The Eyes Flashcards
Ophthalmic history: redness
Associated factors, e.g. watering, discharge- mucopurulent discharge suggests bacterial infection.
Pain- sharp, dull? aching- anterior segment inflammation, acute glaucoma.
Foreign body sensation- epithelial defect, foreign body.
Photophobia.
Blurred vision.
Contact lens wear.
History of trauma.
Ophthalmic history: diplopia
Is it actually double or blurred? Duration/age of onset. Monocular or binocular? Variable or constant? Horizontal, vertical, or mixed? - horizontal = III, VI nerve palsies. - vertical = IV nerve palsy. - variable = myasthenia gravis. - progressive = thyroid eye disease.
Ophthalmic history: visual loss
Unilateral or bilateral?- uniocular = suggestive of ocular or optic nerve pathology; binocular = lesions at or posterior to the optic chiasm.
Extent: severe visual loss can occur with optic neuropathies; unilateral, segmental visual loss = retinal disorders such as retinal detachment and branch retinal vein occlusion.
Speed of onset: sudden suggests ischaemic changes, gradual is more typical of compressive causes, progression over a few hours to days can occur in optic neuritis.
Ophthalmic history: colour vision abnormalities
Often a feature of optic nerve disease.
Congenital red-green colour discrimination deficiency is seen in 5-8%.
Blue-yellow is rarely due to congenital colour deficiency so a causation should be sought.
Ophthalmic history: flashing lights
Photopsia is the perception of light in the absence of a light stimulus.
Monocular or binocular?- monocular is typically due to vitreoretinal pathology, binocular is usually a cortical phenomenon.
Causes:
-Mechanical retinal stimulation (posterior vitreous detachment, tears) or external compression.
-Subretinal pathology (choroidal neovascularisation, uveitis, choroidal tumours).
-Cortical ischaemia.
-Visual hallucinations.
Ophthalmic history: symptoms to ask about
Redness. Diplopia. Visual loss. Colour vision abnormalities. Flashing lights. Glare. Haloes or starbursts. Floaters. Night-driving problems. Increased myopia.
Ophthalmic history: causes of eye pain
Gritty, sharp pain: corneal epithelial defect (abrasion, keratitis).
Ache, photophobia: iritis.
Pain on eye movement: optic neuritis.
Scalp tenderness, jaw claudication: temporal arteritis.
Nausea, vomiting: acute angle closure glaucoma, raised intracranial pressure (papilloedema).
Ophthalmic history: causes of floaters
Weiss ring following posterior vitreous detachment.
Vitreous condensation.
Vitreous haemorrhage.
Liberated pigment cells associated with retinal tears.
Inflammatory cells.
Tumour cells.
Asteroid hyalosis.
Ophthalmic history: systems enquiry
Use this to explore symptoms that may point to a systemic disease with ocular manifestations.
MS: weakness, paraesthesia, bladder dysfunction.
Thyroid eye disease: heat intolerance, weight loss, irritability, anxiety.
Myasthenia gravis: dysphagia, weakness worse at the end of the day.
Embolic disease: atherosclerotic disease, arrhythmias.
Acoustic neuroma: hearing loss, tinnitus, balance problems.
Rheumatological and collagen vascular disease: arthralgia, rashes.
Ophthalmic history: past medical history
Diabetes.
Hypertension.
Atopy (allergic conjunctivitis).
Rheumatological disease (dry eye, corneal melt, scleritis).
Neurological diseases (VII palsy, exposure keratopathy).
Metabolic disease (hypercalcaemia).
Ophthalmic history: past ocular history
Past ophthalmic surgery: intraocular (endothelial dysfunction) or refractive (post-laser-assisted stromal in situ keratomileusis LASIK, dry eye, flap dehiscence).
Does the patient wear glasses?
Does the patient wear contact lenses? type? overnight wear? cleaning regimen? swimming?
Trauma (physical, chemical, radiation).
Infection: herpes simplex keratitis, herpes zoster ophthalmicus.
Ophthalmic history: drug history
Topical steroid (cataract, glaucoma, herpetic geographic ulcer).
Toxicity to preservatives/drop allergy.
Ethambutol, isoniazid, amiodarone, and ciclosporin can cause optic neuropathy.
Recreational drug use- particularly in atypical pupil abnormalities.
Ophthalmic history: family history
FHx of MS common in patients with optic neuritis.
Contact with infection, conjunctivitis.
Inherited corneal dystrophies.
Glaucoma.
Ophthalmic history: family ophthalmic history
Ask about any eye diseases which run in the family, e.g. glaucoma, inherited retinal dystrophies.
Ophthalmic history: social history
Occupation and hobbies: for visual requirements, e.g. sports, driving, reading.
Country of previous residence (sun exposure, poor sanitation).
Lead and carbon monoxide can cause optic nerve dysfunction.
STD? e.g. syphilis, HIV/AIDS.
Ophthalmic history: causes of diplopia
Horizontal: VI nerve palsy.
Vertical: IV nerve palsy.
Mixed: III nerve palsy.
Mechanical: thyroid eye disease, trauma (orbital wall/floor fracture), idiopathic orbital inflammatory disease, tumour.
Myasthenia gravis.
Decompensating phobia.
Monocular: high refractive disparity between eyes (anisometropia, astigmatism), corneal opacities or ectasias, lens subluxation, iris defects (trauma, laser peripheral iridotomies).
Visual acuity: visual axis, applied anatomy
Light passes through the cornea, anterior chamber, pupil, lens, and vitreous chamber before hitting the retina.
The optic nerve begins at the retina (and is the only part of the CNS that can be directly visualised).
The nerve passes through the optic foramen and joins its fellow nerve from the other eye at the optic chiasm just above the pituitary fossa.
Here, the fibres from the nasal half of the retina decussate.
They continue in the optic tract to the lateral vehicular body.
From there, they splay out such that those from the upper retina pass through the parietal lobe and the others through the temporal lobe.
Fibres from the nasal halves of the retinas cross, so the left side of the brain receives init from the right side of vision (left temporal retina and right nasal retina) and vice versa.
Visual acuity: testing visual acuity
Snellen chart.
In good light conditions, stand the patient 6m from a Snellen chart.
Test each eye in turn unaided or with the glasses they normally use for distance vision.
Repeat the test with a pinhole.
Any improvement in vision implies an uncorrected refractive error (rather than ocular pathology).
Record the lowest line that can be read (allow 2 errors per line).
The number associated with the letters indicates the distance from which a person with normal sight would be expected to read.
Record the visual acuity as the distance from the chart followed by the number at the lowest letters read.
If the patient is unable to see the Snellen chart at all, see if they can count fingers (CF), see hand movements (HM), see light (PL)- if the patient is unable to see light then record as NPL.
Causes of visual loss: cornea
Dry eyes. Corneal abrasion. Corneal ulcer. Herpetic keratitis. Corneal oedema (acute angle closure glaucoma). Keratoconus.
Causes of visual loss: anterior chamber
Iritis.
Hyphaema.
Hypopyon.
Causes of visual loss: lens
Cataract.
Causes of visual loss: vitreous chamber
Vitreous haemorrhage.
Vitritis.
Causes of visual loss: retina
Branch/central artery or vein occlusion. Retinal detachment. Macular degeneration. Macular oedema. Hypertensive retinopathy.
Causes of visual loss: optic nerve
Optic neuritis.
Ischaemic optic neuropathy.
Papilloedema.
Causes of visual loss: optic chiasm
Pituitary tumour.
Meningioma.
Causes of visual loss: optic tract
CVA.
Tumour.
Causes of visual loss: occipital cortex
CVA.
Tumour.
Skills station, model technique: examine this patient’s optic nerve function
Clean your hands.
Introduce yourself.
Explain the purpose of the examination, obtain informed consent.
Sit facing the patient.
Measure visual acuity for distance and near with Snellen chart and something to read up close.
Measure colour vision (Ishihara colour plates).
Check for an RAPD (relative afferent pupillary defect).
Examine the optic disc looking for any disc swelling, haemorrhage, atrophy, collateral vessels, and cupping.
Perform perimetry (confrontation, manual, automated) to detect any characteristic field defects.
Thank the patient.
Visual fields: testing the visual field, for gross defects and visual neglect (inattention)
Sit opposite the patient, 1m apart, eyes level.
Test first for gross defects and visual neglect with both eyes open.
Ask the patient to look directly at you, ‘look at my nose’.
Ask ‘is any part of my face missing?’
Raise your arms up and out to the sides so that one hand is in the upper right quadrant of your vision and one in the upper left.
Move one index finger and ask the patient, whilst looking straight at you, to point to the hand which is moving.
Test with the right, left, and then both hands.
Test the lower quadrants in the same way.
If visual neglect is present, the patient will be able to see each hand moving individually but report seeing only one hand when both are moving (compare with sensory inattention).
Visual fields: testing each eye
Sit opposite the patient, 1m apart, eyes level.
Ask the patient to cover their right eye while you close your left and ask them to look into your right eye.
Test each quadrant individually.
Stretch your arm out and up so that your hand is just outside your field of vision, an equal distance between you and the patient.
Slowly bring your hand into the centre, wiggling a finger, and ask the patient to say ‘yes’ as soon as they can see it.
Make sure they keep looking at your right eye.
You should both be able to see you hand at the same time.
Test upper right and left, lower right and left individually, bringing your hand in from each corner of vision at a time.
Map out any areas of visual loss in detail, finding borders- test if any visual loss extends across the midline horizontally or vertically.
Test each eye in turn, then again with a red pin to map ut areas of visual loss in more detail.
Common visual field defects
Tunnel vision. Enlarged blind spot. Unilateral visual loss. Scotoma. Bitemporal hemianopia. Binasal hemianopia. Homonymous hemianopia. Homonymous quadrantanopia.
Common visual field defects: tunnel vision
A constricted visual field (glaucoma or retinal damage).
Tubular vision is often functional.
Common visual field defects: enlarged blind spot
Caused by papilloedema.
Common visual field defects: unilateral visual loss
Blindness in 1 eye caused by devastating damage to the eye, its blood supply, or optic nerve.
Common visual field defects: scotoma
A ‘hole’ in the visual field (macular degeneration, vascular lesion or toxins).
If bilateral, may indicate a very small defect in the corresponding area of the occipital cortex (e.g. MS).
Common visual field defects: bitemporal hemianopia
The nasal half of both retinas and therefore the temporal half of each visual field is lost.
Damage to the centre of the optic chiasm such as pituitary tumour, craniopharyngioma, suprasellar meningioma.
Common visual field defects: binasal hemianopia
The nasal half of each visual field is lost (rare).
Common visual field defects: homonymous hemianopia
Commonly seen in stroke patients.
The right or left side of vision in both eyes is lost, e.g. the nasal field in the right eye and the temporal field in the left eye.
If the central part of vision (the macula) is spared, the lesion is likely in the optic radiation.
Without macular sparing, the lesion is in the optic tract.
Common visual field defects: homonymous quadrantanopia
Corresponding quarters of the vision are lost in each eye.
Upper quadrantanopias suggest a lesion in the temporal lobe.
Lower quadrantanopias suggest a lesion in the parietal lobe.
Pupil abnormalities
Relative afferent pupillary defect (RAPD).
Horner’s syndrome.
Argyll Robertson pupil.
Holmes-Adie-Moore syndrome, Adie’s pupil.
Pupil involving 3rd nerve palsy.
Pupil abnormalities: relative afferent pupillary defect (RAPD)
This results from lesions in the anterior visual pathway.
Corneal opacities or cataract do not cause a RAPD.
Causes:
- optic neuropathy, e.g. optic neuritis, compressive lesions.
- gross retinal pathology, e.g. central retinal vein occlusion CRVO, retinal detachment.
- optic chiasm and tract lesions- infarcts, demyelination.
Pupil abnormalities: Horner’s syndrome
Oculosympathetic palsy (interruption of the cervicothoracic sympathetic chain at a 1st, 2nd, or 3rd order neuron level).
Multiple causes, depending on site of lesion.
Unilateral mild ptosis.
Ipsilateral anhydrosis.
Ipsilateral iris heterochromia if congenital or long-standing.
Mild miosis.
Normal or slight delay of pupillary dilatation.
No relative afferent pupillary defect.
Pupil abnormalities: Argyll Robertson pupil
Caused by neurosyphilis.
Constricted and irregular pupils (asymmetric).
No reaction to light.
Brisk constriction to accommodation.
Pupil abnormalities: Holmes-Adie-Moore syndrome, Adie’s pupil
Denervation of the sphincter pupillae and ciliary muscles, probably following viral illness.
Usually seen in middle aged females.
Dilated pupil (mydriasis).
Anisocoria (difference in pupil size) greater in the light.
Poor response to light and accommodation.
Deep tendon reflexes may be reduced or absent.
Pupil abnormalities: pupil involving 3rd nerve palsy
Causes include subdural haematoma with uncle herniation, posterior communicating artery aneurysm, tumour, vasculitis.
Fixed dilated pupil, ptosis, eye held ‘down and out’, with restricted eye movements.
Eye movements: overview
Eye movements are controlled by 3 cranial nerves: oculomotor (CNIII), trochlear (CNIV), and abducens (CNVI).
There are also supranuclear centres that control conjugate eye movements or ‘versions’, where both eyes move in synchrony.
Eye movements: applied anatomy, CNIII (oculomotor)
Motor: levator palpebrae superioris, superior rectus, medial rectus, inferior rectus, inferior oblique (all extrinsic muscles of the eye except lateral rectus and superior oblique).
CNIII has 2 motor nuclei: the main motor nucleus and the accessory parasympathetic nucleus (Edinger-Westphal nucleus).
Autonomic: parasympathetic supply to the constrictor (sphincter) pupillae of the iris and ciliary muscles.
The nuclear complex is in the midbrain at the level of the superior colliculus.
Eye movements: applied anatomy, CNIV (trochlear)
Motor: contralateral superior oblique.
Nucleus lies inferior to the CNIII nuclei, at the level of the inferior colliculus in the midbrain.
It receives input from the vestibular system and medial longitudinal fasciculus.
Eye movements: applied anatomy, CNVI (abducens)
Motor: ipsilateral lateral rectus muscle.
The nucleus lies beneath the 4th ventricle.
It connects with the nuclei of the III and IV cranial nerves through the medial longitudinal fasciculus.
Normal and abnormal eye movements: ductions
Normal monocular movements including adduction, abduction, elevation, depression, intorsion, and extorsion.
Normal and abnormal eye movements: versions
Normal binocular, conjugate eye movements where both eyes move in the same direction.
Normal and abnormal eye movements: vergences
Normal binocular eye movements in which the eyes move synchronously in opposite directions, e.g. convergence.
Normal and abnormal eye movements: phorias
Eye deviations which are not obvious during normal binocular vision (when the retinal images are ‘fused’).
They can ‘decompensate’ when the patient is tired and become obvious or can be seen when binocular vision is prevented, e.g. covering one eye.
Normal and abnormal eye movements: tropias
Obvious deviations, e.g. esotropia = inward deviation, exotropia = divergent squint.
Examining eye movements: observe
Position yourself opposite the patient and assess their head posture.
Look for ptosis.
Shine a pen-torch into each eye from a central position in from of the nose and look for asymmetry of the corneal reflections.
Both should be approximately central. If the reflection is nasal to the pupil the eye is exotropic; if it is temporal it is esotropic.
Examining eye movements: cover test
This is used to assess for phorias- eye deviations which are compensated for during normal binocular vision.
Ask the patient to look at a distant target.
Cover each eye in turn with your hand and watch for movement of the other eye.
If the non-covered eye moves to take fixation, there is a phoria and the direction of movement gives a clue as to the type.
Inward movement = exotropia (eye had been outward).
Outward = esotropia (eye had been inward).
Down = hypertropia (eye had been up).
Up = hypotropia (eye had been down).
Examining eye movements: uncover test
Remove the cover and watch for movement in the eye that is revealed.
Inward movement = exotropia (eye had been outward).
Outward = esotropia (eye had been inward).
Down = hypertropia (eye had been up).
Up = hypotropia (eye had been down).
Examining eye movements: alternate cover test
Repeatedly cover each eye for a few seconds moving quickly between each eye so one is always covered.
Watch for any eye deviation and recovery.
Examining eye movements: voluntary eye movements
Ask the patient if they have any diplopia in primary position (looking straight at you).
Sitting opposite the patient, ask them to follow a target (e.g. your fingertip or pen torch) without moving their head. Sometimes, your hand on their chin helps to hold their head still.
Examine the 9 positions of gaze with the H-test.
Avoid the extremes of gaze.
Ask if they have double vision in each position.
Watch for failure of eye movements or abnormal movements, e.g. nystagmus.
Perform a cover test in each position.
Examining eye movements: saccades
Hold 2 targets either side of the patient (your thumb of one hand and a finger of your other hand works well).
Ask the patient to look rapidly between the 2 targets.
Often a quick demonstration helps- movements should be accurate, smooth and rapid.
Repeat for the vertical meridian (targets above and below midline).
Examining eye movements: convergence
Hold a target approximately 1m in front of the patient and ask them to fix on it.
Slowly bring the target towards the patient and watch their eyes.
The eyes should converge slowly, symmetrically, and smoothly.
Skills station, model technique: exam this patient’s eye movements
Clean your hands.
Introduce yourself.
Explain the purpose of examination, obtain informed consent.
Sit facing the patient.
Ask the patient if they have any visual problems.
Perform a brief examination of visual acuity and visual fields.
Ask the patient to look straight at you.
Make note of the patient’s head position and any evidence of ptosis.
Ask the patient to look at your nose- look for any obvious asymmetry in eye position (strabismus).
With the patient’s eyes in neutral position, perform the cover-uncover test.
Examine voluntary eye movements.
Perform the cover-uncover test in each of the 9 positions of gaze (H-test) if necessary.
Test saccadic eye movements.
Test convergence.
Thank the patient.
Oculomotor CNIII palsy: clinical features
Ptosis.
Affected eye is exotropic and hypotropic (down and out).
Ophthalmoplegia in all directions other than laterally and inferiorly.
Mydriasis (pupillary dilation- variable).
Oculomotor CNIII palsy: causes
20-45% microvascular causes (with diabetes and hypertension).
15-20% intracranial aneurysms (often posterior communicating artery).
Trauma.
Tumours.
Demyelination.
Vasculitis.
Congenital.
Trochlear CNIV palsy: clinical features
Vertical diplopia (worse on downgaze).
Slight external rotation of affected eye (head may be tilted to opposite side to compensate).
Hypertropia (eye sits higher than contralateral side).
Worse on contralateral gaze and ipsilateral head tilt.
Limitation of depression in adduction.
Trochlear CNIV palsy: causes
30-40% due to head trauma.
20% microvascular disease (often improves within 3-4 months).
Congenital (common, although not usually symptomatic until adult life).
Others: haemorrhage, infarction, demyelination, tumours, infection.
Abducens CNVI palsy: clinical features
Inability to abduct affected eye.
Diplopia (worse when looking in direction of paretic muscles and worse for distance than near).
Abducens CNVI palsy: causes
Microvascular lesions (most common). Other causes: demyelination, infarction, raised intracranial pressure, tumours, meningeal infection, aneurysm (basilar artery), inflammatory processes.
Nystagmus: overview
Nystagmus is involuntary rhythmic oscillation of the eyes and may have a number of appearances.
Direction: vertical, horizontal, upbeat, downbeat, rotatory.
Speed of away movement: slow, fast.
Speed of corrective movement.
Pendular nystagmus: oscillation is the same speed in both directions.
Jerk nystagmus: different speeds in different directions; the direction is determined by the fast phase.
Nystagmus: types
Sensory deprivation nystagmus. Motor nystagmus. Latent nystagmus. Dissociated nystagmus. Down-beat nystagmus. Gaze-evoked nystagmus. Upbeat nystagmus. Vestibular nystagmus.
Nystagmus: types, sensory deprivation nystagmus
A pendular type of nystagmus due to a lack of visual stimulus.
Seen in a number of conditions including congenital cataract, ocular albinism, aniridia, congenital optic nerve abnormalities.
Nystagmus: types, motor nystagmus
Usually present at birth or very early in life.
Not present whilst asleep.
Decreases with convergence.
Nystagmus: types, latent nystagmus
Bilateral jerk nystagmus which is only present when one eye is covered.
The fast phase of the jerk is away from the occluded eye.
Nystagmus: types, dissociated nystagmus
Different pattern of nystagmus seen in the 2 eyes.
Causes include: INO, posterior fossa pathology.
Nystagmus: types, gaze-evoked nystagmus
Seen in particular directions of gaze and not in the primary position.
If physiological, it should be fatiguable and symmetrical.
Pathological causes: drugs, lesions of the brainstem and posterior fossa.
Nystagmus: types, upbeat nystagmus
Seen in the primary position of gaze.
Causes: Wernicke’s encephalopathy, drugs, lower brainstem lesions.
Nystagmus: types, vestibular nystagmus
Another type of jerk nystagmus secondary to vestibular disease.
Often a rotary component.
The fast phase away is from the side of the lesion.
Check for associated tinnitus, vertigo, or hearing loss.
Nystagmus: types, downbeat nystagmus
A jerk nystagmus.
Fast phase is down, slow upbeat.
Null point in upgaze.
Associated with diseases of the craniomedullary junction: MS, stroke, syringomyelia, Arnold-Chiari malformation, lithium toxicity.
Eye examination: anterior segment examination
Ideally performed with a slit lamp, should be visible with ophthalmoscope.
Set the dial to +10 to focus on the anterior segment.
Check for RAPD.
General inspection: general habitus, facial asymmetry, skin lesions e.g. herpes.
Lids: position (ptosis, entropion inverted lid, ectropion everted lid), examine the lashes (looking for blepharitis or other lesions), look for lumps, erythema, swelling, evert the upper and lower lids, looking at the conjunctiva and fornices, especially for foreign bodies, papillae, follicles, symblepharon.
Conjunctiva: look for hyperaemia, haemorrhage, chemosis (oedema), lumps, abrasions, foreign bodies, pterygia.
Sclera: look for colour, hyperaemia, swelling.
Cornea: raise the lid to examine entire cornea; instil a drop of 2% fluorescein and look for epithelial defects which will fluoresce green under a blue light.
Anterior chamber: gauge the depth; check for cells, fibrin, flare, blood (hyphaema), pus (hypopyon).
Iris: note colour, shape, movement, atrophy; use retroillumination to check for transillumination defects.
Lens: look for cataract, intraocular lens; note position, movement.
Anterior vitreous: focus behind the lens and ask the patient to look up, down, and then straight ahead to view the vitreous; check for cells (small white deposits), ‘tobacco dust’ (pigment indicative of retinal tear), blood.
Eye examination: posterior segment examination, using an ophthalmoscope
Introduce yourself, explain the procedure to the patient, and gain informed consent.
Ensure the room is dimly lit and, ideally, sit opposite the patient.
Familiarise yourself with the ophthalmoscope. Choose a large aperture light and adjust the brightness so as not to dazzle your patient.
Ask the patient to focus on a distant object and keep their eyes still (relaxes accommodation as much as possible).
Set the refraction to +10.
Look through the ophthalmoscope ~30cm away from the patient and bring the light in nasally from the temporal field to land on the pupil.
The pupil will appear red and opacities in the visual axis will appear as black dots or lines.
Approach the patient from 15 degrees, don’t block the view of their other eye.
With the +10 setting you can examine the anterior segment. By gradually reducing the power of the lens you can examine the cornea, iris, and lens in turn.
Ask the patient to look up, down, and then straight ahead to view the vitreous.
As you approach, dial the refraction to 0 or to your own refraction.
Find a blood vessel and adjust the focus as necessary. Follow the blood vessel, as it increases in diameter to the optic disc.
Examine the optic disc, noting: cup:disc ratio, colour, shape, margin, rim, abnormal vasculature.
Examine all 4 quadrants.
Examine the macula- ask the patient to look directly into the light.
Eye examination: what to look for on ophthalmoscopy, vitreous
Cells (small white particles).
Pigment.
Blood.
Asteroid hyalosis (calcium deposits in the vitreous).
Weiss ring (posterior vitreous detachment).
Eye examination: what to look for on ophthalmoscopy, macula
Dot/blot haemorrhages. Microaneurysms. Exudates. Cotton-wool spots. Oedema.
Eye examination: what to look for on ophthalmoscopy, vessels
Venous beading.
Venous loops.
Intraretinal microvascular abnormalities (IRMAs).
New vessels (very thin, tortuous vessels).
Silver wiring (arteries appear to have a shiny, silver strip).
Arteriovenous nipping (veins are pinched as arteries pass over).
Macroaneurysm.
Eye examination: what to look for on ophthalmoscopy, peripheral retina
Degenerations. Tears. Retinal detachment. Pigmentation. Laser/cryotherapy scars. Chorioretinal scars. Tumours.
Eye examination: the red eye, approach
A careful history must be taken, including previous ophthalmic history, systems review, and family history of eye disease. Examine the eyes systematically: - visual acuity. - pupil responses. - lids. - conjunctiva/sclera. - cornea. - anterior chamber. - iris. - lens. Alway record the patient's visual acuity for distance and near with their appropriate prescription, check both eyes. Can the vision be improved with a pin-hole?
Eye examination: the red eye, red flags
A red eye in a contact lens wearer should be assumed to be microbial keratitis until proven otherwise and should be seen by an ophthalmologist the same day.
A significant reduction in visual acuity not corrected by a pin-hole or the patient’s glasses should be regarded as sinister.
Eye examination: the red eye, causes
Conjunctivitis Uveitis Microbial keratitis (corneal ulcer) Herpes simplex keratitis Episcleritis Scleritis Sunconjunctival haemorrhage Acute angle closure
Eye examination: the red eye, causes, uveitis
Inflammation of the uveal tract (iris, ciliary body, and choroid).
Anterior uveitis usually presents with circumcorneal injection and photophobia, watering, blurring of vision.
Aggressive uveitis may lead to the iris sticking to the lens. This posterior synechiae may give the pupil a small, irregular appearance.
In severe cases, pus may form in the anterior chamber (hypopyon).
Eye examination: the red eye, causes, microbial keratitis (corneal ulcer)
Symptoms: discomfort, often history of prolonged contact lens wear, photophobia, blurred vision.
Signs: infected conjunctiva, corneal ulcer, ± anterior chamber cells.
Eye examination: the red eye, causes, herpes simplex keratitis
Symptoms: pain and photophobia, watering, history of cold sores.
Signs: branching dendritic ulcer visible on surface of cornea with fluorescein under cobalt blue light.
Eye examination: the red eye, causes, episcleritis
Inflammation of the layer superficial to the sclera, deep to the conjunctiva.
Symptoms: bruised, tender feeling, watering.
Signs: the inflamed vessels in the episclera are superficial and can be moved by touch unlike the deeper scleral vessels; sometimes nodular.
Eye examination: the red eye, causes, scleritis
May be seen in association with connective tissue disease (Wegener’s granulomatosis, rheumatoid disease, polyarteritis nodosa).
Symptoms: severe eye pain that keeps the patient awake at night.
Signs: the sclera may thin revealing the choroid below as a blue tinge.
Eye examination: the red eye, causes, subconjunctival haemorrhage
Redness is usually the only symptom/sign.
Check for hypertension or a bleeding disorder.
Eye examination: the red eye, causes, acute angle closure
An emergency.
Systemic features include nausea, vomiting, and headache.
Typical history includes blurred vision and haloes around lights.
Clinical features: significant reduction in vision, red, infected eye, fixed, mid-dilated and oval-shaped pupil, hazy cornea due to oedema.
Raised intraocular pressure males the eye feel hard (compare sides).
Eye examination: the red eye, causes, conjunctivitis, types
Bacterial Viral Chlamydial Allergic Ophthalmia neonatorum
Eye examination: the red eye, causes, bacterial conjunctivitis
Symptoms: acute red eye, grittiness, burning, discharge, no visual loss.
Signs: infected conjunctiva, mucopurulent discharge, clear cornea.
Eye examination: the red eye, causes, viral conjunctivitis
Symptoms: acute red eye, watering, often starts in one eye and then spreads to other eye
Signs: red eye, watering, ± chemosis, ± eyelid oedema, ± pseudo-membrane, corneal subepithelial opacities, tender lymphadenopathy.
Eye examination: the red eye, causes, chlamydial conjunctivitis
Symptoms: unilateral or bilateral mucopurulent discharge, red eye (may become chronic), ± urethritis (may be asymptomatic).
Signs: red eye, mucopurulent discharge, ± peripheral corneal infiltrates, tender lymphadenopathy.
Eye examination: the red eye, causes, allergic conjunctivitis
Symptoms: itching is the key symptom, bilateral redness, watering, associated ‘hay fever’ symptoms (sneezing, nasal discharge).
Signs: lid oedema, ‘pinkish’ conjunctiva, papillae.
Eye signs in thyroid disease: examination, inspection
Look at the patient’s eyes from the front, side, and from above.
Note whether the sclera is visible above or below the iris and whether the eyeball appears to sit forward- proptosis, best seen from above.
Note the health of the conjunctiva and sclera, looking especially for any ulceration or conjunctivitis.
Ensure both eyes can close (failure is medical emergency).
Eye signs in thyroid disease: examination, overview
Inspection.
(Visual fields: it is wise to perform a quick screening test of the visual fields.)
Eye movements: test eye movements in all directions.
Lid lag (von Graefe’s sign).
Eye signs in thyroid disease: examination, lid lag
Hold your finger high and ask the patient to look at it and follow it with their eyes as it moves (keeping their head still).
Quickly move your hand downwards- the patient is made to look upwards and then quickly downwards.
Watch the eyes and eyelids: do they move smoothly and together? is white sclera seen above the iris as the eye moves downward?
Eye signs in thyroid disease: examination, findings
Proptosis.
Exophthalmos.
Lid retraction.
Lid lag.
Eye signs in thyroid disease: examination, findings, proptosis
Protrusion of the globes as a result of an increase in retro-orbital fat, oedema, and cellular infiltration.
Eye signs in thyroid disease: examination, findings, exophthalmos
More severe form of proptosis.
Sclera become visible below the lower edge of the iris (inferior limbus).
Patient may not be able to close their eyelids and can develop corneal ulceration, chemosis, conjunctivitis.
Eye signs in thyroid disease: examination, findings, lid retraction
The upper eyelid is retracted such that you are able to see white sclera above the iris when the patient looks forwards.
Caused by increased tone and spasm of levator palpebrae superioris as a result of thyroid hormone excess (Dalrymple’s sign).
Eye signs in thyroid disease: examination, findings, lid lag
Upper eyelid seems to lag behind the movement of the eye, allowing white sclera to be seen above the iris as the eye moves downwards.
Caused by sympathetic overstimulation of the muscles supplying the upper eyelid, seen in thyroid hormone excess.
Eye signs of thyrotoxicosis
Lid retraction.
Lid lag.
Eye signs of Graves’ disease
Periorbital oedema and chemosis.
Proptosis/exophthlamos.
Ophthalmoplegia (particularly of upward gaze).
Lid retraction and lid lag only when thyrotoxicosis is present.
