Ophthalmology History Taking

Overview

1. Main Complaint (Chief Complaint)

2. Characterizing Common Ophthalmic Symptoms

Vision Loss

• Monocular vs. binocular - critical for localization (monocular = pre-chiasmal; binocular = chiasmal or post-chiasmal)
• Central vs. peripheral field loss
• Transient vs. permanent (amaurosis fugax = TIA of the eye)
• Sudden painless - consider vascular (CRAO, CRVO, AION)
• Painful - consider acute angle-closure glaucoma, uveitis, optic neuritis

Floaters & Flashes

• New floaters/flashes = posterior vitreous detachment until proven otherwise; must rule out retinal tear or detachment
• Ask about a "curtain" or "shadow" in the visual field (retinal detachment)

Pain

• Sharp/aching - corneal, anterior segment
• Deep/periorbital - acute angle closure, orbital disease, optic neuritis (pain on eye movement)
• Foreign body sensation/grittiness - conjunctiva, cornea, dry eye

Redness

• Acute vs. chronic; unilateral vs. bilateral
• With or without discharge (purulent = bacterial; watery = viral/allergic)
• Ciliary flush (limbal injection) vs. conjunctival injection - ciliary flush indicates anterior segment inflammation

Diplopia

• Monocular (persists when one eye closed) = lens/corneal problem or functional
• Binocular (resolves when one eye closed) = extraocular muscle or cranial nerve pathology
• Constant vs. intermittent; direction of gaze that worsens it

Other Symptoms to Ask About

• Photophobia (uveitis, keratitis, migraine)
• Epiphora / watering (drainage failure vs. hypersecretion - drainage failure worsens in cold/wind)
• Distortion / metamorphopsia (macular disease)
• Halos around lights (corneal edema, acute angle closure)
• Colour vision changes (optic nerve disease)
• Night blindness / nyctalopia (retinitis pigmentosa, vitamin A deficiency)
• Photopsia (flashes of light - vitreoretinal traction)

3. Past Ocular History

• Previous ocular surgery (cataract, glaucoma, refractive surgery - note: refractive surgery affects IOP readings)
• Previous ocular inflammation (uveitis, keratitis)
• Trauma (blunt or penetrating)
• Refractive status - myopia increases risk of POAG and retinal detachment; hypermetropia increases risk of angle-closure glaucoma
• Previous ocular treatments (laser, injections)
• Use of spectacles or contact lenses; compliance and hygiene

4. Past Medical History

5. Systemic Medications

• Corticosteroids (topical, inhaled, oral, skin creams) - steroid-induced glaucoma and cataract
• Tamsulosin (alpha-blocker for BPH) - intraoperative floppy iris syndrome (IFIS) during cataract surgery
• Oral beta-blockers - may lower IOP and mask glaucoma
• Chloroquine / hydroxychloroquine - bull's eye maculopathy (retinal toxicity)
• Ethambutol - optic neuropathy
• Amiodarone - corneal microdeposits, optic neuropathy
• Vigabatrin - peripheral visual field constriction
• Bisphosphonates - scleritis, uveitis (rare)
• Sildenafil (PDE5 inhibitors) - non-arteritic anterior ischaemic optic neuropathy (NAION)
• Isotretinoin - dry eye, blepharitis
• Topical glaucoma medications - note compliance and side effects

6. Allergies

• Drug allergies - especially to:
  • Antibiotics (topical or systemic)
  • Topical glaucoma medications (e.g., brimonidine causing allergic follicular conjunctivitis)
  • Acetazolamide is contraindicated in sulfonamide allergy
• Contact lens solutions
• Preservatives in eye drops (e.g., benzalkonium chloride)

7. Family History

• Glaucoma (primary open-angle glaucoma - strong hereditary component)
• Macular degeneration (AMD has genetic risk factors)
• Inherited retinal dystrophies (retinitis pigmentosa, Stargardt's, Best disease)
• Strabismus and amblyopia
• Refractive errors (myopia especially)
• Systemic conditions with ocular manifestations (Marfan syndrome, NF1/2)

8. Social History

• Occupation - computer use (dry eye), occupational hazards (trauma risk), visual requirements for work (drivers, pilots)
• Hobbies - contact sports, DIY (foreign body risk)
• Driving - legally required vision standards
• Smoking - significantly increases risk of AMD and is a risk factor for CRVO
• Alcohol intake - toxic/nutritional optic neuropathy (suspect if combined with poor nutrition or tobacco)
• Living alone / social support - important for low vision planning

9. Review of Systems (Selected)

• Headache (raised ICP, giant cell arteritis, migraine)
• Jaw claudication, scalp tenderness, temporal artery tenderness - giant cell arteritis (emergency in patients >50 with sudden visual loss)
• Facial pain (trigeminal)
• Limb weakness, sensory changes (MS, stroke)
• Skin rashes (sarcoid, herpes zoster)

Summary Framework

HISTORY OF PRESENTING COMPLAINT
  → Onset, Duration, Severity, Frequency, Progression
  → Character of visual/ocular symptom (see above)

PAST OCULAR HISTORY
  → Surgery, Trauma, Inflammation, Refractive status

PAST MEDICAL HISTORY
  → Diabetes, HTN, CVS, Autoimmune, Neurological

DRUG HISTORY
  → Steroids, Tamsulosin, Antimalarials, Topical drops

ALLERGIES
  → Drug, preservative, contact lens solution

FAMILY HISTORY
  → Glaucoma, AMD, Retinal dystrophy

SOCIAL HISTORY
  → Occupation, Driving, Smoking, Alcohol

Vision Defects

1. Refractive errors - defects in the optical focusing system of the eye
2. Visual field defects - loss of specific areas of vision due to pathology along the visual pathway

Part 1: Refractive Errors

• Myopia is a risk factor for primary open-angle glaucoma (POAG) and retinal detachment
• Hypermetropia is a risk factor for primary angle-closure glaucoma (PACG) and accommodative esotropia in children
• Refractive surgery (LASIK, PRK) alters corneal curvature and can affect IOP readings - always document in history

Part 2: Visual Field Defects - Classification by Anatomy

• Pre-chiasmal lesions = monocular defects (one eye only)
• Chiasmal lesions = bitemporal defects
• Post-chiasmal (retrochiasmal) lesions = homonymous (same-sided) defects in both eyes

Visual Pathway Diagram

Lesion-by-Lesion Summary

A. Retina

• Causes monocular scotoma - a localized blind spot in one eye only
• Shape corresponds to the retinal area affected
• Almost always accompanied by ophthalmoscopic abnormalities (can be seen on fundoscopy)
• Patients may also complain of metamorphopsia (distortion), micropsia, or photopsias
• Common causes: retinal infarct, retinal detachment, haemorrhage, degeneration, infection

B. Optic Nerve (complete)

• Causes total monocular visual loss (blindness in one eye)
• Relative afferent pupillary defect (RAPD) is present
• Common causes: glaucoma, optic neuritis, anterior ischaemic optic neuropathy (AION), optic glioma, meningioma, trauma, raised intracranial pressure

C. Optic Chiasm

• Causes bitemporal hemianopia - loss of the outer (temporal) halves of both visual fields
• Often asymmetric in practice
• The nasal fibres from each eye cross here - compression disrupts them, leaving only temporal field from each eye
• Common causes: pituitary adenoma (most common), craniopharyngioma, meningioma, hypothalamic glioma

D. Optic Tract / LGN

• Causes contralateral homonymous hemianopia (incongruous - fields not perfectly matched)
• At the LGN, unusual sectoranopias ("keyhole" pattern) can occur
• Common causes: tumour, infarct, demyelination; toxoplasmosis / infection (LGN)

E. Temporal Lobe (Meyer's Loop)

• The lower optic radiations loop through the temporal lobe
• Lesion causes contralateral superior quadrantanopia ("pie in the sky")
• Common causes: MCA inferior division infarct, temporal lobe tumour, abscess, surgery (temporal lobectomy)

F. Parietal Lobe

• The upper optic radiations pass through the parietal lobe
• Lesion causes contralateral inferior quadrantanopia ("pie on the floor")
• Common causes: MCA superior division infarct, parietal tumour

G. Entire Optic Radiation

• Complete damage causes contralateral homonymous hemianopia (similar to optic tract lesion but more congruous)

H/I/J. Primary Visual Cortex (Occipital Lobe - PCA territory)

• Upper bank of calcarine fissure → contralateral inferior quadrantanopia
• Lower bank → contralateral superior quadrantanopia
• Both banks (entire cortex) → contralateral homonymous hemianopia, often with macular sparing
• Common causes: PCA infarct, tumour, haemorrhage, occipital trauma

Macular sparing - seen in cortical lesions; the foveal representation may receive collateral blood supply from both PCA and MCA, so central vision is preserved even when peripheral homonymous hemianopia is present.

Types of Scotomas (Localized Field Defects)

Glaucomatous Visual Field Progression (Kanski)

1. Increased response variability (earliest sign)
2. Paracentral depressions (especially superonasal) - more common in NTG
3. Nasal step (horizontal midline boundary in nasal field)
4. Arcuate scotoma - coalescence of paracentral scotomas, extending from blind spot (10-20° from fixation)
5. Ring scotoma - superior and inferior arcuates merge
6. End-stage - small central island + temporal island of vision

Quick Localization Reference

MONOCULAR defect
  → Retina or Optic nerve (pre-chiasmal)

BITEMPORAL hemianopia
  → Optic chiasm (pituitary region)

HOMONYMOUS hemianopia (same side, both eyes)
  → Optic tract / LGN / optic radiation / cortex (post-chiasmal)
  → Incongruous = more anterior (tract/LGN)
  → Congruous + macular sparing = cortical (occipital)

SUPERIOR quadrantanopia ("pie in sky")
  → Temporal lobe (Meyer's loop)

INFERIOR quadrantanopia ("pie on floor")
  → Parietal lobe or upper calcarine bank