Emergency and Acute Medicine – Mushroom Poisoning

Mushroom poisoning encompasses a wide spectrum of toxic syndromes caused by ingestion of wild or contaminated mushrooms, with clinical severity ranging from mild, self-limited gastrointestinal upset to fulminant hepatic or renal failure and death. Toxicity depends on the mushroom species, the specific toxin involved, the quantity ingested, and the timing of presentation. The most lethal poisonings are associated with delayed symptom onset, particularly those involving amanitin-containing mushrooms.

Amanitin and phalloidin toxins are found in species such as *Amanita phalloides* (death cap), *Amanita virosa* and *Amanita verna* (destroying angels), and some *Galerina* species. These cyclopeptide toxins inhibit RNA polymerase II, resulting in cellular death of gastrointestinal epithelium, hepatocytes, and renal tubular cells. Symptoms are characteristically delayed for 6–36 hours and begin with severe nausea, vomiting, abdominal pain, and diarrhea, followed by a transient asymptomatic phase. Progressive hepatic failure, coagulopathy, hypoglycemia, renal failure, and death may occur within days, making this the most dangerous category of mushroom poisoning.

Gyromitrin poisoning, most commonly from *Gyromitra esculenta* (false morels), interferes with pyridoxal phosphate metabolism and causes neurologic, hepatic, and hematologic toxicity. Early gastrointestinal symptoms are followed by weakness, confusion, seizures, coma, and possible liver injury. Muscarine-containing mushrooms such as *Inocybe* and *Clitocybe* species cause rapid-onset cholinergic toxicity, including salivation, lacrimation, diarrhea, bronchoconstriction, bradycardia, and miosis, typically within one hour of ingestion.

Coprine toxicity, seen with *Coprinus atramentarius* (inky cap), produces a disulfiram-like reaction when alcohol is consumed, leading to flushing, nausea, vomiting, palpitations, and diaphoresis. Ibotenic acid and muscimol, found in *Amanita muscaria* and *Amanita pantherina*, act as GABA agonists and cause hallucinations, ataxia, dysarthria, somnolence, and, in children, seizures. Psilocybin and psilocin-containing mushrooms cause serotonergic effects with hallucinations and perceptual disturbances that typically resolve within hours.

Other toxic syndromes include gastric irritant mushrooms that cause early-onset nausea, vomiting, and diarrhea; orellanine-containing *Cortinarius* species and *Amanita smithiana*, which cause delayed and often severe renal failure days to weeks after ingestion; and *Tricholoma equestre*, associated with acute rhabdomyolysis and renal injury.

Diagnosis relies heavily on history, including time of ingestion, symptom onset, number of mushrooms consumed, preparation method, coingestants, alcohol use, and whether others who ate the same mushrooms are symptomatic. Physical examination focuses on vital signs, mental status, abdominal findings, neurologic deficits, and signs of cholinergic or serotonergic toxicity. Exact mycologic identification is uncommon, but any remaining mushrooms should be stored in a brown paper bag and photographed for expert consultation through poison control.

Laboratory evaluation includes complete blood count, electrolytes, renal function tests, liver function tests, coagulation studies, creatine phosphokinase, glucose, and urinalysis. Serial testing is critical in delayed-onset poisonings. Imaging is generally supportive, and specialized testing such as spore prints requires expert interpretation.

Management begins with airway, breathing, and circulation stabilization, intravenous fluids, and close monitoring. Activated charcoal is recommended early in most cases, particularly with suspected amanitin ingestion, and may be repeated. Poison control consultation is essential in all suspected mushroom poisonings. Amanitin toxicity requires aggressive supportive care, correction of hypoglycemia and coagulopathy, consideration of N-acetylcysteine, silibinin or penicillin G when available, and early liver transplant evaluation for signs of hepatic failure. Gyromitrin toxicity is treated with benzodiazepines for seizures and pyridoxine for severe neurologic symptoms. Muscarinic toxicity responds to atropine. Most other syndromes are managed with supportive care, benzodiazepines for agitation or seizures, and careful monitoring for complications.

All symptomatic patients, particularly those with delayed symptom onset, persistent vomiting, neurologic symptoms, or laboratory evidence of hepatic or renal injury, require hospital admission. Intensive care and early transfer to a tertiary center are indicated for amanitin poisoning or evolving organ failure. Asymptomatic patients may be discharged after a period of observation if reliable follow-up is assured.

A key clinical principle is that delayed onset of symptoms beyond six hours strongly suggests a potentially life-threatening toxin. Early consultation with poison control and timely referral for transplant evaluation when indicated are critical to improving outcomes in severe mushroom poisoning.

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 – 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 – 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 – Necrotizing Soft Tissue Infections




Necrotizing soft tissue infections (NSTIs) are rapidly progressive infections involving any layer of the skin and underlying soft tissues, characterized by widespread necrosis, severe systemic toxicity, and a high mortality rate. These infections spread quickly along tissue planes, often causing extensive fascial and muscle destruction with relative sparing of the skin in early stages. Clinical entities within this spectrum include necrotizing fasciitis, Fournier gangrene, clostridial and nonclostridial myonecrosis, crepitant anaerobic cellulitis, and progressive bacterial gangrene. Despite being uncommon, NSTIs carry mortality rates of 24–34% and are associated with significant morbidity such as amputations, renal failure, and prolonged critical illness.


NSTIs typically arise in the setting of local tissue trauma, ischemia, or impaired host defenses. Risk is increased in older adults, smokers, and patients with chronic systemic disease including diabetes mellitus, obesity, peripheral vascular disease, chronic kidney disease, alcohol abuse, immunosuppression, and intravenous drug use. Type I NSTIs, which account for approximately 80% of cases, are polymicrobial infections involving aerobic and anaerobic organisms and commonly occur after surgery or in patients with chronic illness. Type II NSTIs are usually monomicrobial, most often caused by group A β-hemolytic streptococcus, and can affect young, otherwise healthy individuals; these infections are the classic “flesh-eating” disease. Type III NSTIs are rare but fulminant, frequently clostridial in origin, and often follow penetrating trauma, crush injuries, or injection drug use. Pediatric cases are uncommon but may occur in neonates after omphalitis or circumcision, or in children following recent varicella infection, surgery, or in those with immunodeficiency.


The clinical presentation can be subtle early but deteriorates rapidly. Patients often report fever, malaise, altered mental status, and severe pain at the affected site. A hallmark feature is pain that is disproportionate to physical findings. Within the first 24 hours, localized swelling, warmth, erythema, and tenderness develop, followed over the next 24–48 hours by skin discoloration (purple or blue), hemorrhagic bullae, and foul-smelling, thin drainage due to necrosis of fascia and fat. Systemic toxicity is common and includes tachycardia, tachypnea, hypotension, fever, and mental status changes. Crepitus, while pathognomonic, is present in only a minority of cases. In children, localized pain and rash are the most common presenting features, while hypotension and shock are less frequent early findings.


Diagnosis is challenging and relies heavily on clinical suspicion, particularly in high-risk patients who appear severely ill or have pain out of proportion to examination findings. Laboratory abnormalities may include leukocytosis, electrolyte derangements, renal dysfunction, hypocalcemia from fat necrosis, and evidence of disseminated intravascular coagulation. Imaging studies such as plain radiographs, CT, MRI, or ultrasound may demonstrate soft tissue gas, fascial thickening, or fluid along fascial planes, but absence of these findings does not exclude NSTI. Importantly, imaging should never delay surgical intervention. Definitive diagnosis is established by surgical exploration with deep tissue biopsy and cultures, which remains the gold standard.


Management of NSTIs is a true surgical emergency. Initial stabilization focuses on airway protection, aggressive fluid resuscitation, oxygenation, and correction of metabolic disturbances. Broad-spectrum intravenous antibiotics must be initiated immediately, targeting aerobic gram-positive and gram-negative organisms, anaerobes, and methicillin-resistant Staphylococcus aureus until culture results are available. Clindamycin should be started early, particularly when group A streptococcal infection is suspected, due to its ability to suppress toxin production. However, antimicrobial therapy alone is insufficient; early and aggressive surgical debridement of all necrotic tissue with fasciotomy and drainage is the cornerstone of treatment and must not be delayed. Adjunctive therapies such as hyperbaric oxygen and intravenous immunoglobulin may be considered in select cases, though their roles remain controversial.


All patients with NSTI require hospital admission, typically to an intensive care setting, for ongoing surgical management, intravenous antibiotics, and close monitoring for complications such as acute respiratory distress syndrome, renal failure, myocardial dysfunction, and disseminated intravascular coagulation. No patient with NSTI is appropriate for discharge. Key clinical pearls include maintaining a high index of suspicion, recognizing pain out of proportion to examination as a critical clue, and understanding that mortality approaches 100% if treatment is limited to antibiotics without prompt surgical debridement.