Marcus Gunn PupilMANAGEMENT

ENT AND MAXILLOFACIAL PRESENTATIONS · 12 SECTIONS

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736 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Acute laryngitis Acute pharyngitis Auricular hematoma Bezold's Abscess Cerumen impaction Dry socket Ear foreign body Epistaxis (anterior)Epistaxis (Posterior)Labyrinthitis Ludwig's Angina Malignant Otitis Externa Marcus Gunn Pupil Mastoiditis Meniere's Disease Nasal Bone Fracture Nasal foreign body Nasal Septal Hematoma Otitis externa Otitis Media Post-tonsillectomy hemorrhage Sialolithiasis and sialadenitis Sinusitis Sudden Sensorineural Hearing Loss TMJ dislocation Tympanic membrane perforation Vestibular Neuronitis

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp40

Vision-threatening emergencies

›Cannot-miss emergencies requiring immediate action

›Central retinal artery occlusion

›Stroke equivalent with 4.5-hour thrombolysis window

›Sudden painless profound vision loss

›Activate stroke protocol immediately

›Giant cell arteritis with vision loss

›Age >50 with jaw claudication, scalp tenderness, headache

›Risk of bilateral blindness within days if untreated

›Initiate empiric IV methylprednisolone without delay; do not wait for biopsy

›Compressive optic neuropathy from mass lesion

›Progressive vision loss with proptosis or focal neurologic signs

›Neurosurgical consultation urgently

›Traumatic optic neuropathy

›RAPD in setting of head or facial trauma

›Poor prognostic sign for visual recovery

›Intracranial mass with midbrain compression

›New RAPD with altered consciousness or focal neurologic deficits

›Emergent CT head

Monitoring and escalation

›Key monitoring parameters

›Visual acuity each eye separately at presentation and after treatment

›Decline despite treatment triggers urgent ophthalmology

›Contralateral eye vision status

›New involvement indicates bilateral disease progression

›Neurologic status

›Focal weakness, speech, level of consciousness

›Deterioration triggers CT or MRI urgently

02History/hx87

Onset and tempo of vision loss

›Temporal pattern

›Acute onset over seconds

›Central retinal artery occlusion highest concern

›Amaurosis fugax suggests embolic source

›Subacute over hours to days

›Optic neuritis classic tempo

›Ischemic optic neuropathy

›Progressive over weeks to months

›Compressive lesion: meningioma, glioma, pituitary adenoma

›Advanced asymmetric glaucoma

Symptom characterization

›Pain assessment

›Retro-orbital pain worsening with eye movement

›Highly suggestive of optic neuritis

›Temporal headache

›Giant cell arteritis concern

›Painless vision loss

›Ischemic or compressive etiology more likely

›Visual symptom pattern

›Flashes, floaters, curtain defect

›Retinal detachment

›Central scotoma

›Optic neuritis or macular disease

›Altitudinal field loss

›Ischemic optic neuropathy

›Color desaturation

›Optic neuropathy of any cause

Associated symptoms and review of systems

›Neurologic symptoms

›Focal weakness, numbness, gait disturbance

›MS or other demyelinating disease

›Prior episodes of neurologic symptoms

›Relapsing-remitting pattern of MS

›Rheumatologic and systemic symptoms

›Jaw claudication

›Pathognomonic for GCA

›Scalp tenderness over temporal region

›GCA

›Polymyalgia rheumatica symptoms: shoulder and hip girdle pain

›Strongly associated with GCA

›Fever, weight loss, night sweats

›GCA, malignancy, sarcoidosis

›Vascular history

›Prior TIA or stroke

›Embolic source for retinal artery occlusion

›Cardiovascular risk factors

›Hypertension, diabetes, dyslipidemia, smoking, atrial fibrillation

Risk factors

›Demographic and disease-specific risk

›Optic neuritis risk profile

›Young women, median age 31, 3:1 female predominance

›MS history or family history

›Non-arteritic ischemic optic neuropathy risk profile

›Age >50, hypertension, diabetes, hyperlipidemia

›Small crowded optic disc (disc at risk)

›Obstructive sleep apnea

›GCA risk profile

›Age >50, female sex 6:1 ratio, Northern European descent

›Polymyalgia rheumatica history

›Retinal artery occlusion risk profile

›Atrial fibrillation, carotid stenosis, hypercoagulable states

›Retinal detachment risk profile

›High myopia (>=−6.0 diopters), prior cataract surgery, trauma, diabetes

›Compressive optic neuropathy risk

›Neurofibromatosis type 1 for optic glioma

›Prior intracranial malignancy

Medication and toxic exposure history

›Toxic optic neuropathy agents

›Ethambutol

›TB treatment duration and dose monitoring

›Methanol exposure

›Illicit alcohol, solvent exposure

›Linezolid with prolonged use

›Optic neuropathy risk with courses >28 days

›Nutritional factors

›Vitamin B12 deficiency

›Alcoholism, vegan diet, malabsorption

›Folate deficiency

›Tobacco-alcohol amblyopia

Family and collateral history

›Family history

›MS or autoimmune disease

›Increased susceptibility

›Hereditary optic neuropathies

›Leber hereditary optic neuropathy (LHON): young males, painless

›Glaucoma

›Asymmetric disease can cause RAPD

›Collateral history

›Witnesses to onset timing

›Critical for CRAO: 4.5-hour thrombolysis window

›Social history: alcohol, tobacco, nutritional status

›Toxic and nutritional optic neuropathy risk

03Physical Exam/exam65

Swinging flashlight test

›Test performance (defining examination for RAPD)

›Dimly lit room, patient fixating on distant target

›Prevents accommodation-induced miosis confounding

›Bright light into one eye for less than 5 seconds

›Swing quickly to the other eye

›Normal response: both pupils constrict or maintain size

›Equal afferent input bilaterally

›Positive RAPD: affected pupil dilates when light swings to it

›Indicates reduced afferent input from that eye

›Grading: trace to 4+ based on magnitude of dilation

›Large RAPD has higher specificity for significant optic nerve disease

Visual function assessment

›Visual acuity

›Each eye separately with best correction or pinhole

›Pinhole corrects refractive error

›Persistent reduced acuity despite pinhole suggests structural disease

›Color vision and red desaturation

›Red cap test: patient compares redness of object between eyes

›Washed-out red in affected eye suggests optic neuropathy

›Sensitive for early or subtle optic nerve disease

›Confrontation visual fields

›Altitudinal defect

›Anterior ischemic optic neuropathy pattern

›Central scotoma

›Optic neuritis or macular disease

›Peripheral curtain loss

›Retinal detachment

04Differential Diagnosis/ddx64

Optic nerve causes

›Inflammatory and demyelinating

›Optic neuritis (MS-associated)

›ICD-10 H46.0

›Young women, subacute, painful, recovers over weeks

›NMOSD optic neuritis

›Severe bilateral or sequential optic neuritis

›AQP4-IgG seropositive

›MOGAD optic neuritis

›MOG-IgG seropositive

›Perioptic nerve sheath enhancement on MRI

›Sarcoidosis optic neuropathy

›Granulomatous infiltration of optic nerve

›Ischemic

›Arteritic anterior ischemic optic neuropathy (GCA)

›ICD-10 H34.231

›Disc edema, pale, sudden, age >50

›Non-arteritic anterior ischemic optic neuropathy (NAION)

›ICD-10 H47.01

›Altitudinal field defect, disc at risk, no pain

›Compressive

›Optic nerve sheath meningioma

›ICD-10 D32.0

›Slow progression, optociliary shunt vessels

›Optic glioma

›NF1 association in children

›Pituitary adenoma

›Bitemporal hemianopia, chiasmal compression

05Laboratory Tests/lt48

GCA and inflammatory workup

›Inflammatory markers for GCA

›Erythrocyte sedimentation rate (ESR)

›Markedly elevated in GCA (typically >50 mm/h)

›Normal ESR does not exclude GCA

›C-reactive protein (CRP)

›More sensitive than ESR for GCA activity

›Elevated CRP supports diagnosis

›Complete blood count with platelets

›Thrombocytosis supports GCA

›Anemia of chronic disease

Demyelinating and autoimmune workup

›Antibody panel for atypical optic neuritis

›AQP4-IgG (aquaporin-4 antibody)

›NMOSD: high specificity >99%

›Positive result changes treatment (avoid interferon beta, natalizumab)

›MOG-IgG (myelin oligodendrocyte glycoprotein antibody)

›MOGAD: distinct treatment and prognosis from MS

›ANA and anti-dsDNA

›Lupus-associated optic neuropathy

›ACE level

›Sarcoidosis screening

›RPR and FTA-ABS

›Syphilitic optic neuropathy

›Lyme serologies in endemic areas

›Lyme optic neuropathy

Vascular and embolic workup

›Stroke workup for CRAO

06Diagnostic Tests/dt87

Scoring Systems

›Optic Neuritis Treatment Trial (ONTT) risk stratification

›MRI brain lesion number predicts MS conversion risk

›Zero T2 lesions: 25% 15-year risk of MS

›One or more T2 lesions: 72% 15-year risk of MS

›Guides ophthalmology and neurology follow-up intensity

›High-risk features for MS conversion after optic neuritis

›Multiple white matter lesions on baseline MRI

›Oligoclonal bands in CSF

›Prior clinical demyelinating episodes

›GCA pre-test probability

›ACR/EULAR 2022 classification criteria components

›Age >=50: required

›Morning stiffness of shoulders or neck

›Sudden visual loss or diplopia

›Jaw or tongue claudication

›Scalp tenderness

›Elevated ESR >=50 mm/h or CRP >=10 mg/l

›Halo sign on temporal artery ultrasound

›Clinical diagnosis sufficient to initiate steroids

›Do not delay treatment for biopsy or imaging

›RAPD grading scale

›Subjective grading during swinging flashlight test

›Trace: barely perceptible pupillary escape

›1+: slight dilation

›2+: moderate dilation

›3+: marked dilation with brisk escape

›4+: paradoxical dilation without initial constriction

›Larger RAPD correlates with greater afferent pathway damage

MRI

›MRI brain and orbits with gadolinium contrast

›First-line imaging for suspected optic neuropathy

›Identifies optic nerve enhancement in optic neuritis

›Detects compressive lesions, pituitary masses, meningiomas

›Demyelinating plaques in periventricular, juxtacortical, infratentorial, spinal locations

›Enhancement pattern in optic neuritis

›Short-segment unilateral enhancement: MS-associated optic neuritis

›Long-segment or bilateral enhancement: MOGAD or NMOSD

›Perioptic nerve sheath enhancement: MOGAD characteristic pattern

›Orbital fat-suppressed sequences essential

›STIR and fat-saturated T1 post-contrast

›Identify optic nerve signal change and enhancement

›Brain MRI for MS risk stratification

›Recommended for all new optic neuritis even with typical presentation

›ACR Appropriateness Criteria: Usually Appropriate

›MRI spine when NMOSD or MOGAD suspected

›Longitudinally extensive transverse myelitis pattern for NMOSD

›MRI indications by clinical scenario

›Atypical optic neuritis features

›Severe, bilateral, or rapidly progressive

›Age >50 or no pain

›Poor or no visual recovery

›Compressive neuropathy concern

›Proptosis, restricted motility, disc pallor from outset

›CT head and CTA for vascular emergencies

›Emergent CT head for CRAO

›Rule out hemorrhagic stroke before thrombolysis

›Identify calcified emboli on non-contrast CT

›CT angiography (CTA) of head and neck

›Carotid stenosis and plaque

›Intracranial large vessel occlusion

›Sensitivity and specificity for carotid stenosis >70% high

›CT orbits in trauma

›Orbital wall fractures and retrobulbar hemorrhage

›Optic canal fracture in traumatic optic neuropathy

›Bone windows essential

›CT chest/abdomen/pelvis

›GCA with suspected aortic involvement

›Aortic aneurysm screening in confirmed GCA

›Malignancy workup for compressive lesions

›Staging CT for primary or metastatic tumor

Ultrasound

›Temporal artery ultrasound

›GCA: halo sign (hypoechoic rim around arterial lumen)

›Sensitivity 75-86% for GCA

›Specificity 90-96% for GCA

›Non-compressible halo: diagnostic for GCA in appropriate clinical context

›Bilateral examination of temporal arteries

›Axillary and subclavian arteries in suspected large vessel GCA

›Ocular B-scan ultrasound

›Retinal detachment when fundus view is obscured

›Cataract, vitreous hemorrhage, media opacity

›High sensitivity for retinal detachment detection

›Optic nerve sheath diameter

›Elevated intracranial pressure screen (>5.0 mm)

›Ultrasound pupillometry

›Objective RAPD quantification

›AUC of 1.0 for detecting acute optic neuritis vs controls

›Compares pupillary constriction amplitudes between eyes

›Not routinely available but emerging diagnostic tool

07Disposition/dispo42

Admission criteria

›Immediate hospital admission indications

›GCA with acute vision loss

›IV methylprednisolone protocol initiation

›Temporal artery biopsy coordination within 1-2 weeks of steroid start

›CRAO within thrombolysis window (4.5 hours)

›Stroke unit admission for IV alteplase consideration

›Cardiology monitoring for arrhythmia

›Traumatic optic neuropathy with concurrent head injury

›Neurosurgical monitoring

›High-dose steroid vs observation decision

›Suspected intracranial compressive lesion

›Neurosurgical consultation and monitoring

›Severe optic neuritis

›IV methylprednisolone administration

›MRI brain and orbits urgently

Urgent referral without admission

›Same-day ophthalmology referral

›Retinal detachment

›Surgical repair: vitrectomy, scleral buckle, or pneumatic retinopexy

›CRAO outside thrombolysis window

›Embolic workup coordination

›Cardiovascular risk factor management

›Acute angle-closure glaucoma with RAPD

›Laser peripheral iridotomy or surgical intervention

Discharge with close follow-up

›Outpatient management criteria

›Typical optic neuritis in young patient

08Treatment/t93

Optic neuritis treatment

›IV corticosteroid protocol

›IV methylprednisolone

›1 g IV daily for 3 days

›Accelerates visual recovery; does not improve final visual outcome

›Reduces short-term MS conversion risk

›Oral prednisone continuation

›1 mg/kg/day for 11 days after IV course

›3-day taper to completion

›Do not use low-dose oral prednisone alone: increases recurrence risk

›Oral bioequivalent alternative to IV

›Prednisone 1,250 mg/day for 3 days (oral bioequivalent)

›Use when IV access unavailable or outpatient preferred

›NMOSD and MOGAD optic neuritis

›High-dose IV methylprednisolone as above

›Often requires longer courses in NMOSD

›Plasma exchange for severe steroid-refractory cases

›5-7 sessions in NMOSD

›Avoid interferon-beta and natalizumab in NMOSD

›May worsen disease

Giant cell arteritis treatment

›Empiric corticosteroid protocol

›IV methylprednisolone pulse therapy

›15 mg/kg IV daily for 3 days for vision loss

›Then transition to oral prednisone

›Oral prednisone for GCA without acute vision loss

›>=1 mg/kg/day (typically 40-60 mg/day)

›Do NOT delay for temporal artery biopsy

›Biopsy remains diagnostic up to 2-4 weeks after steroid initiation

›Proton pump inhibitor gastroprotection

›Omeprazole 20 mg daily during steroid course

›Tocilizumab (IL-6 receptor inhibitor)

›Adjunct to prednisone for steroid-sparing

›162 mg subcutaneous weekly

›Class IIa recommendation, reduces relapse and cumulative steroid dose

Central retinal artery occlusion treatment

›Acute intervention within 4.5 hours

›IV alteplase thrombolysis

›0.9 mg/kg IV (maximum 90 mg)

›10% as IV bolus, 90% over 60 minutes

›Consult stroke neurology and ophthalmology

›Standard stroke management

›Antiplatelet therapy (aspirin 325 mg loading)

›ECG monitoring for atrial fibrillation

›Echocardiogram for cardiac embolic source

›Beyond thrombolysis window

›No proven acute vision-restoring therapy

›IOP-lowering maneuvers (digital massage, acetazolamide) of uncertain benefit

›Secondary stroke prevention

›Antiplatelet or anticoagulation based on embolic source

›Statin therapy

›Cardiovascular risk factor management

Retinal detachment treatment

›Surgical repair options

›Pneumatic retinopexy

›Office-based, for superior retinal breaks

›Intraocular gas tamponade

›Scleral buckle

›Encircling or segmental

›For complex detachments or inferior breaks

›Vitrectomy

›Complex detachments, PVR, giant retinal tears

›Hospital-based procedure

›Urgent ophthalmology referral mandatory

›Macula-off detachment: within hours

Traumatic optic neuropathy treatment

›Treatment options (controversial)

›High-dose corticosteroids

›Methylprednisolone 30 mg/kg IV bolus, then 5.4 mg/kg/h for 23 hours

›Evidence weak; International Optic Nerve Trauma Study: no benefit over observation

›Risk-benefit discussion with neurosurgery and ophthalmology

›Surgical decompression of optic canal

›Endoscopic or craniotomy approach

›For compressive hematoma or bony impingement

›Observation

›Reasonable when no mass lesion or compressive component

›Spontaneous recovery possible

NAION treatment

›No proven acute treatment

›Cardiovascular risk factor modification

›Blood pressure control to goal

›Glycemic control (HbA1c <7%)

›Statin therapy for dyslipidemia

›Obstructive sleep apnea treatment

›CPAP therapy reduces risk of fellow eye involvement

›Avoid phosphodiesterase-5 inhibitors

›Sildenafil, tadalafil: associated with NAION

Toxic and nutritional optic neuropathy treatment

›Toxic optic neuropathy

›Ethambutol: discontinue immediately

›Vision often improves after cessation

›Methanol toxicity

›Ethanol or fomepizole as ADH competitive inhibitor

›Fomepizole 15 mg/kg IV loading dose, then 10 mg/kg every 12 hours

›Hemodialysis for severe toxicity or high methanol level

›Nutritional optic neuropathy

›Vitamin B12 replacement

›Cyanocobalamin 1,000 mcg IM daily for 7 days, then weekly for 4 weeks, then monthly

›Folate replacement

›Folic acid 1 mg orally daily

09Special Populations/sp65

Pregnancy

›Optic neuritis in pregnancy

›IV methylprednisolone acceptable in pregnancy

›Risk-benefit favors treatment for severe vision loss

›Neonatology consultation for third-trimester exposure

›MRI without gadolinium preferred in first trimester

›Gadolinium crosses placenta; avoid unless essential

›Non-contrast MRI brain and orbits adequate for most cases

›NMOSD and pregnancy

›High risk of relapse in postpartum period

›Disease-modifying therapy decisions with maternal-fetal medicine

›GCA in pregnancy

›Extremely rare (GCA typically age >50)

›High-dose corticosteroids: prednisone risk-benefit counseling

›Preterm labor and gestational diabetes risks

›Fetal monitoring during high-dose steroid therapy

›Retinal detachment in pregnancy

›Pneumatic retinopexy preferred over vitrectomy when feasible

›Avoids general anesthesia risk

›Optical coherence tomography safe in pregnancy

›No radiation or contrast

Geriatric

›GCA as primary geriatric concern

›Exclusively affects age >50; peak incidence 70-80 years

›Prevalence approximately 18-27 per 100,000 in persons >50 years

›Atypical GCA presentation in oldest old

›Absent ESR elevation in 5-10% of confirmed cases

›Jaw claudication may be absent

10Background/b74

Epidemiology

›Prevalence of RAPD causes

›Optic neuritis incidence

›Approximately 5 per 100,000 per year

›Peak age 15-45 years

›3:1 female predominance

›50% of patients develop MS within 15 years after isolated optic neuritis

›GCA incidence

›18-27 per 100,000 per year in persons >50 years

›Peak incidence 70-80 years

›6:1 female-to-male ratio

›Northern European descent highest prevalence

›NAION incidence

›2.3-10.2 per 100,000 per year

›Most common acute optic neuropathy in adults >50

›CRAO incidence

›Approximately 1-2 per 100,000 per year

›Associated with 90-day stroke risk approximately 10%

›Retinal detachment incidence

›Approximately 12 per 100,000 per year

Pathophysiology

›Afferent pupillary pathway anatomy

›Light reflex pathway

›Retinal ganglion cells to optic nerve

›Optic chiasm: nasal fibers decussate

›Optic tract to pretectal nucleus (dorsal midbrain)

›Bilateral projection from each pretectal nucleus to both Edinger-Westphal nuclei

›Edinger-Westphal to ciliary ganglion via CN III

›Ciliary ganglion to iris sphincter

›Why RAPD indicates prechiasmal or asymmetric chiasmal lesion

›Postchiasmal lesions affect both eyes equally via bilateral pretectal projections

›Exception: optic tract lesions cause contralateral RAPD (Wernicke hemianopic pupil)

›Why RAPD is absent with dense amblyopia

›Amblyopia affects cortical processing, not pretectal light reflex pathway

›Large RAPD with apparent amblyopia demands structural workup

›Disease-specific mechanisms

›Optic neuritis

›Demyelination of optic nerve axons

›Conduction block and slowed conduction velocity

›Inflammation causes axonal injury and retinal ganglion cell loss

›NAION

›Ischemia of the short posterior ciliary arteries

›Crowded optic disc with poor autoregulatory reserve

›Compartment-syndrome-like mechanism within disc

›GCA

›Granulomatous vasculitis of medium-to-large arteries

›Intimal hyperplasia and thrombosis causing ischemia

›Posterior ciliary arteries most commonly affected (producing AION)

›CRAO

›Embolic or thrombotic occlusion of central retinal artery

›Retinal tolerance 90-100 minutes before irreversible ischemia

›Inner retina whitening (cytotoxic edema) with preserved foveal choroidal supply (cherry red spot)

Therapeutic Considerations

›Corticosteroid principles in neuro-ophthalmology

›High-dose IV vs oral in optic neuritis

›ONTT showed IV methylprednisolone accelerates recovery

›Low-dose oral steroids alone associated with increased relapse risk

›Oral high-dose (prednisone 1,250 mg/day) acceptable alternative

›GCA steroid dosing rationale

›Empiric treatment mandatory: risk of bilateral blindness justifies steroid toxicity

›IV pulse for active vision loss; oral adequate for prevention

›Steroid monitoring and toxicity prevention

›Calcium 1,200 mg daily and vitamin D 800-1,000 IU daily with prolonged steroids

›Bisphosphonate therapy when >3 months of prednisone anticipated

›CRAO acute intervention rationale

›Time-critical like ischemic stroke

›Retina tolerates ischemia approximately 90-100 minutes

›Thrombolysis benefit window parallels cerebral stroke (4.5 hours)

›EAGLE trial evidence

›Intra-arterial thrombolysis not superior to IV in CRAO

›IV alteplase remains standard if within window

›Disease-modifying therapy considerations for MS after optic neuritis

›High-risk features (multiple MRI lesions) benefit from early DMT

›Interferon-beta, glatiramer acetate, or natalizumab reduce MS conversion

›Treatment decision requires neurologist input

›AQP4-IgG and MOG-IgG testing before DMT initiation

›Wrong agent in NMOSD may worsen disease

11Patient Discharge Instructions/pdi41

copy discharge instructions

›Marcus Gunn Pupil (Relative Afferent Pupillary Defect) home care instructions

›Your eye exam found a sign called a Marcus Gunn pupil or relative afferent pupillary defect (RAPD)

›This finding means one eye or optic nerve is receiving less light signal than the other

›It is always caused by an underlying condition that your doctors are evaluating

›Your specific diagnosis and prescribed treatment

›Take all prescribed medications exactly as directed

›Complete the full course of any steroids unless told otherwise

›Warning signs: return to emergency department immediately

›Vision loss in the other eye

›Any sudden change in vision in the opposite eye is an emergency

›Sudden severe headache

›Especially with jaw pain, scalp tenderness, or stiff neck

›Sudden worsening of vision in the treated eye

›Floaters, flashes of light, or a curtain across your vision

›Possible retinal detachment requiring same-day surgery

›New weakness, numbness, slurred speech, or difficulty walking

›Signs of stroke or multiple sclerosis relapse

›Eye pain, redness, or a fixed dilated pupil

›Possible acute glaucoma

›Medications at home

›If taking prednisone or other steroids

›Take with food to protect your stomach

›Do not stop suddenly without doctor guidance

›Monitor blood sugar if diabetic; steroids raise glucose

›If prescribed eye drops

›Use exactly as directed

›Wash hands before instilling drops

12References/r30

Guidelines and key sources

›Primary evidence sources used in this document

›Fraser JA, Son M, Vinokurtseva A. Sudden Vision Loss: A Diagnostic Approach. American Family Physician. 2025. PMID 39823616

›Comprehensive diagnostic framework for vision loss including RAPD etiologies

›Biousse V, Newman NJ. Diagnosis and Clinical Features of Common Optic Neuropathies. Lancet Neurology. 2016. PMID 27839652

›Definitive reference for optic neuropathy classification and examination

›Bennett JL, Costello F, Chen JJ, et al. Optic Neuritis and Autoimmune Optic Neuropathies: Advances in Diagnosis and Treatment. Lancet Neurology. 2023. PMID 36155661

›NMOSD, MOGAD, MS-associated optic neuritis treatment updates

›ACR Appropriateness Criteria: Vision Loss. Journal of the American College of Radiology. 2025

›Imaging algorithm for vision loss including MRI and CT indications

›Kovach JL, Bailey ST, Kim SJ, et al. Retinal and Ophthalmic Artery Occlusions Preferred Practice Pattern. Ophthalmology. 2025

›CRAO management including thrombolysis evidence

›Siebald F, Grittner U, Otto C, et al. Ultrasound Pupillometry for the Detection of RAPD. PLoS One. 2024. PMID 39792831

›AUC 1.0 for ultrasound pupillometry in acute optic neuritis

›Hutchinson AK, Morse CL, Hercinovic A, et al. Pediatric Eye Evaluations Preferred Practice Pattern. Ophthalmology. 2023. PMCID PMC10680450

›Pediatric optic neuropathy and concussion visual evaluation standards

›Chen CJ, Scheufele M, Sheth M, et al. Isolated Relative Afferent Pupillary Defect Secondary to Contralateral Midbrain Compression. Archives of Neurology. 2004

›Postchiasmal RAPD mechanism and pretectal lesion evidence

›Master CL, Bacal D, Grady MF, et al. Evaluation of the Visual System After Concussion. Pediatrics. 2022

›Visual assessment protocol post-concussion in children

›Kawasaki A, Miller NR, Kardon R. Pupillographic Investigation of RAPD Associated With a Midbrain Lesion. Ophthalmology. 2010. PMID 19923003

›Pupillographic evidence for postchiasmal RAPD mechanisms

Coding references

›ICD-10 codes for RAPD etiologies

›H46.0: Optic papillitis

›H47.01: Ischemic optic neuropathy (non-arteritic)

›H34.10: Central retinal artery occlusion, unspecified eye

›H33.00: Unspecified retinal detachment with retinal break

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Comprehensive Clinical Review

Structured, evidence-informed, long-form analysis for deeper understanding.

Evidence & Review

Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.