FRCS Ophthalmology: Cakewalk Mamta Mittal
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Examination TechniquesChapter 1

Main Topics
  • 1.1 Ptosis Exam
  • 1.2 Pupillary Exam
  • 1.3 Orbit Exam
  • 1.4 Cover/Uncover Tests
  • 1.5 Ocular Motility Exam
  • 1.6 Nystagmus
  • 1.7 Cranial Nerve Exam
  • 1.8 Visual Acuity Exam
  • 1.9 Visual Field Exam
  • 1.10 Examination of Enucleated Socket
 
1.1 PTOSIS EXAMINATION
 
 
History Taking
  • Age of onset/duration
  • Unilateral or bilateral
  • Any head posture
  • Diplopia
 
Examination
Examine right eye first then left eye:
  • Steps
  • Observe
  • Measure
  • Surgical exam
 
Additionals Test
Jaw-winking, cover tests, extraocular movements, pupils.
 
Observe
  • Anisocoria/heterochromia
  • Ocular alignment
  • Scars on the forehead or lids from previous surgery
  • 2Brow position
  • Spectacles: Prisms
  • Pseudoptosis: Check other eye (large/small eye, lid retraction, eno/exophthalmos)
  • Shake hands: Check for myotonia.
 
Measure Ptosis
  • Palpebral aperture
  • Measure the palpebral fissure in pupillary plane by getting the patient to look at distance
  • Margin reflex distance
  • Request the patient to look at your pen torch
  • Measure distance between upperlid margin and corneal reflection
  • Levator excursion
  • Press the brow of the patient with the eyes in downgaze
  • Patient then looks up as far as possible and the amount of excurtion is measured with the rule
  • Measure upper lid creases in both eyes
  • Distance between lid margin and lid crease in downgaze
  • Pretarsal show
  • Distance between lid margin and skin fold in primary position
  • Measure upper lid creases in both eyes
    • Distance between lid margin and lid crease in downgaze
  • Pretarsal show
    • Distance between lid margin and skin fold in primary position.
 
Surgical Exam and Additional Tests
  • Lagophthalmos: Ask patient to close the eye, look for scleral show
  • Bell's phenomenon: Manually open both the lids, observe upward rotation of the eye ball. It is the prognostic indicator of possible exposure problems
  • Increased innervation: Elevate ptotic lid, look for a droop in opposite lid
  • Orbicularis function: Request your patient to close eyes gently first and then squeeze the eye shut. Try to open his eyes against resistance.
  • 3RD Nerve functions: Corneal sensation, ocular motility, pupil reaction
  • Check Marcus Gunn sign: Ask patient to simulate chewing. Note any change in ptosis
  • Check for Myasthenia Gravis:
    • Fatiguability: Ask patient to look up for 1 min without blinking, look for worsening of ptosis
    • Cogan twitch: Ask patient to look rapidly from downgaze to a target held in primary positon, look for overshoot.
 
Likely cases
  • Pseudoptosis (Blow out fracture patient)
  • Congenital ptosis (May be an adult patient)
  • Mechanical ptosis (Lump on the lid)
  • 3Neurogenic (3rd Nerve palsy, Horners, M Gravis, Aberrant 3rd Nerve)
  • Aponeurotic ptosis
 
IMPORTANT VIVA QUESTIONS
  • Tell me about Marcus Gunn Jaw winking syndrome
    The MG jaw winking syndrome is an uncommon cause of congenital ptosis:
    • Synketic innervation of levator and pterygoid muscle by V CN
    • Movement of jaw (to opposite side) leads to retraction or wink
    How do you manage this?
    • Treatment depends on severity of ptosis versus degree of winking
      • For severe ptosis and severe winking, consider levator excision or disinsertion plus brow suspension
      • For mild ptosis and mild winking, levator resection alone may be sufficient.
  • Tell me about the blepharophimosis syndrome
    • AD inheritance, causes congenital ptosis
    • Defined as a narrowing of the horizontal palpebral aperture (note: NOT vertical!)
    • 5 classical features:
    • Epicanthus inversus
    • Ptosis with poor levator function and absent lid crease
    • Telecanthus (note: defined as medial canthal distance > half the interpupillary distance)
    • Ectropian of lower eyelid
    • Hypoplasia of nasal bridge and orbital rim
    Treatment depends on severity of ptosis, other lid problems and presence of amblyopia
    • Correct lid defects first (telecanthus and epicanthus inversus)
    • Correct ptosis later (bilateral brow suspension).
  • What are the causes of acquired ptosis?
    • Neurogenic ptosis: Innervational defect (third nerve) and oculosympathetic palsy (Horner syndrome), M gravis, MS
    • Myogenic ptosis: Myopathy of the levator muscle itself, or by impairment of transmission of impulses at the neuromuscular junction (neuromyopathic) – Myasthenia gravis, myotonic dystrophy and progressive external ophthalmoplegia
    • Aponeurotic ptosis: Defect in the levator aponeurosis.
    • Mechanical ptosis: Gravitational effect of a mass or scarring (Plexiform neurofibroma)
  • What is aponeurotic ptosis?
    • Occurs due to disinsertion or attenuation of the levator aponeurisis.
    • Features-abnormally high lid crease, mild to moderate ptosis (3-4 mm), good levator function (> 10 mm), no lid lag on down gaze, thin eyelid tissue.
 
What are the Differences between Congenital and Senile Ptosis?
Congenital Ptosis
Acquired/Senile Ptosis
Cause
Levator maldevelopmentreplaced by fibrous/fatty tissue
Ageing, trauma, rubbing eyes, rigid contact lens wearers, surgery
4
Laterality
Unilateral
Bilateral, asymmetric
Severity
Severe
Mild
Upper lid crease
Absent
Present, high
On downgaze
Lid lag
Ptosis worse
Levator function
Poor
Good
Other signs
SR weakness, amblyopia, chinup head posture
Thin of upper lid skin
Deep upper lid sulcus
Treatment
Brow suspension
Aponeurotic repair
  • What is pseudoptosis? Causes?
    • A false impression of ptosis is called pseudoptosis.
    • Causes: Contralateral lid retraction, ipsilateral enophthalmos, hypertropia, microphthalmos, brow ptosis, Duane's syndrome, and dermatochalasis.
  • Describe Tensilon test
    • A Tensilon test is indicated in all patients when myasthenia gravis is suspected.
    • The test is performed by giving 2 mg (0.2 mL) intravenous as a test dose to ensure the patient does not have a reaction, followed 30 seconds later by 8 mg (0.8 mL), and observing the patient's lid position.
    • If the patient has myasthenia gravis, there will be a significant elevation in lid position within 1 to 5 minutes after giving the test dose.
  • How do you manage a patient with ptosis?
    It can be conservative or surgical.
    • Factors to consider:
      • Cause of ptosis
      • Severity of ptosis
      • Levator function
      • Amblyopia management
    • Type of surgery
      Levator function good (> 10 mm):
      • Ptosis severe (> 2 mm) - Aponeuretic repair
      • Ptosis Mild (< 2 mm) - Fasanella Servat (tarsomullerectomy)
    • Levator function moderate (4 to 10 mm): Levator resection.
    • Levator function poor (< 4 mm): Brow suspension (frontalis sling-autogenous/preserved fascia, silicone), Whitnall's sling +/− superior tarsectomy.
  • What are complications of ptosis surgery?
    • Corneal exposure due to lagophthalmos
    • Over and undercorrection
    • Contour defects, lid crease asymmetry
    • Less common complications:
      • Lash ptosis and entropian
      • Lash eversion and ectropian
      • Conjunctival prolapse
      • Scarring, wound dehiscence, granuloma formation
      • Orbital hemorrhage.
 
Common Viva and Case Scenarios for Practice
5
  • Unilateral ptosis in young female (You notice aberrant 3rd nerve regeneration). Discuss about the management and possible ptosis surgeries required by the patient.
  • Perform the measurements for the levator function in unilateral ptosis.
  • Picture of a case with bilateral Ptosis. Tell differential diagnosis.
  • Sudden unilateral ptosis in old man. How will you manage?
  • 40 yrs male headache and ptosis. How to assess and examine this case. How to differentiate medical vs surgical lesion? If he develops 4th n palsy, how do you check?
  • Picture of a girl with bilateral ptosis, left eye exotropia. Differentials (mysthenia, CPEO). How would you manage. What is Kearns syre syndrome? What would you find in the heart? How to diagnose. What is mitochondrial inheritance? Where else in ophthalmology (Leber's hereditary optic neuropathy). Which is the enzyme to look for in the blood?
 
1.2 PUPILLARY EXAM
 
 
Examination
  • Step 1 Observe:
    Normal size of pupil in room light is 4-5 mm
    Look for:
    • Anisocoria (the most cases being Horner's, Adie's, third nerve palsy)
    • Less commonly siderosis bulbi and traumatic. 20% cases have physiological anisocoria
    • Heterochromia (congenital Horner's syndrome and siderosis bulbi)
    • Ptosis (Horner's syndrome and third nerve palsy)
    • Ocular misalignment (3rd n)
    • Abnormal pupil shape (posterior synechia).
  • Step 2 Slit lamp exam:
    To determine local factors as the cause of anisocoria – sphincter teras, pupil synaechiae, retroillumination defects, vermiform movements.
  • Step 3 Alter illumination of the room:
    • If no local factors identified for anisocoria, request to alter the illumination of the room - To accentuate differences in pupil size in light and shade.
    • Reduce light: Accentuates sympathetic palsy (dark corners-Horner's) smaller pupil is abnormal
    • Bright light: Accentuates parasympathetic palsy (bright ideas-Aides) larger pupil is abnormal.
      Inference:
      • If anisocoria remains same in bright and dim light-physiologic anisocoria (< 2 mm difference in both pupils in both the situtations)
      • If anisocoria is more in dim light then work up for Horner's syndrome
      • If anisocoria is more in bright light then work up for adie's, CN 3 palsy.
  • Step 4 Check pupillary reactions:
    • Reaction to direct (afferent pathway) and consensual light (efferent pathway).
      6Technique
      • Direct Reaction:
        1. Ambient Illumination in the room, (enough to be able to see other pupil)
        2. Ask patient to focus on distant target. (6 m)
        3. With hand held bright light (Not direct ophthalmoscope), diffusely illuminate pupils from below the nose or from temporal side. Do not obstruct patient's vision
        4. Note the size, shape and position of each pupil.
      • Consensual Reaction:
        • Same technique, but observe other eye.
    • Swinging light test for afferent pupillary defects
      Technique:
      • Move light from right to left eye in 300 msec and dwell on each eye for 2-5 sec
      • Repeat only once or twice
      • Then Grade RAPD depending on reaction in abnormal eye:
        • Immediate dilatation + + +/++ ++
        • 1-2 sec later +/++
        • Subtle escape to slightly large pupil - Trace.
    • Reaction to accommodation (light near dissociation–better response to near than light)
      Technique:
      • Only done when light reflex is abnormal
      • Fixate patient at a target at 6 m
      • Then swiftly present a near target (Langs stick) at 20-30 cm just below horizontal
      • And tell them to fixate the target
      • Observe the pupils.
 
Additional Examination According to Probable Diagnosis
  • RAPD (this indicates optic nerve disease or extensive retinal dysfunction)
  • Look for optic disc pallor, advanced glaucoma cupping or total retinal detachment
  • Horner's syndrome (neck or chest scar)
  • Third nerve palsy (ocular motility) – ptosis, limited motility, mid-dilated pupil, decreased accomodation, no light near dissociation
  • Adie's pupil (slit-lamp for vermiform iris movement and knee jerk)
  • Argyll-Robertson's pupil (interstitial keratitis, deafness).
 
IMPORTANT VIVA QUESTIONS
  • Differential diagnosis of anisocoria
    • Afferent pathway:
      • Optic nerve: Glaucoma, AION, compression
      • Retina: CRVO, CRAO, detachment
    • 7Efferent pathway:
      • Adies
      • 3rd nerve
      • Horners
    • Light near dissociation
      • Unilateral: Afferent defects, Adies, HZO, aberrant regeneration of 3rd nerve
      • Bilateral: Neurosyphilis, Type1 DM, myotonic dystrophy, Perinaud DMS, Familial amyloidosis, Encephalitis, chronic alcoholism.
    • Miscellaneous
      • Traumatic, pharmacological, physiological, congenital, postr synechia, prosthesis
      • Amaurotic pupil.
  • Describe pupillary pathways
    • Parasympathetic pathway (light response):
      • 2nd n-pretectalnucleus-E Wnucleus-3rd nerve-ciliary ganglion-short ciliary nerve-constrict.
    • Sympathetic pathway
      • Posterior hypothalamus-C8-T2 (ciliospinal center of budge)-white ramisuperior cervical ganglion-pericarotid plexes-nasociliary branch of 5N-long ciliary nerve-Dilate
    • Near response pathway
      • Not well defined:
        1. lst order: Retina (ganglion cells)-optic nerve-optic tract
        2. 2nd order: LGB-optic radiation
        3. 3rd order: Visual cortex-visual association areas [Prestriate cortex (area 19)–internal capsule– brain stern]
        4. 4th order: Oculomotor nucleus (MR nucleus and Edinger Westphal nucleus)–short ciliary nerve-ciliary muscle: iris sphincter 30:1 ratio–constrict and, acccomodate
        5. Prestriate cortex (area 19): Ventral to EW nucleus-oculomotor-ciliary ganglion
  • What is the Marcus Gunn pupil?
    • Marcus Gunn pupil is also known as the relative afferent papillary defect.
    • It is elicited with the swinging torchlight test.
  • What is Horner's syndrome? Causes?
    • Etiology: Disruption of oculosympathetic pathway.
    Clinical features:
    • Classic triad of ptosis, miosis (accentuated in dark), anhydrosis on same side
    • Normal reactions to light and near
    • Slight elevation of the inferior eyelid (reverse ptosis)
    • Hypochromic heterochromia (congenital)
    • Low IOP. Conjunctival injection.
 
Causes of Horner Syndrome
8
Central (First-Order Neuron)
Preganglionic (Second-Order Neuron)
Postganglionic (Third-Order Neuron)
  • Brainstem disease (tumour, vascular, demyelination)
  • Syringomyelia
  • Pancoast tumour
  • Cluster headaches (migrainous neuralgia)
  • Lateral medullary (Wallenberg) syndrome
  • Carotid and aortic aneurysm and dissection
  • Internal carotid artery dissection
  • Spinal cord tumour
  • Neck lesions (glands, trauma, postsurgical)
  • Nasopharyngeal tumour
  • Diabetic autonomic neuropathy
  • Otitis media
  • Cavernous sinus mass-prolactinoma, tolosa hunt syndrome
  • Herpes zoster virus
 
Describe Pharmacological Investigations for Horner's Syndrome
Drug
Mechanism
Effect
Cocaine
  • Blocks the reuptake of NA at the postganglionic sympathetic nerve endings
  • Dilates normal pupil only
  • Confirms presence of Horner's syndrome
Hydroxyamphetamine
  • Potentiates the release of NA from postganglionic nerve endings
  • Dilates preganglionic and normal pupil differentiates pre and post-ganglionic lesion
Adrenaline
  • Adrenaline is not broken down due to the absence of monoamine oxidase
  • Dilates postganglionic only
  • Reverses anisocoria.
 
What is Tonic Pupil and How is it Different from AR Pupil?
Tonic / Adie's Pupil
Argyll Robertson Pupil
Demography
Young female
Old male
Pupil
  • Dilated, regular
  • Unilateral
  • Slow reaction to direct light and accomodation
  • Constricts with 2.5% mecholyl or 0.125% pilocarpine due to denervation hypersensitivity
  • Miosed, irregular
  • Bilateral, asymmetrical
  • Normal reaction
  • Doesn't dilate in dark
  • Atropine/cocaine induce mydriasis (unlike Horners)
9
Associations
  • Deep tendon reflexes diminished
  • Autonomic nerve dysfunction
Commoncauses
  • Viral illness leading to denervation of the postganglionic supply to the sphincter pupillae and the ciliary muscle
  • Neurosyphilis
 
Tell me the Causes of Dilated and Constricted Abnormal Pupil
Dilated (Mydriatic) Pupil
Constricted (Miosed) Pupil
3rd CN palsy
Horner's syndrome
Tonic pupil (Holmes Adie syndrome)
Brainstem stroke
Pharmacological mydriasis
Pancoast syndrome
Iris abnormalities
Cluster headache
Trauma
Argyll Robertson pupil
Pharmacological
Iris abnormalities (posterior synechia)
Pontine hemorrhage
  • What is pharmacological mydriasis?
    • Pupil dilated > 7 mm, no light or near response, anisocoria worse in light, no ptosis, normal acuity. Doe1s not constrict with 1% pilocarpine.
  • What is RAPD? Where do you find this?
    • Pupil with afferent defect dilates on swinging flash light test
    • Can be quantified by neutral density filters
    • Magnitude does not correlated with VA
    • Etiology-unilateral or asymmetric ON disease, large macular lesions, asymmetric chiasmal disease, optic tract or LGB lesion.
 
COMMON VIVA AND CASE SCENARIOS FOR PRACTICE
  • RAPD in old male with optic atrophy. What is your D/D. Discuss about AION. Causes, diagnosis, monitoing, differentiate from NAION.
  • Photo of middle aged patient with left side mild ptosis and miosis. Tell me the causes. Discussion on Horner syndrome including pharmacological testing.
  • Examine pupils of a female patient (with an obvious afferent pupillary defect). Now perform direct ophthalmoscopy to examine optic nerves (You notice bilateral optic nerve pallor one side more than the other). Tell differentials (optic neuritis, SOL, trauma, radiation, AION, NAION, toxic, etc.). How you would investigate?
  • Examine pupil of the patient. Discuss causes of RAPD. How will you check for central field?
  • 10Pupil examination in an elderly female (if RAPD LE). Discuss possible etiologies. Slit lamp 90 D in the same patient. What do you expect (optic atrophy)? If the other eye has same finding, why is she still have RAPD? (Asymmetry glaucoma damage).
  • Pupil for RAPD examination. Tell D/D and your approach in the case.
 
1.3 ORBIT EXAMINATION
 
 
Examination of the Case
History: Onset and duration of symptoms, decreased vision, double vision, pain/anesthesia/paresthesia, causes of exacerbation or improvement, progression
  • Observe:
    • Spectacles
    • Unilateral or bilateral problem
    • Direction of globe displacement, if any
    • TED–lid retraction, red eye, chemosis
    • Arterialisation of scleral vessels
    • Tropia
    • Prosthesis
    • Other periorbital changes-ecchymosis, eczema, S-shaped lid.
  • Confirm direction of globe displacement from side and behind and above
  • Palpate the orbit margins for:
    • Heat: Infection, inflammation
    • Tenderness: Infection, inflammation
    • Shape of the mass: Cystic or irregular, focal or diffuse, fixed or mobile, bag of worms?
      (plexiform neurofibroma)
    • Retroplusion
    • Palpate lymph nodes
  • Pulsations:
    • Vascular orbital tumour with arterial component
    • Bony orbital defect transmitting brain pulsation
    • Valsalva maneuvre may increase proptosis if varix is present.
  • Perform exophthalmometry:
    Check globe position with Hertel's exophthalmometer:
    • Explain to the patient, what you are going to do
    • Ensure exophthalmometer is placed firmly on lateral orbital rim at the level of lateral canthi
    • Shut your right eye (to examine pt rt eye)
    • Ask patient to look into your open eye (left) and measure the patient's right eye to tip of corneae
    • Repeat for left eye
    • Measurement > 20 mm or difference of > 2 mm between globes is suggestive of proptosis.
    If proptosis check if axial or non-axial with 2 ruler test:
    • Place the ruler horizontally over bridge of nose at the level of lateral canthi
    • Measure with ruler distance between nasal limbus of both eyes from center of nose
    • 11With horizontal ruler in place, look for and measure the vertical displacement of orbit from horizontal meridian (1st ruler) to inferior limbus of both eyes.
  • Auscultation for bruit
  • Additional tests:
    • Corneal sensation
    • Infraorbital sensation
    • Bending forward and coughing (for orbital varix).
  • Full ophthalmic examination including ocular motility, cover test, fundus exam
  • Optic nerve function:
    • Visual acuity
    • RAPD
    • Colour vision
    • Brightness
    • Optic disc:
      • Swelling, atrophy, optociliary shunts
      • Visual fields.
 
IMPORTANT VIVA QUESTIONS
  • What are the common causes of proptosis?
    (Vein-vascular, inflammatory, endocrine, neoplastic)
 
According to Age
Children
Adults
Orbital cellulitis
Thyroid ophthalmopathy
Rhabdomyosarcoma
Cavernous hemangioma/lymphangioma
Dermoid/epidermoid cyst
Orbital inflammatory syndrome
Capillary hemangioma/lymphangioma
Lymphocytic lesions
Optic nerve glioma
Meningioma
Leukemia
Lacrimal gland lesions
Orbital inflammatory syndrome
Dermoid/epidermoid cysts.
Neurofibroma
Carotid cavernous fistula
Metastatic neuroblastoma
Retinoblastoma
 
According to Signs and Symptoms (Six Ps)
  • Painful
    • Inflammatory (Tolosa Hunt syndrome, Wegner's), orbital haemorrhage
    • Malignant lacrimal gland tumours, orbital cellulitis, nasopharyngeal carcinoma.
  • Proptosis:
    Unilateral:
    • Axial: TED, cavernous hemangioma, glioma, meningioma, metastasis, a-v malformations
    • 12Superior: Maxillary sinus tumour
    • Inferomedial: Dermoid cyst, lacrimal gland tumour
    • Inferolateral: Frontoethmoidal mucoceles, abcesses, osteoma, frontal sinus CA
    Bilateral:
    • Developmental: Cranial dysostosis
    • Endocrine: TED
    • Inflammatory: Vasculitis, pseudotumours, cavernous sinus thrombosis
    • Neoplastic: Lymphomas, leukemia, metastatic neuroblastoma, metastasis from breast and lungs
    • Traumatic: Carotid cavernous fistulas.
  • Progression:
    • Minutes to hours: Varix, lymphangioma, orbital hemorrhage
    • Days to weeks: IOID, TED, orbital cellulitis, hemorrhage, cavernous sinus thrombosis, CCF, rhabdomyosarcoma, neuroblastoma, granulocytic sarcoma
    • Months to years: Dermoid, benign tumours, cavernous hemangioma, neurogenic tumours, lymphomas, CCF, metastatic tumours.
  • Palpation:
    • Superonasal quadrant: Mucoceles, encephaloceles, neurofibroma, dermoid, lymphoma, orbital abcess
    • Superotemporal quadrant: Dermoid, prolapsed lacrimal gland, lacrimal gland tumour, IOID, orbital abcess
    • Inferonasal quadrant: Dacryocystitis, lacrimal sac tumour, invasive sinus tumour.
  • Pulsation:
    • Without bruit: Neurofibroma, menigoencephaloceles, orbital roof defects
    • With/without bruit: CCF, Dural AVF, orbital AVF.
  • Periorbital Changes
    Sign
    Etiology
    Salmon colored mass in cul-de-sac
    Lymphoma
    Lid retraction and lag
    TED
    Vascular congestion on insertion of recti
    TED
    Corkscrew conjuctival vessels
    AVF
    Vascular anomaly of eyelid skin
    Lymphangioma, varix, capillary hemangioma
    S-shaped eyelid
    Plexiform neurofibroma
    Anterior uveitis
    Pseudotumour, sarcoid
    Eczematous lesion of eyelid
    Mycosis fungoides (T-cell Lymphoma)
    Ecchymosis of eyelid skin
    Neuroblastoma, leukemia, amylodosis
    Prominent temple
    Sphenoid wing meningioma
    Edematous swelling of lower lid
    Meningioma
    Frozen globe
    Metastasis, phycomycoses
    Black crust
    Phycomycoses
    Facial asymmetry
    Fibrous dysplasia, NF
  • 13Examination of a patient with hyperthyroidism:
    • Observe: Exophthalmos, goitre, neck scar, thyroid acropachy, pretibial myxoedema.
    • Get patient to stretch out hands for tremor (put a piece of paper on the dorsum if the tremour is not obvious).
    • Feel the hands for warmth and check pulse for rate and character.
    • Examine the neck and feel the goitre (get patient to swallow some water), listen for bruit.
    • Examine the eyes for lid lag.
    • Examine the tendon reflexes.
  • What is pseudoproptosis?
    False impression of proptosis seen in facial asymmetry, severe ipsilateral enlargement of the globe (e.g. high myopia or buphthalmos), ipsilateral lid retraction or contralateral enophthalmos.
  • Tell common causes of:
    • Acute proptosis: Orbital emphysema, orbital hemorrhage
    • Intermittent proptosis: Orbital varices, orbital vascular tumours
    • Pulsating proptosis: Carotid cavernous fistula
  • Causes of enophthalmos:
    • Structural abnormalities of the orbital walls: Congenital, posttraumatic (blowout fractures of the orbital floor)
    • Atrophy of orbital tissues: Postradiotherapy, scleroderma or eye poking (oculodigital sign) in blind infants
    • Sclerosing orbital lesions: Metastatic schirrous carcinoma, chronic inflammatory orbital disease.
  • Causes of lid retraction:
    • Thyroid eye disease
    • Neurogenic: Contralateral unilateral ptosis, unopposed levator action due to facial palsy
    • Third nerve misdirection, Marcus Gunn jaw-winking syndrome
    • Collier sign of the midbrain (Parinaud syndrome), Parkinsonism
    • Infantile hydrocephalus (setting sun sign), sympathomimetic drops
    • Mechanical: Surgical over-correction of ptosis, scarring of upper lid skin
    • Congenital: Duane retraction syndrome, Down syndrome
    • Miscellaneous: Prominent globe (pseudo-lid retraction).
  • What is embryonal sarcoma (Rhabdomyosarcoma)?
    • The most common primary orbital malignancy of childhood
    • Typical age at diagnosis 7-8 years
      Etiology: The tumour is derived from undifferentiated mesenchymal cell rests (EOM precursor cells).
      Presentation:
      • Sudden onset and rapid evolution of proptosis
      • Periorbital ecchymosis
      • Globe displacement
      • Ptosis and lid edema (skin not warm)
      • Mass palpable–mostly in superonasal orbit
      • Pain uncommon
      • Nasal stuffiness/sinusitis and frequent nosebleeds reported.
    14Metastasis: Lung, bone
    D/D: Orbital cellulitis, inflammatory pseudotumour, orbital lymphangioma, neuroblastoma and myeloi sarcoma
    Investigations:
    • CT orbit: Bone destruction later in the disease
    • MRI with contrast: Irregular well circumscribed mass
    • Prompt orbital biopsy and electron microscopy: To assess histopathologic type and prognosis
    • Systemic investigations: For evidence of metastatic spread include chest X-ray, liver function tests, bone marrow biopsy, lumbar puncture and skeletal survey.
    Treatment:
    • Radiotherapy: EBRT
    • Chemotherapy with vincristine, actinomycin and cyclophosphamide
    • Surgical excision: For small well circumscribed tumours, debulking of large resistant tumours
  • What is pseudotumour?
    • Inflammatory, non-neoplastic space occupying lesion of the orbit.
    • Unilateral in adults, bilateral in children.
    • Signs and symptoms: Acute onset, pain, lid edema, chemosis, conjuctival congestion, limited ocular motility and proptosis
    • Management: Spontaneous resolution, NSAIDS, systemic steroids, radiotherapy (if no improvement in 2 weeks), antimetabolites.
  • What is Tolosa-Hunt syndrome?
    • Nonspecific granulomatous inflammation of the cavernous sinus, superior orbital fissure and/or orbital apex
    • Signs and symptoms: Diplopia, ipsilateral periorbital or hemicranial pain. Mild proptosis, unilateral ophthalmoplegia with pupil involvement, sensory loss alongst 1st and 2nd division of trigeminal nerve
    • Treatment: FNAC, systemic steroids, immunosupressents.
  • Tell clinical features of a patient having orbital varix:
    • Unilateral proptosis, intermittent, induced by bending forward, increases on crying and coughing, reducible.
 
1.3.1 THYROID EYE DISEASE
 
What is Graves's Disease?
Commonest cause of hyperthyroidism in which IgG antibodies bind to thyroid stimulating hormone (TSH) receptors in the thyroid gland and stimulate overproduction of thyroid hormones
 
What is Hashimoto's Thyroiditis? Commonest Cause of Hypothyroidism
  • What is the pathogenesis of proptosis in TED?
    • Orbital fibroblasts are the targets of autoimmune process, which turn into adipocytes and stimulate cytokine release and glycosaminoglycan production leading to increased orbital fat, EOM volume, and inflammatory response.
    • 15Are all patients with TED hyperthyroid?
      • Only 80%. 10% may be hypothyroid, another 10% may have subclinical hyper thyroidism.
    • Risk factors: Female sex, middle age, smoking, family history, HLADR3, HLAB8
    • How does a patient of thyrotoxicosis present?
      Symptoms:
      • Weight loss despite good appetite, increased bowel frequency, sweating, heat intolerance, nervousness, irritability, palpitations, weakness and fatigue.
      Signs:
      • Ocular: Proptosis, lid retraction, lid lag on downgaze, conjuctival chemosis, superior limbic keratoconjunctivitis, exposure keratopathy, restrictive myopathy, compressive optic neuropathy
      Systemic:
      • Goitre, fine hand tremors
      • Finger clubbing (thyroid acropachy) and onycholysis (Plummer nails)
      • Pretibial myxoedema
      • Palmar erythema, warm and sweaty skin
      • Myopathic proximal muscle weakness but brisk tendon reflexes
      • Sinus tachycardia, atrial fibrillation and premature ventricular beats
      • High output heart failure.
 
How do You Assess a Case of Thyrotoxicosis with Ocular Signs?
  • Rundle's curve: Records disease activity in terms of active phase, regression phase and an inactive plateau phase
  • Mourits system: Assesses disease activity based on clinical signs of pain, redness, sewlling, and impaired function
  • NOSPECS classification: Assesses disease severity.
N
O
S
P
E
C
S
Score
0
1
2
3
4
5
6
Clinical severity
No signs and symptoms
Only signs, no symptoms
Soft tissue involved
Proptosis
EOM involved
Cornea involved
Sight loss
 
How will You Investigate such Cases?
  • Abnormal thyroid function: Serum free T4 (raised), TSH (reduced)
  • Thyroid auto antibodies: TSH receptor antibody, antithyroid peroxidase and antithyro-globulin antibodies
  • Orbital imaging: CT orbit (better bony resolution, preferred before decompression), MRI (T2 weighted STIR) better soft tissue resolution and identifies active disease (Enlarged bellies of EOM, tendons spared, incidence IR > MR> SR)
  • Orthoptic review: Visual fields, colour vision
 
What is the Diagnostic Criteria for TED?
16
  • Eyelid retraction with thyroid dysfunction/exophthalmos/ON dysfunction/EOM dysfunction or
  • Thyroid dysfunction with exophthalmos, ON dysfunction or EOM involvement.
 
Do all Patients Require Orbital Imaging?
No, only those with optic N-compression suspicion, evaluation for orbital decompression surgery, unclear diagnosis.
 
What is the Treatment of Hyperthyroidism? Side effects of the Antithyroid Medication? Complications of Radioiodine Treatment and How to Prevent Them?
  • Carbimazole (15-40 mg), propylthiouracil (200-400 mg)–to block production of thyroid hormones, until patient is euthyroid. Risk of agranulocytosis (so check FBC, if they develop infection like sore throat), caution during pregnancy can cross placenta-cause foetal hypothyroidism.
  • Propranolol-to reduce anxiety, BP.
  • Radioactive iodine - I131, single dose: Patient instructed to avoid contact with children. Warned of subsequent hypothyroidism (so thyroxine replacement required) and worsening of TED (prophylactic oral steroids may be given)… contraindicated in pregnancy.
  • Partial thyroidectomy: For large goitres, usually proceeded by radioactive iodine to shrink the goitre.
 
When are Systemic Steroids used in Management of TED?
  • To decrease orbital inflammation acutely:
    • Mostly to prevent threatened visual loss from ON compression.
    • To decrease severe proptosis resulting in corneal exposure.
 
Which Patients Require Surgery? In What Sequence?
  • Emergency decompression in c/o threatened ON compression or corneal exposure.
  • Elective procedures to correct proptosis, diplopia from restrictive myopathy, or eyelid retraction.
  • Decompression is done first, then muscle surgery followed by eyelid retraction repair and then blepharoplasty.
 
What is Orbital Decompression?
  • Orbital decompression involves removal of bone and/or fat to reduce proptosis. Indicated in cases of threatened.
  • On compression or corneal exposure. Antero ethmoidal decompression is the most common method.
  • When is muscle surgery done? What are the alternatives to muscle surgery? What type of surgery is done?
  • 17When inflammation is quiet and patients motility pattern is stable and he is still complaining of diplopia in primary gaze.
  • Prisms can be used as an alternative. Recession of muscle (mostly IR, MR) is done with adjustable sutures under LA/GA.
 
How does Eye Muscle Surgery Affect Eyelids?
Recession of IR muscle improves upper eyelid retraction (reduces overactivity of SR and LPS muscles).
 
What Kind of Eyelid Surgery is Required?
  • Lid position surgery: Lid retraction repair, tarsorraphy
  • Blepharoplasty to remove excess fatty tissue and skin.
 
Common Viva and Case Scenarios for Practice
  • Picture of a female with bilateral axial proptosis. CT shows intraconal mass. Tell me your clinical approach and differentials. How will you use an exophthalmometer?
  • Lady with Right proptosis and left enophthalmous and asymmetrical face. How will you approach the case?
  • Photo of patient with unilateral congestive proptosis. Discuss the D/D. How to differentiate these diagnoses from the history, examination and investigations.
  • Bilateral proptosis in young female. Discussions on D/D, investigations.
  • Color photo of unilateral proptosis + Lid retraction: Management in TED, Role of Radiotherapy and how does it work?
  • A case of unilateral proptosis of a young man. Discuss about the signs present and the differential diagnosis, the investigations needed the causes of vision affection and how to manage in details. Draw the site of incision of orbitotomy and the complications of angular vein injury and why this vein is in particular dangerous?
 
1.4 COVER/UNCOVER TESTS
 
 
Examination of the Case
Always inquire visual acuity of the patient before proceeding:
  • Observe:
    • Abnormal head posture:
      • Face turn (sixth nerve palsy, Duane's syndrome)
      • Head tilt (fourth nerve palsy)
      • Chin up (vertical muscle weakness, V and A pattern strabismus, ptosis)
    • Obvious tropia
    • Spectacles: Hypermetropis/myopia/prism.
  • Perform corneal reflection tests
    • Hirshberg test:
      • Pentorch is shown into patient's eye at the arms length. Patient is asked to fixate the light. Observe corneal reflexes in primary position–rough estimate of manifest deviation.
  • 18Look for deviation with:
    • With and without glasses
    • With or without abnormal head posture.
  • Cover/uncover tests:
    Give the most accurate assessment of deviation:
    • Use pen torch, not very bright, kept 14-18 inches from the child
    • Distance: Smallest letter on Snellens chart which patient can see
    • Near: Langs stick/toy at 1/3 m
    • Cover Test: Watch uncovered eye for movement – manifest deviation
    • Uncover Test: Watch eye which is being uncovered for movement-latent deviation.
    • Alternate cover test:
      • Allow adequate time for fixation: Full deviation
      • Right eye covered for 2 sec. Occluder is quickly shifted to left eye for 2 sec.
      • After cover is removed, note the speed and smoothness of recovery
      • Phoria: Straight eye before and after the test
      • Tropia: Manifest deviation.
      Movements noticed:
      • Temporal: Esotropia/phoria, nasal-exo
      • Downward: Hypertropia/phoria, upward-hypo
      • Look for DVD, nystagmus also in infantile esotropia.
      Assessment of angle of deviation:
      • 1 mm deviation of corneal reflex = 15 D = 7 0
      • Reflex at limbus: 45 degrees
      • Reflex at pupil margin: 15 degrees
      • Reflex halfway between pupil margin and limbus = 300
      • Note fixation preference and strength of fixation for both eyes.
 
PRISM TESTS
  • Apex of prism to point in direction of deviation.
  • Krimsky: Manifest deviation (no latent component): Prism in front of fixating eye till corneal reflex become symmetrical.
  • Prisms cover test: Total deviation.
  • Alternate cover test performed first.
  • Prisms of increasing strengths are placed in front of one eye (apex towards deviation).
  • ACT performed continuously. Until ocular movements are negated.
  • Angle of deviation is equal to strength of prism.
 
IMPORTANT VIVA QUESTIONS
  • Describe milestones in fixation behaviour in small kids
    • By 6 weeks: Good fixation behavior
    • By 2-3 months: Interested in bright objects
    • By 3-4 months: Good horizontal following
    • After 4 months: No disconjugate movements persist.
  • 19Indications for cover tests:
    • Assess binocular alignment in patients with suspected strabismus
    • Determine the eye preferred for fixation
    • Distinguishes monocular and binocular diplopia
    • Diagnose latent nystagmus
    • Distinguishes tropic from phoric component of the deviation
    • Assess monocular excursion in DVD
  • Contraindications of cover tests:
    • Profound visual loss in one or both eyes
    • Insufficient cooperation for fixation on accommodative target.
 
Common Viva and Case Scenarios for Practice
  • Perform Cover/uncover test of a young patient having alternate exotropia/esotropia.
  • Demonstrate the technique in a normal person.
  • Name some situations where these tests do not work or give false results.
  • Name some situations which can be accurately diagnosed with these tests only.
 
1.5 OCULAR MOTILITY EXAM
 
 
Examination of the Case
  • Observe
    Age
    Nystagmus
    Spectacles
    Flat maxilla
    Manifest misalignment
    Swollen periorbita
    Head posture
    Scars
    Ptosis
    1. Ask if the examiner wants you to begin with Hershberg test then cover/uncover test.
    2. Explain to the patient to follow the light, keep head still, inform if he sees double.
  • Examine the eye movements in the nine cardinal positions:
    1. Horizontal Movement:
      • Keep pentorch about arms length from patient.
      • Check patient's left gaze first and then the right gaze.
      • Perform cover test in each position.
      • Observe: Any limitation of motility in any direction:
        • Nystagmus
        • AV pattern
        • Pupil
        • Associated signs such as lid narrowing/widening or ocular retraction.
    2. Oblique Movement:
      • Dextroelevation and depression and laevoelevation and depression
      • Back to primary position between each direction of gaze
      • You may be asked to comment on which muscles are acting.
      20
      Direction
      Muscle Acting
      Up left
      Right IO, Left SR
      Up right
      Right SR, left IO
      Down left
      Right SO, Left IR
      Down right
      Right IR, Left SO
    3. Vertical Movement:
      • From primary position, directly down (hold the lid up to observe the globe only when fully down
      • Then directly up and hold for fatigue (Myasthenia Gravis)
      • Look for Cogan's twitch
      • Observe AV pattern.
  • Check saccades both horizontal and vertical:
    • Technique:
      • Hold hand at arms length from patient subtending about 90-120 degrees
      • Ask patient to fixate either hand alternately as fast as they can
      • Repeat for vertical movements with about 90 degree subtended
      • Observe adduction lag, fatigue, and hypometria/dysmetria.
  • Check pursuits:
    • Technique:
      • Ask the patient to keep watching the target without moving their head.
      • Then move the target slowly from side to side and up and down.
      • The eyes should be able to follow the target smoothly without lagging behind or jerking to catch up with the target.
  • Examine convergence:
    • Show the patient near accommodative target
    • Ask them to maintain fixation as you slowly bring target closer to the patient until he loses fixation and image blurs.
  • Examine Doll's eye movement
    • The vestibulo-ocular reflex is obtained by having the patient visually fixate on an object straight ahead
    • Then rapidly turning the patient's head form side to side and up and down
    • The eyes should stay fixed on the object and turn in the opposite direction of the head movement.
  • Optokinetic nystagmus
    • Use a tape with repeating shapes on it and ask the patient to look at each new object as it appears as you run the tape between your fingers to the right, left, up, and down.
    • The patient will have brief pursuit eye movements in the direction of the tape movement with quick saccades or jerks in the opposite direction. The resetting saccades are easier to observe than the brief pursuit movement.
  • If vertical deviation noticed perform the parks–Helveston three step test
 
Technique
21
1st Step
  • Primary position without head posture
  • Identify high eye
  • Paretic eye
2nd Step
  • Lateral gaze (away from paretic eye)
  • Increased vertical deviation
  • Ipsilateral-inferior msls
  • Contralateral-superior msls
3rd Step
  • Head tilt to side of high eye (towards paretic eye)
  • Increased vertical deviation
  • Ipsi-oblique
  • Contra-rectus
 
Common Cases Encountered in the Exam
  • Third nerve palsy
  • Fourth nerve palsy
  • Sixth nerve palsy
  • Blow out fracture
  • Duane's syndrome
  • Brown's syndrome
  • Internuclear ophthalmoplegia
  • Accommodative esotropia
  • Exotropia
  • Infantile esotropia.
 
COMMON VIVA AND CASE SCENARIOS FOR PRACTICE
  • Perform ocular motility in this case-old blow out fracture/TED/Browns/Duanes/INO.
  • A young girl for motility test. She has Brown's. What are the differentials of Brown's and how to distinguish it with IO PALSY?
  • A young man with restrictive movements for ocular motility examination. (Duanes) (Please remember-kids with Duanes do grow up). Management? What is force duction test? How do you do it?
  • An elderly gentleman with Facial nerve LMN palsy. What examinations you want to proceed with? Tell me what are the causes? How do you manage?
  • To check the ocular motility in a young patient (left Duan retraction syndrome, type 1). What is the Duane's mechanism of retraction of globe and how do you manage such case?
  • Why there is incresead deviation in 3rd step of Park e step test? (Based on the fact that Superior muscles intorts and inferior muscles extort the eye).
 
1.6. NYSTAGMUS
 
 
Examination of the Case
 
Aim
  • To describe the signs correctly
  • To localize the site of pathology
 
Examination
22
  • Inquire visual acuity before proceeding
  • Observe
    Spectacles
    Gait
    Albinism
    Scars
    Head turn
    Buphthalmos
    Speech
  • Describe (DWARF)
    • Direction:
      • Fast phase describes direction of nystagmus:
        • Right, left, up, down, rotatory, seesaw.
    • Waveform: Jerk or pendular
    • Amplitude:
      • How many degrees of movement from start of drift away to beginning of the fast corrective phase?
      • Small, medium, large.
    • Rest: primary position/gaze evoked
    • Frequency:
      • Number of beats in a given time
      • Fine, moderate, coarse.
  • Examine nystagmus under:
    • Occlusion
    • Convergence
    • Distance
    • Near.
  • Describe effects of:
    • Extraocular movements
    • Gaze evoked
    • Null region.
  • Slit lamp exam:
    • Assess waveform more correctly
    • Albinism
    • Congenital glaucoma
    • Congenital cataract.
 
Discussion
 
Classification of Nystagmus
Physiological
Congenital
Acquired
End point
Albinism
Cerebellar-gaze evoked
OKN
Aniridia
Vestibular peripheral-horizontal
Vestibular central-vertical
23
Caloric
Congenital cataract
Chiasmal-seasaw
Rotational
Optic nerve disease
Dorsal midbrain-convergence retraction
INO-dissociated
Brainstem-upbeat
Jn of medulla and spinal chord-downbeat
 
COMMON VIVA QUESTIONS AND CASE SCENARIOS
  • Cerebellar jerk nystagmus
  • Congenital pendular nystagmus
  • Down-beat nystagmus
  • Seesaw nystagmus:
    • Ataxic nystagmus (internuclear ophthalmoplegia) is usually seen in ocular motility examiantion
    • And latent nystagmus in infantile esotropia is usually presented in cover/uncover tests.
  • What is nystagmus? What is null point?
    • A repetitive eye movement is nystagmus. Null zone is the direction of gaze that minimizes the amplitude and frequency of nystagmus
  • Does nystagmus mean that patient is blind?
    • No, some vision must be there to develop nystagmus.
  • What is the etiology of nystagmus?
    • Inability to maintain fixation
    • Loss of inhibitory control over EOM
    • Loss of normal symmetric input from vestibular pathways to oculomotor nuclei.
  • Clinical approach to congenital nystagmus
    • Look for features/history:
      • Noticed in first few months of life
      • Binocular, horizontal, conjugate
      • No oscillopsia, near normal VA
      • Abolished in sleep
    • Check in different directions of gaze:
      • Null point
      • Uniplanar in all directions of gaze
      • Dampens on convergence, but increases by distant fixation
      • Jerk or pendular pattern.
    How will you proceed?
    • Will ask patient for history of onset of nystagmus and whether patient has symptoms of oscillopsia
    • Test for paradoxical response to OKN drum (reversal of OKN response due to shifting of null point)
    How would you manage this patient?
    • Conservative
    • 24Refract and prescribe glasses (reading is not impaired)
    • Prescribe contact lens if glasses are not suitable
    • Give base-out prism to induce convergence.
  • Tell me about the optokinetic response
    • Optokinetic (OKN) nystagmus is induced by looking at the rotation of a striped drum–the OKN drum.
    • There is the initial slow pursuit eye movement following the direction of the rotation
    • This is followed by the fast saccade corrective movement in the opposite direction.
  • Use of OKN
    • Diagnosis of congenital nystagmus (paradoxical response)
    • Detect internuclear ophthalmoplegia (rotate drum in direction of the eye with adduction failure)
    • Detect Parinaud's syndrome (rotate drum downwards to elicit convergence retraction nystagmus)
    • Differentiate organic or nonorganic blindness
    • Differentiate vascular or neoplastic cause in patient with homonymous hemianopia:
      • If vascular, lesion is usually confined to occipital lobe (OKN response is symmetrical)
      • If neoplastic, lesion may extend to parietal lobe (OKN response is asymmetrical).
  • What is latent nystagmus?
    • Horizontal conjugate jerk nystagmus, appears when one eye is closed. Fast phase is towards viewing eye.
  • What is manifest latent nystagmus?
    • Nystagmus presents under binocular viewing condition.
  • What is spasmus nutans?
    • Appears in first year of life, intermittent, binocular, small amplitude, high frequency, pendular
    • Head nodding
    • Torticollis.
  • What is gaze evoked nystagmus?
    • Elicited in far horizontal gaze (end gaze) with no other features.
  • How do you manage Nystagmus?
    • Medical treatment: Discontinue any causative medication, correct refractive errors, baseout prisms, image stabilization methods.
    • Pharmacologic: Gabapentin, baclofen, valproate, memantine
    • Surgical: EOM surgery to shift null point into primary position.
 
1.7 CRANIAL NERVE EXAM
General exam
  • Muscle wasting, facial asymmetry, loss of expression
Cranial N 1 olfactory
  • Ask about sense of smell
Cranial N 2 optic nerve
  • Visual acuity, visual fields, fundoscopy, pupil reaction to light and accomodation
25
Cranial N 3, 4, 5 – oculomotor, trochlear, abducens
  • Inspect resting gaze, look for ptosis, test eye movements, look for nystagmus, check diplopia
Cranial N5 trigeminal
  • Light touch (ophthalmic, maxillary, mandibular)
  • Corneal reflex
  • Motor (palpate temporalis, masseter)
  • Move jaw from side to side (pterygoid)
Cranial N 7 facial nerve
  • Raise eyebrow (frontalis)
  • Tightly close eye (orbicularis oculi)
  • Smile and show teeth (orbicularis oris)
  • Blow out cheeks (buccinators)
Cranial N 8 (vestibulocochlear)
  • Whisper test for hearing, Rennie, Weber test
Cranial N 9 and 10-glossopharyngeal, vagus
  • Cough, soft palate movement, gag reflex
Cranial N 11 accessory
  • Shrug shoulder
  • Turn head to each side
Cranial N 12 hypoglossal
  • Protrude tongue, tongue movement, wasting and fasciculations
 
1.8 VISUAL ACUITY EXAMINATION
 
 
Discussion
  • Normal visual acuity is 1min of arc
  • Vernier acuity up to 5 sec of arc
  • Pin hole neutralizes up to 3DS of refractive error.
  • LogMar charts are more accurate than Snellens chart because:
    • 6/6 in Log Mar chart equates to 1min of arc (compared to S1nelllens chart where 6/6 equates to 5 min of arc), so better resolution
    • There is logical geometric progression of resolution
    • Controls crowding phenomenon with 5 letters in each line and appropriate spacing.
 
Vision Testing
  • Select appropriate test considering Age, Language, Literacy
  • Check distance acuity first (Each Eye): Unaided, then with distance prescription, pin-hole if aided VA <6/9
  • Check near acuity (Each Eye): Unaided, with near prescription.
 
Selecting Appropriate Test
Patient
Distance
Near
Adult literate
Snellen
Test type N chart
LogMar/Bailey–Lovie Chart
26
Adult illiterate
E chart
Reduced Sheridan Gardinar Landholt ring
Sheridan Gardinar
Older children
Log Mar Chart
Preferable at risk amblyopia cases
Children >3years
Sheridan Gardiner
Keeler logMar
Sonsken-Silver
Children >2yrs
Kays picture
Reduced Kays picture
Babies
Clinical tests:
  • Fixing and following
  • Objection to occlusion
  • 10 D verticalprism
  • Prefential looking tests-Keeler Teller, Cardiff tests
  • Rotation tests
  • Pattern VEP test
 
Testing Contrast Sensitivity
  • The Pelli Robson chart:
    • Viewed at 1m
    • Equal size of letters in all rows.
    • Decreasing contrast of 0.15 log unit for each group of 3 letters.
  • Cambridge chart:
    • Viewed at 6 m
    • Square wave gratings.
  • Vistech chart:
    • Viewed at 45 cm and 3 m
    • Rows of broken circles
    • Decrease in contrast and size across the rows.
 
Testing Colour Vision
Test
Comments
Ishihara
Viewed at 2/3 m in patients with VA > 6/18
Screens congenital red and green defects
Does not test blue color blindness
First test plate is seen by all with sufficient VA
Hardy-Rand Ritter
Detects all 3 congenital color defects
City university
Farnsworth-Munsell100 hue
Detects congenital and acquired color defects
Most sensitive
Farnsworth D15 hue discrimination test
Screening test, e.g. in military
 
Testing Binocular Status and Stereopsis
27
  • Measured in seconds of arc
  • Normal spatial acuity 1 m
  • Normal stereoacuity-60 sec (= 1 m)
  • Lower the value better the acuity.
Test
Mechanism
Comments
Titmus
  • Polaroid glasses
  • Dissociated 2D tests
  • Based on ARC, monocular cues
TNO
  • Red-green glasses
  • Dissociated 2D tests
  • Random dot tests
  • No monoocular clues
  • Test BSV and stereopsis after age of 4 yrs
Lang
  • Intrinsic cylinder lens
  • Dissociated 2D tests
  • Superior in testing stereopsis in young children
  • No Monocular clues
  • No need for glasses
Frisby
  • Intrinsic plate thickness
  • True 3D test
  • Test BSV and stereopsis after age of 4 yrs
Synaptophore
  • Separate eyepieces
  • Tests BSV
 
Normal Milestones of Visual Development
  • Horizontal gaze full at birth
  • Neonates after exotropic, with variable ocular alignment
  • Response to light in early infancy
  • Good foveal fixation and following light by 8-12 weeks
  • Vertical gaze full by 3 months
  • Stable ocular alignment-4-6 m.
  • Stereopsis is the last to develop:
    • Visual standards for driving
    • A binocular visual acuity > 6/10 on the Snellen chart
    • The minimum visual field for safe driving is a field of vision of at least 120° on the horizontal meridian (the Goldmann perimeter).
    NOTE: Post PRP patients must give informed consent as they may not be able to drive after the laser.
    • No significant field defect in the binocular field which encroaches within 200 of fixation either above or below the horizontal meridian.
    NOTE: Homonymous or bitemporal defects which come within 200 of fixation, whether hemianopic or quadrantanopic, are not accepted as safe for driving.
    • Monocular vision is not a cause for disqualification, providing the visual field in the remaining eye is within the above definition
    • Diplopia in the primary position presents an extreme hazard to safe driving, but if it can be remedied by prisms or a patch.
28The Esterman binocular field test is the least stringent test fulfilling the required standard as it:
  • Allows some enhancement of the binocular field
  • Allows fixation by the dominant eye.
 
IMPORTANT VIVA QUESTIONS
  • How do you manage refractive errors?
    • Nonsurgical methods: Eyeglasses, CL, orthokeratology
    • Surgical:
      • Laser vision correction
      • Photorefractive keratectomy (PRK), LASEK, Epi-LASIK: Removes central corneal epithelium followed by photoablation of lenticule of stromal tissue by excimer laser.
      • LASIK and Femto LASIK: Creates hinged flap, followed by photoablation of lenticule of stromal tissue by excimer laser, and then repositioning of flap.
    • Incisional surgery:
      • Astigmatic keratotomy: Flattens the corneal meridian with arcuate and linear incisions
      • Intrastromal corneal ring segments-to correct low level of myopia or for high astigmatism
      • Phakic implants: For correcting high levels of myopia
      • Clear lens extraction: For correcting high levels of myopia.
    • What is amblyopia? How do you manage it?
      • Amblyopia: Poorer vision in one eye that is not improved with refraction and not entirely explained by an organic lesion.
      • The involved eye nearly always has a higher refractive error.
      • The decrease in vision develops during the first several years of life. Central vision is primarily affected, while the peripheral visual field usually remains normal.
      • Usually Asymptomatic, found when decreased vision is detected by vision testing in each eye.
      • A history of patching, strabismus, or muscle surgery as a child may be elicited.
      • Individual letters are more easily read than a full line (crowding phenomenon).
      • In reduced illumination, the visual acuity of an amblyopic eye is reduced much less than an organically diseased eye (neutral-density filter effect).
      • Etiology: Strabismus, anisometropia (large difference in refractive error (usually >1.5 diopters), occlusion (ptosis or lid hemangioma), sensory deprivation (media opacity).
 
 
Treatment
If Patient < 10 yrs
  • If orthophoric:
    • Appropriate spectacle correction (full cycloplegic refraction or reduce the hyperopia in both eyes symmetrically by 1.50 diopters).
    • Patching: Patch the eye with better corrected vision 2 to 6 hours/day for 1 week per year of age with at least one hour of near activity. Continue patching until 29the vision is equalized or shows no improvement after three compliant cycles of patching.
    • Penalization with atropine: Atropine 1% once daily (used with glasses) has been shown to be equally effective with patching in mild to moderate amblyopia (20/100) or better. Child can wear full hyperopic correction with a + 2.50 bifocal during school.
  • In strabismic amblyopia: Patching first and then strabismus surgery (only after maximal vision has been obtained in the amblyopic eye)
  • In occlusive/sensory deprivation-immediate surgery of affected eye and then patching advised.
 
If Patient >10 years
  • A trial of spectacle correction, patching and/or atropine may be considered if not attempted previously
  • If treatment of amblyopia fails, protective glasses should be worn to prevent accidental injury to the nonamblyopic eye.
  • How do you manage a patient with low vision?
    • Counseling: To address emotional and psychosocial impact
    • Referral: To appropriate medical, vocational, educational professional.
    Optical aids:
    • Spectacle prescription based on low vision refraction
    • Magnification: Enlarge (fonts on the phone, books prints), bring closer (high plus reading glasses), magnify image (Magnifiers, telescopes)
    • Prisms: For image relocation
    • Lighting and glare control: Absorptive lens, illumination control
    • Contrast enhancement: Using high contrast materials, selective transmission filters, closed circuit TV
    • Computers-Reading: Speech output, font enlargement, writing–speech input, keyboard
    • Vision substitution: Auditary aids (talking watches, books), tactile aids (Braille)
    • Skills development: Mobility training, reading with devices.
  • What is legal blindness?
    • A visual acuity of worse than 20 in 200 and/or a visual field of 20 degrees or less, despite best correction is termed legal blindness.
    • The patients are regarded as being disabled and unable to do many types of work, so is usually entitled to various benefits to help them cope financially. They may also qualify for aids such as a dog for the blind or specially adapted equipment, such as a Braille keyboard and speech recognition system for a computer.
  • What is total blindness?
    A term used to describe someone who is completely unable to perceive any light or color at all in either eye.
 
COMMON VIVA QUESTIONS FOR PRACTICE
  • Amblyopia in children: Types, treatment
  • Discuss methods of vision assessment in children
  • 30What are the criteria for low vision with regard to the visual fields? What are low vision aids?
  • You may be given retinoscopy readings and asked for spectacle prescription. Asked about the rules of transposition.
 
1.9 VISUAL FIELD EXAMINATION
The most common cases are:
  • Bitemporal hemianopia (also look for evidence of pituitary abnormality such as acromegaly or hypopituitarism).
  • Homonymous hemianopia/quadrinopia (look for any evidence of hemiparesis).
  • Central scotoma (the patient may have multiple sclerosis, look for spastic paresis or nystagmus).
 
Examination-Confrontational Visual Field
  • Observe
    Wheelchair
    Headturn
    Hemiplegia
    Acromegaly
    Speech
  • Check visual acuity: To adjust target size
  • Check binocular field: To check gross homonymous defects.
    Technique
    • Sit directly opposite patient with eyes at same level 1-2 m apart.
    • Ask patient to focus on your face and inquire if he can see all of your face or is any bit missing.
  • Check uniocular field: Patient with non testing eye occluded.
    Technique:
    • Sit opposite the patient 1-2 m apart with eyes level
    • Ensure background is blank without windows
    • Ask pt to cover his left eye with palm of his hand
    • Ask him to fix on your open right eye and shut your left eye
    • Confirm he can see the target by holding it up in the midline
    • Counting fingers
    • Hold up 1or 2 fingers in 4 quadrants
    • Hand should be perpendicular to visual axis, and half way between pt and yourself
    • Place hand first, and then present the fingers
    • Repeat for other eye.
  • Check for peripheral defects:
    • Check that patient can see out of each eye by covering each eye in turn and present the object for confrontation.
    • Map out the visual field of each eye with white pin. Urge patient to inform when he sees the white pin oming from unseen to seen area.
  • Finally Check if the lesion obeys the midline, congruity, macular sparing.
  • 31Check central field abnormality with a red pin:
    Technique
    Macular sparing:
    • Show pt a red pin and confirm that they can see it
    • Ask pt to say red when they actually see it red and, gone when it disappears
    • Slowly move the pin from nonseeing to seeing area along the line of fixation
    • If patient sees the pin before it crosses the midline, it is macular sparing.
    Obeying midline:
    • Bring red pin in slowly from the nonseeing field
    • The pin should only appear once the midline (horizontal or vertical) has been crossed.
    Central field:
    • Slowly bring pin in from periphery diagonally through each quadrant.
    Blind spot:
    • Slowly move the red pin from periphery horizontally along the line of fixation
    • Confirm the horizontal extent of blind spot, and then while within the blind spot confirm the vertical extent.
    Reporting findings:
    • What side?
    • Type-homonymous/heteronymous
    • Complete/incomplete
    • Congruity
    • Macular sparing
    • Obey meridia.
  • Summary of VF defects
Lesion
Visual Field
Optic nerve
  • Central, cecocentral, altitudinal defects
Optic chiasm
  • Anterior-junctional
Body, posterior-bitemporal hemianopia
Optic tract
  • Incongruous homonymous hemianopia
Optic radiation
  • Internal capsule: Congruous homonymous hemianopia
  • Temporal lobe: Superior quadrantanopia
  • Parietal lobe: Inferior quadrantanopia
Occipital lobe
  • Posterior: Congruous homonymous hemianopia
  • Anterior: Monocular contralateral temporal defect
 
COMMON VIVA QUESTIONS AND CASE SCENARIOS
  • How do you approach a case of bitemporal hemianopia?
    • Most probable clinical diagnosis is a pituitary lesion.
    • I'll like to take a multidisclplinary approach. Include a neurologist and an endocrinologist in the management plan
    • Ask history of diplopia (nonparetic), metamorphopsia, visual hallucination.
  • 32Look for features of hypersecretion from an adenoma:
    • Growth hormone (acromegaly)
    • Prolactin (history of amenorrhea, galactorrhea, infertility in females or impotence in males).
  • Assess for etiology of pituitary lesion-ask for history of:
    • Trauma
    • Radiation
    • Shock, blood loss during pregnancy (pituitary apoplexy)
    • Check EOM (seesaw nystagmus, CN palsies)
    • Check fundus (bow-tie atrophy, papilloedema)
    • Confirm visual field on Humphery perimeter
    • Perform lab tests–GH, ACTH, TSH, prolactin levels
    • Perform MRI Scan–Axial, sagittal and coronal view
    • Treatemt will be given according to the etiology.
  • How do you manage a case of right homonymous hemianopia?
    • Most probable clinical diagnosis is a left postchiasmal lesion.
    • I'll like to take a multidisclplinary approach. Include a neurologist in the management plan:
      • Check fundus (optic atrophy, papilledema)
      • Perfom full Humphrey VF to assess for congruity of lesion.
      • Left optic tract:
        • Incongruous right homonymous quadrantanopia
        • RAPD in right eye.
      • Left parietal lobe:
        • Incongruous right lower homonymous quadrantanopia
        • Check EOM (ipsilateral persuit deficit)
        • Check for right hemiparesis or hemianesthesia
        • Assess reading (alexia) and writing (agraphia)
        • OKN asymmetry (move drum towards left).
      • Left temporal lobe:
        • Incongruous right upper homonymous hemianopia (pie in the sky)
        • Formed visual hallucination
        • Auditary symptoms.
      • Left occipital lobe:
        • Congruous right homonymous hemianopia
        • OKN symmetry
        • Unformed visual hallucination
        • Assess visual attention (inattention) and visual recognition (agnosia).
  • What is internuclear ophthalmoplegia? What are the features?
    INO is motor abnormality cause by lesions in the medial longitudinal fasiculus.
    • Classic Triad
      • Failure of adduction of ipsilateral eye
      • Ataxic nystagmus of contralateral eye
      • Normal convergence.
  • 33What is cecocentral scotoma?
    • A lesion involving blind spot and the macular area
    • Causes: Dominant optic atrophy, Leber's optic atrophy, toxic optic neuropathy, optic nerve pit.
  • What are the causes of central acotoma?
    • Macular disease
    • Optic neuritis
    • Ischemic optic neuropathy (more typically produces an altitudinal field defect)
    • Optic atrophy (e.g. from tumor compressing the nerve, toxic/metabolic disease)
    • An occipital cortex lesion.
  • What is pie in the sky lesion?
    • Homonymous hemianopia involving superior quadrant.
  • Where is physiological blind spot located? Causes of blind spot enlargement?
    • In temporal visual field. 15 degree temporally and just below horizontal plane.
  • Causes of blind spot enlargement
    Papilledema
    Myelinated (medullated) nerve fibers off the disc
    Glaucoma
    Drug toxicity
    Optic nerve drusen
    Myopic disc with a crescent
    Optic nerve coloboma
  • What are the causes of ring scotoma?
    • Advanced glaucoma
    • Retinitis pigmentosa or other peripheral retinal disorders (e.g. gyrate atrophy)
    • Chronic papilledema
    • After panretinal photocoagulation
    • Central retinal artery occlusion with cilioretinal artery sparing
    • Bilateral occipital lobe infarction with macular sparing
    • Nonphysiologic visual loss
    • Carcinoma-associated retinopathy
    • Medications (e.g. phenothiazines).
  • What are the causes of bitemporal hemianopia?
    • Chiasmal lesion (e.g. pituitary adenoma, meningioma, craniopharyngioma, aneurysm, glioma).
    • Tilted optic discs. Nasal retinitis pigmentosa.
  • What are the causes of altitudinal, arcuate and binasal scotoma?
    Altitudinal field defect:
    • Ischemic optic neuropathy
    • Hemibranch retinal artery or vein occlusion
    • Optic neuritis
    • Glaucoma
    • Optic nerve or chiasmal lesion
    • Optic nerve coloboma.
    34Arcuate scotoma:
    • Glaucoma
    • Ischemic optic neuropathy (especially nonarteritic)
    • Optic disc drusen
    • High myopia
    • Optic neuritis.
    Binasal field defect:
    • Glaucoma
    • Bitemporal retinal disease (e.g. retinitis pigmentosa)
    • Bilateral occipital disease
    • Tumor or aneurysm compressing optic nerves or chiasm
    • Chiasmatic arachnoiditis.
  • How can you localize a lesion on the basis of visual fields?
    • Monocular defects are prechiasmal except for anterior occipital lesions (which represent far temporal visual field seen by only one eye)
    • Lesions posterior to chiasm do not cross vertical meridian by more than 15 degrees
    • There normal visual acuity, pupillary reactions and fundus exam in post chiasmal defects.
  • What is kinetic perimetry?
    • A moving stimulus of known luminance is presented from a non-seeing to seeing area.
    • Done on tangent screen, Goldmann perimeter.
  • What is static perimetry?
    Static on–off stimuli of variable luminance is presented throughout the visual field.
    Protocols:
    • Humphrey: Full field testing
    • Swedish Interactive Threshold Algorithm (SITA): Similar to Humphrey but fast
    • Short Wavelength Automated Perimetry (SWAP): Blue test object on yellow background, detects early glaucoma damage
    • Frequency Doubling Perimetry (FDP): Measures the function of magnocellular pathway (M-cell). Helps in early detection of glaucoma, independent of refractive errors up to +/-7D.
  • What is the difference between suprathreshold and threshold testing?
    • Suprathreshold Test: Quickest, calculates the threshold adjusted for age by testing few predetermined spots using 4-6 db steps. Used for screening only and should not be used for monitoring glaucoma.
    • Threshold Test: Used for detailed assessment of visual field by presenting a stimulus at threshold luminance value. Used for monitoring glaucoma.
  • What are the visual fields defects seen in glaucoma?
    • Earliest: Increased variability of responses in areas that subsequently develop defects with slight asymmetry between the two eyes.
    • Paracentral, occur within 10 degrees of fixation most commonly supero-nasally results from loss of nerve fibers on temporal aspect of the disc.
    • Nasal (Roenne) step represents a difference in sensitivity above and below the horizontal midline in the nasal field. Represent loss of nerve fibers at superior or inferior pole of the disc.
    • 35Arcuate-shaped defects develop between 10° and 20° of fixation as a result of upward extensions from the blind spot around fixation (Bjerrum area). Represents loss of nerve fibers bundles from ST or IT disc.
    • A ring scotoma develops when arcuate defects in upper and lower halves of the visual field join.
    • Altitudinal defect: Represents near complete loss of superior or inferior hemifield.
    • Temporal wedge: Loss of temporal field with its apex at blind spot. Represents local NFL loss at nasal side of the disc.
    • End-stage changes with small island of central vision and an accompanying temporal island. The temporal island is usually extinguished before the central.
  • How do you confirm glaucoma by Humphery visual field test?
    • Visual field is always interpreted in conjunction with the clinical findings.
    • There should be presence of at least one of the following defects on Humphrey visual field testing (Anderson's criteria) for diagnosing glaucoma:
      • Glaucoma hemifield test outside normal limits on at least two consecutive occasions.
      • Cluster of three or more non-edge points in a location typical for glaucoma, all of which are depressed on PSD at a P < 5% level and one of which is depressed at a P < 1% level, on two consecutive occasions
      • CPSD that occurs in less than 5% of normal individuals on two consecutive fields.
  • What are reliability indices?
    • Reflect the reliability of field results:
      • Fixation loss: If patient responds to stimuli presented in blind spot. >20% is unreliable
      • False positive: If patient responds to sound alone. Seen in trigger happy patient. Most sensitive
      • False negative: If patient fails to respond to brighter light at a prerecorded threshold point.
  • What is pattern and total deviation? What is probability value (p)?
    • Total deviation: Compares patient's meaurement with agematched controls. Upper display is numerical in dB, lower one is in grey scale
    • Pattern deviation adjusts for any generalized depression in overall field (e.g. cataract, corneal opacity, and miosis)
    • Probability value: Indicates significance of defects. Lower p value-greater clinical significance.
  • What is the significance of global indices?
    • Provide summary of results in a single number used to monitor progression of glaucomatous damage
    • Mean Deviation (MD): A measure of overall field loss
    • Pattern standard deviation (PSD): A measure of focal field loss.↑PSD > reliable than MD
    • Short-term fluctuations (SF): Indicates consistency of response
    • Corrected pattern standard deviation (CPSD): A measure of variability within field after correcting for SF.
 
COMMON VIVA QUESTIONS AND CASE SCENARIOS FOR SELF-ASSESSMENT
36
  • Perform confrontation test in a man in fifty age (a case of RT lower altitudinal defect)
  • Tell me about post-chiasmal visual field defects, defects of higher visual function and effects of internal carotid artery and verebrobasal artery strokes
  • How patient with pituitary tumor will present to you?
  • Tell me about craniopharygiomas - the typical visual field defects and management
  • What is acromegaly? Signs? Management?
  • Confrontational Visual Field on female patient. You notice bitemporal hemianopia with a nasal defect on one side. Tell differential diagnosis (tumour compressing optic chiasm most likely pituitary adenoma). What is the clinical picture of a patient with prolactinaemia?
  • Elderly gentleman who had atherosclerotic risk factors and his optometrist told him his ‘side vision’ was becoming poor. Inspect the patient and demonstrate visual fields
  • VF 24-2 humphrey showing nasal defect, d/d of such a defect, assess, exam findings
  • 48 yrs old lady with inferior field loss for 6 days and now has complete loss of vision. How do you assess, and manage this case
  • A gentleman with bitemporal hemianopia. Questions on what part of history you want to cover, systemic features and of course possible pathology
  • Visual Fields: What do the reliability indices mean? What is MD, PSD, GHT, etc.
  • You are presented with HFA of hemianopia; respecting vertical midline. Where is the level of lesion if one eye is involved? If the other eye having same type of field defect (chiasmal and retrochiasmal lesions). What you do for this pt?
  • A HVFA of a patient with superior altitudinal field defect, Q give the description of the field. Causes?
  • Field with RT side temporal field defect and similar type of defect in Lt Eye. Tell D/D with site of lesion
  • Discussion over a couple of sets of field tests about the error percentages, blink bar, MSD/PSD, GHT.
 
1.10 EXAMINATION OF ENUCLEATED SOCKET
 
Examination of the Contracted Socket
  • Observe the eye for post enucleation syndrome
    • Deep upper lid sulcus
    • Pseudoptosis
    • Enophthalmos
    • Lower lid laxity (ptosis of lower lid).
  • Examine the orbital area and eyelids for any abnormalities and check eyelid closure
  • Test the tone of the orbicularis and tarsal sulci.
  • Check Prosthesis:
    • Fit, size and its appearance with respect to fellow eye
    • Observe the movement of prosthetic eye
    • Remove prosthesis and look for discharge, granulation tissue or any growth
    • 37Presence of any chronic inflammation or infection
    • Cicatrical bands and degree of contracture
    • Whether the socket is dry or wet (dry fibrosed conjunctiva may indicate poor vascularity).
  • Area of the socket and assessment of the fornices especially the inferior
  • Volume of the socket by noting the depth of the socket compared to the fellow eye
  • Movements of the muscles are looked for
  • Associated bony contracture
  • Replace prosthesis
  • Examine other eye.
 
COMMON VIVA QUESTIONS
  • What is contracted socket?
    • Contracted socket is defined as the shrinkage and shortening of all or a part of orbital tissues causing a decrease in depth of fornices and orbital volume ultimately leading to inability to retain prosthesis.
  • What are the causes of contracted socket?
    • Etiology related:
      • Alkali burns
      • Radiation therapy.
    • Surgery related:
      • Fibrosis from the initial injury
      • Poor surgical techniques during previous surgical nucleation/evisceration with extensive dissection of the orbital tissue
      • Excessive sacrifice of the conjunctiva and tenons capsule
      • Traumatic dissection within the socket leading to scar tissue
      • Multiple socket operations.
    • Others:
      • Cicatrizing conjunctival diseases
      • Chronic inflammation and infection
      • Not wearing a conformer/prosthesis
      • Ill fitting prosthesis.
  • What are the characterstics of contracted socket?
    Extensive loss of conjunctival surface area, deep cicatrix formation, atrophy of the orbital fat, fornix contraction and volume redistribution leading to post enucleation syndrome (superior sulcus depression, pseudoptosis of upper lid and ptosis of lower lid.
  • How can you prevent contracted socket?
    • Proper dissection at the time of initial procedure
    • Preserving maximum possible conjunctiva and tenon's capsule
    • Secured closure of all layers over the implant without
    • Avoidance of ill-fitting or roughened prosthesis
    • Elimination of any source of chronic infection
    • Identification of conjunctival cicatrizing diseases like pemphigoid, Stevens-Johnson syndrome.
 
COMMON VIVA QUESTIONS FOR PRACTICE
38
  • Picture of a patient with artificial Left eye. What are the possible aetiologies? What do you know about types of prosthetic eyes? How do you choose?
  • Scenario: A young girl with a prosthetic eye with contracted socket, Discuss the causes for these contraction, preventive measures and detailed surgical options for the patient.