Ophthalmology, Neuro-Ophthalmology & Otolaryngology (ENT) Emergencies

Primary Open-Angle Glaucoma (POAG) (90% of cases; risk factors: African American race, advanced age, family history, myopia, diabetes, chronic corticosteroid use) results from gradual resistance to aqueous outflow through a microscopically degenerating but anatomically open trabecular meshwork; patients are completely asymptomatic until late-stage painless bilateral peripheral (“tunnel”) vision loss occurs. First-line pharmacotherapy is a topical prostaglandin F2-alpha analog (latanoprost, bimatoprost, travoprost), which increases uveoscleral outflow (side effects: darkening of iris brown pigmentation and eyelash hypertrichosis), or a topical beta-blocker (timolol, which decreases ciliary aqueous production; contraindicated in asthma/heart block). Conversely, Acute Angle-Closure Glaucoma (AACG) occurs in anatomically predisposed patients (hyperopia/farsightedness, shallow anterior chamber, older age, Asian/Inuit heritage) when pupillary dilation—triggered by entering a dark movie theater, sympathomimetics (phenylephrine), or anticholinergic medications (atropine, ipratropium, oxybutynin, TCAs, antihistamines)—pushes the peripheral iris against the trabecular meshwork, abruptly blocking all aqueous outflow. Patients present with sudden, severe unilateral ocular pain, frontal headache, nausea/vomiting, blurred vision with colored halos around lights, conjunctival ciliary injection, a steamy/cloudy cornea, a mid-dilated (4–6 mm) fixed nonreactive pupil, and a rock-hard globe on palpation. Confirm immediately with tonometry (IOP >40–60 mmHg) and gonioscopy; emergency medical stabilization combines topical timolol (beta-blocker), apraclonidine (alpha-2 agonist), and pilocarpine (direct M3 muscarinic agonist that constricts the pupil to pull the iris out of the angle) PLUS systemic intravenous acetazolamide or mannitol, followed by definitive laser peripheral iridotomy in BOTH eyes (to prevent an attack in the fellow eye; mydriatics/atropine are strictly contraindicated!). In central vision loss in older adults (>60 yr), Age-Related Macular Degeneration (AMD) spares peripheral vision while destroying the macula (causing central scotoma and straight lines appearing wavy [metamorphopsia] on the Amsler grid): Dry (non-exudative) AMD (85%) shows subretinal yellowish drusen deposits and geographic RPE atrophy (treated with AREDS2 antioxidant vitamins: C, E, Lutein, Zeaxanthin, Zinc, Copper—never beta-carotene in smokers due to lung cancer risk!), whereas Wet (exudative) AMD (15%) results from VEGF-driven choroidal neovascularization causing rapid subretinal hemorrhage (treated with intravitreal anti-VEGF injections: ranibizumab, bevacizumab, aflibercept).

Evaluating an acute red eye relies on visual acuity, pupillary reaction, and fluorescein slit-lamp examination: (1) Conjunctivitis has normal visual acuity, normal pupillary light response, and no photophobia: Viral (Adenovirus) is the most common overall (watery discharge, preauricular lymphadenopathy, follicular tarsal reaction, sequential bilateral spread after URI); Bacterial (S. aureus, S. pneumoniae, H. influenzae) causes thick yellow-green purulent discharge crusting the lashes shut in the morning (note: in a contact lens wearer, rapidly progressive painful corneal ulceration is Pseudomonas aeruginosa keratitis—treat immediately with topical fluoroquinolone [ciprofloxacin/moxifloxacin] drops and never patch the eye!; hyperacute copious purulent conjunctivitis within 24 hours of exposure or on Day 2–5 of life is Neisseria gonorrhoeae—treat with IM ceftriaxone). (2) Herpes Simplex Virus (HSV-1) Keratitis shows a pathognomonic branching dendritic corneal ulcer on fluorescein staining (treat with topical ganciclovir/trifluridine or oral acyclovir; topical corticosteroids are strictly contraindicated as they worsen viral ulceration!). (3) Anterior Uveitis (Iritis) (associated with HLA-B27 spondyloarthropathies, sarcoidosis, Behcet, JIA) presents with ocular pain, photophobia, a constricted (miotic) pupil, perilimbal ciliary flush, and inflammatory leukocytes (“cell and flare”) or layered WBCs (hypopyon) in the anterior chamber (treat with topical corticosteroids). (4) Episcleritis vs. Scleritis: Episcleritis causes mild irritation with superficial vessel injection that blanches with topical phenylephrine, whereas Scleritis (50% associated with Rheumatoid Arthritis or GPA vasculitis) causes deep, boring ocular pain radiating to the brow/jaw that worsens with eye movement, a violaceous/bluish sclera (thinning exposing the dark choroid), and vessels that do NOT blanch with phenylephrine. (5) Traumatic Hyphema (blood pooling in the anterior chamber after blunt orbital trauma) requires shielding the eye, elevating the head of the bed 30–45 degrees (so RBCs settle inferiorly away from the visual axis and trabecular meshwork), topical cycloplegics, and screening African American patients for sickle cell trait/disease (which clogs the trabecular meshwork and contraindicates carbonic anhydrase inhibitors that acidify aqueous humor and promote sickling).

(1) Central Retinal Artery Occlusion (CRAO) (“stroke of the eye”) is caused by a cholesterol embolus (Hollenhorst plaque from an ipsilateral internal carotid artery plaque) or cardiogenic embolus occluding the central retinal artery (a branch of the ophthalmic artery from the internal carotid). Patients present with sudden, painless, profound monocular vision loss and a relative afferent pupillary defect (Marcus Gunn pupil); fundoscopy reveals a diffusely pale, opaque retina, attenuated arterioles with “boxcar” segmentation, and a pathognomonic macular cherry-red spot (spared choroidal perfusion via posterior ciliary arteries). Treatment within 90 minutes includes ocular massage, high-flow O2/carbogen, anterior chamber paracentesis/IOP lowering, and full stroke workup (carotid duplex ultrasound, echocardiogram). (2) Central Retinal Vein Occlusion (CRVO) occurs in patients with hypertension, diabetes, glaucoma, or hyperviscosity/hypercoagulability due to thrombosis of the central retinal vein at the lamina cribrosa; fundoscopy reveals a dramatic “blood and thunder” retina with diffuse 4-quadrant intraretinal flame hemorrhages, dilated tortuous retinal veins, cotton-wool spots, and optic disc edema (treated with intravitreal anti-VEGF injections for macular edema). (3) Retinal Detachment (separation of the inner neurosensory retina from the outer retinal pigment epithelium [RPE] and choroidal blood supply; risk factors: severe myopia, prior cataract surgery, trauma, proliferative diabetic retinopathy) presents with sudden painless monocular photopsia (flashing lights) and a shower of floaters followed by a “dark curtain or veil” drawn across the visual field; fundoscopy and ocular ultrasound show an elevated, gray, crinkled retinal fold (surgical emergency treated with laser photocoagulation, cryopexy, pneumatic retinopexy, scleral buckle, or pars plana vitrectomy). (4) Diabetic Retinopathy progresses from Non-proliferative (microaneurysms, dot-blot hemorrhages, hard lipid exudates, cotton-wool nerve-fiber infarcts; managed with glycemic control and laser/anti-VEGF for macular edema) to Proliferative (retinal hypoxia drives VEGF-mediated neovascularization on the optic disc/retina, which ruptures to cause vitreous hemorrhage [loss of red reflex and dark fundus] and tractional retinal detachment; treated with panretinal laser photocoagulation and intravitreal anti-VEGF).

The fibrous orbital septum separates superficial eyelid tissues from the deep orbit: Preseptal (Periorbital) Cellulitis (anterior to the septum; caused by skin trauma/insect bite with S. aureus or S. pyogenes) presents with eyelid erythema and swelling WITHOUT proptosis, WITHOUT pain on extraocular movement, and WITH completely normal visual acuity and full extraocular motility (managed with oral outpatient antibiotics: TMP-SMX + amoxicillin-clavulanate). Conversely, Orbital (Postseptal) Cellulitis (posterior to the septum; 90% caused by contiguous spread of acute bacterial ethmoid sinusitis through the paper-thin lamina papyracea) presents with fever, eyelid swelling PLUS the cardinal triad of (1) Painful ophthalmoplegia (pain and restriction with extraocular eye movements), (2) Proptosis (chemosis), and (3) Decreased visual acuity or afferent pupillary defect. Confirm immediately with CT of the orbits and sinuses with IV contrast (to identify a subperiosteal orbital abscess requiring surgical drainage) and admit for intravenous vancomycin plus ceftriaxone (or ampicillin-sulbactam/piperacillin-tazobactam). Posterior extension via valveless ophthalmic veins into the Cavernous Sinus causes Septic Cavernous Sinus Thrombosis—presenting with bilateral headache, fever, periorbital edema, proptosis, and paralysis of Cranial Nerves III, IV, V1, V2, and VI (where CN VI [abducens, lateral rectus] is affected earliest because it runs freely inside the sinus alongside the internal carotid artery!). On neuro-ophthalmology vignettes: (1) Oculomotor (CN III) palsy causes a “down-and-out” eye with ptosis—if the pupil is dilated and nonreactive (“surgical CN III”), external compression of superficial dorsal parasympathetic fibers by a posterior communicating artery (PCOM) aneurysm or uncal herniation is present (order an emergent CTA/MRA of the head!), whereas a pupil-sparing CN III palsy (“medical CN III”) reflects microvascular ischemia of the central nerve trunk in diabetes/hypertension; and (2) Internuclear Ophthalmoplegia (INO) results from a demyelinating (Multiple Sclerosis) or ischemic lesion of the Medial Longitudinal Fasciculus (MLF): on attempted contralateral conjugate gaze, the ipsilateral eye fails to adduct while the contralateral abducting eye exhibits horizontal nystagmus, with convergence completely intact.

High-yield causes of Conductive Hearing Loss include cerumen impaction, acute otitis media / serous otitis media with effusion (note: unilateral middle ear effusion in an adult without URI is nasopharyngeal carcinoma obstructing the torus tubarius of the Eustachian tube until proven otherwise!), tympanic membrane perforation, Otosclerosis (autosomal dominant sclerotic bony fixation of the stapes footplate to the oval window presenting in young women aged 20–40 years—often worsening during pregnancy—with progressive conductive hearing loss, normal tympanic membrane [or reddish Schwartze sign], and paradoxical improvement of speech discrimination in noisy environments [paracusis Willisii]; treated with stapedectomy or hearing aids), and Cholesteatoma (an locally destructive keratinizing squamous epithelial cyst in the superior pars flaccida of the tympanic membrane secondary to chronic negative middle-ear pressure/Eustachian tube dysfunction, presenting with painless chronic foul-smelling otorrhea and a pearly white mass or retraction pocket with granulation tissue; lytic enzymes erode the middle-ear ossicles, mastoid air cells, tegmen tympani, and facial nerve [CN VII], requiring CT temporal bone and surgical tympanomastoidectomy). High-yield causes of Sensorineural Hearing Loss include Presbycusis (age-related symmetric bilateral high-frequency hearing loss worse in crowded background noise due to degeneration of hair cells at the base of the cochlea), Noise-induced hearing loss (loss of outer hair cells with a characteristic audiogram notch at 4,000 Hz), ototoxic drugs (aminoglycosides, cisplatin, loop diuretics, salicylates), and Vestibular Schwannoma (Acoustic Neuroma)—a benign S-100+ Schwann cell tumor of CN VIII at the cerebellopontine angle presenting with unilateral SNHL, unilateral tinnitus, and disequilibrium (plus facial numbness CN V and facial weakness CN VII as it expands; bilateral vestibular schwannomas are diagnostic of Neurofibromatosis Type 2 [Chr 22, merlin]; diagnosed by gadolinium-enhanced brain MRI).

True vertigo (the illusion of rotational spinning accompanied by nystagmus and nausea) must first be differentiated into Peripheral (CN VIII / inner ear semicircular canals) versus Central (brainstem / cerebellar posterior circulation stroke [PICA/AICA] or multiple sclerosis) using the bedside HINTS exam (Head Impulse, Nystagmus, Test of Skew), which is more sensitive than early diffusion MRI in the first 24 hours: a Central (Stroke) cause is indicated by a Normal head impulse test (eyes stay fixed on the examiner without a corrective saccade!), Direction-changing or purely vertical/torsional nystagmus that is not suppressed by visual fixation, or Vertical skew deviation on alternate cover testing (plus any brainstem/cerebellar 5 D's: Dysarthria, Diplopia, Dysphagia, Dysmetria/ataxia, or Dizziness). Peripheral vertigo is stratified strictly by episode duration and presence/absence of auditory symptoms (hearing loss or tinnitus): (1) Benign Paroxysmal Positional Vertigo (BPPV): brief episodes lasting <1 minute triggered strictly by head position changes (rolling over in bed, looking up) with NO hearing loss/tinnitus, caused by calcium carbonate otoconia (canaliths) dislodged into the posterior semicircular canal; diagnosed by the Dix-Hallpike maneuver (reproduces latent torsional/upbeating nystagmus) and cured at the bedside by the Epley canalith repositioning maneuver; (2) Vestibular Neuritis: a single, continuous severe episode lasting several days following a recent viral URI with NO hearing loss or tinnitus (treated with a short course of vestibular suppressants [meclizine] and corticosteroids); (3) Acute Labyrinthitis: identical post-viral continuous vertigo lasting days, PLUS acute unilateral sensorineural hearing loss and/or tinnitus; and (4) Ménière Disease: recurrent episodes lasting 20 minutes to 12 hours caused by endolymphatic hydrops (distension of the endolymphatic compartment of the inner ear), presenting with the classic triad of episodic vertigo, unilateral aural fullness/roaring tinnitus, and fluctuating low-frequency sensorineural hearing loss (first-line prophylaxis: strict low-sodium diet [<1.5–2 g/day], avoidance of caffeine/alcohol/nicotine, and thiazide diuretics [hydrochlorothiazide]).

Four life-threatening deep neck infections must be distinguished on board vignettes: (1) Peritonsillar Abscess (Quinsy) occurs in adolescents and young adults as a polymicrobial (GAS, Staphylococcus aureus, Fusobacterium) suppurative complication of tonsillitis between the palatine tonsillar capsule and superior pharyngeal constrictor; patients present with unilateral severe sore throat, fever, muffled “hot-potato” voice, drooling, trismus (inability to open the mouth due to medial pterygoid spasm), and unilateral inferior-medial tonsillar bulge with CONTRALATERAL deviation of the uvula; treat with needle aspiration or incision and drainage PLUS IV ampicillin-sulbactam or clindamycin. (2) Retropharyngeal Abscess occurs primarily in children <5 years old (before the retropharyngeal lymph nodes of Rouviere atrophy, or after penetrating posterior pharyngeal trauma from a lollipop stick/fishbone); children present with high fever, odynophagia, drooling, muffled voice, stridor, and refusal to extend the neck (painful neck extension / torticollis); a lateral neck radiograph shows widening of the prevertebral soft-tissue space (>1/2 the width of the adjacent cervical vertebral body at C2–C4 or >7 mm at C2) with air-fluid levels, confirmed by contrast neck CT and treated with urgent surgical drainage and IV ampicillin-sulbactam/clindamycin (to prevent rupture into the carotid sheath or posterior mediastinal “danger space”). (3) Ludwig Angina is a rapidly progressive, bilateral polymicrobial cellulitis of the submandibular and sublingual spaces originating from an infected mandibular 2nd or 3rd molar (tooth roots extend below the mylohyoid line!); patients present with fever, drooling, trismus, and board-like (“woody”) brawny induration of the floor of the mouth that displaces the tongue superiorly and posteriorly against the palate—secure the airway IMMEDIATELY via awake fiberoptic nasotracheal intubation or tracheostomy plus IV ampicillin-sulbactam/meropenem + vancomycin. (4) Acute Epiglottitis (caused by Haemophilus influenzae type b in unimmunized children or Streptococcus in adults) presents with abrupt high fever, toxic appearance, tripod positioning (sitting upright leaning forward with chin hyperextended), drooling, dysphagia, muffled voice, and inspiratory stridor; do NOT agitate the child or examine the throat with a tongue depressor—proceed immediately to the operating room for endotracheal intubation under direct visualization, followed by IV ceftriaxone plus vancomycin (lateral neck X-ray in stable patients shows the classic swollen “thumbprint sign” of the epiglottis, contrasted with the subglottic “steeple sign” of parainfluenza viral croup).

Anterior Epistaxis (90%; arises from Kiesselbach's plexus on the anteroinferior nasal septum, supplied by the anterior ethmoidal, sphenopalatine, greater palatine, and superior labial arteries) is managed by having the patient sit upright and lean forward while pinching the soft nasal alae continuously for 10–15 minutes, applying topical oxymetazoline (alpha-1 vasoconstrictor), and performing silver nitrate chemical or electrocautery (or anterior nasal packing—always prescribe prophylactic cephalexin/amoxicillin-clavulanate against S. aureus toxic shock syndrome while nasal packing is in place!). Posterior Epistaxis (10%; arises from the sphenopalatine artery [branch of the maxillary artery] in older hypertensive/anticoagulated patients) causes brisk bleeding down the posterior pharynx refractory to anterior pressure and requires a posterior balloon catheter, Foley tamponade, or sphenopalatine artery embolization/ligation. In the salivary glands, Sialolithiasis (calcium phosphate duct stones) occurs 85% in the Submandibular gland (Wharton's duct) because its secretions are thick/mucinous and flow uphill (presenting with postprandial pain/swelling relieved by lemon drop sialagogues and massage), whereas acute bacterial Suppurative Parotitis (S. aureus in dehydrated elderly/post-op patients on anticholinergics) occurs in the Parotid gland (Stensen's duct). The universal salivary tumor rule is: the smaller the salivary gland, the higher the likelihood that a mass is malignant (parotid masses are 80% benign, submandibular 50% benign, sublingual/minor 80% malignant). The #1 salivary tumor overall is the benign Pleomorphic Adenoma (mixed chondromyxoid stroma + epithelium; painless mobile mass at the angle of the jaw; recurrences or malignant transformation into carcinoma ex pleomorphic adenoma damage CN VII); the #2 benign tumor is Warthin Tumor (papillary cystadenoma lymphomatosum; 10% bilateral, strongly linked to smoking, contains lymphoid germinal centers); and the #1 malignant tumor of the parotid is Mucoepidermoid Carcinoma (while Adenoid Cystic Carcinoma exhibits classic perineural invasion along CN VII with a cribriform “Swiss-cheese” pattern).

True Strabismus is differentiated from benign pseudostrabismus (wide epicanthal folds with a broad nasal bridge in infants that creates the optical illusion of esotropia) using two bedside tests: (1) the Hirschberg Corneal Light Reflex Test (in pseudostrabismus, the corneal light reflection falls symmetrically in the center of both pupils; in true esotropia, the light reflex is displaced temporally in the deviated eye), and (2) the Cover-Uncover Test (covering the normal fixating eye forces the deviated strabismic eye to snap back to midline to pick up fixation). First-line treatment of strabismic or anisometropic Amblyopia is occlusion therapy (patching the normal/strong eye) or cycloplegic penalization (1% atropine drops in the normal eye) to force the visual cortex to use and develop pathways from the amblyopic eye, plus corrective lenses (or strabismus extraocular muscle surgery). Distinguish congenital glaucoma (presenting with the triad of epiphora [tearing], photophobia, and blepharospasm with an enlarged cloudy cornea [buphthalmos]) from benign Congenital Nasolacrimal Duct Obstruction (Dacryostenosis, failure of the valve of Hasner to canalize, presenting with unilateral tearing and morning crusting without photophobia, conjunctival redness, or corneal enlargement; managed with Crigler nasolacrimal sac massage until spontaneous resolution by 6–12 months, or surgical probing if persistent past 1 year).

Neonatal conjunctivitis (Ophthalmia Neonatorum) is stratified by the exact day of onset after birth: (1) Day 1 (First 24 hours): Chemical Conjunctivitis secondary to silver nitrate prophylaxis (rare today because 0.5% erythromycin ophthalmic ointment is routine at birth; presents with mild bilateral watery irritation resolving spontaneously within 48 hours). (2) Days 2 to 5: Neisseria gonorrhoeae Conjunctivitis—a hyperacute ophthalmic emergency presenting with severe bilateral eyelid edema, chemosis, and profuse purulent exudate capable of penetrating intact corneal epithelium to cause corneal ulceration, perforation, and permanent blindness within 24 hours! Diagnose immediately via Gram stain (intracellular Gram-negative diplococci) and NAAT, and treat immediately with a single dose of systemic IV or IM Ceftriaxone (25–50 mg/kg) (or Cefotaxime if the neonate has hyperbilirubinemia, because ceftriaxone displaces bilirubin from albumin and precipitates with IV calcium!) plus frequent saline eye irrigation (note: topical erythromycin ointment at birth prevents gonococcal ophthalmia, NOT chlamydial!). (3) Days 5 to 14: Chlamydia trachomatis Inclusion Conjunctivitis—presents with watery-to-mucopurulent discharge and eyelid swelling; because 50% of infants have concomitant nasopharyngeal colonization that can progress to afebrile staccato cough pneumonia at 4–12 weeks of age, topical therapy alone is inadequate—treat with a 14-day course of oral Erythromycin (which carries a risk of infantile hypertrophic pyloric stenosis) or 3 days of oral Azithromycin.

Salivary gland neoplasms obey the surgical inverse size-malignancy rule: the smaller the salivary gland, the higher the probability that a mass is malignant (~20% of parotid masses, ~50% of submandibular masses, and ~80% of sublingual/minor salivary gland masses are malignant!). Overall, the most common salivary gland tumor (70–80% of all tumors, most frequently in the superficial lobe of the parotid gland) is the benign Pleomorphic Adenoma (Benign Mixed Tumor): a painless, slow-growing, firm, mobile mass behind the angle of the mandible composed of chondromyxoid stroma and epithelial/myoepithelial cells; it requires superficial parotidectomy with wide margins (simple enucleation leads to high recurrence, and long-standing untreated tumors can undergo malignant transformation into carcinoma ex pleomorphic adenoma presenting with sudden rapid growth and ipsilateral CN VII facial nerve paralysis!). The second most common benign parotid tumor is Warthin Tumor (Papillary Cystadenoma Lymphomatosum): a benign cystic tumor with dense lymphoid stroma and germinal centers occurring almost exclusively in older male smokers (10% bilateral/multifocal). The most common malignant salivary gland tumor overall is Mucoepidermoid Carcinoma (composed of mucinous and squamous cells; parotid gland), whereas the most common malignant tumor of the submandibular and minor salivary glands is Adenoid Cystic Carcinoma (characterized by a cribriform “Swiss-cheese” histology and a notorious propensity for painful perineural invasion along cranial nerves!). Differentiate neoplasms from acute Sialolithiasis (a radiopaque calcium phosphate stone in Wharton's duct of the submandibular gland [80–90% of stones due to uphill course and alkaline mucinous saliva] causing episodic colicky postprandial jaw pain and swelling when eating or smelling sour food; managed with sialogogues [lemon drops], warm compresses, hydration, and gland massage, or antistaphylococcal antibiotics if complicated by suppurative sialadenitis).

Any patient presenting with persistent hoarseness (dysphonia) lasting >2–4 weeks requires direct visualization via flexible fiberoptic laryngoscopy before prescribing empiric therapies. Laryngeal innervation derives entirely from the vagus nerve (CN X): (1) the External Branch of the Superior Laryngeal Nerve (accompanying the superior thyroid artery) innervates only the cricothyroid muscle, which tenses the vocal cord (injury during superior thyroid pole ligation causes loss of high-pitched voice projection and easy voice fatigability in singers); and (2) the Recurrent Laryngeal Nerve (RLN) (accompanying the inferior thyroid artery; the left RLN loops under the aortic arch near the ligamentum arteriosum, making it vulnerable to left upper lobe bronchogenic carcinoma [Pancoast/hilar mass], thoracic aortic aneurysm, or mitral stenosis left atrial enlargement [Ortner syndrome]) innervates all intrinsic laryngeal muscles EXCEPT the cricothyroid (crucially including the posterior cricoarytenoid muscle, the sole abductor of the vocal cords!). Consequently, Unilateral RLN Paralysis causes a paramedian immobile vocal cord with a hoarse, breathy voice and bovine cough, whereas Bilateral RLN Paralysis leaves both vocal cords adducted near the midline, causing acute inspiratory stridor and life-threatening upper airway obstruction requiring emergent tracheostomy! In infants, the #1 cause of chronic congenital stridor is Laryngomalacia (flaccid supraglottic epiglottis/arytenoids that collapse inward during inspiration, producing high-pitched inspiratory stridor that worsens when supine or crying and improves when prone; laryngoscopy shows a classic omega-shaped [Ω] epiglottis; >90% resolve spontaneously by 12–18 months).