Side Effects of Medications Flashcards
Amiodarone. What is it?
<ul> <li>Medication used to control heart rhythm disturbances</li> <li>Ophthalmic side effect: whorl opacities in cornea (cornea verticillata)</li> <li>Usually does not disturb vision </li> <li><a>Ischemic optic neuropathy</a> linked to amiodarone use, but evidence of causation weak</li> </ul>
Amiodarone. How does it appear?
<ul> <li>Patients usually have no visual symptoms</li> <li>May rarely report mildly blurred vision or haloes </li> <li><a>Curved golden brown or gray-white lines</a> originate below center of cornea in both eyes </li> <li>Visible to naked eye but better seen with slit lamp </li> <li>Corneal whorls are subepithelial phospholipid deposits </li> </ul>
Amiodarone. What else looks like it?
<ul> <li>Fabry disease: glycolipidosis caused by deficiency of the alpha-galactosidase A, but... </li> <li>Patients with Fabry disease have characteristic visceral and vascular manifestations </li> </ul>
Amiodarone. How do you manage it?
<ul> <li>Be aware that these deposits are signature of amiodarone use but have no other medical importance</li> <li>Be aware that medical literature links ischemic optic neuropathy to amiodarone use, so if patient has only one sighted eye, consult ophthalmologist about prescribing amiodarone</li> <li>If patient develops sudden vision loss, refer to ophthalmologist to rule out ischemic optic neuropathy</li> </ul>
Amiodarone. What will happen?
<ul> <li>Corneal whorls appear within months of starting medication and disappear within months of stopping it</li> <li>Litigation has occurred against physician prescribers of amiodarone, alleging that this medication causes ischemic optic neuropathy, but evidence not convincing</li> </ul>
Anticholinergics. What is it?
<ul> <li>Systemically-administered medications used to treat gastric distress, spastic bladder, and side effects of anti-psychotic medications</li> <li>Most common ophthalmic side effect: loss of accommodation ("iatrogenic <a>presbyopia</a>")</li> <li>Loss of accommodation results from paralysis of ciliary muscle</li> <li>Topical installation (but not systemic use) may rarely provoke <a>angle-closure glaucoma</a></li> </ul>
Anticholinergics. How does it appear?
<ul> <li>Blurred vision at reading distance in patients aged under 55 years</li> <li>Slightly dilated pupils that constrict weakly to bright light</li> <li>Elevated intraocular pressure if <a>angle-closure glaucoma</a> has occurred </li> </ul>
Anticholinergics. What else looks like it?
<ul> <li>Anticholinergics accidentally or deliberately instilled in eyes, but they cause more widely dilated pupils that will not constrict to bright light </li> <li>Common offenders: scopolamine patch for seasickness, aerosolized medications for respiratory secretions, plant substances, or cycloplegic eye drops (atropine, homatropine, scopolamine, cyclopentolate, tropicamide)</li> <li>Systemic dysautonomias can mimic effects of anticholinergic medications</li></ul>
Anticholinergics. How do you manage it?
<ul> <li>Anticipate loss of accommodation and warn patients that reading glasses may be necessary</li> <li>Recognize that dilated pupils may result from accidental contact and cause unnecessary alarm, especially in patients on respiratory therapy </li> <li>Recognize that unacknowledged instillation of anticholinergic medications may be part of factitious illness</li> </ul>
Anticholinergics. What will happen?
<ul> <li>Blurred vision at reading distance can be fully corrected with glasses</li> </ul>
Bisphosphonates. What is it?
<ul> <li>Medications that inhibit bone resorption and are used to prevent osteoporosis</li> <li>Most commonly used medications: pamidronate, alendronate, risedronate</li> <li>Most common ophthalmic side effects: <a>acute conjunctivitis</a>, <a>anterior uveitis</a>, orbital myositis, <a>episcleritis</a>, <a>scleritis</a> within days to weeks of starting medication </li> </ul>
Bisphosphonates. How does it appear?
<ul> <li>Eye pain</li> <li>Blurred and double vision</li> <li>Red eye</li> <li>Lid swelling</li> <li>Proptosis</li> </ul>
Bisphosphonates. What else looks like it?
<ul> <li><a>Orbital cellulitis</a></li> <li><a>Idiopathic orbital inflammation</a></li> <li><a>Graves disease</a></li> <li><a>Conjunctivitis</a></li> <li><a>Episcleritis</a></li> <li><a>Scleritis</a></li> </ul>
Bisphosphonates. How do you manage it?
<ul> <li>Anticipate these ophthalmic manifestations </li> <li>Refer to ophthalmologist urgently</li> </ul>
Bisphosphonates. What will happen?
<ul> <li>Discontinuing medication brings about recovery, but...</li> <li>Treatment with topical or oral corticosteroid or nonsteroidal anti-inflammatory drug (NSAID) often needed to hasten relief </li> </ul>
Chloroquine and Hydroxychloroquine. What is it?
<ul> <li>Chloroquine prevents malaria</li> <li>Hydroxychloroquine treats rheumatic illnesses</li> <li>Most common ophthalmic side effect: damage to retinal pigment epithelium, causing irreversible vision loss</li> <li>Retinal toxicity uncommon with chloroquine and even less common with hydroxychloroquine as long as proper dose limits observed</li> <li>Ophthalmologic monitoring protects against severe toxicity</li> </ul>
Chloroquine and Hydroxychloroquine. How does it appear?
<ul> <li>Blurred vision in both eyes</li> <li>Pericentral scotomas on special visual fields </li> <li>Fading of orange color of retina around fovea ("<a>bull’s eye maculopathy</a>"), appearing well after visual symptoms begin</li> <li>Optical coherence tomography and multifocal electroretinography may reveal abnormalities before they are visible with ophthalmoscope and perhaps even before patient develops symptoms</li> </ul>
Chloroquine and Hydroxychloroquine. What else looks like it?
<ul> <li>Genetically-determined storage diseases</li> <li>Healed choroiditis</li> </ul>
Chloroquine and Hydroxychloroquine. How do you manage it?
<ul><li>Have patients treated with chloroquine undergo baseline ophthalmic examination and be monitored by ophthalmologist every 3-6 months after starting it </li> <li>Have patients treated with hydroxychloroquine undergo baseline ophthalmic examination and be monitored yearly starting at 5 years of medication use </li><li>Keep chloroquine daily dose at <u><</u>3 mg/kg/day and cumulative dose at <u><</u>460 gm to reduce chances of retinopathy </li> <li>Keep hydroxychloroquine daily dose at <u><</u>5.0mg/kg/day and cumulative dose at <u><</u>1000gm to reduce chances of retinopathy </li> <li>Recognize that patients with renal failure are at unusually high risk of retinal toxicity </li> <li>Stop medication at first suggestion of retinal toxicity </li> </ul>
Chloroquine and Hydroxychloroquine. What will happen?
<ul> <li>Chloroquine and hydroxychloroquine retinopathy rare if recommended dose limits followed </li> <li>Once visual symptoms develop, they cannot be reversed, and may worsen even if medication stopped</li> <li>Monitoring with visual fields, optical coherence tomography, and electroretinography allows earlier detection of toxicity and may prevent disabling vision loss</li> </ul>
Cyclosporine. What is it?
<ul> <li>Calcineurin inhibitor (includes tacrolimus and sirolimus) that fights organ transplant rejection and autoimmune disorders </li> <li>Most common ophthalmic side effect: posterior reversible encephalopathy syndrome (PRES) producing binocular vision loss</li> <li>Caused by toxicity to vascular endothelium and high blood pressure, which provoke vascular leakage into brain</li> <li>Damage greatest in distribution of posterior cerebral artery</li> </ul>
Cyclosporine. How does it appear?
<ul> <li>Acute or subacute onset of visual impairment</li> <li>Unilateral or bilateral homonymous hemianopia</li> <li>Normal eye examination </li> <li>Confusional state</li> <li>Headache</li> <li>Seizures</li> <li>High blood pressure</li> <li><a>High T2/FLAIR MRI signal</a> concentrated around visual cortex</li> <li>No abnormalities on <a>diffusion-weighted MRI</a></li></ul>
Cyclosporine. What else looks like it?
<ul> <li>Stroke</li> <li>Hypertensive encephalopathy</li> <li>Reversible cerebal vasoconstriction (Call-Fleming) syndrome</li> <li>Non-convulsive status epilepticus</li> <li>Dural venous sinus thrombosis</li> <li>Encephalitis</li> <li>Posterior ischemic optic neuropathy</li> <li>Occult retinopathy</li> <li>Pituitary apoplexy</li> </ul>
Cyclosporine. How do you manage it?
<ul> <li>Anticipate this common side effect </li> <li>Refer urgently to ophthalmologist or emergency room</li> </ul>
- Medication must be promptly discontinued and blood pressure lowered
- These measures will lead to recovery within days, but...
- If PRES has persisted for too long, stroke may occur, producing permanent occipital blindness, so...
- Diagnosis is urgent!
- Medication that binds iron and treats iron overload occurring after frequent blood transfusions
- Most common ophthalmic side effect: damage to retinal pigment epithelium, photoreceptors, retinal ganglion cells
- Patient complains of impaired visual acuity, visual field, night vision, color vision
- Symptoms develop after acute or chronic administration of deferoxamine
- Ophthalmoscopy normal at symptom onset
- Ophthalmoscopy later shows fine retinal speckled pigmentation or pale optic discs
- Once ophthalmoscopic signs have appeared, visual dysfunction may be irreversible even if medication stopped
- Electroretinography detects abnormalities before ophthalmoscopy
- Hereditary photoreceptor dystrophy ("retinitis pigmentosa")
- Toxicity from thioridazine
- Congenital rubella syndrome
- Refer patients for baseline ophthalmological examination before starting medication
- Refer for reexamination every three months while on treatment
- Refer promptly for reexamination if patient develops visual symptoms
- If toxicity diagnosed early, visual loss may be reversible or non-disabling
- Medication must be stopped at diagnosis of ocular toxicity and later resumed at lower dose or replaced with alternative iron chelator, depending on visual manifestations
- Medication used to treat mycobacterial diseases, including tuberculosis
- Most common ophthalmic side effect: bilateral optic neuropathy
- Optic neuropathy develops in 2% to 5% treated with more than 15mg/kg/day, and in up to 25% treated with more than 25mg/kg/day
- Slowly progressive visual loss in both eyes, appearing within 3 months of starting medication
- Reduced visual acuity in both eyes
- Central scotomas on visual field testing
- Reduced color vision
- Ophthalmoscopy normal at first, later disclosing mildly pale optic discs at their temporal portions
- May be mistaken for cataract or uncorrected refractive error
- Other optic neuropathies
- Refer patient for baseline eye examination
- Repeat ophthalmic examinations every 3 months while patient being treated
- Avoid daily doses of greater than 15mg/kg especially in those with impaired kidney function
- Discontinue medication promptly if optic neuropathy discovered
- Visual loss irreversible and may worsen after medication discontinued, so...
- Early detection critical to preserve vision
- Delayed diagnosis common because visual loss symmetrical, very slowly progressive, and painless
- Antibiotic derived from tetracycline used against wide variety of bacteria
- Treats refractory acne vulgaris
- Most common ophthalmic side effect: papilledema (from increased intracranial pressure)
- Headache, neck pain, transient or persistent loss of vision, and...
- Loss of vision even WITHOUT headache or other symptoms
- Symptoms begin within weeks to months after starting standard doses of minocycline
- Swollen optic discs (papilledema)
- Visual fields abnormal, reflecting axonal damage from chronically elevated intracranial pressure
- Brain imaging normal
- Lumbar puncture discloses high opening pressure and normal cerebrospinal constituents
- Isotretinoin-induced increased intracranial pressure
- Idiopathic intracranial hypertension (pseudotumor cerebri)
- Brain tumor
- Meningitis
- Hydrocephalus
- Optic neuritis
- Ischemic optic neuropathy in giant cell arteritis
- Compressive or infiltrative optic neuropathy from cancer
- Refer promptly to ophthalmologist any patient with visual symptoms and/or headache who is using minocycline
- Consider baseline ophthalmologic screening and routine screening every 3-6 months because papilledema can exist at first without causing visual symptoms
- Vision loss may be delayed because axonal damage in papilledema proceeds slowly and initially spares visual acuity
- Vision loss reversible if papilledema detected early
- Vision loss permanent and disabling if papilledema detected late
- Corticosteroid used to treat inflammatory conditions
- Most common ophthalmic side effect: posterior subcapsular cataract, developing in 25% of patients who use prednisone 15 mg/day for 1 year or more, or equivalent doses of other corticosteroids
- Slowly progressive visual loss in both eyes, but may be asymmetric in two eyes
- Opacity on posterior portion of crystalline lens, usually visible only with ophthalmoscope or slit lamp biomicroscope
- Cataract as part of aging, intraocular inflammation, eye trauma
- Refractive error, retinal or visual pathway disorder
- Warn patients that cataract is likely complication of chronic prednisone use
- Refer patients who report visual impairment and are using prednisone chronically
- Discontinuing prednisone does not reverse cataract but may halt its progression
- Cataract extraction has high chance of restoring vision provided there are no other causes of vision loss
- Phosphodiesterase inhibitor used to treat erectile dysfunction or prolong normal erection
- Most common ophthalmic side effect: temporary alteration in vision, presumed to be effect on retinal photoreceptors or their connections
- Possible ophthalmic side effect: ischemic optic neuropathy
- Ophthalmic side effects reported for all phosphodiesterase inhibitors
- Blurred, bright, dim, blue discoloration of vision starting within 30 minutes of taking medication and ceasing within hours
- Sudden, persistent loss of vision occurring within 24 hours of medication use, associated with swollen optic disc and afferent pupil defect in ischemic optic neuropathy
- Temporary alteration in vision has no other explanation
- Persistent vision loss may be caused by ischemic optic neuropathy unrelated to phosphodiesterase inhibitor use, non-ischemic optic neuropathy, or retinopathy
- Reassure patient that alteration in vision common, temporary, and benign
- Refer to ophthalmologist urgently any patient with persistent vision loss occurring within day of using medication
- Warn users that ischemic optic neuropathy has been associated with phosphodiesterase inhibitor use and discourage its use in those with only one sighted eye
- Discoloration of vision always temporary, may recur with repeated phosphodiesterase inhibitor use, but causes no permanent vision impairment
- Ischemic optic neuropathy causes irreversible and untreatable vision loss
- Medication used to treat some forms of breast cancer
- Most common ophthalmic side effect: accumulation of white crystalline deposits around fovea
- Less common ophthalmic side effect: blurred vision from cystoid macular edema mostly in patients treated with 120mg twice daily and after cumulative dose of 100gm
- Perifoveal white crystalline deposits
- Blurred vision
- Cystoid macular edema
- Macular hard exudates in diabetes mellitus
- Hereditary maculopathy
- Cystoid macular edema of other causes
- Perform baseline ophthalmic examination if treatment with high doses is anticipated
- Refer patient with visual symptoms
- Discontinue medication if tamoxifen retinopathy confirmed
- Visual loss usually reversible
- Crystalline deposits sometimes reversible
- Selective alpha-1A antagonist used to treat symptoms in benign prostatic hypertrophy
- Most common ophthalmic side effect: floppy iris syndrome
- Dome-shaped anterior displacement of iris
- Prolapse of iris during cataract surgery, requiring special measures to prevent surgical complications
- Occurs in up to 60% of patients
- Nothing
- Discontinue medication within week of anticipated intraocular surgery
- Floppy iris syndrome must be anticipated by cataract surgeon to avoid complications
- Special maneuvers usually allow safe lens extraction
- Medication used to treat seizures and migraine
- Most common ophthalmic side effect: angle-closure glaucoma caused by edema of the ciliary body
- Incidence of this side effect estimated at 2%
- Sudden eye pain
- Blurred vision
- Red eye with ciliary flush
- Hazy cornea
- Shallow anterior chamber (note that iris surface nearly touches peripheral cornea); compare to normal depth of anterior chamber
- Angle-closure well shown on ultrasound; compare to normal anterior chamber depth
- Avoid prescribing topiramate if ophthalmologist has documented that patient has narrow anterior chamber angle
- Refer emergently to ophthalmologist any patient with acute eye pain or visual symptoms who is taking topiramate
- Discontinue topiramate if angle closure glaucoma is confirmed
- Intraocular pressure must be lowered promptly with aqueous suppressants, cycloplegia, topical corticosteroids
- Peripheral iridectomy, standard approach to angle closure glaucoma not caused by topiramate, does not work here
- Permanent vision loss has resulted from angle closure precipitated by topiramate even when diagnosis and treatment are undertaken promptly
- Anti-epileptic agent used mainly for refractory childhood seizure disorder called infantile spasms
- Most such children are cognitively impaired
- Ophthalmic side effect: visual field constriction
- Attributed to effect of excess neurotransmitter GABA on retinal photoreceptors and ganglion cells
- Children do not report symptoms because they are neurologically impaired and vision deficits are subtle
- Ophthalmoscopy normal unless damage advanced
- Visual field constriction and optic disc pallor indicate advanced damage
- Electroretinography may disclose abnormalities
- Try not to exceed daily dose of 100mg/kg
- Withdraw this medication if ineffective
- FDA requires that children undergo baseline and serial ophthalmic examinations, but
- These children not able to cooperate for visual function testing or electroretinography, so...
- Serial ophthalmoscopy may be only way to monitor for retinal toxicity, yet...
- Ophthalmoscopy insensitive to toxicity
- Peripheral visual field loss may occur but unlikely to be disabling, and...
- Visual field loss may be reasonable trade-off for seizure control
