This document provides an overview of the diagnostic approach for acute loss of vision. It discusses the three main causes of acute loss of vision and lists specific conditions that can cause acute loss of vision with or without eye pain. For each condition, it describes suggestive clinical findings and the recommended diagnostic approach. Physical examination focuses on a complete eye exam including visual acuity, visual fields, pupil examination, and ophthalmoscopy. The interpretation of exam findings can provide clues to retinal abnormalities, retinal detachment, vein occlusion or artery occlusion. The summary aims to efficiently convey the key information on evaluating and diagnosing different causes of acute loss of vision.
Ischemic optic neuropathy constitutes one of the major causes of blindness or seriously impaired vision among the middle-aged and elderly population.
Ischemic optic neuropathy is due to acute ischemia of the optic nerve. it can be classified into two, depending upon the part of the optic nerve involved:
1.Anterior ischemic optic neuropathy (AION)
-AION is due to acute ischemia of the front (anterior) part of the optic nerve (also called optic nerve head), which is supplied mainly by the posterior ciliary arteries.
-AION is divided into two types, depending on what causes it:
1.Arteritic AION: This is the most serious type and is due to a disease called giant cell arteritis or temporal arteritis.
2. Non-arteritic AION: This is the usual, most common type, with many different causes but not associated with giant cell arteritis.
2.Posterior ischemic optic neuropathy (PION). -
-PION is a much less common type. It is due to acute ischemia of the back (posterior) part of the optic nerve, located some distance behind the eyeball; this part of the optic nerve is NOT supplied by the posterior ciliary arteries
(Hayreh, 2009)
Ischemic optic neuropathy constitutes one of the major causes of blindness or seriously impaired vision among the middle-aged and elderly population.
Ischemic optic neuropathy is due to acute ischemia of the optic nerve. it can be classified into two, depending upon the part of the optic nerve involved:
1.Anterior ischemic optic neuropathy (AION)
-AION is due to acute ischemia of the front (anterior) part of the optic nerve (also called optic nerve head), which is supplied mainly by the posterior ciliary arteries.
-AION is divided into two types, depending on what causes it:
1.Arteritic AION: This is the most serious type and is due to a disease called giant cell arteritis or temporal arteritis.
2. Non-arteritic AION: This is the usual, most common type, with many different causes but not associated with giant cell arteritis.
2.Posterior ischemic optic neuropathy (PION). -
-PION is a much less common type. It is due to acute ischemia of the back (posterior) part of the optic nerve, located some distance behind the eyeball; this part of the optic nerve is NOT supplied by the posterior ciliary arteries
(Hayreh, 2009)
Slides include
Basic anatomy of optic nerves
Background & epidemiology of optic neuritis
Classification of optic neuritis
Clinical features
Investigations
Diagnosis
Differential diagnosis
Managements
Prognosis
1.BRIEF ANATOMY OF EYE
2.OPTIC NEUROPATHY
3. SIGNS OF OPTIC NEUROPATHY
4. CLASSIFICATION OF OPTIC NEUROPATHY
5. IN DETAIL ABOUT DIFFERENT OPTIC NEUROPATHY
6. MANAGEMENT OF OPTIC NEUROPATHY
Metabolic optic neuropathies
The three subcategories of metabolic optic neuropathies are
•Heredodegenerative (such as leber's hereditary optic neuropathy).
•Nutritional deficiencies (such as vitamins B12 or folic acid).
•Toxicities (such as ethambutol or cyanide).
Slides include
Basic anatomy of optic nerves
Background & epidemiology of optic neuritis
Classification of optic neuritis
Clinical features
Investigations
Diagnosis
Differential diagnosis
Managements
Prognosis
1.BRIEF ANATOMY OF EYE
2.OPTIC NEUROPATHY
3. SIGNS OF OPTIC NEUROPATHY
4. CLASSIFICATION OF OPTIC NEUROPATHY
5. IN DETAIL ABOUT DIFFERENT OPTIC NEUROPATHY
6. MANAGEMENT OF OPTIC NEUROPATHY
Metabolic optic neuropathies
The three subcategories of metabolic optic neuropathies are
•Heredodegenerative (such as leber's hereditary optic neuropathy).
•Nutritional deficiencies (such as vitamins B12 or folic acid).
•Toxicities (such as ethambutol or cyanide).
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Acute loss of vision
1. ACUTE LOSS OF VISION
DIAGNOSTIC APPROACH
Yasser Alzainy
10/4/2018
AL-AZHAR UNIVERSITY
Faculty of Medicine
Neurology Department
2. Acute loss of vision has 3 general causes:
Opacification of normally transparent structures (eg, cornea, vitreous)
Retinal abnormalities
Abnormalities affecting the optic nerve or visual pathways
3. ACUTE LOSS OF VISION
Without eye pain
Amaurosis fugax (transient)
Arteretic ischemic optic neuropathy
Non arteritic ischemic optic neuropathy
Retinal artery occlusion
Ocular migraine
TIA or Stroke
Retinal detachment
Retinal vein occlusion
Macular hemorrhage
Viterous hemorrhage
Functional
With eye pain
Acute angle closure glaucoma
Corneal ulcer
Endophthalmitis
Optic neuritis
4. HISTORY
History of present illness: is the visual loss:
Monocular or binocular?
Transient or permanent?
Pattern of onset? (acute / sudden)
Associated symptoms
Flashing lights?
Eye pain ( constant or with eye movement)?
Diplopia
Hemihyposthesia
5. Review of systems should seek extraocular symptoms of possible causes
Jaw or tongue claudication, temporal headache, proximal muscle pain, and stiffness (giant cell arteritis)
headaches (ocular migraine).
Past medical history should seek known risk factors for
Eye disorders (contact lens use, severe myopia, recent eye surgery or injury),
Vascular disease (eg, diabetes, hypertension)
Hematologic disorders (eg, sickle cell anemia or disorders such as Waldenström macroglobulinemia or multiple
myeloma that could cause a hyperviscosity syndrome).
Family history
migraine headaches.
6. PHYSICAL EXAMINATION
If the diagnosis of a transient ischemic attack or ischemic stroke is under consideration, a complete
neurologic examination is done.
The temples are palpated for pulses, tenderness, or nodularity over the course of the temporal artery.
However, most of the examination focuses on the eye.
7. EYE EXAMINATION
Visual acuity.
Color vision is tested with color plates.
Peripheral visual fields are assessed by confrontation.
Central visual fields are assessed by Amsler grid.
Direct and consensual pupillary light reflexes.
Ocular motility is assessed.
Color vision is tested with color plates.
8. EYE EXAMINATION
The eyelids, sclera, and conjunctiva are examined using a slit lamp if possible.
The cornea is examined with fluorescein staining.
The anterior chamber is examined for cells and flare in patients who have eye pain or conjunctival
injection.
The lens is checked for cataracts using a direct ophthalmoscope, slit lamp, or both.
Intraocular pressure is measured.
Ophthalmoscopy
9. INTERPRETATION
Retinal abnormalities that are severe enough to cause acute loss of vision are detectable during
ophthalmoscopy
Retinal detachment may show retinal folds
Retinal vein occlusion may show marked retinal hemorrhages
Retinal artery occlusion may show pale retina with a cherry-red fovea.
13. GENERAL RULES
Monocular symptoms suggest a lesion anterior to the optic chiasm.
Bilateral, symmetric (homonymous) visual field defects suggest a lesion posterior to the chiasm.
Constant eye pain suggests a corneal lesion (ulcer or abrasion), anterior chamber inflammation, or
increased intraocular pressure, whereas eye pain with movement suggests optic neuritis.
Temporal headaches suggest giant cell arteritis or migraine.
14. AMAUROSIS FUGAX
Suggestive findings
Monocular blindness lasting minutes to hours
Typically less than 5 minutes
Diagnostic approach
Carotid U/S
Echo
MRI
ECG / Holter ECG
15. ARTERITIC ISCHEMIC OPTIC NEUROPATHY (AION)
Suggestive findings
Headache
Jaw or tongue claudication
Temporal artery tenderness or swelling
Pale and swollen disk with surrounding
hemorrhages
Occlusion of retinal artery or its branches
Proximal myalgia (PMR)
Diagnostic approach
ESR, C-reactive protein (CRP), platelet count
Temporal artery biopsy
16. NONARTERITIC ISCHEMIC OPTIC NEUROPATHY
Suggestive findings
Optic disk oedema and haemorrhages
Sometimes loss of inferior and central visual
fields
Risk factors (e.g. diabetes, hypertension,
hypotensive episode)
Diagnostic approach
ESR, CRP, and platelet count
Consideration of temporal artery biopsy to
exclude giant cell arteritis
17. OCULAR MIGRAINE
Suggestive findings
Scintillating scotomata, mosaic patterns, or
complete loss of vision lasting usually 10–60 min
and often followed by headache
Often in young patients
Diagnostic approach
Clinical evaluation
19. RETINAL ARTERY OCCLUSION
Suggestive findings
Nearly instantaneous onset, pale retina, cherry-
red fovea, sometimes Hollenhorst plaque
(refractile object at the site of arterial occlusion)
Risk factors for vascular disease
Diagnostic approach
ESR, CRP, and platelet count to exclude giant
cell arteritis
Carotid ultrasonography
Echocardiography
Consideration of MRI or CT
ECG
Continuous monitoring of cardiac rhythm
21. TIA OR STROKE
Suggestive findings
Bilaterally symmetric (homonymous) field
defects, no effect on visual acuity in the intact
parts of the visual field (bilateral occipital lesions
are the exception and are uncommon but can
occur due to basilar artery occlusion)
Risk factors for atherosclerosis
Diagnostic approach
Carotid ultrasonography
Echocardiography
Consideration of MRI or CT
ECG
Continuous monitoring of cardiac rhythm
23. OPTIC NEURITIS
Suggestive findings
Mild pain with eye movement, afferent pupillary
defect (occurs early)
Visual field defects, typically central
Abnormal color vision testing results
Sometimes optic disk edema
Diagnostic approach
Gadolinium-enhanced MRI to diagnose multiple
sclerosis and related disorders
24. FUNCTIONAL LOSS OF VISION (UNCOMMON)
Suggestive findings
Normal pupillary light reflexes, positive
optokinetic nystagmus, no objective
abnormalities on eye examination
Often inability to write name or bring
outstretched hands together
Sometimes indifferent affect despite severity of
claimed loss of vision
Diagnostic approach
Clinical evaluation
If diagnosis is in doubt, ophthalmologic
evaluation and visual evoked responses