Syphilis: venereal disease research laboratory (VDRL), line immunoassay IgM and IgG
(LIA-IgG and LIA-IgM)
— Tuberculosis: Mantoux, chest X-ray (CXR)
⚬ Immune status:
— Human immunodeficiency virus (HIV), CD4/CD8 counts
• Aqueous or vitreous tap: tetraplex polymerase chain reaction [cytomegalovirus (CMV), herpes
simplex virus (HSV), varicella zoster virus (VZV), toxoplasmosis]
Q
1.5 What are the treatment options?
• Systemic
⚬ Systemic antivirals: intravenous ganciclovir or oral valganciclovir
• Ocular
⚬ Intravitreal ganciclovir or foscarnet
⚬ Barrier laser retinopexy, vitrectomy (if retinal tears/retinal detachment develops subsequently)
2.
A 50-year-old comes in with a complaint of floaters.
Figure 4.2
Q
2.1 What are the signs?
• Pigmented subretinal scar (black arrow)
• Adjacent areas of chorioretinitis (white star)
• Vascular sheathing (yellow arrows)
• Vitritis (headlight-in-the-fog appearance)
Q
2.2 What is your diagnosis?
• Reactivation of toxoplasmosis with chorioretinitis adjacent to the scar
Q
2.3 What are the treatment options?
• Triple therapy: pyrimethamine, folinic acid, sulphadiazine
• Steroids can be added once infection is under control
3.
A 40-year-old presents with painful red eyes.
Figure 4.3
Q
3.1 What are the signs?
• Dilated deep scleral vessels
• Bluish violaceous hue
Q
3.2 What is your diagnosis?
• Anterior scleritis
Q
3.3 What are the systemic associations?
• Granulomatosis with polyangiitis (GPA) (previously known as Wegener’s syndrome)
• Polyarteritis nodosa (PAN)
• Rheumatoid arthritis (RA)
• Relapsing polychondritis (RP)
• Systemic lupus erythematosus (SLE)
Q
3.4 What ocular investigation would you perform?
• B-scan: T sign (suggestive of posterior scleritis)
Q
3.5 What are the potential complications?
• Scleral melt
• Corneal melt
• Cataract
• Glaucoma
• Exudative retinal detachment
4.
A 45-year-old complains of bilateral eye discomfort.
Figure 4.4 A–C
Q
4.1 What are the signs?
• Multifocal serous retinal detachments
• Mutton fat keratic precipitates
Q
4.2 What are your differential diagnoses for multifocal serous retinal detachment?
• Vogt-Koyanagi-Harada disease (VKH)
• Sympathetic ophthalmia (SO)
• Multifocal central serous chorioretinopathy (CSCR)
• Posterior scleritis
• Infection: tuberculosis
• Tumours: choroidal metastasis, lymphoma
Q
4.3 What ocular investigations will you perform?
• B scan
• Fundus fluorescein angiogram (FFA)
• Indocyanine green (ICG)
Q
4.4 What are the treatment options for Vogt-Koyanagi-Harada disease?
• Oral prednisolone
• Intravenous methylprednisolone
• Immunomodulatory therapy
NEURO-OPHTHALMOLOGY
1.
A 60-year-old lady comes in with sudden-onset diplopia.
Figure 5.1
Q
1.1 What are the signs?
• Right partial ptosis, not obscuring the visual axis
• Right eye deviated laterally and inferiorly
Q
1.2 What is your diagnosis?
• Right cranial nerve III palsy
Q
1.3 What are some worrying features?
• Absence of vascular risk factors
• Absence of spontaneous recovery
• Aberrant regeneration: lid elevation on adduction or downgaze, pupil constriction on adduction or downgaze
• Incomplete cranial nerve III palsy
• Multiple cranial nerve palsies
• Pupil movement
• Progression of pupil involvement
• Young age
Q
1.4 What are the causes?
• Medical
⚬ Diabetes mellitus
⚬ Giant cell arteritis
⚬ Inflammatory
⚬ Miller-Fisher syndrome
⚬ Ophthalmic migraine
⚬ Tolosa-Hunt syndrome
• Surgical
⚬ Cerebral aneurysm
⚬ Raised intracranial pressure with uncal herniation
⚬ Tumour
Q
1.5 What investigations will you perform?
• Medical
⚬ Autoimmune markers
⚬ Complete blood count (CBC)
⚬ Erythrocyte sedimentation rate (ESR)
⚬ Fasting blood sugar level
⚬ Venereal disease research laboratory (VDRL), fluorescent treponemal antibody absorption (FTA-ABS)
• Surgical
⚬ Computed tomography angiography (CTA), magnetic resonance angiography (MRA) or four-vessel
angiography
2.
A 50-year-old man comes in with sudden-onset horizontal diplopia.
Figure 5.2A–B
Q
2.1 What are the signs?
• Right esotropia in primary gaze
• Right abduction deficit
Q
2.2 What is your diagnosis?
• Right sixth nerve palsy
Q
2.3 What else do you look for on examination?
• Extraocular movements (involvement of cranial nerve III)
• Check ability to intort on abduction (failure would suggest involvement of cranial nerve IV)
• Check pupils (involvement of cranial nerve II)
• Check fundus for papilledema (false localizing sign of raised intracranial pressure, idiopathic intracranial
hypertension)
• Check ears for battle sign (petrous bone fracture)
• Examine neurologically
⚬ Contralateral hemiparesis (Raymond’s syndrome)
⚬ Cranial nerve VII palsy and contralateral hemiparesis (Millard-Gubler syndrome)
⚬ Cranial nerve V, VII and VIII palsy, cerebellar signs (Cerebellopontine angle tumour — acoustic neuroma)
⚬ Horizontal gaze palsy, cranial nerves V and VII palsy, Horner’s syndrome (Foville’s syndrome)
Q
2.4 What are your differential diagnoses?
• Convergence spasm
• Divergence insufficiency
• Duane’s syndrome
• Longstanding esotropia
• Myasthenia gravis
• Medial wall fracture
• Thyroid eye disease
Q
2.5 What are the causes?
• Gradenigo syndrome: mastoiditis/petrositis
• Raised intracranial pressure: space occupying lesion, idiopathic intracranial hypertension
• Tumours: nasopharyngeal carcinoma
• Vascular: ischaemia, giant cell arteritis
3.
A 50-year-old lady complains of vertical diplopia.
Figure 5.3 A–E
Q
3.1 What are the signs?
• Right hypertropia
• Limitation of downward movement of right eye in down and left gaze
• Over-elevation of the right eye in up and left gaze
Q
3.2 What Investigations or examination will you perform?
• Park’s three-step test
• Double Maddox rod test (excyclotorsion)
• Examine old photos (differentiate congenital versus acquired cranial nerve IV palsy)
• Vertical fusional range (increased in congenital cranial nerve IV palsy)
Q
3.3 What is your diagnosis?
• Right cranial nerve IV palsy
Q
3.4 What are your differential diagnoses?
• Myasthenia gravis
• Orbital fracture
• Partial cranial nerve III palsy
• Skew deviation
• Thyroid eye disease
Q
3.5 What are the treatment options?
• Bangerter foil
• Patching
• Fresnel prism
• Surgery: if stable over six months
4.
A 45-year-old man complains of droopy eyelids that worsen at the end of the day.
Figure 5.4
Q
4.1 What are the signs?
• Left partial ptosis obscuring the visual axis
Q
4.2 What are other ocular features of the likely diagnosis?
• Ptosis
⚬ Asymmetrical
⚬ Cogan’s lid twitch
⚬ Fatigability of the lids on upgaze
⚬ Shifting (between left and right eyes)
⚬ Variable (between different times of day)
• Ophthalmoplegia
⚬ Normal pupil examination
⚬ Not consistent with single cranial nerve palsy
⚬ Variable strabismus
• Orbicularis oculi weakness
⚬ ‘Eye lash’ sign (failure to bury eyelashes)
⚬ ‘Eye peek’ sign (failure of full lid closure)
Q
4.3 What is your diagnosis?
• Ocular myasthenia gravis
Q
4.4 What investigations will you perform?
• Clinical tests: ice pack test
• Blood tests
⚬ Anti-acetylcholine receptor antibody
⚬ Anti-smooth muscle antibody
⚬ Anti-muscle specific kinase antibody
⚬ Thyroid function tests
• Electrodiagnostic tests
⚬ Repetitive nerve fibre stimulation
⚬ Single-fibre electromyography
• Anti-cholinesterase tests
⚬ Prostigmine test
⚬ Tensilon test
• Imaging
⚬ Computed tomography (CT) or magnetic resonance imaging (MRI) scan of the thorax (looking out for
thymoma)
Q
4.5 What are the treatment options?
• Systemic
⚬ Anti-acetylcholinesterase: pyridositgmine (Mestinon)
⚬ Immunosuppresive therapy: prednisolone, azathioprine
⚬ Plasmapheresis
⚬ Thymectomy
• Ocular complications
⚬ Lid crutches for ptosis
⚬ Prisms for ophthalmoplegia-induced diplopia
5.
A 45-year-old lady complains of right-sided neck and face pain.
Figure 5.5
Q
5.1 What are the signs?
• Anisocoria with the right pupil smaller than the left
• Right partial ptosis (right upper lid lifted up to expose the visual axis)
Q
5.2 What is your diagnosis?
• Right Horner’s syndrome
Q
5.3 What are the causes?
• Central (first order)
⚬ Brainstem cerebrovascular accident
⚬ Multiple sclerosis
⚬ Spinal cord tumour
⚬ Trauma
• Preganglionic (second order)
⚬ Pancoast tumour
⚬ Subclavian aneurysm
⚬ Thyroid cancer
⚬ Trauma
⚬ Vertebral metastasis
• Postganglionic (third order)
⚬ Carotid dissection
⚬ Cluster headache
⚬ Cavernous sinus syndrome
Q
5.4 How do you confirm the diagnosis?
• Apraclonidine 0.5% eye drops (reversal of anisocoria)
• Cocaine 10% (failure to dilate in the Horner’s pupil)
Q
5.5 How do you localize the lesion?
• Hydroxyamphetamine 1%
• Phenylephrine 1%
• Decreased sweating over hemi-face of the affected side
Q
5.6 What imaging would you perform?
• Magnetic resonance imaging (MRI) of brain and neck
• Magnetic resonance angiography (MRA)
• Computed tomography (CT) of thorax
Q
5.7 What are the causes of small pupils?
• Horner’s syndrome
• Longstanding Adie
• Neurosyphillis (Agryll Robertson)
• Pharmacological
• Uveitis
6.
A 30-year-old man comes in for routine eye screening, showing anisocoria worsening in the light
with full extraocular movements.
Figure 5.6
Q
6.1 What are the signs?
• Anisocoria with the right pupil larger than the left
Q
6.2 What is the most likely diagnosis?
• Tonic pupil
Q
6.3 What are other features of this condition?
• Light near dissociation
• Slow constriction and dilatation of the pupil
• Vermiform movements of the iris (constriction of the iris in segments)
Q
6.4 How do you confirm the diagnosis?
• 0.125% pilocarpine (constriction of tonic pupil secondary to denervation hypersensitivity)
Q
6.5 Where is the lesion?
• Ciliary ganglion or short ciliary nerves
Q
6.6 What are the causes?
• Primary
⚬ Holmes-Adie pupil
⚬ Holmes-Adie syndrome (associated with areflexia)
• Secondary
⚬ Degenerative
⚬ Diabetes mellitus
⚬ Iatrogenic/trauma
⚬ Myotonia dystrophica
⚬ Parkinson’s disease
⚬ Progressive supranuclear palsy
⚬ Syphilis
⚬ Tumour
7.
A young lady complains of painful blurring of vision in the left eye.
Figure 5.7
Q
7.1 What are the signs?
• Optic disc vessels obscured
• Obliterated cup
• Swollen and hyperaemic optic disc with blurred disc margins
Q
7.2 What are the causes?
• Autoimmune
• Compressive optic neuropathy
• Ischaemic optic neuropathy
• Infiltrative: leukaemia, sarcoidosis
• Optic neuritis: demyelinating, infectious, para-infectious
• Ocular causes: retinal vein occlusion, diabetic papillopathy, posterior scleritis
• Orbital causes: thyroid eye disease, orbital inflammatory syndrome, orbital tumours
Q
7.3 What features would suggest a demyelinating cause?
• Dysarthria/dysphagia/ataxia
• Motor/sensory dysfunction
• Lhermitte’s sign
• Pulfrich phenomenon
• Uhthoff phenomenon
Q
7.4 What investigations will you perform?
• Autoimmune screening
• Infectious screening
• Steroid workup
• Magnetic resonance imaging (MRI) of the brain and anterior visual pathways with contrast
• Lumbar puncture
Q
7.5 What are the treatment options for optic neuritis?
• Intravenous methylprednisolone for three days followed by oral prednisolone for 11 days
Q
7.6 What are the complications of steroids?
• Ocular
⚬ Cataract, glaucoma, exacerbation of infection (e.g. HSV)
• Systemic
⚬ Cardiac: arrhythimia, heart failure
⚬ Ischaemic necrosis of the femur
⚬ Malignant hypertension, hyperglycaemia, herpetic failure
⚬ Neutropenia, infection: reactivation of tuberculosis
⚬ Psychosis
⚬ Skin changes: hirsutism, acne, moon facies, buffalo hump
⚬ Suppression hypothalamic-pituitary-adrenal axis: shock
⚬ Ulcer: gastric ulcers, bleeding of gastrointestinal tract
8.
A 30-year-old obese lady presents with progressive blurring of vision.
Figure 5.8 A–B
Q
8.1 What are the signs?
• Bilateral optic disc swelling
• Discs are hyperemic with blurred margins and obliterated cups
Q
8.2 What are the causes?
• Life threatening
⚬ Dural venous sinus thrombosis
⚬ Malignant hypertension
⚬ Meningitis
⚬ Space-occupying lesion
• Idiopathic intracranial hypertension
• Bilateral optic neuritis
• Hereditary optic neuropathy
• Infiltrative: sarcoidosis, leukaemia
• Orbital: thyroid eye disease, carotid-cavernous fistula
• Ocular: diabetic papillopathy, posterior uveitis
• Pseudopapilloedema
Q
8.3 What is the likely diagnosis?
• Idiopathic intracranial hypertension (IIH)
Q
8.4 What are the risk factors for IIH?
• Medications
⚬ Tetracycline, vitamin A, nalidixic acid, cyclosporin, oral contraceptives pills, steroids
• Systemic
⚬ Addison’s disease
⚬ Chronic obstructive pulmonary disease
⚬ Hypoparathyroidism, hypothyroidism
⚬ Obesity
⚬ Renal failure
Q
8.5 What investigations would you perform?
• Blood pressure, temperature
• Lumbar puncture
• Magnetic resonance imaging (MRI) of brain and anterior visual pathways with contrast and magnetic resonance
venography (MRV)
Q
8.6 What are the treatment options?
• Conservative: weight loss, stop offending agents, treat systemic disorders
• Oral acetazolamide, frusemide or topiramate
• Surgery: lumbo-peritoneal or ventriculo-peritoneal shunt
9.
A 70-year-old man comes in with sudden loss of vision.
Figure 5.9
Q
9.1 What are the signs?
• Occlusion of the cilio-retinal artery with associated retinal infarction
• Pale, swollen disc
• Peripapillary flame haemorrhages
Q
9.2 What else will you ask for in the history?
• Fever/malaise
• Headache
• Jaw claudication
• Polymyagia rheumatica
• Scalp tenderness
Q
9.3 What investigations will you perform?
• Complete blood count (CBC): thrombocytosis
• Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)
• Pre-steroid work-up
• Temporal artery biopsy
Q
9.4 What are the treatment options?
• Optimize cardiovascular risk factors
• IV methylprednisolone
• Oral prednisolone: gentle tapering of the dosage with serial ESR monitoring
10. A 70-year-old man comes in with a six-month history of painless blurring of vision.
Figure 5.10
Q
10.1 What are the signs?
• Pale disc
Q
10.2 What are the causes?
• Life-threatening cause: compressive optic neuropathy, infiltrative neuropathy
• Hereditary, e.g. Leber’s hereditary optic neuropathy (LHON)
• Infectious optic neuropathy
• Ischaemic optic neuropathy
• Nutritional optic neuropathy: vitamin B12 deficiency, folate deficiency
• Previous optic neuritis
• Radiation optic neuropathy
• Trauma optic neuropathy
• Toxic optic neuropathy: ethambutol, methanol
• Ocular: pan-retinal photocoagulation, previous central retinal artery occlusion
• Orbital: thyroid eye disease
11.
A 45-year-old lady comes in with longstanding blurring of vision.
Figure 5.11
Q
11.1 What are the signs?
• Central core of white glial tissue
• Large disc with a funnel-shaped excavation
• Peripapillary atrophy and pigmentation
• Vessels emerge radially from the disc in ‘spokes of wheel’ fashion
Q
11.2 What is your diagnosis?
• Morning glory disc
Q
11.3 What are the systemic associations?
• Frontonasal dysplasia
• Moyamoya disease
• Neurofibromatosis type 2
• PHACES syndrome
Q
11.4 What are the ocular complications?
• Choroidal neovascularisation (CNV)
• Serous retinal detachment
Q
11.5 What investigations will you perform?
• Magnetic resonance imaging (MRI) of the brain
• Magnetic resonance angiography (MRA)
12. A 25-year-old man comes in with poor vision in the right eye since young.
Figure 5.12
Q
12.1 What are the signs?
• Inferior peripapillary atrophy
• White bowl-shaped excavation involving the inferior disc
Q
12.2 What is the diagnosis?
• Optic disc coloboma
Q
12.3 What are the potential complications?
• Peripapillary choroidal neovascularisation (CNV)
• Serous retinal detachment
Q
12.4 What are the systemic associations?
• Brain malformation: agenesis of corpus callosum, anencephaly
• CHARGE syndrome
• Chromosomal anomalies: trisomy 13, 18, 22
• Goldenhar syndrome
13. A 45-year-old lady comes in with strange-looking discs.
Figure 5.13
Q
13.1 What are the signs?
• Yellow, lumpy lesions at the disc not obscuring the optic disc vessels
Q
13.2 What is your diagnosis?
• Optic disc drusen
Q
13.3 What investigations can you perform to confirm the diagnosis?
• Autofluorescence
• B-scan with low gain settings
• Computed tomography scan: calcification of optic nerve
Q
13.4 What are the potential complications?
• Choroidal neovascularisation
• Central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO)
• Limited loss of visual field
14. A 70-year-old lady is referred for routine eye screening.
Figure 5.14
Q
14.1 What are the signs?
• Optociliary shunt (black arrow)
Q
14.2 What are the causes?
• Central retinal vein occlusion
• Chronic papilloedema
• Meningioma
• Optic glioma
Q
14.3 What other examinations will you perform?
• Dilated fundus examination
• Extraocular movements
• Hertels exophthalmometer
• Optic nerve function
• Fellow eye
15. A 50-year-old lady complains of difficulty driving.
Figure 5.15 A–B
Q
15.1 What are the signs?
• Bitemporal hemianopia respecting the midline
Q
15.2 What are your differential diagnoses?
• Infective: tuberculosis
• Infiltrative: sarcoidosis
• Tumour: pitutary tumour/apoplexy, craniopharyngioma, parasellar meningioma
Q
15.3 What investigations will you perform?
• Blood: Hormone level — prolactin [others: oxytocin, follicle-stimulating hormone (FSH), luteinising
hormone (LH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), growth hormone (GH),
antidiuretic hormone (ADH)]
• Magnetic resonance imaging (MRI) of brain and anterior visual pathway with contrast
Q
15.4 What are the treatment options?
• Co-manage with the endocrinologist to optimise any endocrine dysfunction
• Hormonal therapy: bromocriptine, cabergoline, somatostatin analogues (for prolactinoma)
• Gamma knife stereotactic radiosurgery
• Surgery: transphenoidal or transethmoidal resection
16. A 45-year-old man complains of frequent bumping into objects.
Figure 5.16A–B
Q
16.1 What are the signs?
• Left superior homonymous quadrantinopia
Q
16.2 Where is the lesion?
• Right retro-chiasmal lesion (likely temporal or inferior occipital lesion)
Q
16.3 What investigations will you perform?
• Magnetic resonance imaging (MRI) of brain with contrast
Q
16.4 What features would suggest an occipital cortex lesion?
• Congruence
• Optokinetic nystagmus (OKN) symmetry
• Unformed visual hallucinations
Q
16.5 What are features of a parietal lobe lesion?
• Dominant lobe:
⚬ Agraphia
⚬ Acalculia
⚬ Apraxia
⚬ Finger agnosia
⚬ Right-left disorientation
• Non-dominant lobe
⚬ Hemi-neglect
⚬ Impaired constructional ability (constructional apraxia)
⚬ Dyscalculia
Q
16.6 What are features of a temporal lobe lesion?
• Auditory hallucination
• Déjà vu hallucination
• Formed visual hallucination
• Seizures
OCULOPLASTICS
1.
A 50-year-old lady is referred for bilateral bulging eyes.
Figure 6.1
Q
1.1 What are the signs?
• Bilateral proptosis
• Conjunctival injection
• Lid retraction and oedema
• Superior and inferior scleral show
Q
1.2 What else will you examine for?
• Optic nerve function
• Lid lag, lagophthalmos, Bell’s reflex, cornea sensation
• Extraocular movements, Hertel exophthalmometer
• Slit lamp:
⚬ Conjunctival chemosis
⚬ Exposure keratopathy
⚬ Intraocular pressure
⚬ Fundus examination: disc swelling, choroidal folds
• Systemic features:
⚬ Neck: goitre, neck scar
⚬ Hand: atrial fibrillation, tremor, palm sweatiness, thyroid acropachy
⚬ Legs: pretibial myxedema
Q
1.3 What is your diagnosis?
• Bilateral active thyroid eye disease
Q
1.4 How is activity assessed?
• Clinical activity score: patients with at least three out of the following seven criteria are
considered to have the active disease:
⚬ Conjunctival injection
⚬ Chemosis
⚬ Caruncular oedema
⚬ Lid oedema
⚬ Lid erythema
⚬ Pain at rest
⚬ Pain with eye movement
Q
1.5 What are the sight-threatening complications?
• Compressive optic neuropathy
• Exposure keratopathy
• Glaucoma
Q
1.6 What investigations will you perform?
• Blood:
⚬ Pre-steroid workup
⚬ Thyroid function test
⚬ Thyroid antibodies or immunoglobulins (thyroid receptor antibody (TrAb), thyroid stimulating
immunoglobulin (TSI)
• Computer tomography (CT) scan of the orbits
• Facial photos
• Humphrey visual field (HVF)
Q
1.7 What are the treatment options?
• General: Co-manage with the endocrinologist to optimise thyroid function, stop smoking
• Active disease:
⚬ Intravenous steroids/systemic immunosuppressants
⚬ Orbital radiation
⚬ Orbital decompression: bone/fat
• Exposure keratopathy: intensive lubricants, moist chamber goggles
• Glaucoma: intraocular pressure-lowering medications
• Restrictive myopathy: patching or prism, surgical correction
2.
A 40-year-old lady comes in with a two weeks’ history of diplopia.
Figure 6.2
Q
2.1 What are the signs?
• Right hypoglobus
• Fullness of the right upper lid particularly temporally
• Lacrimal gland enlargement
Q
2.2 What are your differential diagnoses?
• Lacrimal gland:
⚬ Tumours (pleomorphic adenoma, pleomorphic adenocarcinoma, adenoid cystic carcinoma)
⚬ Inflammation (dacryoadenitis)
• Orbital causes:
⚬ Haematological: lymphoma
⚬ Inflammatory: orbital inflammatory disease
⚬ Soft tissue: dermoid cyst, mucocele, encephalocele
⚬ Tumours: meningioma, neurofibroma, metastasis
⚬ Vascular: lymphangioma, orbital varix, arteriovenous malformation (AVM)
Q
2.3 What investigations will you perform?
• Imaging: computed tomography (CT) scan of the orbits
• Blood: infective, inflammatory, pre-steroid work-up
3.
A 45-year-old lady comes in with a two-day history of painful left eye.
Figure 6.3
Q
3.1 What are the signs?
• Periorbital erythema and oedema
• Complete ptosis
Q
3.2 What else will you examine for?
• Inspect: chalazion, pimples, open wounds, insect bites
• Palpate the eye: masses, chalazion, collection of abscess
• Extraocular movement
• Optic nerve function
• Hertel exophthalmometer for proptosis
• Slit lamp:
⚬ Chemosis and conjunctival injection
⚬ Intraocular pressure
⚬ Optic disc swelling
Q
3.3 What is your diagnosis?
• Orbital cellulitis
Q
3.4 What are your differential diagnoses?
• Diabetes mellitus: mucormycosis, aspergillosis
• Orbital inflammatory syndrome
• Ruptured dermoid cyst
• Trauma
Q
3.5 What are the sources of infection?
• Haematogenous
• Contiguous spread from chalazion, pimples, sinusitis
• Skin wound secondary to trauma, insect bites
Q
3.6 What are the potential complications?
• Abscess formation: subperiosteal, intraobital
• Cavernous sinus thrombosis
• Exposure keratopathy
• Intracranial extension: meningitis or encephalitis
• Increased intraocular pressure
• Optic neuropathy
Q
3.7 What investigations will you perform?
• Blood: complete blood count (CBC), erythrocyte sedimentation rate (ESR), C reactive protein
(CRP), blood culture
• Conjunctival swabs for microscopy and cultures
• Computed tomography (CT) scan of the orbits with contrast
Q
3.8 What are the treatment options?
• Intravenous augmentin and cloxacillin ± metronidazole
• Incision and drainage of the abscess
4.
A 30-year-old lady comes in with a two-day history of left lower lid swelling.
Figure 6.4
Q
4.1 What are the signs?
• Swelling inferior to the medical canthal tendon
• Surrounding erythema and induration
Q
4.2 What is your diagnosis?
• Left dacryocystitis
Q
4.3 What will you want to exclude?
• Orbital cellulitis
Q
4.4 What investigations will you perform?
• Blood: complete blood count (CBC), erythrocyte sedimentation rate (ESR), C reactive protein
(CRP), blood culture
• Imaging: computed tomography (CT) scan of the orbits if the suspicion of orbital cellulitis is
high
Q
4.5 What are the treatment options?
• Topical antibiotics: tobramycin
• Intravenous augmentin
• Aspiration for decompression
• Dacryocystorhinostomy (DCR) when the disease is quiescent.
5.
A five-year-old boy presents with droopy right eye since birth.
Figure 6.5
Q
5.1 What are the signs?
• Right ptosis obscuring the visual axis
• Absence of lid crease
Q
5.2 What else will you examine for?
• Bell’s reflex
• Corneal sensation
• Extraocular movement
• Lagophthalmos
• Lid measurements: palpebral aperture, levator function, marginal reflex distance-1 (MRD1)
• Pupils: anisocoria
• Visual acuity
• Cycloplegic refraction
Q
5.3 What is the likely diagnosis?
• Congenital ptosis
Q
5.4 What are the treatment options?
• Treat amblyopia
• Ptosis surgery: frontalis suspension
6.
A mother notices an enlarging mass appearing over her baby’s left upper lid
for the past three months.
Figure 6.6
Q
6.1 What are the signs?
• Bluish red mass on the left upper eyelid
• Partial ptosis obscuring visual axis
Q
6.2 What is your diagnosis?
• Capillary haemangioma
Q
6.3 What are the ocular complications?
• Amblyopia: occlusive, astigmatism
• Proptosis: exposure keratopathy, increased intraocular pressure, compressive optic neuropathy
Q
6.4 What are the treatment options?
• Treat amblyopia
• Oral propranolol, topical beta blockers
• Topical or intralesional steroids
• Surgical excision
Q
6.5 What is the prognosis?
• Good prognosis
• 70% resolved spontaneously by seven years of age
7.
A 70-year-old man comes in with a six-month history of right eye discomfort.
Figure 6.7
Q
7.1 What are the signs?
• Inward turning of the lower lid margin
• Corneal-lash touch
Q
7.2 What is your diagnosis?
• Right lower lid entropion
Q
7.3 What are the causes?
• Acute spastic
• Cicatricial
• Involutional
Q
7.4 What are the treatment options for involutional entropion?
• Lubricants
• Epilation, electrolysis of lash follicles
• Everting sutures
• Surgery
8.
A 70-year-old man with a history of Bell’s palsy comes in with left ocular
discomfort.
Figure 6.8
Q
8.1 What are the signs?
• Lower lid ectropion
• Poor lid globe apposition
Q
8.2 What are the underlying mechanisms?
• Horizontal lid laxity
• Laxity of medial and lateral canthal ligament
• Weakness of pretarsal orbicularis
Q
8.3 What are the causes of ectropion?
• Cicatricial
• Involutional
• Mechanical
• Paralytic: facial nerve palsy
Q
8.4 How do you assess for horizontal lid laxity?
• Distraction test
• Snap back test
9.
A 50-year-old man complains of a lump over the lower lid that has been present for
the last six months.
Figure 6.9
Q
9.1 What are the signs?
• Rodent ulcer occupying medial one-third of lower lid
• Rolled pearly edges
• Destruction of the normal lid architecture
Q
9.2 What else will you examine for?
• Extraocular movements
• Fixation to deep tissue or bone
• Punctal involvement
• Proptosis
• Optic nerve function
Q
9.3 What is your diagnosis?
• Basal cell carcinoma
Q
9.4 What are your differential diagnoses?
• Keratoacanthoma
• Melanoma
• Squamous cell carcinoma
• Sebaceous cell carcinoma
Q
9.5 What investigations will you perform?
• Incisional biopsy for diagnostic confirmation
10. A 40-year-old man complains of recurrent styes.
Figure 6.10
Q
10.1 What are the signs?
• Yellow lumpy lesion located at the medial one-third of upper lid region
• Destruction of normal lid architecture
• Localised madarosis
Q
10.2 What is the diagnosis?
• Sebaceous cell carcinoma
Q
10.3 What investigations will you perform?
• Incisional biopsy
• Send fresh specimen to be stained with Oil Red O stain
11. A 30-year-old man comes in with blunt trauma to the left eye.
Figure 6.11
Q
11.1 What are the signs?
• Conjunctiva injection
• Eyelid oedema
• Periorbital bruising
Q
11.2 What else would you examine for?
• Decreased visual acuity
• Loss of colour vision
• Extraocular movement limitation
• Elevated intraocular pressure
• Relative afferent pupillary defect
• Crepitus
• Infraorbital paresthesia
• Step deformity
• Globe integrity
• Traumatic hyphema and iritis
• Iridodialysis
• Retinal tear/detachment
Q
11.3 If the intraocular pressure is greatly elevated, what is the diagnosis?
• Left retrobulbar haemorrhage
Q
11.4 What are the treatment options?
• Lateral canthotomy with inferior cantholysis
• Intraocular pressure-lowering medications
12. A 30-year-old man comes in with injuries sustained in a fight.
Figure 6.12
Q
12.1 What are the signs?
• Full-thickness lower and upper lid laceration
Q
12.2 What structure may be damaged?
• Lower and upper canaliculus
Q
12.3 What is the potential complication?
• Epiphora
Q
12.4 What are the treatment options?
• Direct closure with stenting
• Options of stenting: bicanalicular (Crawford stent) or monocanalicular (mini-monoka stent)
Q
12.5 What are some causes of tearing?
• Hypersecretion:
⚬ Aberrant regeneration
⚬ Dry eyes
⚬ Eyelids: trichasis, ectropion, entropion
⚬ Reflex tearing
• Obstruction:
⚬ Partial versus complete blockage
• Lacrimal pump failure:
⚬ Facial nerve palsy
Q
12.6 How do you assess a patient with tearing?
• Eyelids: punctum, lids for entropion, ectropion, distichiasis/trichiasis, lash cornea touch
• Cornea: tear break-up time, punctate epithelial erosions
• Special test:
⚬ Dye disappearance test
⚬ Naso-lacrimal irrigation: syringing and probing
⚬ Schirmer’s test
PAEDIATRICS
1.
A three-year-old boy presents with in-turning of the left eye.
Figure 7.1
Q
1.1 What are the signs?
• Left esotropia (ET) with about 30 prism diopters of deviation
Q
1.2 What are your differential diagnoses?
• Comitant:
⚬ Accommodative esotropia (esotropia secondary to hyperopia)
⚬ Congenital esotropia
⚬ Consecutive esotropia
⚬ Convergence spasm
⚬ Divergence insufficiency
⚬ Sensory esotropia (esotropia secondary to poor vision in the affected eye)
• Incomitant:
⚬ Abducens nerve (CN VI) palsy
⚬ Duane’s syndrome
⚬ False localising sign (raised intracranial pressure)
⚬ Myasthenia gravis
⚬ Orbital fracture
⚬ Thyroid eye disease
Q
1.3 What else do you look for on examination?
• Visual acuity: using age-appropriate methods
• Pupil light reflex and red reflex
• Extraocular movement
• Cover/uncover/alternate cover test with prism cover test (taking measurements for distance/near
with and without the aid of full refractive correction)
• Stereopsis
• Cycloplegic refraction
• Anterior and posterior segment examination
• Old photos: family album tomography
Q
1.4 What are the treatment options for accommodative esotropia?
• Full correction with glasses
• Executive bifocals (for patients with excessive convergence)
• Surgery for residual deviation that glasses are unable to correct
2.
A four-year-old boy presents with outward deviation of the eyes.
Figure 7.2
Q
2.1 What are the signs?
• Left exotropia (XT) with about 50 prism diopters of deviation
Q
2.2 What are your differential diagnoses?
• Congenital exotropia (rare, usually associated with intracranial abnormalities)
• Acquired exotropia
⚬ Comitant:
â–ª Consecutive exotropia (e.g. resultant overcorrection post-squint operation for esotropia)
â–ª Convergence insufficiency
â–ª Divergence excess
â–ª Intermittent exotropia
â–ª Sensory exotropia (exotropia secondary to poor vision in the affected eye)
⚬ Incomitant:
▪ Duane’s syndrome
â–ª Internuclear ophthalmoplegia
â–ª Myasthenia gravis
â–ª Oculomotor nerve (CN III) palsy
â–ª Orbital fracture
â–ª Thyroid eye disease
Q
2.3 What examination will you perform for intermittent exotropia?
• Measure angle of deviation for distance and near using prisms
• Refraction
• Stereopsis
3.
A six-year-old girl is brought in for strange-looking eyes.
Figure 7.3 A–C
Q
3.1 What are the signs?
• Narrowing of palpebral aperture in the right eye on left gaze
• Right abduction deficit
Q
3.2 What is your diagnosis?
• Right duane’s syndrome (type 1)
Q
3.3 What are the systemic and ocular associations?
• Systemic associations:
⚬ Central nervous system: epilepsy
⚬ Deafness
⚬ Goldenhar syndrome
⚬ Klippel-Feil anomaly of spine
⚬ Wildervanck syndrome
• Ocular associations:
⚬ Epibulbar dermoids
⚬ Lid coloboma/iris coloboma
⚬ Ptosis
⚬ Optic disc and fovea hypoplasia
⚬ Nystagmus
4.
A 1-week old neonate is brought in with sticky discharge.
Figure 7.4
Q
4.1 What are the signs?
• Bilateral oedematous and erythematous lids
• Copious purulent discharge
Q
4.2 What is your diagnosis?
• Ophthalmia neonatorum
Q
4.3 What else do you want to know from the history?
• Birth history: mode of delivery, birth weight, antenatal, perinatal and postnatal history
• Contact history
• Onset of symptoms
• Sexual history from parents: any sexually transmitted disease
Q
4.4 What are the causes?
• First 24 hours: silver nitrate
• Third to fifth day: gonorrhoea
• Fifth to seventh day: chlamydia
• Seventh to 14th day: viral (herpes simplex virus), bacterial (haemophilus, Staphylococcus
aureus, Streptococcus pneumoniae)
Q
4.5 What are the treatment options?
• Refer the parents to the communicable disease centre (if the swab/cultures are positive, start
contact tracing and family counselling)
• Copious eye irrigation
• Neisseria gonorrhea:
⚬ Systemic: intravenous ceftriaxone
⚬ Ocular: topical tobramycin
• Chlamydia trachomatis:
⚬ Systemic: oral erythromycin
⚬ Ocular: topical tetracycline/erythromycin ointment
• Herpes simplex virus:
⚬ Intravenous acyclovir
⚬ Topical acyclovir ointment
5.
A 2-year-old presents with abnormal-looking eyes.
Figure 7.5
Q
5.1 What are the signs?
• Right leukocoria
Q
5.2 What are your differential diagnoses?
• Chronic retinal detachment
• Coat’s disease
• Congenital cataract
• Persistent fetal vasculature
• Retinoblastoma
• Retinopathy of prematurity
Q
5.3 What are the genetics of retinoblastoma?
• Mutation of RB1 gene in chromosome 13q14
• Knudson 2 hit hypothesis
• Heritable (40%) versus non-heritable (60%)
Q
5.4 What investigations will you perform if you suspect the patient has
retinoblastoma?
• Bone marrow aspiration
• Blood test for genetic testing
• Lumbar puncture
• Magnetic resonance imaging (MRI) of the orbit and brain
Q
5.5 What are the secondary tumours the patient is at risk of?
• Brain and nerve: pinealoma, medulloblastoma, neuroblastoma
• Bone or soft tissue: ewing’s sarcoma, rhabdomyosarcoma, osteogenic sarcoma
• Blood: leukaemia
• Skin tumours: squamous cell carcinoma, malignant melanoma
Q
5.6 What are the treatment options for retinoblastoma?
• Co-manage with paediatric oncologist for systemic work-up
• Systemic chemotherapy
• Intra-arterial chemotherapy
• Focal therapy: laser/cryotherapy/plaque radiotherapy
• Enucleation
6.
A 31-week neonate is referred for eye screening.
Figure 7.6
Q
6.1 What are the signs?
• Peripheral area of avascular retina (1)
• Peripheral ridge (2)
• Extrafoveal fibrovascular proliferation (3)
• Vitreous haze
• Dilated veins and tortuous arterioles
Q
6.2 What is your diagnosis?
• Retinopathy of prematurity (ROP)
Q
6.3 What are the risk factors?
• Birth weight < 1.5 kg
• Gestational age: 32 weeks or less
• Intraventricular haemorrhage
• Necrotising enterocolitis
• Use of supplemental oxygen
• Respiratory distress syndrome
Q
6.4 What are the potential complications?
• Amblyopia
• Cataract
• Dragged disc
• Glaucoma
• Refractive error (anisometropia/myopia/astigmatism)
• Retinal detachment
• Vitreous haemorrhage
Q
6.5 What are the treatment options?
• Laser/cryotherapy to the areas of avascular retina
• Intravitreal antivascular endothelial growth factor (anti-VEGF)
• Vitreoretinal surgery (if retinal detachment occurs)
7.
A 1-year-old baby is brought in with injuries suffered when he rolled off the bed.
Figure 7.7
Q
7.1 What are the signs?
• Multiple intraretinal haemorrhages
• Pre-retinal haemorrhage
Q
7.2 What else will you examine for?
• Ocular:
⚬ Anterior segment:
— Hyphema
— Iritis
— Iridodialysis
— Traumatic cataract
— Subluxated lens
— Glaucoma
⚬ Posterior segment:
— Retinal tear/detachments
• Systemic:
⚬ Head injury
⚬ Skeletal survey for fractures
⚬ Signs of raised intracranial pressure (bulging fontanelles, lethargy, hypotonia)
Q
7.3 What are your differential diagnoses?
• Non-accidental injury
• Haematological anomalies: haemophilia, leukaemia
• Infective: infective endocarditis
• Meningitis
• Trauma: birth trauma, head injury
Q
7.4 What is the prognosis?
• Poor
• Cortical blindness occurs in up to 15% of patients who suffers non-accidental injuries
8.
A 6-month-old boy is brought in with tearing and blepharospasm.
Figure 7.8
Q
8.1 What are the signs?
• Slightly hazy cornea
• Right buphthalmos
Q
8.2 What are your differential diagnoses?
• Congenital glaucoma
• Corneal abrasion
• Megalocornea
• Naso-lacrimal duct obstruction (NLDO)
Q
8.3 What is the classical triad of symptoms of congenital glaucoma?
• Blepharospasm
• Photophobia
• Tearing
Q
8.4 What are the signs of congenital glaucoma?
• Buphthalmos
• Cloudy cornea
• Descemet’s break: Haab’s striae
• Disc cupping
• Enlarged cornea diameter
• Myopia
• Raised intraocular pressure
Q
8.5 What are the causes of paediatric glaucoma?
• Primary congenital glaucoma
• Secondary:
⚬ Systemic disorders:
— Chromosomal: neurofibromatosis, sturge-weber syndrome
— Metabolic: lowe syndrome
⚬ Ocular anomalies:
— Anterior: aniridia, anterior segment dysgenesis
— Posterior: retinopathy of prematurity, familial exudative vitreoretinopathy, retinal and uveal
tumours
⚬ Acquired conditions:
— Steroid, following cataract surgery, uveitis
Q
8.6 What are the treatment options?
• Medical: anti-glaucoma medications (temporising)
• Surgical: goniotomy, trabeculotomy, trabeculectomy, glaucoma drainage devices
9.
A 5-year-old boy is brought in with decreased red reflex in one eye.
Figure 7.9
Q
9.1 What are the signs?
• Discrete round opacity in the lens
• Obscuration of the visual axis
Q
9.2 What is your diagnosis?
• Congenital cataract
Q
9.3 What are the causes/associations?
• Systemic:
⚬ Chromosomal disorders: down syndrome
⚬ Intrauterine infections: TORCH infections
⚬ Metabolic disorders: galactosemia, lowe syndrome
• Ocular:
⚬ Aniridia, nanophthalmos, persistent fetal vasculature
⚬ Trauma, tumours, steroid use
Q
9.4 What are the treatment options if it is visually significant?
• Lens aspiration with primary posterior capsulotomy and anterior vitrectomy
Q
9.5 What are the options for aphakia correction?
• Intraocular lens
• Aphakic glasses
• Contact lens
10. A 2-year-old child is referred by the general practitioner for an eye check.
Q
10.1 How do you assess visual acuity in pre-verbal children?
• Qualitative tests:
⚬ Fixation and following
⚬ Objection to occlusion
⚬ Optokinetic nystagmus drum
⚬ Catford drum
• Quantitative tests:
⚬ Forced preferential testing/Teller acuity (1)
⚬ Cardiff acuity cards
Figure 7.10
Q
10.2 How do you assess visual acuity in verbal children?
• Kay’s pictures
• HOTV chart
• Snellen chart
• Sheridan gardiner singles
Q
10.3 How do you assess stereopsis?
• Frisby (2)
• Lang test (3)
• Titmus test
• TNO random dot: requires red-green glasses (4)
Q
10.4 What are the causes of amblyopia?
• Refractive
• Occlusive (stimulus deprivation)
• Strabismus
Figure 7.11
Figure 7.12
Figure 7.13
Q
10.5 What are the treatment options for amblyopia?
• Refractive:
⚬ Atropine penalisation
⚬ Cyclorefraction: spectacles
⚬ Patching
• Stimulus deprivation:
⚬ Surgery to remove obstruction
• Strabismus-related:
⚬ Spectacles
⚬ Patching
⚬ Surgery
IMAGING
1.
Look at Figure 8.1 and answer the questions.
Figure 8.1
Q
1.1 What imaging modality is this?
• Optical coherence tomography scan of the macula
Q
1.2 What do you see?
• Cystoid macula oedema and subretinal fluid involving the fovea
Q
1.3 What are the causes?
• Vascular:
⚬ Diabetic macula oedema (DME), retinal vein occlusion, choroidal neovascularisation
• Inflammation/infection:
⚬ Uveitis
⚬ Endophthalmitis/panophthalmitis
• Surgery/lasers:
⚬ Irvine-Gass (post-cataract surgery)
⚬ Post-vitrectomy
⚬ Laser photocoagulation
• Drugs:
⚬ Prostaglandin analogues
⚬ Epinephrine eyedrops
• Tractional:
⚬ Vitreomacular traction
⚬ Epiretinal membrane
• Others:
⚬ Retinitis pigmentosa
⚬ X-linked retinoschisis
2.
Look at Figure 8.2 and answer the questions.
Figure 8.2
Q
2.1 What do you see?
• Subretinal fluid
Q
2.2 What are causes of subretinal fluid accumulation?
• Inflammatory and autoimmune diseases:
⚬ Posterior scleritis
⚬ Sarcoidosis
⚬ Sympathetic ophthalmia
⚬ Systemic lupus erythematosus
⚬ Vogt-Koyanagi-Harada disease
⚬ Wegener’s granulomatosis
• Infectious diseases:
⚬ Lyme disease
⚬ Syphilis
⚬ Tuberculosis
• Neoplastic disorders:
⚬ Choroidal melanomas
⚬ Metastatic choroidal lesion
⚬ Retinal or choroidal haemangiomas
⚬ Retinoblastoma
• Vascular diseases:
⚬ Central serous chorioretinopathy
⚬ Eclampsia/preeclampsia
• Congenital abnormalities:
⚬ Optic disc pit
⚬ Retinal colobomas
⚬ Morning glory syndrome
⚬ Nanophthalmos
• Degenerative:
⚬ Polypoidal choroidal vasculopathy
⚬ Choroidal neovascularisation
• Others:
⚬ Drugs: interferon, ribavirin
⚬ Uveal effusion syndrome
3.
Look at Figure 8.3 and answer the questions.
Figure 8.3
Q
3.1 What do you see?
• Epiretinal membrane
Q
3.2 What are the causes?
• Primary: idiopathic
• Secondary:
⚬ Cryotherapy
⚬ Pan-retinal photocoagulation
⚬ Retinal tears
⚬ Retinal tumours: angioma, harmatoma
⚬ Retinal vascular diseases: diabetic retinopathy, retinal vein occlusion, macroaneurysm
⚬ Retinitis pigmentosa
Q
3.3 What are the treatment options?
• Conservative:
⚬ Mild with good visual acuity
• Surgery: vitrectomy with membrane peel:
⚬ Decreased visual acuity
⚬ Metamorphopsia
⚬ Vitreomacular traction
⚬ Cystoid macula oedema
4.
Look at Figure 8.4 and answer the questions.
Figure 8.4
Q
4.1 What imaging modality is this?
• Anterior segment optical coherence tomography (ASOCT)
Q
4.2 What do you see?
• Narrow angles
• Shallow anterior chamber
Q
4.3 What are causes of narrow angles?
• Pupil block:
⚬ Idiopathic
⚬ Iris bombe secondary to seclusio/occlusio pupillae
⚬ Silicone oil fill
• Iris block:
⚬ Iris cysts
⚬ Peripheral anterior synechiae, e.g. neovascular glaucoma or uveitis
⚬ Plateau iris
• Lens block:
⚬ Swollen lens
⚬ Subluxed lens
• Retrolental:
⚬ Choroidal effusion
⚬ Malignant glaucoma
⚬ Suprachoroidal haemorrhage
Q
4.4 How else is this imaging modality used?
• Cornea scar depth: planning for surgery
• Cornea grafts, e.g. attachment of endothelial grafts
• Post-LASIK, e.g. residual stromal bed
5.
Look at Figure 8.5 and answer the questions.
Q
5.1 What imaging modality is this?
• Corneal topography: Orbscan
Q
5.2 What do you see?
• Elevated anterior float (A)
• Elevated posterior float (B)
• Inferior corneal steepening (C)
• Thinning at the apex (D)
Q
5.3 What is the diagnosis?
• Keratoconus
Q
5.4 What other features on the scan will suggest the diagnosis?
• Asymmetric bow-tie (irregular astigmatism)
• Inferior cornea steeper than superior cornea
• Disparity in central steepening between both eyes
• Large difference in keratometric values between apex and periphery
Figure 8.5
6.
Look at Figure 8.6 and answer the questions.
Figure 8.6
Q
6.1 What do you see?
• Depressed anterior float
• Flattened central cornea
• Thinning of the central cornea (436 microns)
Q
6.2 What is the diagnosis?
• Post-myopic LASIK ablation
Q
6.3 What are the complications of LASIK?
• General:
⚬ Dry eyes
⚬ De-centred ablation
⚬ Glare
⚬ Halos
⚬ Undercorrection/overcorrection
⚬ Infectious keratitis
⚬ Post-LASIK ectasia
• Flap related:
⚬ Flap striae
⚬ Traumatic flap dislocation
• Interface related:
⚬ Diffuse lamellar keratitis (Sands of Sahara)
⚬ Epithelial ingrowth
Q
6.4 What are the contraindications for LASIK?
• Patient factors:
⚬ Drug use: amiodarone, accutane
⚬ Immunodeficiency
⚬ Pregnancy (unstable refraction)
• Ocular factors:
⚬ Corneal ectasia: keratoconus
⚬ Previous herpetic eye disease
⚬ Thin corneas
7.
Look at Figure 8.7 and answer the questions.
Figure 8.7
Q
7.1 What imaging modality is this?
• B-scan
Q
7.2 What is the diagnosis?
• Retinal detachment
Q
7.3 What are the principles of its use?
• Based on the reflection of sound waves at the interface between tissues of different acoustic impedances
• Ultrasound of 8–10 MHz is produced by the piezoelectric transducer
• Reflected sound waves are detected by the transducer and converted to an electric signal
Q
7.4 What are the indications for its use?
• Diagnostic:
⚬ Choroidal detachment
⚬ Intraocular foreign body
⚬ Optic disc drusen
⚬ Posterior scleritis
⚬ Retinal detachment
⚬ Intraocular tumours, e.g. retinoblastoma, choroidal melanoma
• Measurements:
⚬ Axial length, biometry
• Poor view of fundus:
⚬ Dense cataracts
⚬ Hyphaema
⚬ Vitreous haemorrhage
⚬ Vitritis
8.
Look at Figure 8.8 and answer the questions.
Figure 8.8
Q
8.1 What imaging modality is this?
• Specular microscopy (endothelial cell count)
Q
8.2 What do you see?
• Increased coefficient of variation (normal < 40)
• Guttata
• Reduced cellular density
• Reduced hexagonality index (6A): pleomorphism (normal > 60)
Q
8.3 What is your diagnosis?
• Fuch’s endothelial dystrophy
Q
8.4 What are other indications for its use?
• Monitoring: post-corneal transplant, cytomegalovirus (CMV) uveitis
• Prognostic: assess risk of corneal decompensation post-cataract surgery
Q
9.1 Look at Figure 8.9 and answer the questions.
Q
9.1 What imaging modality is this?
• Fundus fluorescein angiogram (FFA)
Q
9.2 What do you see?
• Hypofluorescence temporally, filling defect
• Neovascularisation
• Leakage
Q
9.3 What is your diagnosis?
• Branch retinal vein occlusion
Figure 8.9
Q
9.4 What are the principles of its use?
• Fluorescence:
⚬ The ability of a substance to emit light energy of a longer wavelength when stimulated by light of a shorter
wavelength
• Blood-retinal barrier
⚬ Inner: tight junctions of retinal capillary endothelial cells
⚬ Outer: tight junctions of retinal pigment epithelial (RPE) cells
Q
9.5 What are the causes of hyperfluorescence?
• Pre-injection:
⚬ Autofluorescence
⚬ Pseudofluorescence
• Window defect, e.g. RPE atrophy, RPE tear, chorioretinal atrophy, peripapillary atrophy
• Leak: e.g. choroidal neovascularisation, cystoid macular oedema, vasculitis, retinal neovascularisation
• Pooling, e.g. central serous chorioretinopathy, pigment epithelial detachment
• Staining, e.g. drusen, scar
Q
9.6 What are the causes of hypofluorescence?
• Blocked fluorescence, e.g. blood, hard exudates, melanin
• Vascular filling defect, e.g. retinal vein occlusion, retinal artery occlusion
10. Look at Figure 8.10 and answer the questions.
Figure 8.10
Q
10.1 What imaging modality is this?
• Indocyanine green (ICG) angiography
Q
10.2 What do you see?
• Multiple polypoidal lesions around the fovea (within red square)
Q
10.3 What is your diagnosis?
• Polypoidal choroidal vasculopathy (PCV)
Q
10.4 What advantage does it have over fundus fluorescein angiogram (FFA)?
• Allows imaging of the choroidal circulation which is otherwise prevented by poor transmission of fluorescence
through fundus pigmentation, subretinal fluid, lipid exudation
Q
10.5 How is it useful in other conditions?
• Central serous chorioretinopathy: identify areas of choroidal hyperpermeability
• Choroidal haemangioma: identify intrinsic vascular pattern
• Choroidal melanoma: identify tumour vessels (dual circulation)
INDEX
age-related macular degeneration, 41
angle closure, 23, 24
anisocoria, 76–78
blebitis, 30
B-scan, 138
carcinoma, 106, 107
congenital cataract, 117, 123
congenital glaucoma, 122
cornea, 1, 3, 4, 7, 15
corneal topography, 134
cytomegalovirus, 64
dacryocystitis, 100
detachment, 35, 36, 38, 43, 48, 50, 52, 56, 57, 60
diabetic retinopathy, 42, 46, 59, 61
diplopia, 69, 71, 73, 76
disc swelling, 81
dystrophy, 7, 8, 10, 52
ectropion, 105, 110
endophthalmitis, 2, 18
entropion, 104, 110
esotropia, 111–113
exotropia, 113, 114
fundus fluorescein angiography, 140, 143
glaucoma, 21, 28, 32–34
glaucoma drainage device, 32
graft, 8, 9, 14, 15
Humphrey visual field, 22, 34
hyphema, 28, 29
keratic precipitates, 68
keratoconus, 11
lacrimal gland swelling, 97
leukocoria, 117
myopia, 36
neuro-ophthalmology, 69
oculoplastics, 95
ophthalmia neonatorum, 115
optical coherence tomography, 129, 133
paediatric, 111, 118, 122
pale disc, 85
pigment dispersion, 26
proptosis, 95, 99, 103, 106
pseudoexfoliation, 28
pterygium, 13, 14
ptosis, 69, 74–76
red eyes, 19
retina, 35, 50
retinopathy of prematurity, 117, 119, 122
specular microscopy, 140
tumour, 45
trauma, 99, 108
uveitis, 63
vascular occlusion, 52
vitritis, 65