Eyes and Vision
A. Vision
Sudden visual loss is an emergency.
1. H&P: Time course of visual loss, eye pain, headache, fevers, joint pain, DM, check BP, ocular and carotid bruits, fundi (disc pallor, papilledema, retinopathy, arterial occlusion or cholesterol plaque, cherry red spot), red desaturation, pinhole correction, Amsler grid for metamorphopsia, size of blind spot.
a. Whenever you use dilating drops to examine the fundi, note it clearly in the chart so the next examiner will not think the pt is herniating.
2. Poor acuity: See eye chart, back endpapers. Suggests eye or optic nerve problem. If acuity corrects to normal with pinhole, the problem is in the media of the eye, not nerve.
3. Binocular blindness: Usually from a lesion at the optic chiasm (e.g., pituitary mass) or in both occipital lobes (e.g., bilateral PCA infarcts), or toxic/metabolic/nutritional—unless both eyes have been exposed to the same insult (e.g., shower of emboli).
4. Monocular blindness: Transient (TMB) or permanent loss, sudden and nontraumatic.
a. Causes:
1) TMB: Embolus or thrombus, often from carotid lesion. 11% of TMB pts later have stroke, 41% of them within 1 wk. Temporal arteritis or other vasculitis….
2) Sudden permanent monocular blindness: All causes of TMB, plus optic neuritis, intraocular bleed, retinal detachment, acute angle closure glaucoma, infection….
b. Types of retinal infarct:
1) Central retinal artery: Cherry red spot seen in fundus after 6 h.
2) Branch retinal artery: Fundus pallor along that branch.
3) Anterior ischemic optic neuropathy: Often idiopathic; sometimes arteritis.
c. Tests: ESR, CRP, fibrinogen, TEE, temporal artery biopsy (within days of starting steroids). See also Stroke workup, p. 20.
d. Rx of TMB:
1) Prednisone: 60 mg qd until artery biopsy results are back. Vessel inflammation can be patchy, so if clinical suspicion is high, continue prednisone and rebiopsy.
2) IV heparin: See Anticoagulants, p. 160.
3) Decrease intraocular pressure to help move a possible embolus through the eye. Hypercarbia probably does not help.
a) Massage eye: Have pt. press hard × 4 sec; off × 4 sec.
b) IV mannitol 50 g, or IV acetazolamide 400 mg. Watch BP.
c) Anterior paracentesis by ophthalmologist.
e. Rx of optic neuritis: See Demyelinating Disease, p. 33.
5. Visual field defects:
a. Monocular scotoma: Prechiasmal lesion, e.g., glaucoma, retinal hemorrhage, optic neuritis, retinal detachment.
b. Noncongruent bilateral scotomata: Chiasm + nerve lesion.
c. Bitemporal defect: Chiasmal lesion, e.g., aneurysm or pituitary mass. Consider glaucoma.
d. Homonymous defect (same side in both eyes): Postchiasmal.
1) Sparing macula: Visual cortex.
2) Including macula: Optic radiations.
3) Superior quadrant defect: Optic radiations in inferior temporal lobe that can be affected by mastoid infection causing cerebritis.
4) Inferior quadrant defect: Optic radiations in parietal lobe.
6. Higher visual system abnormalities:
a. Anton’s syndrome: Bilateral occipital lesions cause blindness, but pt denies he is blind.
b. Bonnet’s syndrome: Visual deprivation hallucinations (formed, stereotyped, no other signs of delirium).
c. Motion and visuospatial processing: Dorsal, occipitoparietal “where” pathway.
1) Balint’s syndrome: Visual disorientation (simultanagnosia), optic ataxia (deficit of visual reaching), ocular apraxia (deficit of visual scanning). From bilateral occipitoparietal lesion.
d. Object recognition: Ventral, occipitotemporal “what” pathway lesions cause visual agnosia.
1) Prosopagnosia: Inability to recognize faces; from bilateral inferior visual association cortex lesions.
2) Word blindness: Alexia without agraphia. Seen in left hemisphere lesion near splenium of callosum. Usually with R homonymous hemianopsia and color anomia or achromatopsia.
3) Achromatopsia vs. color anomia: In former, pt. cannot perceive colors; in latter, pt. can perceive them but not name them.
B. Pupils
1. Causes of anisocoria: (unequal pupils)
a. Horner’s syndrome: see p. 12.
b. Third nerve lesion:
1) H&P: Unilateral large pupil; also ophthalmoplegia and ptosis. Anisocoria is worse in light (vs. Horner’s). Ask about time course, comorbid conditions (e.g., DM).
2) DDx: Aneurysm (especially P-comm) > ischemia (e.g., DM or HTN) > trauma, uncal herniation, tumor, etc. In an alert pt., a fixed dilated pupil is almost never herniation.
a) Pupil involvement: Suggests compression because pupillary parasympathetic fibers are the most superficial.
b) Pupil sparing: Suggests ischemic third nerve. But only consider a lesion pupil sparing if it is otherwise a complete third nerve palsy (ophthalmoplegia and ptosis). Otherwise you may be fooled by an early compressive third.
c) R/O P-comm aneurysm: Immediate CT and LP to r/o bleed, consider angiogram. May not need this if deficit is clearly pupil sparing.
c. Drug effects:
1) Dilators (mydriatics): From sympathetic agonists, e.g., atropine, scopolamine, phenylephrine, tropicamide, albuterol. Test with 1% pilocarpine (a parasympathetic agonist); it will not constrict pupil if the pupil was previously drug dilated, but will in third nerve compression or Adie’s syndrome.
2) Constrictors: From parasympathetic agonists, e.g., pilocarpine.
d. Acute glaucoma: Fixed pupil, about 6 mm. Also decreased acuity; red, painful eye; hazy cornea; blurred vision; shallow ant. chamber if side-illuminate with penlight.
1) Rx: Emergent IV acetazolamide or mannitol; topical pilocarpine.
e. Adie’s (tonic) pupil: One large pupil, reacts poorly to light, with better constriction to near; then redilates sluggishly. Often sudden, in young woman, with decreased DTRs.
1) Test: Dilute pilocarpine (0.1%) will constrict Adie’s pupil but not normal pupil.
f. Argyll-Robertson: Small, irregular, unequal (sometimes equal) pupils, constrict to near better than light.
1) DDx: Syphilis, diabetic pseudotabes….
g. Old ocular surgery or trauma.
h. Physiologic anisocoria: Should be less than 1 mm difference in both light and dark, briskly reactive.
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