Causes of Sudden Loss of Vision Flashcards

1
Q

Sudden loss of vision in a quiet eye without preceding history of trauma or globe changes is not uncommon.

T/F

A

T

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2
Q

AMAUROSIS FUNGAX /TRANSIENT ISCHAEMIC ATTACK (TIA)

Transient reversible unilateral visual obscurations lasting for a short duration attributable to a ____________________.

TIA can be due to ingestions of the following drugs: _________,_________,_________ and ______________.

A

visual cortical disturbance

Chloral hydrate, Nalidixic acid, Ethyl alcohol & Bromocriptine

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3
Q

TIA may occur prior to the ___________________ in arteritic ischaemic optic neuropathy. It may be a precursor to __________________.

_____________ episodes are implicated.

A

infarction of the Optic Nerve head

irreversible blindness

Thromo-embolic

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4
Q

OPTIC NEURITIS
Optic neuritis or __________ is used for the ______________________ associated with a decrease in vision or visual field.

It can be mostly ____lateral or rarely ____lateral but not synonymous with ____________________________.

A

papillitis

inflammation of the Optic nerve

uni; bi

unilateral or bilateral disc oedema (papilloedema).

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5
Q

OPTIC NEURITIS

Most common aetiology is _______ & less common cause is ___________________.

Other rare causes are ____________ ,_____________ , Connective tissue disorder, other bacterial; Viral; Fungal & Parasitic infections.

A

idiopathic

Multiple Sclerosis (MS)

HIV (Syphilis/CMV), Sarcoidosis

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6
Q

Howbeit, it is said that Euroids of Northern European extraction are more susceptible to MS than those of the Mediterranean while the ________ and ________ are the least susceptible.

A

Negroids & Asians

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7
Q

Mean age at onset of idiopathic ON: _______ years & mostly among (men or women?).

A

20-40

Women

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8
Q

ON is sometimes incorrectly diagnosed in _____ patients _____ years & above. Other ophthalmic ailment like ______________ are commonly implicated for acute or subacute loss of vision in this age group.

A

Older; 50

ischaemic optic neuropathy

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9
Q

ON symptoms include loss of vision (____–______), (ipsi or contra?) lateral eye ____ (Whitnall’s hypothesis; retrobulbar neuritis) & _____________

A

6/9; PL/NPL

ipsi; pain

dyschromatopsia

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10
Q

dyschromatopsia is??

A

Colour desaturation

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11
Q

OPTIC NEURITIS DIFFERENTIAL DIAGNOSIS

_____________
COMPRESSIVE _________________
ANTERIOR ____________
TOXIC ____________ (ALCOHOL, TOBACCO, PERNICIOUS ANAEMIA, ETHAMBUTOL, ISONIAZIDE, PHENOTHIAZINES, ANTINEOPLASTIC DRUGS)
HYSTERIA / HYPOCHONDRIASIS
LEBER’S HEREDITARY OPTIC NEUROPATHY
______________ , CENTRAL SEROUS RETINOPATHY, DISC DRUSEN, _____________.

A

Papilloedema
Optic neuropathy
ISCHAEMIC OPTIC NEUROPATHY

AMBLYOPIA

POSTERIOR UVEITIS; glaucoma

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12
Q

Treatment for ON
Longitudinal Optic Neuritis Study (LONS) recommended intraveinous ____________ (250mg every 6 hours) for ______ days, followed by _________ (1mg/kg/day) for ___ days accelerated visual recovery but provided no advantage to long-term visual recovery and outcome.

Neurologist & Neuroradiologist back up is essential considering the risk of __________ & progression to ______.

A

methylprednisolone

three; oral prednisolone; 11

steroid therapy; MS

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13
Q

PSEUDOTUMOR CEREBRI

Elevated ______________ without _________ or ____________ , and with normal ___________________ .

______ induced papilloedema secondary to _____________ thus the pseudonyms ‘Idiopathic or Benign Intracranial Hypertension’ attributable to idiopathic causes (90%) and medications (10%)

A

intracranial pressure

ventriculomegaly or mass lesion

CSF composition; Drug; intracranial hypertension

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14
Q

Pseudomtor cerebri
Drug induced papilloedema secondary to intracranial hypertension thus the pseudonyms ‘Idiopathic or Benign Intracranial Hypertension’ attributable to idiopathic causes (90%) and medications (10%) like :-

________ - Prednisolone, Triamcinolone (Withdrawal)
Tetracyclines
________ acid
amiodarone
_________/_____________
Oral contraceptives
Carbidopa/levodopa
Growth hormone
Chronic bromide intoxication

A

Corticosteroids

Nalidixic

Hypervitaminosis A / Hypovitaminosis A

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15
Q

CAUSES OF VISUAL LOSS IN idiopathic intracranial Hypertension

Chronic (atrophic) ____________
__________ folds
_______ ________ or exudates
___________ infarction
Subretinal peripapillary haemorrhage extending through the fovea
Subretinal peripapillary neovascular membrane

A

papilloedema; Chorioretinal

macula oedema

Optic nerve head

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16
Q

PREDICTIVE FACTORS FOR VISUAL LOSS IN IIH
Recent ________
________ papilloedema
_________ papilloedema
Subretinal ____________
Significant ______________ at presentation
______________

A

weight gain

High-grade ; Atrophic

haemorrhage; visual field loss

Hypertension

17
Q

Mimickers of IIH

_________________ thrombosis/ __________ cerebri/Neoplastic or Infective leptomeningeal infiltration may escape neuroimaging & CSF analysis.

A

Cerebral veinous sinus

Gliomatosis

18
Q

IIH Management

Multidisciplinary management: Neurosurgeons, Neurologists, Neuroradiologists, Dieticians
____________
Repeated ______________ (but can lead to _____________)
_____________ inhibitors
?______________

A

Weight reduction

lumbar puncture

low pressure headache

Carbonic anhydrase

Corticosteroids

19
Q

SURGICAL APPROACH
_________________________

______________ procedures –Lumboperitoneal shunt/Ventriculoperitoneal shunt

A

Optic Nerve Sheath Decompression

CSF diversion

20
Q

Ischaemic optic neuropathy

Occlusion of the vascular supply to the ____________ resulting in partial or total infarction.

A

Optic Nerve head

21
Q

Non-arteritic ischaemic optic neuropathy (___________________ arteries) usually in ________ decades with sudden, (painful or painless?) ____nocular visual loss commonly on _______________, suggesting associated _________________.

A

short posterior ciliary

6th -7th ; painless

mo; waking up from sleep

nocturnal hypotension

22
Q

Arteritic ischaemic optic neuropathy is caused by ____________, a granulomatous necrotizing arteritis involving large & medium-size arteries – superficial temporal, ophthalmic, posterior ciliary & proximal vertebral. Scalp __________, headache, polymyalgia rheumatica, TIA, malaise, weight loss, night sweats are not uncommon. _____________ is the main treatment

A

giant cell arteritis

tenderness

Steroid therapy

23
Q

CENTRAL RETINAL ARTERY OCCLUSION
(CRAO)

____________ or _____________-related thrombosis at the level of _____________ is the commonest cause in about 80% with arteriolar narrowing and poor panretinal perfusion .

Incidence increases with age, accelerated by hypertension, hyperlipidaemia, diabetes mellitus, sickle cell disease, obesity, oral contraceptives, tobacco smoking, hyperhomocysteinaemia, giant cell arteritis (painful), glaucoma & sedentary life style.

A

Microangiopathic or atherosclerosis

lamina cribrosa

24
Q

CRAO

‘__________________’ in fresh CRAO

____________ may occur earlier than in CRVO , __________ compared to 3 months.

A

CHERRY RED SPOT

Rubeosis iridis

4-5 weeks; 3 months

25
Q

Acute retinal artery occlusion is an emergency since it will eventually leads to _______________ except retinal circulation and perfusion is re-established within __________.

A

irreversible visual loss

6 hours

26
Q

In acute retinal artery occlusion

Following may be tried with guarded prognosis:

____________ may help (improve perfusion)
_____________ (to Dislodge thrombo-embolus)
____________________ (Dislodge & hypotony)
Topical apraclonidine 1%, timoptol 0.5% & IV acetazolamide 500mg (Dislodge & hypotony)
Sublingual _____________ (Arteriolar dilatation)
______________________to increase respiratory acidosis
Breathing carbogen (95% oxygen + 5% carbon dioxide) Transluminal Nd:Yag laser embolysis (Vitreous haemorrhage)
Thrombolysis (Radiological intervention with canulation of ophthalmic artery via supraorbital artery)

A

Supine position

Ocular massage

Anterior chamber paracentesis

isosorbide dinitrate ; Rebreathing in to a paper bag

27
Q

CENTRAL RETINAL VEIN OCCLUSION(CRVO)

Sudden ____lateral _________ with ______________ of all branches of the central retinal vein involving all the four quadrants.

A

uni; blurred vision

tortuosity & dilatation

28
Q

CRVO

____________ CRVO (Commonest, 75%) with _____ prognosis

_____________ CRVO associated with rapid onset veinous occlusion with poor retinal perfusion, capillary shut down and retinal hypoxia resulting in neovascularization – Vascular Endothelial Growth Factor (VEGF) release,vascular leakage, rubeosis iridis & neovascular (90-day)glaucoma.

A

Non-ischaemic; good

Ischaemic

29
Q

Retinal Neovascularization

Not uncommon following ____________,__________,_______,________,_________

_______________________________ are implicated

A

diabetes mellitus retinopathy, CRVO, CRAO, BRAO & HRVO

Vascular Endothelial Growth Factor (VEGF)

30
Q

Retinal Neovascularization

Management will include strict control of the systemic co-morbidities like diabetes mellitus, hypertension, cessation of smoking among others.

_________ injections of ________ / biodegradable _______ implants, ______ inhibitors – Ranibizumab, Pegaptanib, Bevabizumab

_________ _______________ with diode or argon green laser.

A

Intravitreal; triamcinolone

Steroid; VEGF

Panretinal photocoagulations

31
Q

VITREOUS HAEMORRHAGE

Sudden loss of vision may occur following ______________________ - _______ (retrohyaloid) & ______ following leaks from friable ‘new vessels’ as seen in proliferative diabetic retinopathy, sickle cell retinopathy, ischeamic CRVO, CRAO, HRVO & BRAO.

Management approach is multidisciplinary with stabilization of the systemic co-morbidities by speacialist physicians and vitreo-retinal surgeons.

B ultrasound, panretinal photocoagulation, intravitreal anti-VEGF and posterior vitrectomy.
Management of vitreous haemorrhage patient is

A

bleeding into the vitreous spaces

preretinal; intragel