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MarttiIlvesmäki

Impaired Vision

Essentials

  • If the cause of acute visual impairment remains unclear, consult an ophthalmologist urgently. The faster the loss of vision, the quicker actions are required. Symptoms that have developed slowly may also sometimes require prompt referral (for example exudative age-related macular degeneration, giant cell arteritis, greatly elevated intraocular pressure, iritis with severe symptoms).
  • The most urgent situations are those where it is possible to save vision by a rapid start of medication or by surgery. For classification of urgency, see table T2.

Causes of impaired vision

  • See table T1.

Causes of impaired vision

LateralityPainRednessOther eye symptoms or findingsOther symptoms or things to be noticed
  1. In hours, days, weeks, months, years
  2. Both eyes may be affected at different times and recurrently; ALWAYS suspect systemic disease if symptoms are bilateral.
Sudden, in minutes-hours
Acute angle-closure glaucomaUnilateralYesYesBlurred vision, reduced visual acuity, intraocular pressure may be > 30 mmHgHeadache, abdominal pain, nausea
Giant cell arteritis (previously temporal arteritis)Uni-or bilateralNoNoVisual acuity ↓-↓↓↓Headache, impaired general condition, weight loss
Central artery occlusionUnilateralNoNoVisual acuity ↓↓↓; cherry-red spot in the macula, pale retinaNo general symptoms
Intoxication (methanol, quinine)BilateralNoNoVisual acuity ↓↓↓, tunnel visionGeneral symptoms
Non-arteritic anterior ischaemic optic neuropathy (NAION)Unilateral (bilateral)NoNoVisual acuity ↓-↓↓↓, sectoral visual field defectNo other eye symptoms (cardiovascular diseases as predisposing factors)
Central vein occlusion or branch vein occlusion affecting the maculaUnilateralNoNoVisual acuity ↓-↓↓, flame- or patch-shaped retinal haemorrhages and oedema, often also microinfarctionsNo other eye symptoms (predisposing factors hypertension, hypercholesterolaemia, diabetes / metabolic syndrome, coagulation disorders, malignant diseases)
Vitreous haemorrhageUnilateralNoNoVisual acuity ↓-↓↓↓; flashing and veil-like visual disturbance: vitreous detachmentNo other eye symptoms (predisposing factors diabetes, cardiovascular diseases, anticoagulant treatment, trauma)
Haemorrhage in the foveaUnilateralNoNoVisual acuity ↓↓↓↓; myopiaNo other eye or systemic symptoms
Retinal detachmentUnilateralNoNoVisual acuity ↓-↓↓↓; often preceding symptoms of vitreous detachment; myopiaNo other eye symptoms (predisposing factors injury, intraocular operations)
Epidemic nephropathyBilateralNoNo/YesVisual acuity ↓-↓↓; transient myopia, possibly increase in intraocular pressure (usually decreases)General symptoms of epidemic nephropathy
Hypo- or hyperglycaemiaBilateralNoNoVisual acuity ↓-↓↓; in case of hyperglycaemia, possibly transient myopia (impaired distance vision)Undiagnosed diabetes
Periodic (with typical duration)
Papilloedema (seconds, attacks of blurred vision less than one second long)BilateralNoNoVisual acuity ↓-↓↓↓; may be transient, of a few seconds' durationHeadache and nausea in the morning as general symptoms of increased intracranial pressure
Amaurosis fugax (minutes)Uni- (or bilateral)NoNoThere may be transient total vision loss (of usually several minutes)No general symptoms
Migraine (ca. 15-20 min., up to 1-2 hours)(Uni- or) bilateralNoNoVisual acuity ↓-↓↓; serrated figures, transient visual field defect; transient diplopia possible(Unilateral) headache, nausea
Dry eyes(Uni- or) bilateralMildNo/YesVisual acuity ↓↓Elderly persons; predisposing factors (medication, such as isotretinoin) and locations, significantly prolonged visual display terminal use
Rapid or gradual (speed of development) 1)
Keratitis (days)Unilateral (bilateral)YesYesVisual acuity ↓-↓↓No other eye symptoms (predisposing factors prior injury or wearing of contact lenses)
Recurrent corneal erosionUnilateralYesYes/NoVisual acuity ↓-↓↓Severe pain often with onset at night; often with prior injury; may also occur in the morning when opening the eyes
Corneal oedema (hours-days)Uni- or bilateralNo/YesNo/YesVisual acuity ↓-↓↓If corneal oedema is due to acute angle-closure glaucoma, intraocular pressure is elevated (often more than 50-80 mmHg).
Endophthalmitis (hours-days)UnilateralYesYesVisual acuity ↓-↓↓↓No other eye symptoms (predisposing factors prior ophthalmic operation, intravitreal injection, injury or immunosuppression)
Iridocyclitis (days)Unilateral (bilateral)2) YesYesVisual acuity ↓-↓↓↓, photophobia, pain, small pupil, redness around the corneaGeneral symptoms associated with systemic diseases possible (predisposing factors rheumatic diseases, various systemic diseases)
Macular oedema (hours-days)Uni- or bilateralNoNoVisual acuity ↓-↓↓↓Other eye symptoms also possible (macular oedema may occur after diabetic retinopathy, central or branch venous thrombosis, uveitis, cataract surgery, for example)
Age-related macular degeneration (days, weeks)Uni- or bilateralNoNoVisual acuity ↓-↓↓↓, central dim area; line distortionNo other eye or systemic symptoms
Macular hole and preretinal fibrosis (“puckering of the macula”)UnilateralNoNoVisual acuity ↓-↓↓, line distortion, missing lettersNo other eye or systemic symptoms (macular hole and preretinal fibrosis are often associated with incomplete posterior vitreous detachment)
Cataract (hours-days)(Uni- or) bilateralNoNoVisual acuity ↓-↓↓↓, glare, blurred vision, often increased myopia, monocular diplopiaNo other eye symptoms (rapidly developing form associated with strongly varying blood sugar levels)
Openn-angle glaucoma (years)Uni- or bilateralNoNoVisual acuity ↓-↓↓, visual field defectsNo other eye or systemic symptoms
Optic neuritis (a day-days)Unilateral (bilateral)2) YesNoVisual acuity ↓-↓↓, the papilla may be indistinctly definedPossibly symptoms of MS; eye pain and tendernesson eye movement
Compressive lesion of the optic nerve/ optic pathway (months-years)Uni- or bilateralNoNoVisual acuity ↓-↓↓, papillary stasis possibleGeneral symptoms possible: symptoms of a brain tumour or an aneurysm
Chorioretinitis (days-weeks)Unilateral2) No/YesNoVisual acuity ↓-↓↓↓, retinal inflammatory changesGeneral symptoms possible
Hereditary retinal degeneration, e.g. retinitis pigmentosa http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Expert=791BilateralNoNoVisual acuity ↓-↓↓, often deterioration of night vision, narrowing of the visual fieldGeneral symptoms possible (syndromes, such as Usher's syndrome also associated with loss of hearing)
Adverse effect of a drug (such as ethambutol, thioridazine, chloroquine, amiodarone, tamoxifen, gentamicin)BilateralNoNoVisual acuity ↓-↓↓Other possible adverse effects

Urgency of treatment

  • See Table T2

Urgency of treatment of eye diseases

Emergency treatment the same day (at any time of the day)Emergency treatment or treatment no later than the following morningBy appointment at an outpatient clinic
Angle-closure glaucomaRetinal detachmentUrgent referral (appointment within 7 days*):
Chemical lesion (acid/base), burnOptic neuritisVitreous detachment
Open penetrating eye injuryIIridocyclitisRetinal tears
Intoxication (methanol, quinine)Blunt eye injuryExudative age-related macular degeneration
Papilloedema (refer to a neurologist)Eyelid and lacrimal duct woundsOther macular oedema of unclear origin
Giant cell arteritis with eye symptomsCorneal foreign body / rustVitreous haemorrhage associated with diabetes in a patient with a history of laser treatment of the fundus
Amaurosis fugax (refer to a neurologist)Corneal erosion of unclear originUrgent referral (appointment within 30 days*):
Central artery occlusionVitreous haemorrhage with no known predisposing factor (such as proliferative diabetic retinopathy)Other
Branch artery occlusion (refer to a neurologist)Sudden diplopia or strabismus (emergency referral, if there is ptosis or there is a difference in pupil size)
Suspected intraocular inflammation after eye surgery (endophthalmitis)Fracture of the bony orbit
Bacterial keratitisHigh-pressure open-angle glaucoma with no response to medication
Acute orbit, i.e. optic-nerve compression due to retrobulbar haematoma, abscess or foreign bodyLoss of vision more than 6 hours ago
Orbital cellulitis
Dirty eyelid wounds
Loss of vision less than 6 hours ago
Sudden diplopia with concomitant ptosis or difference in pupil size (refer to neurologist/neurosurgeon - suspected aneurysm)
* The timelines (7 or 30 days) presented here are based on the practice in Finland. Timelines may vary across countries.

History

  • Is the vision impaired in one or both eyes?
  • Did the vision become impaired in seconds, minutes, hours, days, months or years?
  • Preceding or accompanying symptoms
    • redness of the eye
    • pain in the eye, pain on eye movement
    • pain in the temple region, headache or jaw claudication (pain when chewing or moving the jaws)
    • fever and generalized aches
    • Weight loss
    • other changes in visual function (floaters, flashing, micropsia, macropsia, metamorphopsia, diplopia, visual field defects).
  • Other diseases and medication: diabetes, hypertension, blood dyscrasias, polymyalgia rheumatica and other connective tissue diseases, infections (e.g. HIV, borreliosis), etc. The causes vary according to geographical location: ask about the country of origin (immigrants) and travel history (e.g. onchocerciasis Filariases, malaria Diagnosis and Treatment of Malaria, leprosy Bacterial Diseases in Warm Climates, trachoma).

Clinical examination

  • Visual acuity (using patient's distance glasses, both eyes examined separately)
  • Visual field (finger perimetry)
  • Eye movements, diplopia
  • Pupillary reactions (direct and indirect)
  • Ophthalmoscopy (dilate pupillae if not contraindicated; notice especially neurological patients)
    • Red fundus reflex, vitreous body, optic papilla, retina, and particularly the macula
  • Intraocular pressure measurement
  • Fluorescein staining

Sudden visual loss lasting seconds

Papilloedema (caused by increased intracranial pressure)

  • Aetiology
    • Increased intracranial pressure Increased Intracranial Pressure that spreads via the subarachnoidal space into the optic nerve sheath causing axonal flow stasis.
    • The most common cause is benign increase in the intracranial pressure (idiopathic intracranial hypertension, formerly called pseudotumor cerebri Headache in Children), occurs particularly in young over-weight women who have headache as symptom.
    • The cause may also be a brain tumour, subdural or subarachnoid haemorrhage, meningitis, encephalitis, brain abscess or hydrocephalus.
  • Symptoms and findings
    • Occasionally diplopia
    • Vertigo, headache, nausea and (especially in the morning) vomiting
    • Papilloedema is often visible on ophthalmoscopy (picture 1).
      1. Early: blurred margins, central cupping is present, no venous pulsation is observable (distinguishing it from intrapapillary drusen)
      2. Definite: optic papilla raised, very blurred margins, veins dilated, haemorrhages, retinal infarctions
      3. Chronic: dilated capillaries
      4. Atrophic: optic atrophy, impaired vision
  • Differential diagnosis
    • Severe hypertensive retinopathy: bilateral
    • Central vein occlusion: unilateral, more extensive haemorrhages in the ocular fundus
    • Papillitis: unilateral, in children often (70%) bilateral
    • Pseudopapilloedema (hyperopic eye, drusen and other disc anomalies); consult with an ophthalmologist if the diagnosis is uncertain.
    • Giant cell arteritis may sometimes resemble papilloedema, possibly causing malfunction of several cranial nerves.
  • Refer a patient with papilloedema to a neurologist.
  • NB: one optic disc may be atrophic (visual acuity decreased) and no longer reacts with oedema, although the underlying cause is increased intracranial pressure.

Sudden visual impairment, painless

Central retinal artery occlusion

  • Try to restore the retinal circulation by pressing the eye strongly with the side of the fist and by other means of lowering the intraocular pressure, if the patient has come for treatment the same day the vision was lost.
  • The cause of the arterial occlusion should be identified and treated (compare with TIA as a risk sign for a disorder of the cerebral circulation).
    • Emergency referral to a neurologist, if the patient presents within 2 weeks after the occlusion and has not already him-/herself sought care by a neurologist.
  • See Central Retinal Artery Occlusion.

Non-arteritic anterior ischaemic optic neuropathy (NAION)

  • The circulatory disturbance is in the optic nerve itself.
  • Aetiology
    • The most common cause of sudden optic neuropathy in a person over 50 years of age.
    • The risk is increased by diabetes, sleep apnoea, hypertension, dyslipidaemia, smoking (arteriosclerosis), drusen, small tight optic nerve ending).
    • Always remember the possibility of giant cell arteritis, see below.
    • Occurs also in younger persons with the aforementioned predisposing factors.
  • Findings
    • Direct pupillary reaction to light is decreased (relative afferent pupillary defect, i.e. positive Marcus Gunn).
    • Oedematous optic papilla, flame-shaped haemorrhages
    • Horizontal visual field defect
  • Differential diagnosis
    • Papillary stasis (bilateral, normal or only slightly impaired vision)
    • Arteritic anterior ischaemic optic neuropathy (AAION) caused by giant cell arteritis
  • Treatment
    • Treat the predisposing factor.
    • Systemic glucocorticoid therapy to prevent the visual loss in the other eye is indicated if giant cell arteritis cannot be ruled out.

Sudden visual loss with headache or general symptoms

Giant cell arteritis, polymyalgia rheumatica

  • See Giant Cell (Temporal) Arteritis.
  • Symptoms and findings
    • The most typical patient is a woman over 70 years of age. If the patient has a history of giant cell arteritis, note the approx. 50% risk of recurrence.
    • Pain in the temple, headache or jaw pain when eating (ischaemia of the jaw muscles)
    • Tenderness of the temples on palpation
    • Decreased visual acuity
    • Fever, weight loss, muscle pain for weeks or months
  • The most important investigations: urgently ESR (if available) and CRP
  • Confirming the diagnosis
    • Temporal artery biopsy, if readily available. Treatment should be started before the biopsy.
    • A Doppler scan of the temporal artery may also possibly confirm the diagnosis.
  • Treatment

Sudden visual impairment associated with consumption of toxic substances

  • Methanol intoxication Alcohol Poisoning
    • Even a small amount of methanol causes toxic optic neuropathy and acute visual impairment.
    • The optic disc is hyperaemic.
    • Diagnosis is based onsuspected methanol ingestion.
    • Refer immediately to the intensive care unit: treat the acidosis.
  • Quinine-induced blindness
    • A high dose of quinine may cause a severe and only partly reversible visual impairment within 6-24 hours of drug ingestion.

Painless visual impairment over several hours

Central retinal vein occlusion

  • Occlusion of the central retinal vein by circulatory disturbance or thrombosis usually at the level of the lamina cribrosa in the optic nerve
  • Painless unilateral gradual visual impairment, usually noticed in the morning
  • Examination of the ocular fundus often reveals widespread haemorrhages (flame- or patch-shaped) and often also microinfarcts, congested and tortuous veins, with retinal oedema and often also papilloedema.
  • There is no consensus on emergency treatment. Aspirin is recommended if there are no contraindications.
  • A more specific diagnosis should be based on ophthalmological workup. Differential diagnostic alternatives:
    • diabetic retinopathy with widespread haemorrhages
    • ocular ischaemic syndrome with haemorrhages predominantly at the mid-periphery.
  • If the workup (OCT) reveals oedema in the area responsible for fine detail vision (macular oedema), it can be treated with vascular endothelial growth factor (VEGF) inhibitor injections.
  • See Retinal Venous Thrombosis.

Vitreous haemorrhage

  • The patient experiences a sudden painless onset of a fog screen in the visual field; the screen moves when the patient moves the eyes or the head.
  • If the patient has no known underlying disease predisposing to VH, he/she should be referred to an ophthalmologist immediately, or at least the next morning in order to identify the cause of the bleeding. In case of an injury, immediate referral is indicated.
  • If the patient has diabetes which has required laser panphotocoagulation, urgent referral for an appointment within a week at an outpatient clinic is indicated.
  • See Vitreous Haemorrhage (Vh).

Hypertensive retinopathy

  • Aetiology
    • A sudden increase in blood pressure causes arterial constriction in the retina (autoregulation) and a prolonged increase causes hypertrophy of the smooth muscle in the arterial walls (arteriolosclerosis which reflects the degree of the patient's systemic arteriosclerosis).
      • Other causes include aging and e.g. diabetes, smoking and stress.
    • Hypertensive retinopathy occurs in connection with pre-eclampsia and malignant hypertension and in chronic hypertension when the hypertension is poorly controlled.
  • Findings
    • In the acute type: extremely narrow arterioles in the retina, oedema of the optic papilla and retina, retinal haemorrhages (flame, spot or patch-shaped) and lipid exudates, macular oedema (often star-shaped; picture 2)
    • In the chronic type: general and focal narrowing of the retinal arterioles (artery/vein ratio < 2/3), increased light reflexes (in advanced disease so-called copper and silver wiring), arteriovenous crossing changes (general arteriosclerosis), as well as retinal haemorrhages and lipid exudates
  • Treatment
    • The acute form is an emergency; refer to a internal medicine unit.
    • Visual prognosis is good.
  • Prevention

Visual impairment within hours accompanied by a headache and gastrointestinal symptoms

Acute angle closure glaucoma

  • See Glaucoma.
  • The patient has intense eye pain and/or headache, sometimes in the beginning a rainbow halo around lights due to corneal oedema.
  • Nausea and vomiting is common.
    • In differential diagnosis consider acute abdomen and the aetiologies of headache, such as subarachnoid haemorrhage.
  • The eye is usually intensely red, the cornea (often) dim, pupil mid-dilated, vertically oval, non-reactive to light, and the anterior chamber is shallow.
  • Intraocular pressure is very high (generally > 60 mmHg).
  • First aid
    • Acetazolamide 500 mg i.v. provided that the patient is not allergic to sulphonamides.
    • Refer the patient immediately to an ophthalmology unit where a fluid drainage channel can be created through the iris using laser (laser iridotomy).

Visual impairment within days accompanied with initially mild ocular pain

Iridocyclitis

  • Typical symptoms include dull eye pain, photophobia
  • If iridocyclitis is suspected, the patient should be referred to an outpatient clinic of ophthalmology or to the patient's own ophthalmologist within 24 hours.
  • If a patient with iritis has simultaneously significantly elevated intraocular pressure (exceeding 30 mmHg), the patient should be referred immediately to an ophthalmologist.
  • See Iridocyclitis (Iritis).

Chorioretinitis

  • Possible causes include Toxoplasma (picture 3), Toxocara, tuberculosis, and in immunocompromised/-suppressed patients cytomegalovirus or HIV. In recent years, the share of tuberculosis and syphilis has increased.
  • The symptoms are impaired vision and floaters.
  • The diagnosis requires fundus examination under mydriasis. Usually treated at an ophthalmology unit.
  • If there is suddenly significantly reduced vision, and retinitis is suspected, the patient should be referred immediately to an ophthalmology unit.

Retinitis

  • Seen in, for example, Lyme borreliosis
  • Herpes viruses can cause so-called acute retinal necrosis syndrome.
  • Acute retinal necrosis requires emergency referral to an ophthalmology unit.

Endophthalmitis

  • Infection inside the eye caused by bacteria (acute: Staphylococcus epidermidis, S. aureus, streptococci, pseudomonas; chronic: Propionibacter acnes) or fungi.
  • Predisposing factors include recent intraocular surgery (e.g. after cataract surgery slightly less than 0.1% of eyes), open globe injury, perforating corneal ulcer, systemic diseases such as diabetes or immunosuppression, abuse of intravenous drugs.
  • Symptoms and findings
    • Marked lid oedema
    • Intense hyperaemia
    • Pain and usually rapidly decreasing vision
    • Hypopyon (white blood cells in the inferior part of the anterior chamber)
    • Loss of the red reflex
  • The patient must be referred immediately to an ophthalmic unit to save vision.
  • Treatment
    • Intravitreal and local antimicrobials
    • Paraocular and systemic glucocorticoids

Sympathetic ophthalmia

  • Granulomatous uveitis of the other eye (the sympathizing eye) several days to years after an open globe injury.
  • Symptoms and findings
    • Clinical picture similar to iridocyclitis: circumcorneal injection, pain, photophobia. Cells and flare in the anterior chamber.
  • Refer the patient to an ophthalmologist.

Visual impairment over days and a shadow in the visual field

Retinal detachment

  • A common vision-threatening eye disorder occurring already in young adults especially if they are myopic, becomes more common with age; also occurs after eye injuries and intraocular interventions, e.g. cataract surgery.
  • Treatment is usually surgical; a small local detachment can be limited by laser photocoagulation.
  • In case of retinal detachment, the patient should be referred to an ophthalmological unit without delay; do not hesitate to consult an ophthalmologist. If the diagnosis is certain or probable, the following morning will often be soon enough. If the diagnosis is uncertain, emergency ophthalmological examination may be necessary.
  • See Retinal Detachment.

Visual impairment over a few days with dull pain aggravated by eye movements

Retrobulbar optic neuritis, papillitis

  • Aetiology
    • Often unknown
    • Occurs more often in women
    • The most common identifiable aetiology is multiple sclerosis (MS). The patient may have been diagnosed with multiple sclerosis (MS), or retrobulbar neuritis may be the first manifestation of MS already years before other manifestations of the disease.
    • Optic neuromyelitis
    • Myelin oligodendrocyte glycoprotein (MOG) optic neuritis
    • Viral infections
    • Bacterial infections (e.g. syphilis, tuberculosis, borreliosis, bartonella)
    • Other autoimmune diseases (sarcoidosis, vasculitides, e.g. SLE, polyarteritis nodosa, granulomatosis with polyangiitis)
  • Symptoms and findings
    • Slight impairment of visual acuity, often with a central visual field defect. Sometimes vision is reduced to seeing only hand movement.
    • Altered colour vision (lowered sensitivity to red colour) and contrast sensitivity
    • Impaired direct light reaction or relative afferent pupillary defect is present even if visual acuity is almost normal (Marcus Gunn positive).
    • The optic papilla may be swollen and hyperaemic if the neuritis is anterior (papillitis) or pale and atrophic after a neuritis.
    • Otherwise the eye is normal.
  • Differential diagnosis
    • Papillary stasis (usually bilateral)
    • Brain tumour (meningioma) or other cause of compression of the optic nerve (neuroimaging is usually always indicated)
    • Optic disc drusen - vision not impaired
    • Anterior ischaemic optic neuropathy (AION; usually elderly patients)
    • Giant cell arteritis (elderly patients)
  • Treatment

Distortion of lines (metamorphopsia), distortion of size (micropsia, macropsia)

  • Metamorphopsia always necessitates referral to an ophthalmologist (e.g. for optical coherence tomography of the ocular fundus). Patients with diabetes and some patients with age-related macular degeneration require laser therapy or treatment with a vascular endothelial growth factor (VEGF) inhibitor. Patients with age-related degeneration need urgent therapy; treatment of exudative age-related macular degeneration should start within 2 weeks after the onset of symptoms.
  • Visual disturbance appear within days or weeks.
  • Oedema in the centre of the macula causes distortion of the lines and changes the perceived size of images. These symptoms can be very confusing to the patient.
  • Aetiology
    • If the patient has diabetes the cause is most probably leakage from the capillaries to the fovea (diabetic macular oedema).
    • In age-related macular degeneration, blood is exuded from the new vessels that have grown from the choroid underneath the retina.
    • In disturbances of retinal venous circulation, central vision is impaired by oedema and haemorrhages.
    • Macular hole, preretinal fibrosis (“puckering of the macula”) caused by "incomplete" vitreous detachment, or fibrosis due to oedema
    • After cataract surgery as well as in patients with diabetes, retinitis or recurrent uveitides, fluid may be accumulated in the fovea in cyst-like pockets (cystoid macular oedema).
    • Strong myopia may lead to rupture of the Bruch's membrane and neovascularization.
    • So-called central serous chorioretinopathy is seen in working-aged stressed and busy persons or in pregnant women. The condition may heal spontaneously over months.

Impaired vision developing slowly over months or years

Cataract

  • See Cataract.
  • Symptoms
    • Painless visual impairment
    • Sometimes uniocular diplopia or polyopia
    • Development of myopia at a later age
    • Glare from the lights of oncoming cars
  • Red reflex is uneven, locally invisible or totally absent (picture 4). The fundus of the eye is difficult or impossible to see.
  • In diabetics and patients on glucocorticoids or after blunt ocular trauma, cataract may develop early and rapidly, but it is mostly seen after the age of 60 years. Smoking is one of the risk factors.
  • The timing of surgery is determined by the deterioration of visual acuity and by the patient's vision requirements (occupation and daily activities).

Refractive errors

Myopia

  • The patient squints when looking at distant objects, whereas seeing close up is normal. The patient may have problems watching TV from the same distance as others or seeing the blackboard at school.
    • Examine both distance vision (impaired) and near vision (normal) separately. Pinhole occluder improves distance vision.

Hyperopia

  • Usually symptomless until the early presbyopic age. Sometimes symptoms in school children or students, headache that worsens towards the evening, dull ache in the forehead, the eyes are tired, even a foreign body sensation in the eyes (asthenopia). The symptoms are caused by excessive accommodation.
  • Depending on the grade of hyperopia, both distance and near vision or just near vision may be impaired. Hyperopia may be accompanied by esotropia particularly during attempts to look at close objects.
  • Significantly increased near work may increase visual symptoms due to hyperopia. A person with a history of mild hyperopia may experience blurring of vision and eye pain after long periods of near work.

Strabismus

  • Manifest and latent strabismus may cause impaired vision.
  • Eye strain and visual problems from long-term near work may be due to untreated latent strabismus.
  • Manifest strabismus can be seen in the cover test, latent strabismus in the cover-uncover test.
  • Strabismus should be treated under the supervision of an ophthalmologist. Treatment consists of glasses, eye patching or squint surgery, as necessary.
  • See Adult Strabismus (Squint)

Astigmatism

  • Text is occasionally unclear or may be blurred in some areas.
  • Astigmatism can be treated by suitable correcting glasses (cylindrical lens), contact lenses or eye surgery.

Visual impairment over months or years associated with a progressive visual field defect

Chronic open-angle glaucoma

  • Glaucoma is a progressive neuropathy of the optic nerve leading to typical defects of the optic papilla, the nerve fibre layer and eventually the visual field.
  • In most patients the changes caused by the disease progress slowly over the years.
  • Central visual acuity often remains good for a long time if the defects do not reach the central area.
  • The patient may not experience the defect as a black hole in the visual field but as loss of objects or targets in traffic, for instance (the visual field of the contralateral eye completing the missing section, the background may appear intact but an object may be lost).
  • See Glaucoma.

Hereditary degenerations of the retina

  • A group of progressive diseases that are often part of a syndrome
  • Symptoms include glare and photophobia (intolerance to light), night blindness (nyctalopia) and progressive narrowing of the visual fields. Central vision may remain for a long time or deteriorate in early adulthood.
  • Findings include narrowed visual field, pale optic disc, narrow retinal arterioles and bone spicule pigment clumpings.
  • Refer the patient to an ophthalmologist for the diagnosis, to discuss the prognosis, and for the treatment of possible associated diseases (myopia, cataract, glaucoma, macular oedema) and for fitting of assistive devices and rehabilitation.
    • Hereditary degenerations of the retina is among the the most common causes of visual loss or impairment in working-age people in industrialized countries.

Adverse effects of drugs

  • Ethambutol, amiodarone and vigabatrin may cause toxic optic neuropathy.
  • Thioridazine, chloroquine and hydroxychloroquine may cause toxic retinopathy.
  • Tamoxifen may cause changes in the area responsible for seeing fine detail (macula).
  • Gentamicin may cause a toxic reaction in the retina.
  • Sildenafil may cause disturbances of colour vision.
  • Interferon alfa may cause intraretinal haemorrhages.
  • Isotretinoin used for the treatment of acne may cause severely dry eyes and impaired vision even long after stopping using it.