Emergency and Acute Medicine – Neck Trauma, Blunt, Anterior




Blunt anterior neck trauma can result in injury to multiple critical structures, including vascular, laryngotracheal, pharyngoesophageal, neurologic, and cervical spine components. Vascular injuries may involve the carotid or vertebral arteries and include intramural hematoma, intimal tear, thrombosis, pseudoaneurysm, hemorrhage, or expanding neck hematoma. Laryngotracheal injuries include fractures of the hyoid bone, thyroid or cricoid cartilage, cricotracheal separation, vocal cord disruption, arytenoid dislocation, and tracheal hematoma or transection. Pharyngoesophageal injuries may present as hematoma or perforation of the pharynx or esophagus. Neurologic injury can involve the thoracic sympathetic chain causing Horner syndrome, the vagus or recurrent laryngeal nerves, cervical nerve roots, or spinal cord. Cervical spine fractures or dislocations may also be present.


The most common etiology is motor vehicle collisions, particularly frontal impacts in unrestrained occupants striking the dashboard or steering wheel (“padded dash syndrome”), or from shoulder harness–related shearing injury. Other causes include assault with blows to the anterior neck, “clothesline injuries” from motorcycles or recreational vehicles striking suspended wires or cords, and strangulation. In children, the proportionally larger head increases risk for acceleration–deceleration injury, and intraoral trauma to the soft palate may lead to carotid artery thrombosis.


Clinical presentation varies by injured structure. Vascular injury may cause hemorrhage, ecchymosis, edema, carotid bruit or thrill (highly suggestive of vascular injury), and delayed neurologic deficits. Laryngotracheal injury may present with hoarseness, aphonia, dyspnea, inspiratory stridor, labored breathing, air hunger, subcutaneous emphysema, and anterior neck tenderness. Pharyngoesophageal injury may cause dysphagia, odynophagia, hematemesis, blood in saliva, and delayed infection or sepsis. Neurologic injury may manifest as central or peripheral deficits. History should focus on mechanism, force, associated symptoms, and injuries beyond the neck, as blunt neck trauma is commonly associated with head and chest injuries.


Physical examination must prioritize airway protection and patency. The neck should be inspected for hemorrhage, hematoma, ecchymosis, edema, and anatomic distortion, auscultated for carotid bruits or stridor, and palpated for tenderness or subcutaneous emphysema. A complete neurologic examination is essential to detect ischemic events, spinal cord injury, or peripheral nerve damage, along with a full trauma examination for associated injuries.


Workup depends on clinical findings. Laboratory studies may include type and cross-match, CBC, and renal function prior to contrast imaging. Cervical spine and lateral neck radiographs have limited value but may show prevertebral swelling, subglottic narrowing, subcutaneous air, or calcified cartilage fractures. Chest radiograph is useful for detecting pneumothorax or pneumomediastinum. Carotid duplex ultrasonography is a rapid, noninvasive screening tool but is operator dependent and limited above the bifurcation. CT is useful in stable patients to evaluate laryngotracheal injury, cartilage disruption, and cervical spine trauma. CT angiography and magnetic resonance angiography have high specificity but limited sensitivity; four-vessel angiography remains the gold standard for arterial injury evaluation. Indications for angiography include carotid bruit, expanding neck hematoma, neurologic deficit with normal head CT, Horner syndrome, or decreased level of consciousness. Fiberoptic laryngoscopy can assess airway injury and assist with intubation, while suspected esophageal injury should be evaluated initially with a contrast swallow study. Unstable patients require immediate surgical intervention.


Prehospital and initial management focus on vigilant airway monitoring, as edema or hematoma may rapidly compromise the airway. Orotracheal intubation is preferred, while blind nasotracheal intubation should be avoided due to distorted anatomy and risk of hematoma rupture. Cervical spine stabilization is mandatory. Immediate airway control is indicated for respiratory distress, stridor, air hunger, or expanding neck hematoma. Cricothyrotomy or emergent tracheostomy may be required if intubation fails, but is contraindicated when bruising or hematoma overlies the thyroid or cricoid cartilage. Unstable patients should proceed directly to the operating room.


Emergency department management requires early surgical consultation for suspected vascular, tracheal, or esophageal injuries, with immediate repair for symptomatic vascular, tracheal, pharyngeal, or esophageal injuries. Laryngeal injuries may not always require immediate surgery. Anticoagulation is often recommended for vascular injuries to reduce thrombosis and improve neurologic outcomes, but only after surgical consultation. Prophylactic antibiotics with anaerobic coverage are indicated when esophageal injury is present.


Patients who are symptomatic, have abnormal imaging, or sustained significant blunt mechanisms require admission and observation for at least 24 hours, with ICU admission for suspected airway or vascular injury. Patients on anticoagulation should be observed for delayed neck hematoma. Only those with trivial injury and negative evaluation may be discharged with strict return precautions for delayed airway, vascular, or neurologic symptoms. Key pitfalls include underestimating delayed vascular injury, failing to anticipate a difficult airway, and missing associated injuries; preparation for airway deterioration and early specialty involvement are essential.

Emergency and Acute Medicine – Nasal Fractures




Nasal fractures are the most common fractures of the facial skeleton and of the body overall. They usually result from blunt trauma, most commonly due to motor vehicle crashes, sports injuries, and interpersonal altercations. Lateral forces are more likely to cause displacement than direct frontal blows. Although many nasal fractures are isolated and uncomplicated, certain historical and physical features suggest more serious associated injuries, including high-force trauma, loss of consciousness, obvious facial bone injury, frontal bone crepitus, or cerebrospinal fluid (CSF) leakage.


The etiology of nasal fractures is overwhelmingly direct trauma. In adults, altercations are the most frequent cause, whereas in children, sports-related direct blows predominate. Because the pediatric nasal skeleton is more cartilaginous and flexible, significant injury may be present even when deformity appears minimal.


Patients typically present with nasal pain, swelling, deformity, asymmetry, ecchymosis, and epistaxis. Periorbital ecchymosis (“raccoon eyes”) may indicate injury to branches of the ethmoidal artery and raises concern for nasofrontoethmoid complex fractures. Palpable irregularities, sharp edges, crepitus, or abnormal mobility of nasal bones strongly suggest fracture. A critical associated finding is a septal hematoma, which appears as a bluish, fluctuant swelling of the nasal septum; failure to promptly identify and drain it can lead to septal necrosis and permanent deformity. Flattening of the nasal bridge with widening of the intercanthal distance (telecanthus) suggests a serious nasofrontoethmoid injury. Clear rhinorrhea raises concern for a CSF leak, which may be delayed, and anosmia suggests more significant trauma.


History should focus on the mechanism of injury, presence of epistaxis, visual or olfactory changes, and other associated injuries. Physical examination must include careful inspection and palpation of the nose and midface, with particular attention to identifying a septal hematoma and signs of telecanthus. Examination for CSF rhinorrhea is essential; blood-tinged CSF may produce a “double-ring” sign on filter paper, though this finding is not fully reliable.


Routine imaging is rarely required for simple nasal fractures, as radiographs seldom change management. Gross deformities warrant specialist referral regardless of imaging findings, and nondisplaced fractures are treated conservatively even if radiographically evident. Computed tomography is the imaging modality of choice when facial bone fractures, nasofrontoethmoid injuries, or skull base fractures are suspected, and clinicians should have a low threshold for ordering CT when associated injuries are possible.


Initial management prioritizes airway and cervical spine protection, especially in patients with multisystem trauma. Nasotracheal intubation is contraindicated; if airway control is required, orotracheal intubation or cricothyroidotomy should be performed. Epistaxis is often controlled with direct pressure but may require topical anesthetics and vasoconstrictors, cauterization, or nasal packing. Patients with nasal packing should receive prophylactic antibiotics to reduce the risk of sinus and staphylococcal infections.


Definitive reduction of displaced nasal fractures is usually deferred until swelling subsides, typically within 3–5 days, and is performed by an ENT, plastic surgeon, or oral and maxillofacial surgeon. Immediate reduction in the emergency department is generally unnecessary unless airway compromise exists. In contrast, septal hematomas require urgent drainage in the ED, followed by bilateral nasal packing and antibiotic therapy to prevent reaccumulation and infection.


Most patients with isolated nasal fractures can be discharged once epistaxis is controlled and no associated injuries are identified, provided they have reliable follow-up. Admission is reserved for patients with nasoethmoid fractures, CSF leaks, or significant craniofacial injuries. All patients should receive clear instructions to follow up with a specialist within 3–5 days, or sooner (within 24 hours) if a septal hematoma was drained. Careful documentation of the absence or presence of a septal hematoma is essential in every case, as missed hematomas are a common and preventable cause of long-term complications.

Emergency and Acute Medicine – Myocardial Contusion

Myocardial contusion, also referred to as blunt cardiac injury (BCI), is a form of cardiac trauma resulting from blunt force to the chest. Pathologically, it is characterized by a discrete, well-demarcated area of myocardial hemorrhage, most commonly involving the subendocardium. In some cases, the injury may extend in a pyramidal, transmural fashion. Due to its anatomic position, the anterior wall of the right ventricle or right atrium is most frequently affected.

The etiology of myocardial contusion is blunt chest trauma. High-speed motor vehicle collisions are the most common cause, although injuries have been reported at speeds as low as 20–35 mph. Other mechanisms include auto–pedestrian accidents, falls, explosions, crush injuries, and prolonged closed-chest cardiac massage. Injury may occur through direct compression of the heart between the sternum and vertebral column, deceleration forces causing the heart to strike the sternum, or upward displacement of abdominal viscera transmitting force to the heart. Concussive forces may also contribute. Myocardial contusion may be associated with serious complications, including life-threatening dysrhythmias, cardiogenic shock, congestive heart failure, hemopericardium with tamponade, valvular or myocardial rupture, intraventricular thrombus, thromboembolic events, and, rarely, coronary artery occlusion due to intimal injury or edema.

Clinical presentation is highly variable and often nonspecific. Patients may complain of chest pain, develop cardiogenic shock, or exhibit only subtle electrocardiographic changes without symptoms. The most common clinical finding is sinus tachycardia that appears disproportionate to the degree of trauma or blood loss. Retrosternal chest pain, often unrelieved by nitroglycerin, may be delayed for up to 24 hours and may respond to supplemental oxygen. Other findings include friction rubs (rare), signs of thoracic trauma such as contusions or abrasions, crepitus, flail chest segments, or sternal fractures. Importantly, isolated sternal fracture with a normal ECG and negative serial troponin I does not predict blunt cardiac injury. Symptoms may be masked by other traumatic injuries. A history of syncope or loss of consciousness raises concern for dysrhythmia. In elderly patients, pre-existing cardiac disease and medications must be carefully considered, while in pediatric patients significant cardiac injury may occur despite minimal external signs due to the compliance of the chest wall.

There is no single diagnostic test that definitively confirms myocardial contusion. Electrocardiography is the best initial screening tool and should be obtained in all patients with suspected blunt cardiac injury. Sinus tachycardia is the most common finding, but ECG abnormalities may include nonspecific ST changes, right bundle branch block, or premature atrial or ventricular contractions. A normal ECG does not exclude myocardial injury, and repeat ECGs are recommended because abnormalities may evolve over time. Cardiac troponin I is the preferred laboratory marker and should be obtained in conjunction with ECG findings; levels should be repeated at 6–8 hours after injury. Any elevation warrants admission. Echocardiography is indicated in patients with ECG abnormalities or elevated troponins to assess for wall-motion abnormalities, effusions, or structural injury. Transesophageal echocardiography is more sensitive than transthoracic echocardiography but is more invasive. FAST examination should be performed to assess for pericardial effusion and associated intra-abdominal injuries. CT or MRI may assist in evaluating associated thoracic injuries but have no pathognomonic findings for myocardial contusion.

Management in the emergency setting focuses on supportive care and treatment of complications. Airway management, oxygen supplementation, intravenous access, and continuous cardiac monitoring are essential. Dysrhythmias are treated using standard protocols for nontraumatic arrhythmias, and prophylactic antiarrhythmic therapy is not recommended. Cardiogenic shock should be managed with cautious fluid resuscitation and inotropic support when necessary, with intra-aortic balloon counterpulsation reserved for severe cases. There is no specific therapy to reverse myocardial contusion itself; treatment is directed toward hemodynamic stabilization and management of associated injuries.

Disposition decisions require caution, as adverse outcomes—particularly dysrhythmias—most often occur within the first 24 hours. All patients in whom myocardial contusion is strongly suspected should be admitted to a monitored setting. Admission is indicated for any ECG abnormality, elevated cardiac enzymes, hemodynamic instability, or imaging suggestive of cardiac injury. Asymptomatic patients with normal ECGs and normal serial troponin I levels after 6–8 hours of observation may be safely discharged with close follow-up within 24 hours.

Key clinical pearls include the importance of obtaining an ECG in all patients with significant chest trauma and performing a FAST examination to assess for pericardial effusion. External signs of chest wall injury should heighten suspicion for blunt cardiac injury, while their absence—especially in pediatric patients—does not exclude it. Thrombolytic therapy should not be administered for ST-elevation myocardial infarction following trauma. A normal ECG combined with a negative troponin I level makes clinically significant blunt cardiac injury unlikely.

Emergency and Acute Medicine – Myasthenia Gravis

Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by painless, fluctuating, and fatigable skeletal muscle weakness. Weakness typically worsens with repeated activity and improves with rest. The disease may present in an ocular form or as generalized myasthenia gravis. Ocular involvement, affecting the eyelids and extraocular muscles, is the most common initial presentation and accounts for approximately 60% of cases. Although symptoms may initially be limited to the eyes, nearly 80% of patients with ocular MG will progress to generalized disease within two years.

Generalized myasthenia gravis involves proximal limb muscles, axial musculature, and bulbar muscles, including those responsible for speech, chewing, and swallowing. The disease often follows an acute or subacute course with relapses and remissions. Thymic abnormalities are common, with thymic hyperplasia present in approximately 65% of patients and thymoma in about 15%. A life-threatening complication, known as myasthenic crisis, occurs when respiratory muscle weakness or bulbar dysfunction leads to respiratory failure or inability to protect the airway. Common triggers include infection, surgery, trauma, pregnancy, and medication changes, particularly rapid tapering of corticosteroids.

The pathophysiology of myasthenia gravis involves antibodies directed against nicotinic acetylcholine receptors at the neuromuscular junction, resulting in impaired neuromuscular transmission. Up to 20% of patients may be seronegative for acetylcholine receptor antibodies. Certain medications can induce or worsen myasthenic weakness, including aminoglycosides, macrolides, fluoroquinolones, beta-blockers, calcium-channel blockers, anticonvulsants, antipsychotics, and neuromuscular blocking agents. Penicillamine is a well-recognized cause of drug-induced MG.

Clinically, patients report fluctuating weakness that worsens with activity. Ocular symptoms include ptosis and diplopia, often noted during prolonged visual tasks such as reading or driving. Bulbar involvement leads to slurred or nasal speech, difficulty chewing, swallowing, and maintaining jaw closure. Limb weakness commonly affects proximal muscles, causing difficulty climbing stairs, rising from a seated position, or lifting objects overhead. On physical examination, ptosis, diplopia, and facial weakness may be evident, while reflexes and sensation remain normal. Repetitive testing of affected muscle groups typically reproduces weakness.

Emergency evaluation focuses on identifying respiratory compromise and precipitating factors such as infection. Diagnostic testing includes basic laboratory studies, thyroid function tests, and antibody testing for acetylcholine receptor antibodies. Imaging of the chest with CT is essential to evaluate for thymoma. Bedside diagnostic tools include the ice test, in which application of ice to the eyelid transiently improves ptosis, supporting the diagnosis. The edrophonium (Tensilon) test may produce short-lived improvement in strength but requires cardiac monitoring and atropine availability due to the risk of bradycardia and increased secretions.

Management in the emergency setting prioritizes airway protection and respiratory support. Patients in myasthenic crisis require early intubation and mechanical ventilation. Objective indicators of impending respiratory failure include reduced vital capacity and weak inspiratory pressures. In crisis, acetylcholinesterase inhibitors are typically withheld, and treatment includes plasmapheresis or intravenous immunoglobulin (IVIG), along with high-dose corticosteroids. Infections and other triggers must be identified and treated aggressively. Atropine may be used to counteract muscarinic effects in suspected cholinergic crisis.

Hospital admission is required for new-onset disease, diagnostic uncertainty, worsening weakness, or any evidence of respiratory compromise. Intensive care admission is mandatory for myasthenic crisis or borderline respiratory status. Patients who demonstrate improvement and have stable respiratory function may be discharged in consultation with neurology, with close outpatient follow-up arranged.

A key clinical pearl is that any patient with known myasthenia gravis presenting to the emergency department should be carefully evaluated for signs of myasthenic crisis and secondary precipitants. Early recognition and aggressive supportive management are essential to prevent respiratory failure and improve outcomes.

Emergency and Acute Medicine – Munchausen Syndrome

Munchausen syndrome is a severe and chronic form of factitious disorder in which patients intentionally fabricate or induce signs and symptoms of illness without external incentives such as financial gain or avoidance of responsibility. The primary motivation is the psychological need to assume the sick role. It represents the most dramatic end of the factitious disorder spectrum and predominantly involves physical complaints rather than psychological symptoms. Although difficult to study systematically, associated risk factors include male sex, being unmarried, middle age, underlying personality disorders, histories of childhood illness, and early experiences of rejection or abuse.

The disorder is defined by intentional production of physical or psychological signs, motivation to be perceived as ill, and absence of obvious external rewards. Patients with classic Munchausen syndrome often demonstrate repeated hospitalizations, extensive peregrination between medical facilities, and elaborate, inconsistent medical histories. Clinical patterns include self-induced infections, simulated illnesses without objective disease, chronic nonhealing wounds, and self-medication to provoke abnormal findings. Pediatric and geriatric variants include Munchausen syndrome by proxy, in which a caregiver induces or fabricates illness in a dependent, most commonly a child, to gain attention or sympathy through the patient’s illness. Separation of the victim from the caregiver typically results in resolution of symptoms.

Patients frequently present with unusual or inappropriate emergency department utilization, numerous prior admissions, and dramatic but inconsistent complaints. They may provide intricate, false narratives known as pseudologia fantastica, alter personal identifiers, use aliases, and demonstrate extensive medical knowledge. Escalating demands for diagnostic tests or invasive procedures are common, as is hostility when providers question inconsistencies. Many tolerate painful interventions with little distress and may appear more comfortable than expected given the purported severity of illness. Common behaviors include self-inflicted wounds, ingestion or injection of substances to alter laboratory results, swallowing blood to simulate gastrointestinal bleeding, and manipulation of specimens.

Physical examination may reveal signs inconsistent with the reported history, such as multiple scars from prior procedures, foreign bodies in wounds or body orifices, unexplained infections, or fever caused by manipulation or contamination. Establishing the diagnosis requires careful, methodical investigation, including retrieval of outside medical records, verification of prior histories, communication with family members or prior providers, and, when appropriate, supervised observation. Definitive diagnosis requires clear evidence of intentional deception.

Laboratory abnormalities may reflect deliberate manipulation, such as hematuria from added blood, hypoglycemia from insulin administration, abnormal coagulation profiles from anticoagulant ingestion, or thyroid abnormalities from exogenous hormone use. Imaging and invasive procedures should be avoided unless objective findings clearly justify intervention, as unnecessary testing increases the risk of iatrogenic harm.

The differential diagnosis includes true medical illness, malingering with external gain, conversion disorder, somatic symptom disorders, and psychiatric or neurologic conditions that may result in self-injury or unreliable histories. In the emergency setting, management focuses on treating genuine medical conditions and stabilizing life- or limb-threatening consequences of self-harm. Thorough documentation of observed behaviors, inconsistencies, known aliases, and patterns of presentation is essential to reduce future harm and improve continuity of care.

Disposition decisions are guided by medical stability and safety. Admission may be required for injuries resulting from self-harm, observation to gather evidence, protection of dependents in suspected Munchausen by proxy cases, or management of serious complications. Psychiatric admission may be beneficial but is often refused. Discharge is appropriate when the patient is medically stable, not actively self-harming, and appropriate follow-up is arranged. Long-term management relies on coordinated care with a single provider when possible, cautious engagement with psychiatric services, and ongoing efforts to minimize unnecessary medical interventions, recognizing that prognosis is generally poor and relapse is common.
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