Medical School · Year 3 · Emergency Medicine · includes a quiz and discussion video

Seminar 15: Ophthalmologic and ENT Emergencies

Emergency Medicine Clerkship

Learning Objectives

By the end of this seminar, students will be able to:

1. Evaluate and classify the causes of acute vision loss and initiate time-sensitive interventions for reversible etiologies
2. Perform appropriate initial management of ocular trauma including chemical burns, globe rupture, hyphema, and corneal injuries
3. Differentiate emergent from non-emergent causes of the red eye using a systematic approach to history and examination findings
4. Manage epistaxis through stepwise interventions including direct pressure, cautery, anterior packing, and posterior packing
5. Distinguish peripheral from central vertigo using bedside clinical examination maneuvers including the HINTS examination
6. Recognize and manage life-threatening ENT emergencies including peritonsillar abscess, epiglottitis, Ludwig's angina, and airway foreign bodies

Seminar Outline

Section 1: Acute Vision Loss

Acute vision loss is one of the most alarming presentations in emergency medicine, and the differential diagnosis spans a wide range of conditions that vary drastically in urgency. Central retinal artery occlusion (CRAO) presents as sudden, painless monocular vision loss and is the ocular equivalent of an ischemic stroke. On fundoscopic examination, the retina appears pale with a characteristic cherry-red spot at the macula, and an afferent pupillary defect is typically present. CRAO is exquisitely time-sensitive, with a treatment window of approximately 90 to 120 minutes, during which interventions such as ocular massage, anterior chamber paracentesis, or experimental fibrinolytic therapy may be attempted. Because CRAO is typically embolic in origin, a thorough cardiac and carotid workup is indicated.

Acute angle-closure glaucoma represents another ophthalmologic emergency that demands immediate recognition and treatment. Patients present with severe eye pain, headache, nausea, visual halos, and decreased visual acuity. Examination reveals a fixed mid-dilated pupil and a hazy, edematous cornea. Intraocular pressure is markedly elevated, often exceeding 40 mmHg when normal is below 21 mmHg. Emergency treatment involves a multi-drug approach including timolol to decrease aqueous humor production, pilocarpine to constrict the pupil and open the trabecular meshwork, acetazolamide to reduce intraocular pressure systemically, and intravenous mannitol for osmotic pressure reduction. Definitive treatment is laser iridotomy performed by an ophthalmologist.

Giant cell arteritis (GCA) is a vasculitis affecting medium and large arteries, predominantly in patients over 50 years of age. The classic presentation includes headache, jaw claudication, scalp tenderness, and visual symptoms that may be preceded by transient episodes of vision loss known as amaurosis fugax. Laboratory evaluation reveals elevated erythrocyte sedimentation rate and C-reactive protein. The critical management principle is that high-dose prednisone must be initiated immediately upon clinical suspicion without waiting for temporal artery biopsy results, as untreated GCA can progress to permanent bilateral blindness. Temporal artery biopsy should be obtained within two weeks of starting steroids, as histologic findings remain present during this window.

Other emergent causes of acute vision loss include retinal detachment, which presents with floaters, photopsia (flashes of light), and a progressive curtain-like visual field deficit requiring urgent ophthalmology evaluation. Vitreous hemorrhage presents with sudden floaters and decreased vision, necessitating same-day ophthalmology consultation to evaluate for underlying retinal pathology. The emergency physician must recognize that painless acute vision loss is always emergent until proven otherwise, and the pattern of pain, laterality, and associated symptoms guides the differential toward the correct diagnosis and appropriate time-critical interventions.

<image>Panel A: Fundoscopic appearance of central retinal artery occlusion showing a pale retina with a cherry-red spot at the macula and attenuated retinal vessels. Panel B: Slit lamp examination of acute angle-closure glaucoma demonstrating a fixed mid-dilated pupil, corneal edema with a hazy appearance, and conjunctival injection. Panel C: Clinical photograph of a patient with giant cell arteritis showing a prominent, tender, nodular temporal artery with overlying scalp erythema. Panel D: Fundoscopic view of retinal detachment showing an elevated, undulating retinal fold with a grayish appearance separating from the underlying retinal pigment epithelium.</image>

Section 2: Ocular Trauma

Chemical burns to the eye represent a true ophthalmologic emergency where immediate action takes precedence over all other aspects of evaluation. The most critical initial step is copious and continuous irrigation with normal saline or water, requiring at least two liters of fluid, and this must begin before any formal assessment is completed. The pH of the ocular surface should be checked both before and after irrigation, with a target pH of 7.0 to 7.4 indicating adequate decontamination. Alkali burns are significantly more dangerous than acid burns because alkaline substances undergo liquefactive necrosis, penetrating deeply into ocular tissues and continuing to cause damage long after the initial exposure. Acid burns, by contrast, cause coagulation necrosis that forms a protein barrier limiting further penetration. All chemical burns require emergent ophthalmology consultation regardless of the causative agent.

Globe rupture is a sight-threatening injury that occurs following blunt or penetrating trauma to the eye. Clinical signs include an irregularly shaped pupil, a shallow anterior chamber, visible prolapse of uveal tissue through the wound, and a positive Seidel test in which fluorescein is seen streaming away from the site of perforation due to leaking aqueous humor. Management of suspected globe rupture follows strict protective principles: a rigid eye shield must be placed over the affected eye without any pressure, the patient should be kept NPO in anticipation of surgical repair, and antiemetics should be administered to prevent Valsalva-induced extrusion of intraocular contents. Tonometry and any form of direct pressure on the globe are absolutely contraindicated, and emergent ophthalmologic surgical repair is required.

Hyphema refers to the accumulation of blood in the anterior chamber of the eye, most commonly resulting from blunt ocular trauma. The severity is graded by the proportion of the anterior chamber occupied by blood, ranging from a microhyphema with only circulating red blood cells to a complete eight-ball hyphema filling the entire chamber. Treatment includes cycloplegic drops to reduce ciliary spasm, topical steroids to decrease inflammation, a rigid eye shield for protection, and head-of-bed elevation to promote layering and absorption of blood. A significant concern is the risk of rebleeding, which peaks at three to five days after the initial injury and can lead to secondary glaucoma. Patients with sickle cell disease or trait are at substantially higher risk for complications, as sickling within the anterior chamber can obstruct aqueous outflow and cause dangerously elevated intraocular pressure even with relatively small hyphemas.

Corneal abrasions and foreign bodies are among the most common ocular complaints in the emergency department. Patients present with pain, tearing, foreign body sensation, and photophobia. Diagnosis is made by fluorescein staining, which reveals the epithelial defect under cobalt blue light, and slit lamp examination allows detailed evaluation of the cornea. Foreign bodies should be removed under direct visualization, and any retained metallic foreign body should have its associated rust ring removed to prevent ongoing corneal irritation. Treatment consists of topical antibiotic prophylaxis, with fluoroquinolone drops specifically indicated for contact lens wearers due to the elevated risk of Pseudomonas keratitis. Eye patching is no longer recommended for corneal abrasions, as studies have demonstrated it does not improve healing rates and may actually decrease patient comfort.

<image>Panel A: Emergency irrigation of a chemical eye burn using a Morgan lens delivering continuous normal saline flow across the ocular surface with pH testing strips shown beside the setup. Panel B: Slit lamp photograph of a globe rupture demonstrating an irregular pupil, shallow anterior chamber, and positive Seidel test with fluorescein streaming from the wound site. Panel C: Slit lamp view of a layered hyphema in the anterior chamber showing a visible blood-fluid level with clear cornea above the blood layer. Panel D: Fluorescein-stained corneal abrasion under cobalt blue illumination showing a bright green epithelial defect with sharp margins and surrounding uptake pattern.</image>

Section 3: Red Eye

The differential diagnosis of the red eye is broad, and the emergency physician must systematically evaluate pain, vision, discharge, and pupil findings to distinguish benign from sight-threatening conditions. Conjunctivitis typically presents with minimal pain, normal vision, and discharge, with a normal pupil. Corneal abrasion causes pain and decreased vision with tearing but maintains a normal pupil. Iritis produces pain, decreased vision, and no discharge, with a characteristically constricted pupil. Acute angle-closure glaucoma causes severe pain, decreased vision, and no discharge, with a fixed dilated pupil. Scleritis produces severe pain that may be out of proportion to examination findings, with vision that may be normal or decreased, no discharge, and a normal pupil. This systematic approach using key clinical features allows the clinician to rapidly narrow the differential and guide appropriate management.

Conjunctivitis is classified into viral, bacterial, allergic, and hyperacute subtypes, each requiring distinct management. Viral conjunctivitis, the most common form, presents with watery discharge and often an associated preauricular lymph node; treatment is supportive with cold compresses and artificial tears. Bacterial conjunctivitis produces purulent discharge and is treated with topical antibiotics such as erythromycin ointment or fluoroquinolone drops. Allergic conjunctivitis is characterized by prominent itching, bilateral involvement, and seasonal patterns, managed with antihistamine or mast cell stabilizer drops. Hyperacute conjunctivitis, presenting with copious purulent discharge and rapid onset, should raise immediate concern for gonococcal infection and requires systemic antibiotic therapy with ceftriaxone in addition to topical treatment, along with evaluation for concurrent chlamydial infection.

Iritis, also termed anterior uveitis, is an inflammation of the iris and ciliary body that presents with pain, photophobia, tearing, and a characteristic ciliary flush consisting of a ring of injection surrounding the limbus. Slit lamp examination reveals cells and flare in the anterior chamber, representing inflammatory cells and protein leak respectively, along with miosis due to ciliary spasm. The causes of iritis include trauma, autoimmune conditions such as HLA-B27-associated spondyloarthropathies, infections including herpes simplex and syphilis, and idiopathic inflammation. Emergency department treatment includes cycloplegic drops such as cyclopentolate or homatropine to relieve ciliary spasm and prevent posterior synechiae, and topical corticosteroid drops should be initiated with ophthalmology follow-up arranged within 24 hours for ongoing management.

Distinguishing periorbital from orbital cellulitis is critical because these two conditions carry vastly different morbidity profiles. Periorbital (preseptal) cellulitis is an infection anterior to the orbital septum, presenting with eyelid erythema and swelling but preserving normal extraocular movements, vision, and globe position; it is typically treated with oral antibiotics on an outpatient basis. Orbital (postseptal) cellulitis, by contrast, involves infection posterior to the orbital septum within the orbit itself, producing proptosis, painful or limited extraocular movements, and potential visual compromise. Orbital cellulitis requires emergent CT imaging to evaluate for orbital abscess, intravenous broad-spectrum antibiotics, and often surgical drainage. Complications of orbital cellulitis include cavernous sinus thrombosis, meningitis, intracranial abscess, and permanent vision loss, making timely differentiation between these two entities essential.

<image>Panel A: Comparison chart of red eye differential diagnosis showing conjunctival injection patterns in conjunctivitis with diffuse injection, iritis with ciliary flush, and acute glaucoma with diffuse injection and corneal haze. Panel B: Clinical photographs comparing the four types of conjunctivitis showing watery discharge in viral, purulent discharge in bacterial, chemosis with lid swelling in allergic, and copious purulent discharge in hyperacute gonococcal. Panel C: Slit lamp photograph of anterior uveitis demonstrating cells and flare in the anterior chamber with a constricted pupil and ciliary flush around the limbus. Panel D: CT scan comparison of periorbital cellulitis showing preseptal soft tissue swelling with normal orbital contents versus orbital cellulitis showing proptosis, fat stranding, and a subperiosteal abscess.</image>

Section 4: Epistaxis

Epistaxis is one of the most common ENT emergencies encountered in the emergency department, and the initial assessment must distinguish between anterior and posterior sources because management differs significantly. Anterior epistaxis, accounting for approximately 90 percent of cases, originates from Kiesselbach's plexus on the anterior nasal septum, where branches of the anterior ethmoid, superior labial, sphenopalatine, and greater palatine arteries form an anastomotic network. Anterior bleeds are typically less severe and more amenable to conservative measures. Posterior epistaxis, comprising the remaining 10 percent, originates from branches of the sphenopalatine artery in the posterior nasal cavity. Posterior bleeds tend to be more severe, are more common in elderly or anticoagulated patients, and often require ENT consultation for definitive management.

Initial management of epistaxis follows a systematic stepwise approach. The patient should lean forward to prevent aspiration of blood, and direct pressure should be applied by firmly pinching the nasal alae together for 10 to 15 continuous minutes without releasing to check for hemostasis prematurely. After the pressure period, the nasal cavity should be carefully inspected. If a discrete bleeding vessel is identified, chemical cautery with silver nitrate can be applied directly to the site. Topical vasoconstrictors such as oxymetazoline or phenylephrine on cotton pledgets can be placed to achieve local hemostasis. It is important to apply cautery to only one side of the septum at a time to avoid the risk of septal perforation from bilateral cauterization.

When initial conservative measures fail to control anterior epistaxis, nasal packing is the next intervention. Absorbable packing materials include gelatin sponge (Gelfoam) and oxidized cellulose (Surgicel), which dissolve over time and do not require removal. Non-absorbable options include compressed hydroxylated polyvinyl acetate sponges (Merocel) and pneumatic nasal tampons (Rapid Rhino), which expand upon contact with saline or inflation to provide tamponade against the bleeding site. Balloon-based devices expand with saline to fill the nasal cavity and apply direct pressure. Nasal packing is typically left in place for 24 to 72 hours, and prophylactic antibiotics should be considered while packing is in place to reduce the risk of sinusitis and, rarely, toxic shock syndrome.

Posterior epistaxis is recognized when anterior measures fail to control bleeding and blood is seen flowing posteriorly in the pharynx. Management requires posterior packing using a dual-balloon device or a Foley catheter placed through the naris with the balloon inflated in the nasopharynx to tamponade the posterior source. Patients with posterior packing must be admitted to a monitored setting because of the risk of respiratory compromise, including the nasopulmonary reflex that can cause hypoventilation and hypoxemia. ENT consultation is essential, and definitive treatment options include endoscopic cauterization of the sphenopalatine artery, angiographic embolization of the internal maxillary artery, or surgical ligation of the offending vessel. Patients on anticoagulation should have their coagulation status assessed and corrected as clinically appropriate.

<image>Panel A: Anatomical diagram of the nasal septum showing Kiesselbach's plexus at the anterior septum with its contributing arterial branches (anterior ethmoid, superior labial, sphenopalatine, and greater palatine arteries) and the posterior sphenopalatine artery territory. Panel B: Stepwise illustration of initial epistaxis management showing patient positioning leaning forward, two-finger pinch technique on the nasal alae, and silver nitrate cautery application to a visible vessel on the anterior septum. Panel C: Comparison of anterior nasal packing devices including a Merocel sponge before and after saline expansion, a Rapid Rhino device with inflated balloon, and absorbable Gelfoam pledgets. Panel D: Dual-balloon posterior nasal packing device in situ showing the posterior balloon inflated in the nasopharynx and the anterior balloon occluding the anterior nasal cavity with the catheter secured externally.</image>

Section 5: Vertigo

The evaluation of vertigo in the emergency department centers on distinguishing peripheral causes, which are generally benign, from central causes, which may represent life-threatening posterior circulation stroke or mass lesions. Peripheral vertigo is characterized by horizontal-rotary nystagmus that suppresses with visual fixation, may be accompanied by hearing loss, and is notable for the absence of neurologic signs. Central vertigo may present with vertical or direction-changing nystagmus that does not suppress with fixation, is rarely associated with hearing loss, and is accompanied by cerebellar or brainstem neurologic deficits such as dysarthria, diplopia, dysphagia, or ataxia. Peripheral causes include benign paroxysmal positional vertigo (BPPV), vestibular neuritis, Meniere's disease, and labyrinthitis. Central causes include posterior circulation stroke, cerebellar hemorrhage, and posterior fossa mass lesions.

The HINTS examination is a three-component bedside test that has been demonstrated to be more sensitive than early MRI for detecting posterior circulation stroke in the setting of acute vestibular syndrome. The Head Impulse test assesses the vestibulo-ocular reflex: a corrective saccade during rapid head turning indicates a peripheral lesion, whereas a normal head impulse test (no corrective saccade) is paradoxically the dangerous finding, suggesting a central cause that has spared the reflex arc. The Nystagmus component evaluates the direction of nystagmus: unidirectional nystagmus suggests a peripheral etiology, whereas direction-changing nystagmus with gaze in different directions indicates a central lesion. The Test of Skew evaluates vertical ocular misalignment by alternately covering and uncovering each eye: a vertical refixation movement indicates a central brainstem lesion. Any single central finding on the HINTS examination should prompt urgent neuroimaging and neurology consultation.

The most common peripheral causes each have distinctive features and specific treatments. BPPV is caused by displaced otoconia within the semicircular canals and presents with brief episodes of vertigo triggered by specific head positions, diagnosed by the Dix-Hallpike maneuver and treated with the Epley canalith repositioning maneuver. Vestibular neuritis presents as constant severe vertigo lasting days, often following a viral illness, with unilateral vestibular hypofunction but preserved hearing, managed supportively with possible benefit from corticosteroids. Meniere's disease is characterized by the triad of episodic vertigo, fluctuating sensorineural hearing loss, and tinnitus, with long-term management including dietary salt restriction and diuretics. Labyrinthitis is clinically similar to vestibular neuritis but additionally involves hearing loss, suggesting inflammation of the labyrinth itself, treated with corticosteroids and sometimes antivirals.

Symptomatic treatment of vertigo should be used judiciously and for limited duration. Vestibular suppressants such as meclizine reduce the severity of acute vertiginous symptoms by dampening vestibular nerve activity. Benzodiazepines such as diazepam may be used for severe symptoms refractory to meclizine, providing both vestibular suppression and anxiolysis. Ondansetron is effective for managing the nausea and vomiting that frequently accompany acute vertigo. However, it is critically important that long-term use of vestibular suppressants is avoided, as these medications delay central vestibular compensation, the natural process by which the brain adapts to unilateral vestibular loss. Patients should be counseled that early mobilization and vestibular rehabilitation exercises promote faster recovery than prolonged medication use.

<image>Panel A: Comparison diagram illustrating peripheral versus central vertigo features, showing horizontal-rotary nystagmus on one side and vertical nystagmus on the other, with associated clinical features listed beneath each type. Panel B: Step-by-step illustration of the three-component HINTS examination showing head impulse testing with corrective saccade versus normal response, direction of nystagmus assessment, and the alternate cover-uncover test of skew deviation. Panel C: Dix-Hallpike maneuver and Epley repositioning sequence for posterior canal BPPV, showing patient and examiner positions through each step with arrows indicating the direction of head movement. Panel D: Anatomical cross-section of the inner ear labyrinth showing the semicircular canals, cochlea, and vestibular nerve with annotations indicating the sites of pathology in BPPV, vestibular neuritis, Meniere's disease, and labyrinthitis.</image>

Section 6: Ear Emergencies

Acute otitis media (AOM) is one of the most common infections in pediatric patients and represents a frequent emergency department presentation. Patients present with otalgia, fever, irritability in young children, and middle ear effusion. The diagnosis is confirmed by otoscopic examination revealing a bulging, opacified tympanic membrane with decreased mobility on pneumatic otoscopy. First-line treatment is high-dose amoxicillin at 90 mg/kg/day for children, reflecting the need to overcome increasing beta-lactamase-producing organisms. Observation without antibiotics is an acceptable strategy for children older than two years with mild, unilateral disease and reliable follow-up. Complications of inadequately treated AOM include mastoiditis, characterized by postauricular swelling and erythema with protrusion of the pinna, tympanic membrane perforation, and rarely intracranial extension including brain abscess or meningitis.

Otitis externa, commonly known as swimmer's ear, results from infection of the external auditory canal, typically precipitated by moisture exposure or local trauma such as aggressive ear cleaning. The hallmark examination finding is pain elicited by traction on the pinna or pressure on the tragus, distinguishing it from otitis media. The canal appears erythematous, edematous, and may contain purulent debris. Treatment consists of topical fluoroquinolone drops, often combined with a corticosteroid to reduce inflammation and edema. When canal edema is severe enough to prevent adequate drop penetration, a compressed cellulose wick should be inserted to facilitate medication delivery. Malignant (necrotizing) otitis externa is a serious complication seen predominantly in diabetic and immunocompromised patients, where Pseudomonas aeruginosa infection extends beyond the canal into surrounding bone, causing skull base osteomyelitis that requires prolonged intravenous antibiotics and often surgical debridement.

Foreign bodies in the ear canal are a common pediatric emergency and occasionally present in adults. Adequate visualization with appropriate lighting and an otoscope is essential before attempting removal. Removal techniques include alligator forceps for graspable objects, suction-tipped devices for smooth objects, and irrigation with warm water for non-organic, non-battery objects. Irrigation is strictly contraindicated when a button battery is present, as the alkaline contents can cause rapid liquefactive necrosis of the ear canal and tympanic membrane, and when a tympanic membrane perforation is suspected. Button batteries represent a true emergency requiring immediate removal due to their ability to cause tissue destruction within hours through direct electrical current and alkali leakage. Live insects should be killed prior to removal by instilling mineral oil or lidocaine into the canal to prevent further canal trauma from the insect's movement.

Tympanic membrane perforation can result from direct trauma such as cotton swab insertion or foreign body injury, barotrauma from diving or flying, or infection as a complication of acute otitis media. Patients report sudden pain at the time of perforation followed by hearing loss and possibly bloody or purulent drainage. Examination reveals a visible defect in the tympanic membrane, which may range from a small pinpoint perforation to a large subtotal disruption. Management is conservative in the majority of cases: the ear should be kept dry by avoiding water entry, and most traumatic perforations heal spontaneously within weeks to months. Antibiotic drops are prescribed only if there is evidence of active infection. Patients who do not demonstrate healing on follow-up examination should be referred to an ENT specialist for consideration of tympanoplasty.

<image>Panel A: Otoscopic view of acute otitis media showing a bulging, erythematous tympanic membrane with loss of normal landmarks and purulent middle ear effusion visible through the semi-translucent membrane. Panel B: Otoscopic image of otitis externa demonstrating a narrowed, edematous external auditory canal with erythema, purulent debris, and a wick placed for topical medication delivery. Panel C: Illustration of ear foreign body removal techniques showing alligator forceps grasping a bead, suction-tip device applied to a smooth object, and warm water irrigation with a syringe directed along the canal wall. Panel D: Otoscopic view of a traumatic tympanic membrane perforation showing a well-defined defect in the pars tensa with visible middle ear structures through the perforation and surrounding hemorrhage at the edges.</image>

Section 7: Throat Emergencies

Peritonsillar abscess (PTA), also known as quinsy, is the most common deep space infection of the head and neck and represents the most frequent ENT emergency requiring drainage. Patients present with severe sore throat, often unilateral, progressive dysphagia, trismus (difficulty opening the mouth due to pterygoid muscle spasm), and a characteristic muffled "hot potato" voice. On examination, the affected tonsil appears erythematous and displaced medially with a bulging soft palate, and the uvula is deviated away from the side of the abscess. The diagnosis is primarily clinical, though CT with contrast can be obtained when the diagnosis is uncertain or when extension into deeper neck spaces is suspected. Treatment consists of needle aspiration or incision and drainage of the abscess cavity, combined with systemic antibiotics such as penicillin or clindamycin, and corticosteroids may be administered to reduce edema and improve symptoms.

Retropharyngeal abscess is a deep neck space infection that occurs predominantly in children under six years of age, because the retropharyngeal lymph nodes that suppurate to form these abscesses involute after this age. Patients present with neck pain, stiffness, fever, dysphagia, and may hold the neck in extension to maximize airway patency. A lateral neck radiograph may demonstrate widening of the prevertebral soft tissue space, with a measurement greater than 7 mm at the level of C2 being suggestive of pathology. CT with contrast is the definitive imaging modality, delineating the extent of the abscess and its relationship to surrounding structures including the carotid sheath and airway. The primary dangers of retropharyngeal abscess include airway compromise from mass effect and the potential for rupture leading to aspiration pneumonia or extension into the mediastinum causing mediastinitis, a rapidly fatal complication. Treatment requires intravenous antibiotics with anaerobic and gram-positive coverage and typically surgical drainage.

Epiglottitis is an infection and inflammation of the epiglottis and supraglottic structures that can rapidly progress to complete airway obstruction. The classic presentation includes the four D's: dysphagia, drooling, dysphonia, and distress, along with stridor and a tripod positioning with the patient leaning forward on extended arms to optimize airway patency. In children, it is imperative not to agitate the patient or attempt to examine the throat, as these actions can precipitate acute laryngospasm and complete airway obstruction. Lateral neck radiography may demonstrate the pathognomonic thumbprint sign representing the swollen epiglottis. Management prioritizes airway control, ideally performed in the operating room with both anesthesiology and surgical backup available, followed by intravenous antibiotics covering Haemophilus influenzae and other potential pathogens. Although the incidence in children has declined dramatically since widespread Hib vaccination, epiglottitis in adults is increasingly recognized and may present with less dramatic symptoms, requiring a higher index of suspicion.

Ludwig's angina is a rapidly progressive bilateral cellulitis of the submandibular, sublingual, and submental spaces that represents one of the most dangerous deep neck space infections. The infection most commonly originates from dental sources, particularly lower molar infections that spread through the mylohyoid muscle. Patients present with a firm, brawny swelling of the floor of the mouth and upper neck, tongue elevation and protrusion, drooling, trismus, and a characteristic "bull neck" appearance. The primary threat is airway obstruction from progressive swelling that displaces the tongue posteriorly and superiorly. Management requires immediate assessment and securing of the airway, which may be extremely challenging due to distorted anatomy and may require awake fiberoptic intubation or surgical airway. Broad-spectrum intravenous antibiotics with coverage for oral flora including anaerobes are administered, and surgical drainage or debridement may be necessary for cases with abscess formation or failure to improve.

<image>Panel A: Intraoral examination of a peritonsillar abscess showing a bulging, erythematous soft palate with medial displacement of the tonsil and uvular deviation to the contralateral side, with needle aspiration being performed. Panel B: Contrast-enhanced CT scan of the neck in a child with retropharyngeal abscess showing a rim-enhancing hypodense fluid collection in the retropharyngeal space causing anterior displacement of the airway. Panel C: Lateral neck radiograph demonstrating the thumbprint sign of epiglottitis with a markedly swollen, rounded epiglottis compared to the normal thin epiglottic shadow, alongside a clinical photograph of a child in tripod position. Panel D: Clinical photograph of Ludwig's angina showing massive bilateral submandibular swelling with a tense, erythematous "bull neck" appearance and tongue protrusion with floor-of-mouth elevation.</image>

Section 8: Dental Emergencies

Dental infections represent a spectrum of severity ranging from localized pulpitis to life-threatening deep space infections. Pulpitis is inflammation of the dental pulp, presenting as tooth pain that may be exacerbated by hot or cold stimuli; it is managed with analgesics and dental referral for definitive care. Periapical abscess occurs when pulpal infection extends through the tooth apex into surrounding alveolar bone, presenting as localized swelling, fluctuance, and tenderness at the gum line overlying the affected tooth root. Treatment includes antibiotics, incision and drainage when a fluctuant collection is present, and referral for extraction or root canal therapy. Dental nerve blocks provide effective pain control in the emergency department, with the inferior alveolar nerve block anesthetizing the lower teeth, lower lip, and chin, and the mental nerve block providing anesthesia to the premolar region and anterior lower lip. These infections can progress to Ludwig's angina, parapharyngeal abscess, or other deep space infections that compromise the airway, emphasizing the importance of recognizing dental infections that require emergent rather than elective treatment.

Dental trauma requires prompt assessment and management, particularly for avulsed permanent teeth where reimplantation success is directly time-dependent. An avulsed permanent tooth should be reimplanted as quickly as possible, ideally within 30 minutes, with the best outcomes achieved when reimplantation occurs within 5 minutes of avulsion. If immediate reimplantation is not possible, the tooth should be stored in Hank's balanced salt solution, cold milk, or the patient's own saliva to preserve periodontal ligament cell viability. Critically, avulsed primary (deciduous) teeth should never be reimplanted because reimplantation can damage the developing permanent tooth bud. Subluxated teeth, which are loosened but remain in the socket, are managed with soft diet, avoidance of the affected area, and dental follow-up for possible splinting. Fractured teeth are classified by the Ellis system: class I involves enamel only, class II exposes the yellow dentin, and class III exposes the pink pulp, with classes II and III requiring coverage with calcium hydroxide paste and urgent dental referral.

Post-extraction bleeding is a common dental emergency that can be alarming to patients but is usually manageable with systematic intervention. The initial approach involves direct pressure by having the patient bite firmly on gauze placed over the extraction socket for 20 to 30 minutes. If direct pressure fails, hemostatic agents such as gelatin sponge (Gelfoam) or oxidized cellulose (Surgicel) can be packed into the socket to promote clot formation. Sutures may be placed across the socket to secure packing and provide additional hemostatic compression. Tranexamic acid, either as an oral rinse or soaked into gauze, is an effective adjunctive measure that inhibits fibrinolysis at the local level. Patients with refractory post-extraction bleeding should be evaluated for underlying coagulopathy including platelet disorders, von Willebrand disease, anticoagulant use, or liver disease, and appropriate factor replacement or reversal agents should be administered as indicated.

Temporomandibular joint (TMJ) dislocation typically occurs anteriorly when the mandibular condyle translates forward past the articular eminence and becomes locked in position. Patients present with an inability to close the mouth, often following a wide yawn, dental procedure, or seizure, with the jaw held in an open and sometimes asymmetric position. The reduction technique involves the clinician placing their thumbs on the patient's posterior lower molars (wrapped in gauze for protection), applying steady downward pressure to disengage the condyle from the anterior position, and then guiding the mandible posteriorly as the condyle slides back into the glenoid fossa. Muscle relaxation with benzodiazepines or procedural sedation significantly facilitates reduction by overcoming the masticatory muscle spasm that often prevents manual reduction. Patients should be counseled to avoid wide mouth opening, to support the jaw when yawning, and to follow up if recurrent dislocations occur, as chronic instability may require surgical intervention.

<image>Panel A: Intraoral photograph of a periapical dental abscess showing gingival swelling and erythema overlying the affected tooth root, with illustration of the inferior alveolar nerve block injection technique targeting the mandibular foramen. Panel B: Clinical photograph of a completely avulsed permanent incisor alongside images of appropriate storage media including Hank's balanced salt solution container and a cup of cold milk, with the reimplantation technique demonstrated. Panel C: Step-by-step management of post-extraction socket bleeding showing gauze placement, hemostatic agent (Gelfoam) insertion into the socket, and figure-of-eight suture closure across the socket margins. Panel D: Illustration of TMJ dislocation reduction technique showing the examiner's thumb placement on the posterior molars, directional arrows indicating downward then posterior force application, and before-and-after radiographic appearance of the condyle position.</image>

Section 9: Neck Emergencies

Deep neck space infections represent a spectrum of conditions that share the common threat of airway compromise and potential for extension into the mediastinum. Peritonsillar abscess presents with trismus and deviated uvula, retropharyngeal abscess with neck stiffness predominantly in children, parapharyngeal abscess with lateral neck swelling and potential carotid sheath involvement, and Ludwig's angina with floor-of-mouth elevation and submandibular swelling. Each of these infections can progress rapidly from cellulitis to organized abscess to rupture, with the potential for aspiration pneumonia, mediastinitis, internal jugular vein thrombosis (Lemierre syndrome), or carotid artery erosion. The deep cervical fascia creates interconnected potential spaces that allow infection to track from one compartment to another, explaining why deep neck infections can disseminate widely despite originating from a localized source. Timely imaging with contrast-enhanced CT, broad-spectrum intravenous antibiotics, and surgical consultation for drainage are the cornerstones of management.

Penetrating neck trauma is evaluated using a zone-based system that guides diagnostic and management decisions. Zone I extends from the clavicles and sternal notch to the cricoid cartilage and contains the proximal carotid arteries, subclavian vessels, trachea, esophagus, thoracic duct, and lung apices. Zone II extends from the cricoid cartilage to the angle of the mandible and contains the carotid arteries, jugular veins, larynx, trachea, esophagus, and pharynx. Zone III extends from the angle of the mandible to the skull base and contains the distal carotid and vertebral arteries and pharynx. Hard signs of vascular or aerodigestive injury, including active hemorrhage, expanding hematoma, hemodynamic shock, air bubbling through the wound, massive hemoptysis, or hematemesis, mandate immediate operative exploration regardless of zone. Soft signs such as stable hematoma, dysphagia, hoarseness, or minor hemoptysis warrant observation and further imaging with CT angiography.

Esophageal foreign bodies are a common emergency, particularly in the pediatric population, and occur at predictable anatomic narrowing points. The three physiologic constriction points of the esophagus are the cricopharyngeus muscle (upper esophageal sphincter), the level of the aortic arch, and the lower esophageal sphincter. Children most commonly present with drooling, refusal to eat, and dysphagia after witnessed or suspected ingestion. Button battery ingestion in the esophagus constitutes a true emergency requiring removal within two hours, as the battery can cause full-thickness esophageal necrosis, perforation, and fistula formation to the aorta through direct electrical current, alkali generation, and pressure necrosis. Coins lodged in the esophagus of asymptomatic patients may be observed for up to 24 hours with the expectation of spontaneous passage, but persistent impaction requires endoscopic removal. Sharp or pointed objects necessitate gastroenterology or surgical consultation for planned endoscopic removal due to the risk of perforation.

Airway foreign body obstruction ranges from partial to complete and requires immediate recognition and intervention. Complete obstruction presents with the universal choking sign of hands clutching the throat, inability to speak, breathe, or cough, and rapidly progressive cyanosis. Partial obstruction presents with stridor, a weak cough, and preserved but compromised voice. In conscious adults and children over one year, abdominal thrusts (Heimlich maneuver) are the initial intervention, while back blows alternating with chest thrusts are used for infants. If the patient loses consciousness, standard CPR with chest compressions is initiated and the oropharynx is visually inspected for the foreign body before each ventilation attempt. If these measures fail, direct laryngoscopy with Magill forceps removal should be attempted, followed by bronchoscopy for foreign bodies that have passed beyond the glottis. Chest radiography may not demonstrate the foreign body if it is radiolucent, but findings such as unilateral hyperinflation, atelectasis, or air trapping on expiratory films can provide indirect evidence of obstruction.

<image>Panel A: Anatomical diagram of the deep neck spaces showing the peritonsillar, retropharyngeal, parapharyngeal, and submandibular spaces with arrows indicating potential pathways of infection spread and relationship to the carotid sheath and mediastinum. Panel B: Illustration of the three zones of the neck with zone I below the cricoid cartilage, zone II between the cricoid and mandible angle, and zone III above the mandible angle, with key vascular and aerodigestive structures labeled in each zone. Panel C: Anteroposterior and lateral radiographs showing a coin lodged at the cricopharyngeus level and a button battery in the esophagus with the characteristic double-ring or halo sign on AP view. Panel D: Algorithm for airway foreign body management showing progression from abdominal thrusts in the conscious patient to CPR in the unconscious patient to direct laryngoscopy with Magill forceps to bronchoscopy, with corresponding clinical illustrations at each step.</image>

Section 10: Facial Trauma

Nasal fractures are the most common facial fracture and are diagnosed clinically based on the mechanism of injury, deformity, swelling, and crepitus, with radiographic imaging rarely adding useful information and therefore not routinely indicated. The most critical aspect of the emergency department evaluation is ruling out a septal hematoma, which appears as a boggy, fluctuant, purple swelling on the nasal septum. Septal hematomas must be incised and drained emergently because the accumulated blood separates the septal cartilage from its perichondrial blood supply, leading to avascular necrosis of the septum and subsequent saddle nose deformity if untreated. Management of the nasal fracture itself includes pain control, ice application, and referral to ENT or plastic surgery for definitive reduction, which is optimally performed 5 to 10 days after injury when swelling has subsided but before bony union has occurred.

Mandible fractures are the second most common facial fracture and should be suspected in any patient presenting with malocclusion, trismus, lower lip numbness from inferior alveolar nerve injury, or a palpable step-off along the mandibular border. Because the mandible is a ring structure, fractures frequently occur in two locations, analogous to a pretzel. Imaging is performed with panoramic radiography (Panorex) or CT scan, which provides superior detail of fracture location and displacement. Treatment depends on the location and severity: nondisplaced fractures may be managed with a soft diet and close follow-up, while displaced fractures require open reduction and internal fixation (ORIF) or maxillomandibular fixation (wiring). Fractures that communicate with the oral cavity through the gingiva are considered compound fractures and require prophylactic antibiotics, typically penicillin or clindamycin, to prevent osteomyelitis.

Orbital fractures encompass several patterns that result from blunt facial trauma. Orbital blowout fractures result from direct impact to the globe that transmits hydraulic force to the thin orbital floor or medial wall, producing infraorbital nerve numbness, diplopia from inferior rectus entrapment, and enophthalmos from increased orbital volume. Tripod (zygomaticomaxillary complex) fractures involve the zygomatic arch, orbital floor, and lateral orbital wall, producing lateral facial flattening, trismus, and infraorbital hypoesthesia. Le Fort fractures are classified into three progressively extensive patterns: Le Fort I is a horizontal maxillary fracture, Le Fort II is a pyramidal fracture through the infraorbital rim and nasal bridge, and Le Fort III is complete craniofacial disjunction. CT imaging is the modality of choice for all orbital and mid-face fractures. Surgical intervention is indicated for fractures with significant cosmetic deformity, extraocular muscle entrapment causing restrictive strabismus, or enophthalmos greater than 2 mm.

Septal hematoma warrants special emphasis because it is easily missed and carries significant consequences if untreated. The hematoma forms when blunt nasal trauma shears blood vessels between the septal cartilage and its overlying perichondrium, creating a collection of blood that progressively separates the cartilage from its sole nutritional source. On examination, the nasal septum appears as a boggy, purple, grape-like swelling that is fluctuant to palpation rather than the firm, midline structure of normal septum. Treatment is incision and drainage performed under local anesthesia, with a small incision made through the mucoperichondrium to evacuate the hematoma, followed by placement of bilateral nasal splints or packing to prevent re-accumulation. If the diagnosis is delayed, the cartilage undergoes avascular necrosis leading to septal perforation, loss of dorsal nasal support, and the characteristic saddle nose deformity. Every patient presenting with nasal trauma, regardless of apparent severity, should have an anterior rhinoscopy performed specifically to evaluate for septal hematoma.

<image>Panel A: Clinical photograph of a displaced nasal fracture with associated nasal deviation, periorbital ecchymosis, and epistaxis, alongside an anterior rhinoscopy view showing a septal hematoma as a smooth, purple, fluctuant mass on the nasal septum. Panel B: Panoramic radiograph (Panorex) of bilateral mandible fractures showing fracture lines through the parasymphysis and angle with associated displacement and malocclusion. Panel C: CT scan comparison of orbital fractures showing an orbital floor blowout fracture with herniation of orbital fat and inferior rectus muscle into the maxillary sinus, a tripod fracture with zygomatic displacement, and Le Fort fracture classification diagrams (types I, II, and III) on a skull model. Panel D: Step-by-step illustration of septal hematoma drainage showing the fluctuant septal swelling on anterior rhinoscopy, local anesthetic injection, mucosal incision and hematoma evacuation, and bilateral anterior nasal packing placement to prevent re-accumulation.</image>

Summary

• CRAO presents as painless monocular vision loss with a cherry-red spot on fundoscopy and requires intervention within 90 minutes
• Acute angle-closure glaucoma causes severe pain, halos, and a fixed mid-dilated pupil requiring emergent intraocular pressure reduction with timolol, pilocarpine, and acetazolamide
• Chemical eye burns demand immediate copious irrigation before any other assessment, with alkali burns being more dangerous than acid due to deep tissue penetration
• Globe rupture requires a protective shield without pressure, NPO status, antiemetics, and emergent ophthalmologic surgical repair
• Epistaxis management follows a stepwise approach: pinch for 10 to 15 minutes, cauterize visible vessels, anterior packing if conservative measures fail, and posterior packing with ENT for refractory cases
• The HINTS examination (Head Impulse, Nystagmus, Test of Skew) is more sensitive than early MRI for detecting central vertigo, with a normal head impulse being the dangerous finding suggesting stroke
• Peritonsillar abscess presents with "hot potato" voice, trismus, and deviated uvula and is treated with needle aspiration or incision and drainage
• Avulsed permanent teeth should be reimplanted within 30 minutes and stored in milk or Hank's solution; avulsed primary teeth should never be reimplanted
• Septal hematoma must be drained immediately on diagnosis to prevent avascular necrosis and saddle nose deformity
• Ludwig's angina is a rapidly progressive submandibular cellulitis originating from dental infection that constitutes an airway emergency requiring early airway management

Key Terms

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