Causes of Sudden Loss of Vision Flashcards
Sudden loss of vision in a quiet eye without preceding history of trauma or globe changes is not uncommon.
T/F
T
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 ______________.
visual cortical disturbance
Chloral hydrate, Nalidixic acid, Ethyl alcohol & Bromocriptine
TIA may occur prior to the ___________________ in arteritic ischaemic optic neuropathy. It may be a precursor to __________________.
_____________ episodes are implicated.
infarction of the Optic Nerve head
irreversible blindness
Thromo-embolic
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 ____________________________.
papillitis
inflammation of the Optic nerve
uni; bi
unilateral or bilateral disc oedema (papilloedema).
OPTIC NEURITIS
Most common aetiology is _______ & less common cause is ___________________.
Other rare causes are ____________ ,_____________ , Connective tissue disorder, other bacterial; Viral; Fungal & Parasitic infections.
idiopathic
Multiple Sclerosis (MS)
HIV (Syphilis/CMV), Sarcoidosis
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.
Negroids & Asians
Mean age at onset of idiopathic ON: _______ years & mostly among (men or women?).
20-40
Women
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.
Older; 50
ischaemic optic neuropathy
ON symptoms include loss of vision (____–______), (ipsi or contra?) lateral eye ____ (Whitnall’s hypothesis; retrobulbar neuritis) & _____________
6/9; PL/NPL
ipsi; pain
dyschromatopsia
dyschromatopsia is??
Colour desaturation
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, _____________.
Papilloedema
Optic neuropathy
ISCHAEMIC OPTIC NEUROPATHY
AMBLYOPIA
POSTERIOR UVEITIS; glaucoma
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 ______.
•
methylprednisolone
three; oral prednisolone; 11
steroid therapy; MS
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%)
intracranial pressure
ventriculomegaly or mass lesion
CSF composition; Drug; intracranial hypertension
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
Corticosteroids
Nalidixic
Hypervitaminosis A / Hypovitaminosis A
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
papilloedema; Chorioretinal
macula oedema
Optic nerve head
PREDICTIVE FACTORS FOR VISUAL LOSS IN IIH
Recent ________
________ papilloedema
_________ papilloedema
Subretinal ____________
Significant ______________ at presentation
______________
weight gain
High-grade ; Atrophic
haemorrhage; visual field loss
Hypertension
Mimickers of IIH
_________________ thrombosis/ __________ cerebri/Neoplastic or Infective leptomeningeal infiltration may escape neuroimaging & CSF analysis.
Cerebral veinous sinus
Gliomatosis
IIH Management
Multidisciplinary management: Neurosurgeons, Neurologists, Neuroradiologists, Dieticians
____________
Repeated ______________ (but can lead to _____________)
_____________ inhibitors
?______________
Weight reduction
lumbar puncture
low pressure headache
Carbonic anhydrase
Corticosteroids
SURGICAL APPROACH
_________________________
______________ procedures –Lumboperitoneal shunt/Ventriculoperitoneal shunt
Optic Nerve Sheath Decompression
CSF diversion
Ischaemic optic neuropathy
Occlusion of the vascular supply to the ____________ resulting in partial or total infarction.
Optic Nerve head
Non-arteritic ischaemic optic neuropathy (___________________ arteries) usually in ________ decades with sudden, (painful or painless?) ____nocular visual loss commonly on _______________, suggesting associated _________________.
short posterior ciliary
6th -7th ; painless
mo; waking up from sleep
nocturnal hypotension
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
giant cell arteritis
tenderness
Steroid therapy
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.
Microangiopathic or atherosclerosis
lamina cribrosa
CRAO
‘__________________’ in fresh CRAO
____________ may occur earlier than in CRVO , __________ compared to 3 months.
CHERRY RED SPOT
Rubeosis iridis
4-5 weeks; 3 months
Acute retinal artery occlusion is an emergency since it will eventually leads to _______________ except retinal circulation and perfusion is re-established within __________.
irreversible visual loss
6 hours
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)
Supine position
Ocular massage
Anterior chamber paracentesis
isosorbide dinitrate ; Rebreathing in to a paper bag
CENTRAL RETINAL VEIN OCCLUSION(CRVO)
Sudden ____lateral _________ with ______________ of all branches of the central retinal vein involving all the four quadrants.
uni; blurred vision
tortuosity & dilatation
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.
Non-ischaemic; good
Ischaemic
Retinal Neovascularization
Not uncommon following ____________,__________,_______,________,_________
_______________________________ are implicated
diabetes mellitus retinopathy, CRVO, CRAO, BRAO & HRVO
Vascular Endothelial Growth Factor (VEGF)
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.
Intravitreal; triamcinolone
Steroid; VEGF
Panretinal photocoagulations
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
bleeding into the vitreous spaces
preretinal; intragel
