Clinical Medicine and Surgery I · Exam 2 — Study Guide

Also tested

• Chemical eye injury. This is emergent: copious irrigation starts at once, before visual acuity, imaging or referral calls.

Also tested

• Demonstrating a corneal abrasion. Instill fluorescein and examine under a Wood's lamp with ultraviolet light; this surface fluorescein examination detects abrasions, ulcers and foreign bodies.
• Red flags in a red eye. Reduced vision and true pain move a red eye out of the benign category and separate a dangerous cause from a benign one.
• Fluorescein. Instilled and viewed under a blue light; it pools in epithelial defects and reveals abrasions, ulcers and foreign bodies.

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• Escalation for red, crusted lid margins. Lid hygiene comes first; if there is no improvement after two weeks, add a topical antibiotic, then oral antibiotics.
• Causes of ectropion. Aging, scarring and congenital causes can produce ectropion, and seventh nerve palsy causes ectropion only.
• Entropion and the cornea. The key question with entropion is always whether the lashes have damaged the cornea, assessed by slit lamp examination; an epithelial defect from lash contact means the cornea is now involved.
• Recurrent lid nodule. A nodule that keeps recurring after being treated as a chalazion raises the possibility of sebaceous carcinoma; recurrent lesions, or one persisting beyond two to three months, are referred to rule this out.
• Entropion and ectropion. Slit lamp examination is required to assess corneal involvement, i.e. whether the cornea has been damaged.
• Blepharoplasty coverage. Visual field testing is the assessment that determines coverage, because a demonstrated field deficit is what makes blepharoplasty a covered procedure.
• Seventh nerve palsy and lid position. Seventh nerve palsy causes ectropion, with the lower lid margin turned outward, watering and a red, exposed inner lid surface. Of the two malpositions, it causes ectropion only.
• Yellowish plaques near the inner canthus. Initial workup is lipid, diabetes and liver blood tests: a serum lipid profile, fasting glucose and hemoglobin A1C, and liver function tests. The lesion is a marker of the metabolic issue that is treated.
• Chalazion versus hordeolum. Tenderness separates them: the hordeolum is tender and the chalazion is not.
• Hordeolum referral. Refer to ophthalmology if persistent, for example no improvement in two weeks, for incision and drainage.
• Xanthelasma prognosis. Recurrences are common even after effective local treatment, whatever the local treatment.
• Ectropion treatment. Surgery is the definitive treatment, since only surgery restores lid position permanently; lubrication only protects the surface in the meantime.
• Yellowish plaques on the inner upper eyelids. Workup is a serum lipid profile, together with tests for diabetes mellitus and liver function; the plaques are a marker of an underlying metabolic disorder.
• Xanthelasma. Soft yellow plaques lying in the eyelid skin near the inner corner, typically on both sides.
• Entropion. It produces foreign body sensation because the inward-turned lashes rub the globe.
• Dermatochalasis. Treated with blepharoplasty, the surgical removal of the excess skin.
• Chalazion. A firm, painless, non-tender, slowly enlarging eyelid nodule is managed conservatively first, with warm compresses with gentle massage.

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• Imaging in dacryoadenitis. Contrast computed tomography of the orbits and paranasal sinuses is used when indicated, not automatically on presentation.
• Dacryocystitis needing admission. Fever, systemic illness or an unreliable patient move care to inpatient: intravenous therapy for 48 to 72 hours, then oral therapy to complete 10 to 14 days.
• Mild dacryocystitis. In an afebrile, systemically well, reliable patient it is managed as an outpatient with oral antibiotics for ten days and warm compresses.
• Corticosteroids in painful lid swelling of unclear cause. Infection must be reasonably excluded first; the alternative path is empiric oral antibiotics for 24 hours with reassessment.
• Inflammatory dacryoadenitis. Treat with oral corticosteroids, with a response expected within 48 hours.

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• Pterygium surgery. Refer for surgical excision when a pterygium grows onto the cornea and distorts vision.
• Yellowish raised nasal conjunctival nodule not reaching the cornea. Sun, dust and wind protection with lubricating drops controls symptoms but will not resolve the nodule.
• Pinguecula versus pterygium. The pterygium extends into the cornea; the pinguecula does not involve it. Corneal involvement is the whole distinction.
• Unexplained bright red patch on the sclera. Take a careful history and check blood pressure; history is the priority, and an unexplained bleed warrants a blood pressure check.

Also tested

• Course of viral conjunctivitis. It worsens for about a week, then clears, with resolution taking two to three weeks, and it is highly contagious throughout.
• Viral conjunctivitis education. Strict hand hygiene is the key advice, as the condition is highly contagious; contagious precautions are the central education point.
• Preauricular node in conjunctivitis. Bacterial conjunctivitis otherwise lacks a node, so severe purulent discharge with a node points to gonococcal disease.
• Neonatal purulent conjunctivitis timing. Onset on day 2 of life suggests Neisseria gonorrhoeae, since gonococcal disease presents in the first few days while chlamydial disease presents later, around days 5 to 14.
• Mucous membrane pemphigoid. Chronic red, gritty eyes with progressive scarring of the lower palpebral conjunctiva, fornix shortening and oral erosions indicate it: progressive subconjunctival fibrosis with mucosal involvement elsewhere (the ocular form).
• Trichiasis from trachoma. It requires surgical treatment, because the lashes keep abrading the cornea until they are dealt with surgically.
• Doxycycline counseling. Avoid the sun (photosensitivity) and heed food and mineral interactions: take it with a full glass of water, stay upright, and separate it from antacids and from iron, calcium or magnesium.
• Neonate with marked bilateral lid edema, copious purulent discharge and a preauricular node. Hospitalize and give systemic ceftriaxone as a single dose, with specialty consultation; the untreated risk is corneal perforation.
• Bacterial conjunctivitis risk groups. Immunocompromised, elderly, children and contact lens wearers are at particular risk. Neonates are a separate concern, where gonococcal infection is the worry.
• Allergic conjunctivitis unresponsive to topical treatment. The diagnosis may be wrong, so refer; symptoms usually settle as allergen levels fall.
• Chlamydial conjunctivitis. Beyond treating the eye, arrange evaluation for other sexually transmitted infections and notify partners for evaluation; the eye finding is a sentinel for a usually asymptomatic urogenital infection.
• Stages of trachoma. Trachoma progresses through four stages: follicles, scarring, entropion and opacity.
• Neonatal chlamydial conjunctivitis. Neonates are often treated in hospital because there is often concomitant pneumonia or pneumonitis; the lung involvement is what drives admission.
• Urgent conjunctivitis. Contact lens wear, immunocompromise, recent surgery, a foreign body, corneal opacity or no improvement in 24 hours all make it urgent.
• Trachoma. Caused by Chlamydia trachomatis; it progresses through follicles, tarsal scarring, entropion with trichiasis, and corneal opacity.

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• Scleritis workup. Severe deep eye pain that wakes from sleep, with a bluish hue to the sclera, warrants an autoimmune workup, because scleritis is frequently associated with systemic autoimmune disease, including connective tissue disease.
• Episcleritis. The inflamed tissue is the deep subconjunctival tissue, the episcleral layer.
• Scleritis response to treatment. Decreased pain is the expected first sign of response and comes before any change in appearance, so an unchanged-looking eye is not failure.
• Scleritis referral. Refer to ophthalmology urgently, because the sclera is at risk of perforation and may need a surgical patch.
• Episcleritis. The bedside test is to instill 2.5 percent phenylephrine and look for blanching of the vessels after 15 minutes; episcleral vessels blanch, and mild painless sectoral redness fits episcleritis.
• Episcleritis. It is self-limiting and often needs no specific treatment; management is reassurance, with lubricants for comfort.

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• Contact lens corneal ulcer. Pseudomonas aeruginosa is the organism of greatest concern with contact lens wear, and it can perforate the cornea rapidly.
• Corneal ulcer with intraocular inflammation. A hypopyon, layered white cells in the anterior chamber, indicates significant intraocular inflammation.
• Vesicular rash on forehead and nose tip. The ophthalmic division (V1) of the trigeminal nerve is involved, and involvement of the nose tip signals ocular involvement.
• Hutchinson sign. Vesicles on the tip of the nose indicate a high likelihood of ocular involvement, because the nasociliary branch supplies both the nose tip and the globe.
• Herpes zoster ophthalmicus with deeper involvement. If there is retinitis, choroiditis or optic neuritis, treatment is steroids and intravenous acyclovir.
• Corneal ulcer referral. A corneal ulcer needs ophthalmology emergently, outranking keratitis's 24-hour window.
• Corneal ulcer follow-up. Review is needed the next day after an anti-infective is started, and most ulcers heal over a two to three week course.
• Herpes zoster ophthalmicus. A dermatomal vesicular rash over the forehead and upper lid seen within the ideal 72-hour window calls for an oral antiviral now, plus referral for slit lamp examination and dilated fundoscopy.
• Corneal ulcer position. Prognosis follows both size and position relative to the visual axis; ulcers inside the visual axis carry a poorer outcome.
• Herpes simplex keratitis prognosis. Good, though recurrences are common.
• Corneal ulcer on examination. The patient resists opening the affected eye, because of photophobia and foreign body sensation.
• Nasal-tip vesicle (Hutchinson sign). It indicates nasociliary branch involvement, and therefore a higher risk of ocular involvement.
• Corneal infiltrate with epithelial defect and hypopyon. Urgent referral for scraping and antibiotics is the next step. A hypopyon indicates significant intraocular inflammation and the eye is at risk; treatment is intensive topical antibiotics after corneal scraping.
• Punctate epithelial keratitis. It presents as a painful, photophobic red eye with reduced vision, with diffuse punctate fluorescein staining without an infiltrate, from exposure and surface drying.
• Herpes simplex keratitis. A true dendrite, a branching corneal lesion on fluorescein with terminal end bulbs, is pathognomonic for herpes simplex, and the treatment is oral antiviral therapy for ten days.

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• Recurrent anterior uveitis with inflammatory back pain. Back pain that improves with exercise and worsens with rest points to HLA-B27 spondyloarthropathy, the ankylosing spondylitis association, which is why the systemic history matters.
• Cycloplegic in anterior uveitis. It relieves pain and prevents synechiae by resting the ciliary body and keeping the iris from adhering to the lens.
• Posterior uveitis. It involves the choroid and/or the retina, that is, choroiditis and retinitis.
• Infectious cause of posterior uveitis. Toxoplasma gondii causes chorioretinitis and is a classic infectious cause of posterior uveitis.
• Posterior uveitis treatment. Topical treatment will not work; an intraocular corticosteroid injection may be required, the key management difference from anterior uveitis.
• Posterior versus anterior uveitis course. Posterior uveitis develops a lot more slowly and may last several years, though it can also turn acute and threaten vision.
• Recurrent uveitis with systemic features. Recurrent uveitis with suggestive systemic features warrants a thorough systemic evaluation for an underlying autoimmune condition.
• Anterior uveitis. It involves the iris (iritis), or the iris and ciliary body (iridocyclitis).

Also tested

• Mild pre-septal cellulitis. In a systemically well child with reliable follow-up, manage with oral antibiotics and early review at 24 to 48 hours.
• Progression of pre-septal cellulitis. New pain on eye movement and mild proptosis mean the infection has progressed behind the orbital septum; painful restricted movement and proptosis indicate post-septal disease.
• Post-septal cellulitis. All post-septal disease is admitted for intravenous antibiotics and imaging; computed tomography of the orbits and sinuses defines the extent.
• Hospitalizing pre-septal cellulitis. Admit for moderate to severe or toxic disease, concern for poor compliance, a child of five years or younger, or no improvement after oral antibiotics were started.
• Orbital cellulitis. The usual source of infection is the paranasal sinuses, which is why imaging covers the sinuses as well as the orbits.

Also tested

• Acquired nystagmus in an adult. It suggests an underlying neurological cause; it is not benign and requires investigation.
• Nystagmus present since birth. It warrants evaluation for a cause of poor vision, since congenital nystagmus often reflects an underlying visual deficit.
• Early-onset nystagmus. It is usually asymptomatic if acquired before age eight, which is why onset age matters.
• Monocular or asymmetric nystagmus. Refer for work-up; it is a concerning, non-physiologic pattern.
• Nystagmus in infants and young children. It warrants referral for work-up.
• Upbeat nystagmus. New upbeat nystagmus is classified as concerning and non-physiologic, and it warrants work-up in adults.

Also tested

• Light reflex, afferent limb. Afferent impulses travel along the second cranial nerve: retinal ganglion cells to the optic nerve and tracts.
• Opioid toxicity. The features that matter clinically are reduced consciousness and respiratory depression; the miosis is a clue rather than the danger.
• Pupillary muscles. The iris sphincter constricts and the radial muscle dilates, producing miosis and mydriasis respectively.
• Naloxone reversal. Naloxone may need repeating, because it lasts about two hours and respiratory depression can return.

Also tested

• Pupillary light-near dissociation. It is defined by no reaction to light with a preserved reaction to near.
• Near response. On shifting gaze from distance to near, the lens thickens, the pupils constrict and the eyes converge; it acts on lens, pupil and globes together.

Also tested

• Pharmacologically dilated pupil. Anticholinergics such as atropine, ipratropium, scopolamine and glycopyrrolate can cause it, giving a large pupil that is unreactive to light.
• Physiologic anisocoria. The size difference between the pupils is typically under about half a millimeter and is equal in light and dark.
• Sympathomimetic versus anticholinergic pupil. A sympathomimetic-dilated pupil is only mildly enlarged, unlike the very large anticholinergic pupil.
• Scopolamine patch mydriasis. A unilateral fixed dilated pupil after handling a scopolamine patch will resolve as the drug wears off; pharmacologic mydriasis is transient and needs no imaging.
• Physiologic anisocoria. Mild anisocoria, equal in light and dark, with normal lids and movements, needs only reassurance and no work-up.

Also tested

• Horner syndrome. A droopy lid, small pupil that reacts to light and dry face (ptosis, miosis, anhidrosis) in a smoker with a months-long cough means an apical lung tumor, a Pancoast tumor, must be excluded.
• First-order Horner syndrome. Brainstem stroke fits this level, along with spinal cord lesions above T1.
• Holmes-Adie syndrome. It is accompanied by absent deep tendon reflexes, often the Achilles or patellar reflex.
• Argyll Robertson pupils. Syphilis remains the classic association, but diabetes, alcohol, sarcoidosis and multiple sclerosis can also cause them.
• Horner syndrome anisocoria. The difference between the pupils is most evident within the first few seconds after the lights are dimmed, when a normal pupil would dilate rapidly and actively.
• Apraclonidine in Horner syndrome. It dilates a Horner pupil through alpha-two greater than alpha-one activity, acting on a denervated, supersensitive pupil.
• Adie pupil versus third nerve palsy. An Adie pupil has no ptosis and no extraocular weakness; a third nerve palsy also weakens the levator and extraocular muscles, giving ptosis and a down-and-out eye.
• Adie tonic pupil. It is often benign and asymptomatic, though photophobia and blurred near vision can occur.
• Absent anhidrosis with ptosis and miosis. It does not exclude the diagnosis, since it depends on lesion level: the triad may be incomplete depending where along the pathway the lesion sits.
• Adie pupil. Dilute pilocarpine drops support the diagnosis: the denervated pupil is supersensitive and constricts.
• Relative afferent pupillary defect. Optic neuritis can explain it, because the defect lies in the afferent pathway, which is the optic nerve.
• Acute Horner syndrome with neck pain after chiropractic manipulation. The next step is urgent vascular imaging, because carotid dissection must be identified before it embolizes.
• Argyll Robertson pupil. Small, irregular pupils in both eyes that do not react to light but constrict briskly on near effort: light-near dissociation, "accommodates but does not react".
• Marcus Gunn pupil. The lesion is pre-chiasmal, in the retina or optic nerve.
• Relative afferent pupillary defect. Detected with the swinging flashlight test: moving the light to the affected eye makes both pupils dilate.
• Argyll Robertson pupils. Look for the associated finding of sensory ataxia, from tabes dorsalis with posterior column involvement.

Also tested

• Sixth nerve palsy. Binocular horizontal diplopia that worsens on gaze to one side, with under-abduction of that eye, means a sixth nerve palsy on that side: the lateral rectus abducts, and the deficit is on the side of gaze.
• Patching in congenital palsy. Patching of a young child with a congenital palsy should be supervised by ophthalmology, especially under about five years of age.
• Head tilt in fourth nerve palsy. Tilting the head compensates for the weak muscle: the patient tilts away from the affected side to reduce the vertical deviation.
• Third nerve palsy with a normal, reactive pupil. A normal pupil in ptosis with the eye deviated down and out suggests a microvascular ischemic cause. Pupillary fibers run peripherally and are spared by ischemia but compressed by an aneurysm.
• Sixth nerve palsy. It is a false localizing sign because of its long intracranial course; the palsy does not indicate where the lesion is, since raised pressure anywhere can affect it.
• Third nerve palsy causes. Severe head trauma is a cause, alongside microvascular disease and aneurysm.
• Superior division oculomotor lesion. It causes ptosis and impaired elevation, because the superior division supplies levator palpebrae and superior rectus.
• Third nerve palsy. The eye is "down and out" because of unopposed lateral rectus and superior oblique: the muscles the third nerve does not supply are the ones left working.
• Fourth cranial nerve. It supplies the superior oblique, which depresses the adducted eye, hence vertical diplopia worse on downgaze.
• Peripheral fourth nerve lesion. A peripheral lesion after the nerve exits gives an ipsilateral deficit, in the same side eye.
• Acquired fourth nerve palsy. The likely causes are trauma and microvascular disease, with even mild trauma sufficient.

Also tested

• Eyelid closure. The muscle that closes the eyelids, orbicularis oculi, is supplied by the seventh (facial) cranial nerve.
• Fatigable bilateral ptosis with variable diplopia. This pattern points away from a structural palsy and toward myasthenia, so the next step is referral for neurologic evaluation.
• Ptosis causes. Horner syndrome and third nerve palsy both drop the lid, and each also disturbs the pupil, so ptosis appears alongside anisocoria.
• Ptosis of third nerve palsy versus Horner syndrome. Levator function distinguishes them: it is reduced in third nerve palsy and normal in Horner syndrome.

Also tested

• Homonymous hemianopsia with macular sparing. This pattern suggests a lesion of the occipital cortex; macular sparing is the cortical signature.
• Monocular field defect. The lesion lies anterior to the chiasm; a monocular defect localizes pre-chiasmal.

Also tested

• Tonic pupil in an otherwise well person. Management is reassurance once causes are excluded; it is benign, though the anisocoria may persist.
• Neuro-ophthalmological work-up. After history and examination, head computed tomography or MRI is used if indicated.

Also tested

• Assessing acute vision loss. The initial assessment turns on four questions: one or both eyes, duration, pain, and a description of the symptoms.

Also tested

• Amaurosis fugax source. Painless monocular blackouts lasting under a minute most likely arise from a carotid or cardiac embolus, most commonly a transient ischemic attack of retinal origin.
• Treatment of amaurosis fugax from carotid emboli. Antiplatelet therapy is given for stroke risk, together with endarterectomy for the carotid source.
• Amaurosis fugax. A transient curtain-like loss of vision in one eye with full recovery is a transient ischemic attack of the eye, carries the same stroke risk, and calls for carotid imaging and urgent stroke workup.
• Amaurosis fugax. Loss that descends over the field of one eye like a shade from above is attributed to retinal ischemia.
• Transient monocular vision loss lasting minutes. The mechanism is transient retinal ischemia, usually embolic, most often from carotid atheroma.
• Curtain coming down over vision. This description is a warning sign because more than one condition uses it; it fits amaurosis fugax and retinal detachment.
• Amaurosis fugax. The term for fleeting blindness, meaning monocular episodic visual loss.
• Amaurosis fugax outlook. About 85% recover fully, and the remainder progress to a central retinal artery occlusion.

Also tested

• Secondary angle-closure glaucoma. Drainage can be obstructed by tumor, scarring or other mechanical causes.
• Anticholinergics in angle closure. Systemic anticholinergic medications such as atropine are a risk factor for acute angle closure, in which the iris blocks the drainage circuit and pressure rises, so they can worsen angle-closure glaucoma.
• Intraocular pressure in glaucoma. Pressure may be either normal or elevated in this disease.
• Why open-angle glaucoma is missed. Loss is gradual and the other eye compensates, which is why it is found on screening rather than by symptoms.
• Chronic open-angle glaucoma cause. Idiopathic optic nerve damage, from trabecular meshwork change with aging.
• Evaluating glaucoma. Tonometry and gonioscopy are the two tests: tonometry measures pressure, and gonioscopy views the angle.
• Painful red eye with a hazy cornea. Intraocular pressure is measured first, by tonometry or gonioscopy; expect 40 to 80 mmHg.
• Acute severe eye pain with halos, hazy cornea and fixed dilated pupil. With a shallow anterior chamber and ciliary injection, tonometry is the immediate next step: measuring the intraocular pressure confirms the diagnosis.
• Acute angle-closure glaucoma. A shallow anterior chamber predisposes to it: a crowded angle is what allows closure when the pupil dilates.

Also tested

• Optic neuritis epidemiology. About 75 percent of cases occur in women, in patients aged 18 to 45.
• Optic nerve pallor without cupping. This favors ocular ischemic syndrome, which is underlain by carotid stenosis.
• Optic neuritis course. Vision usually recovers substantially over weeks, though color desaturation may persist.
• Imaging in suspected optic neuritis. Magnetic resonance of the brain and orbits is ordered, with and without contrast.
• Optic neuritis course. Improvement within weeks, normal vision within a year, often without treatment.
• Optic neuritis patient profile. Typically aged 18 to 45 and mostly female; about 75% are women.
• Optic neuritis with demyelinating lesions on imaging. Neurology referral with corticosteroids follows; steroids are given if a demyelinating cause is found. Neuro-ophthalmology is equally appropriate.

Also tested

• Posterior vitreous detachment without a retinal break. Advise return if a curtain or shadow appears; that warning converts this from observation to emergency.
• Holding text further away with unchanged distance vision. The lens stiffens, so accommodation fails.
• Myopia risk factors. Family history and near work are risk factors, and trauma displacing the lens forward can cause myopia.
• Retinal detachment symptoms. Vision changes with head position, which is unusual among causes of acute vision loss, because the detached retina moves.
• Suspected retinal detachment with a poor fundus view. Ocular ultrasound is more sensitive than fundoscopy, and it also types the detachment.
• Retinal detachment with the macula still attached. Central vision is salvageable before the macula goes, so macula-on detachment is the more urgent repair.
• Types of retinal detachment. Rhegmatogenous, traction and serous; the serous form is also called exudative.

Also tested

• Central retinal artery occlusion and general health. Stroke risk is markedly increased, since plaque reaching the retinal artery implies more in the carotids.
• Branch versus central retinal vein occlusion. In a branch occlusion a smaller branch vein is blocked, so only part of the retina is affected, unlike central retinal vein occlusion.
• Sudden painless monocular vision loss. Immediate ophthalmology referral is the next step; it is a stroke of the eye, and the window is measured in minutes to hours.
• Branch versus central retinal vein occlusion. In the branch form the clot is in a branch vein, so hemorrhage is confined to that territory and only part of the retina is affected.
• Central retinal vein occlusion complication. Neovascular glaucoma is monitored for, because ischemia drives new vessel growth at the iris and angle.
• Cherry-red spot. It is the intact choroid showing through the fovea; the surrounding retina is pale from infarction, and the fovea has no inner retinal layers to become edematous.
• Central retinal artery occlusion. Anterior chamber paracentesis is performed to lower the intraocular pressure; fluid is withdrawn from the eye with a needle.
• Central retinal vein occlusion. Look for hypertension, diabetes and hyperviscosity; the venous side reflects systemic vascular and rheological disease.
• Frequency of retinal vascular occlusions. Vein occlusion is more common than central retinal artery occlusion.
• Central retinal artery occlusion. It causes sudden profound painless loss of vision, with a pale, swollen retina and a cherry-red spot at the fovea.
• Arterial versus venous retinal occlusion on fundoscopy. Arterial occlusion shows pallor with a cherry-red spot at the fovea rather than hemorrhages.
• Branch retinal artery occlusion. It causes sudden painless loss of part of the visual field, with a pale wedge of retina in one artery's territory producing loss of the opposite field.
• Central retinal artery occlusion. Profound painless loss of vision in one eye over seconds that does not recover, with a pale retina.
• Central retinal vein occlusion. Sudden painless loss of vision with the "blood and thunder" fundus: disc swelling, dilated, engorged veins, cotton wool spots and hemorrhages in every quadrant.

Also tested

• Papilledema versus optic neuritis. Acuity is preserved in papilledema and reduced in optic neuritis; papilledema is bilateral, while optic neuritis is usually unilateral with an afferent pupillary defect.
• Lumbar puncture in idiopathic intracranial hypertension. With papilledema, the expected finding is a raised opening pressure with normal constituents.

Also tested

• Inflammatory markers in arteritic optic neuropathy. They help rule the diagnosis in or out; erythrocyte sedimentation rate and C-reactive protein are markedly raised.
• Arteritic optic neuropathy outlook. The outlook depends on the duration of symptoms and when steroids began, which is why early therapy is critical.
• Antihypertensive timing in non-arteritic anterior ischemic optic neuropathy. The antihypertensive dose may be moved away from bedtime to avoid nocturnal hypotension, which can worsen the condition.
• Optic disc in anterior ischemic optic neuropathy. Sudden painless vision loss with a swollen, pale disc and loss of side or central vision is the expected picture.
• Arteritic anterior ischemic optic neuropathy. With markedly raised inflammatory markers, treatment starts with intravenous methylprednisolone for three days, then a slow oral taper; early therapy is critical.
• Non-arteritic share of anterior ischemic optic neuropathy. The non-arteritic form accounts for ninety to ninety-five percent of cases and is by far the commoner form.
• Suspected arteritic vision loss. Sudden painless vision loss with scalp tenderness, jaw aching on chewing and a markedly raised erythrocyte sedimentation rate calls for high-dose corticosteroids immediately; treatment precedes biopsy because the other eye is at risk within days.
• Arteritic anterior ischemic optic neuropathy. It affects people aged 55 years and older.
• Non-arteritic anterior ischemic optic neuropathy. It typically affects people aged 40 to 60 years, accounting for 90 to 95 percent of cases.
• Giant cell arteritis with vision loss. Start treatment today rather than waiting for the biopsy, because the fellow eye can be lost within days.
• Non-arteritic anterior ischemic optic neuropathy. Altitudinal field loss on waking, with normal inflammatory markers and no arteritic symptoms such as scalp tenderness or jaw claudication.

Also tested

• Sudden painless monocular vision loss. Urgent ophthalmology involvement is the non-negotiable step, because each of these diagnoses is sight-threatening and time-dependent.

Also tested

• Stakes of untreated idiopathic intracranial hypertension. Permanent vision loss from optic nerve damage is the risk; the vision, not the headache, drives treatment.
• Idiopathic intracranial hypertension workup. Imaging with venography comes first; when it is normal, the next step is lumbar puncture to measure opening pressure, which confirms the diagnosis.
• Idiopathic intracranial hypertension. Classic picture: a woman with a raised body mass index, daily headaches, pulsatile tinnitus, transient visual obscurations, papilledema with bilateral disc swelling, and normal neuroimaging.

Also tested

• Why screen for open-angle glaucoma. It is asymptomatic at onset, and the damage it does cannot be reversed.
• Eye care in diabetes. Annual ophthalmology review should be arranged, because a medical eye risk needs the medical specialist.
• Why open-angle glaucoma goes unnoticed. It is painless and spares central vision early, which is why screening exists.
• Glaucoma drops. Drops protect the vision that remains, because damage already done cannot be reversed.
• Fellow eye in acute angle closure. The other eye receives prophylactic iridotomy, because it shares the crowded anatomy and is anatomically at risk.
• Glaucomatous optic disc damage. Defined by cupping, an excavated disc, with a raised cup-to-disc ratio.
• Who needs a yearly ophthalmologist. A patient with diabetes needs a yearly ophthalmologist rather than an optometrist, because a medical eye problem needs the medical specialist.
• Cupped discs on routine examination. Refer to ophthalmology for assessment; good central vision does not exclude damage.
• Most common form of glaucoma. Primary open-angle glaucoma is the most common form, and it is characteristically painless and slow.
• First-line treatment of open-angle glaucoma. A prostaglandin analog; prostaglandins or beta blockers lead, and cholinergic agents are third or fourth line.

Also tested

• Dry versus wet macular degeneration. About 80 percent of macular degeneration is the dry form, leaving roughly 20 percent wet.
• Sharp worsening of central blur in dry macular degeneration. A rapid change over a week raises concern for conversion to the wet form, in which new vessels bleed.
• Amsler grid. It is a self-monitoring tool to detect distortion or a missing area, which suggests conversion of dry macular degeneration to the wet form.
• Dry form of macular degeneration. About eighty percent of age-related macular degeneration is dry; the wet form accounts for the remaining twenty.
• Gradual painless vision loss in older patients. The three commonest causes, and so the top of the differential, are cataract, macular degeneration and open-angle glaucoma.
• Dry macular degeneration. Defined by drusen, pigment change and atrophy. Neovascular bleeding defines the wet form instead.
• Dense macular scar from previous bleeding. This is wet macular degeneration, because it began with neovascular bleeding. The scar is the end stage of the wet process.
• Wet macular degeneration treatment. Intravitreal anti-VEGF injection, with photodynamic therapy and laser as alternatives.
• Wet macular degeneration with acute distortion and central gray patch. Straight lines distort, with subretinal fluid and hemorrhage at the macula. Give urgent referral for intravitreal anti-VEGF therapy; the wet form is treatable and the window matters.
• Dry to wet macular degeneration. In the wet form, new vessels from the choroid bleed into retina, and the blood organizes into a scar.

Also tested

• Long eyeball. A long eyeball predicts blurred distance vision with clear near vision, because myopia focuses distant objects in front of the retina.
• Lens correcting myopia. Myopia is corrected by a concave lens of negative diopter, which moves the focus back.
• Astigmatism. Uneven curvature gives several focal points, so no single point focus forms, causing blur at every distance.
• Farsightedness. A convex lens corrects it because it converges light onto the retina; the farsighted eye focuses behind the retina.
• Hyperopia. The eye is too short, and accommodative effort at near produces headaches and eye strain when reading, with normal distance vision.
• Hyperopia and ocular emergencies. Hyperopic patients are warned about acute angle-closure glaucoma, because the short eye has a crowded anterior segment.

Also tested

• Double vision that resolves when either eye is covered. Binocular diplopia means misalignment until proven otherwise, so the next step is to assess ocular alignment and cranial nerves.
• Third nerve palsy with pupil involvement. Sudden ptosis, a dilated pupil and an eye deviated down and out require urgent exclusion of an aneurysm compressing the third nerve; pupil involvement makes this an emergency.
• Levels causing strabismus. The cause can lie in the brain, nerve, junction or muscle; causes are found at all four levels.

Also tested

• Amblyopia outcome with patching. Outcome is good, though vision is not always fully normal, and starting treatment before age five is better still.
• Objection to covering one eye. A toddler who cries only when the right eye is covered sees poorly with the left eye, because he objects when his good eye is taken away.
• Occlusion objection test. A child who objects when one eye is covered has amblyopia in the other eye, because the child objects when the good eye is covered.
• Amblyopia treated late. An adult may have good acuity but struggle with 3D films because stereo vision never developed; the brain still uses one eye at a time.
• Amblyopia mechanism. The brain favors one eye and the other fails to develop. Strabismus, refractive difference or deprivation all do this.
• Patching in amblyopia. A patch over the good eye makes the weaker eye work; the stronger eye otherwise does everything.
• Unilateral amblyopia. It is defined by two or more lines of difference between the eyes on best corrected acuity.
• Eyelid hemangioma covering the visual axis. The priority is prompt referral to prevent amblyopia, because the obstruction has to be cleared while vision can still develop.

Also tested

• Timing of cataract surgery. Surgery can be deferred until the cataract affects daily life, unless another eye disease forces the issue.
• Cataract referral urgency. A cataract with uveitis in the same eye needs urgent referral, whereas an isolated cataract is a routine referral.
• Recovery after cataract surgery. Recovery is prompt and near-complete in almost all isolated cases, with complications infrequent overall.
• Improved near vision with nuclear cataract. The lens shifts toward myopia, so suddenly reading without glasses is explained, because nuclear change blurs distance more than near.
• Absent red reflex in an infant. It demands urgent ophthalmology referral, because cataract and retinoblastoma both present this way.
• Age and amblyopia treatment. Treatment works less well as maturity approaches; the earlier amblyopia is treated, the better the outcome.
• Manifest misalignment in a child. An eye that turns inward, with the other eye moving to take up fixation on the cover test, needs referral to ophthalmology to prevent amblyopia.
• Deciding on cataract surgery. The decision is driven by the effect on daily functioning, that is, symptoms and function, rather than by an acuity threshold alone.
• Improved near vision in cataract. A myopic shift from nuclear sclerosis ('second sight') explains it: the hardening lens increases its refractive power.
• Cataract that blocks the retinal exam. Surgery is needed to see behind it, because the cataract blocks diagnosis of other eye disease.
• Posterior vitreous detachment. Cataract surgery, myopia and ocular trauma all make it more likely.

Also tested

• Treatment of cataract. Surgery to replace the lens, deferred until the cataract interferes with daily activities.
• Posterior capsule opacification. Vision clouds again after cataract surgery because residual lens epithelial cells cloud the capsule.

Also tested

• Delayed appointment for suspected retinoblastoma. Call the specialist and get the appointment brought forward, and document the request if they will not.
• Untreated retinoblastoma. It is almost always fatal, which is why referral cannot wait.
• Biopsy in suspected retinoblastoma. Biopsy is avoided because it risks seeding tumor cells, so diagnosis rests on examination and imaging.
• Presentation of retinoblastoma. The two most common presenting features are leukocoria (a white pupil) and strabismus (a squint).
• Bilateral retinoblastoma. It implies a heritable germline mutation, with implications for siblings and for second malignancies.

Also tested

• Iris lesion size concerning for melanoma. A lesion over 3 mm across and over 1 mm deep raises concern for melanoma; a nevus is usually smaller and flat.
• Uveal melanoma outlook by site. Iris melanoma carries a better outlook than ciliary body melanoma, with roughly 4 to 10 percent mortality for the iris against far worse for the ciliary body.
• Growing vascular iris lesion. A raised pigmented iris lesion with a feeder vessel that has grown raises real concern and warrants referral to ophthalmology, likely ocular oncology.
• Ciliary body versus iris melanoma. Ciliary body melanoma does worse because it is hidden and found later, whereas an iris lesion is visible and caught earlier.
• Stable iris nevus. The risk of transformation to cancer is low, but surveillance continues because the risk is not zero.
• Enlarging vascular conjunctival lesion. A raised pigmented conjunctival lesion that has enlarged and has its own feeding vessels needs urgent referral for biopsy, since growth and intrinsic vascularity are the concerning features.
• Stable flat pigmented iris lesion. A lesion unchanged on photographs over five years, with no pupil distortion, is managed with photographic monitoring, as documented stability supports a benign nevus.
• Treated choroidal melanoma follow-up. Surveillance for liver metastasis, because the liver is where it goes.
• Raised pigmented choroidal lesion. With orange pigment and associated subretinal fluid, the next step is urgent ophthalmology referral; orange pigment, thickness and subretinal fluid separate melanoma from a benign nevus.
• Small flat uniformly pigmented choroidal lesion. With drusen on its surface and no subretinal fluid, management is photographic surveillance; flatness, drusen and absent fluid all favor a benign nevus.
• Iris freckles. Flat, multifocal, bilateral surface pigment on the irides, with no stromal involvement.

Also tested

• Small flat pigmented iris spot. A flat, 2 mm, avascular pigmented iris spot is likely benign but should be referred to ophthalmology to document and monitor, as a baseline is needed.
• Enlarging pigmented conjunctival lesion. Refer to ophthalmology for assessment, because growth in a pigmented lesion demands specialist review.
• Iris nevus follow-up. Surveillance with dilated review is more frequent at first, then annual; the early checks confirm the nevus is not growing.
• Ocular trauma red flag. A relative afferent pupillary defect converts a routine review into an emergency referral, because it indicates optic nerve compromise.

Also tested

• Embedded object in the eye. Leave it in place and arrange surgical repair, because it may be tamponading the wound and removal risks extruding intraocular contents.
• Ocular trauma. Dilating the pupil must be avoided in any suspected ocular trauma, because it removes the pupil examination, one of the few windows onto the inside of the eye.
• Ocular trauma epidemiology. Ocular trauma is the leading cause of monocular blindness in young adult men in the United States, so eye protection matters most for them.
• Possible intraocular metal fragment. Computed tomography of the orbit is ordered, since it answers the question without moving the fragment.
• Lid laceration with globe risk. The globe beneath is assessed before any lid repair, since two thirds of full-thickness lid lacerations have an accompanying globe injury.
• Automatic imaging after facial trauma. Anticoagulation (such as warfarin) and confusion both make imaging automatic; computed tomography without contrast is the choice.
• Periorbital penetrating injury. Penetration with metal or organic material carries tetanus risk, so confirm that tetanus immunization is up to date.

Also tested

• Mechanism in ocular trauma. Whether the injury was blunt or sharp, and high or low velocity, most changes the level of concern, because it predicts the injury pattern.

Also tested

• Suspected globe rupture. Immediate management is a rigid shield, nil by mouth, antiemetics and urgent referral; avoid anything that raises intraocular pressure and apply no pressure to the eye.
• Deferring lensectomy after full-thickness eye wall laceration. It is often deferred to let the hyphema and inflammation settle and to measure accurately for an implant.
• Antiemetics in suspected open globe. They are given alongside analgesia because vomiting raises intraocular pressure; keeping the patient from straining protects the eye.
• Suspected open globe. Alongside the shield, give antiemetics, analgesia and tetanus, and obtain computed tomography; keeping the patient from straining protects the eye.
• Lensectomy timing in open globe injury. Lensectomy for a cut lens capsule is required but usually deferred from the globe repair, being performed later once hyphema and inflammation settle.
• Globe rupture. A soft eye with massive hemorrhagic chemosis after blunt force is a globe rupture until proven otherwise; shield the eye and call ophthalmology.
• Globe rupture sites. Ruptures commonly occur behind the muscle insertions, especially superonasally, and also along incisions from earlier intraocular surgery and at the lamina cribrosa.
• Corneal laceration with iris prolapse. Do not attempt repositing the prolapsed iris; manipulation risks further extrusion and infection. Shield the eye and refer in the emergency department.
• Globe rupture risk. Previous intraocular surgery makes rupture more likely at lower force, because old incisions leave a permanent weak point.
• Lens capsule laceration. The lens becomes hydrated, edematous and opaque, as aqueous entering the capsule clouds it.
• Globe rupture. A peaked, teardrop-shaped pupil points toward the rupture site, and the anterior chamber deepens with a posterior rupture.

Also tested

• Corneal abrasion follow-up. Periodic re-examination is required, alongside a topical broad-spectrum antibacterial, to confirm healing and exclude infection.
• Uncomplicated corneal abrasion. A well-defined epithelial defect with no infiltrate is treated with topical antibiotic ointment and analgesia, with follow-up to confirm healing.
• Numbing drops for corneal abrasion. They should not be given to take home, because repeated use is toxic and delays healing, and it masks worsening infection.
• Rust ring. A rust ring remaining after removal of a metallic foreign body is removed with a burr tip drill.
• Conjunctival foreign body. One visible on diffuse light examination is removed with a cotton-tipped applicator, since a conjunctival object lifts off with a swab.
• Corneal abrasion at home. Give analgesia and a topical antibiotic; take-home anesthetic delays healing, masks worsening symptoms and can cause a corneal ulcer.
• Metallic corneal foreign body with rust ring. Remove it and the rust ring, then give antibiotics. The rust ring is removed too, as it perpetuates inflammation.
• After removing a superficial corneal foreign body. Check that there is no deeper injury, because a superficial fragment can accompany a penetrating one.
• Vertical linear corneal scratches. Evert the upper lid to find the object; vertical linear defects mean it is in the tarsal conjunctiva of the upper lid, scraping with each blink.
• Corneal rust ring. A rust ring from iron or copper is removed with a battery-operated burr.
• Corneal abrasion that worsens. Worsening pain and a white spot on the cornea mean a corneal ulcer has developed. This is why abrasions are re-examined, and why anesthetic drops are never sent home.
• Corneal foreign body. Photophobia, tearing and foreign body sensation with nothing on diffuse light call for slit lamp examination as the next step: larger objects show on diffuse light, smaller ones need the slit lamp.

Also tested

• Hyphema instructions. Strenuous activity and bending must be avoided, as both raise the risk of rebleeding.
• Hyphema management. Use upright positioning, a rigid shield and urgent ophthalmology review; keeping the head up lets the blood settle inferiorly and clear the visual axis.
• Hyphema with sickle cell disease. Sickle cell anemia raises the risk of complications in hyphema, where a secondary hemorrhage can cause permanent visual loss.
• Hyphema screening. Sickle cell testing is particularly important in a patient of African ancestry; sickling in the anterior chamber obstructs outflow and raises pressure at lower blood volumes.
• Hyphema. A layer of blood with a fluid level in the anterior chamber is hyphema, and it can itself indicate an open globe; it is not always an isolated injury.
• Hyphema discharge instructions. Avoid aspirin, antiplatelets and straining, since both raise the risk of a secondary hemorrhage.
• Complication of traumatic hyphema. Patients are monitored for rebleeding with a rise in intraocular pressure; the rebleed risk peaks in the first three to five days.

Also tested

• Lid margin laceration. A laceration through the lid margin needs specialist repair with meticulous approximation, because a poor repair leaves a permanent notch and chronic irritation.
• Lid laceration near the medial canthus. The canalicular drainage may be cut, and a missed canalicular injury leaves the person tearing for life.
• Simple orbital contusion. When vision, pupils, eye movements and the globe are all normal, management is supportive: ice, analgesia and review if symptoms change.
• Delayed facial laceration closure. A facial laceration may be left open for 24 hours before closure because the face is highly vascular, which is what permits the delay.
• Partial-thickness lid laceration. One meeting none of the referral criteria is repaired at the initial site, with ophthalmology follow-up in 2 to 3 days; it does not need the specialist to close it.
• Periorbital swelling and ecchymosis after trauma. Beyond supportive care, brain trauma should be excluded, because the force that bruised the orbit reaches the brain.
• Full-thickness lid laceration. Beyond repairing the lid, the globe underneath must be examined, because about two thirds of these lacerations come with a globe injury.
• Lid lacerations repairable in the emergency department. A superficial skin cut sparing the margin can be repaired there; partial-thickness lacerations meeting none of the referral criteria are repaired in the emergency department.
• Black eye after a punch. A relative afferent pupillary defect makes it more than a simple contusion; it indicates optic nerve involvement and changes the urgency entirely.
• Orbital contusion versus periorbital hematoma. Contusion has no hemorrhage; the hematoma bleeds in the orbit. The septum is what keeps the contusion in front of the eye.
• Lid laceration referral. A laceration through the lid margin goes to ophthalmology, because margin involvement is one of the explicit referral criteria.
• Orbital and lid contusion. Lid bruising and swelling with normal vision, equal reactive pupils and full eye movements indicate soft tissue injury with normal ocular function.
• Orbital contusion. Blunt injury fills the surface with hemorrhage and swells the lids, with no open wound.

Also tested

• Macular involvement in retinal detachment. Field defects come first; a drop in central visual acuity indicates that the macula has become involved.
• Retinal detachment urgency. A fresh detachment must be seen by an ophthalmologist within 24 hours; the referral is immediate.
• Retinal detachment presentation. Flashes of light, a shower of floaters and a curtain moving across the vision of one eye, with myopia as the risk factor, suggest rhegmatogenous retinal detachment.
• Rhegmatogenous retinal detachment. The most common type of retinal detachment: full-thickness retinal breaks let liquefied vitreous behind the retina.

Also tested

• Blowout fracture with entrapment. Urgent surgical referral is required because entrapped muscle becomes ischemic and fibroses, and delay risks permanent restriction of eye movement.
• Orbital floor fracture without entrapment or ocular injury. Management is ice, analgesia and review in two to three days.
• Orbital floor fracture. Patients are advised not to blow the nose because it forces sinus air into the tissues; periorbital subcutaneous emphysema is a recognized feature of this fracture.
• Suspected orbital fracture. Computed tomography of the orbits and midface is the imaging study for this fracture.
• Orbital floor fracture with inferior rectus entrapment. A facial trauma surgeon is contacted urgently, because an entrapped muscle can necrose if its blood supply is compromised.

Also tested

• Basilar skull fracture. After head trauma, raccoon eyes, Battle sign and hemotympanum together should raise suspicion of a basilar skull fracture; they are the indirect signs.
• Basilar skull fracture. Suggested by raccoon eyes (bruising around both eyes), Battle sign (bruising behind the ear) and hemotympanum (blood behind the eardrum) together.