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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.
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.
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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.
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.
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Emergency and Acute Medicine – Multiple Myeloma
Multiple myeloma is a malignant disorder arising from transformation of normal hematopoietic stem cells into clonal plasma cells. These abnormal myeloma cells proliferate within the bone marrow, leading to extensive marrow infiltration, bone destruction, and suppression of normal blood cell production. The disease is characterized by several pathologic derangements, including immunodeficiency, anemia, renal dysfunction, and skeletal damage. Plasma cell secretions stimulate osteoclast activity, resulting in bone lysis, pathologic fractures, neurologic compromise, and hypercalcemia, which is often worsened by concurrent renal impairment.
Immunodeficiency in multiple myeloma develops through multiple mechanisms. Normal immunoglobulin production is suppressed, and both T- and B-cell function are impaired. Granulocytopenia and reduced cell-mediated immunity further increase susceptibility to infection. Abnormal monoclonal proteins produced by myeloma cells contribute to hyperviscosity syndromes, amyloidosis, and renal injury. Light chains may accumulate within renal tubules, causing progressive nephron destruction and eventual renal failure. Common complications of the disease include recurrent infections, anemia, hypercalcemia, renal failure, pathologic fractures, and spinal cord compression, which occurs in approximately 10% of patients.
The incidence of multiple myeloma is approximately 4 per 100,000 individuals, accounting for about 1% of all cancers and 15% of hematopoietic malignancies. The mean age at diagnosis is around 70 years, with a slightly higher incidence in men and African Americans. The disease is rare in younger populations, with fewer than 2% of cases occurring in patients under 40 years of age.
Bone pain is the most common presenting symptom and typically involves the ribs, sternum, spine, clavicle, skull, shoulders, or hips. This pain may lead to reduced mobility or neurologic deficits if vertebral involvement is present. Constitutional symptoms such as fatigue, weakness, weight loss, anemia, and recurrent infections are also common. Approximately 20% of patients are asymptomatic at diagnosis, with the condition discovered incidentally during routine laboratory testing. Recurrent episodes of severe infection, particularly from encapsulated organisms such as Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus species, are a major cause of morbidity.
Initial emergency evaluation includes a complete blood count, erythrocyte sedimentation rate, electrolytes, renal function tests, and urinalysis. Imaging should be directed by symptoms, with plain radiographs or skeletal surveys used to evaluate bone pain and detect lytic lesions or fractures. CT or MRI is indicated when pain persists despite normal radiographs or when spinal cord compression is suspected. Diagnostic confirmation relies on serum and urine protein electrophoresis and immunofixation to identify monoclonal proteins, along with bone marrow biopsy demonstrating increased plasma cells.
Laboratory findings often reveal normocytic, normochromic anemia, thrombocytopenia, elevated ESR, hypercalcemia, and renal insufficiency. Peripheral blood smears may show rouleaux formation. Imaging commonly demonstrates lytic bone lesions or compression fractures, while MRI is preferred for detecting spinal cord involvement or soft-tissue plasmacytomas. Bone scans may be falsely negative due to the uncoupling of bone resorption and formation in multiple myeloma.
Emergency management focuses on identifying and treating life-threatening complications. Patients presenting with back pain or neurologic deficits should be presumed to have a pathologic spinal fracture and immobilized appropriately. Hypercalcemia requires aggressive intravenous hydration and bisphosphonate therapy. Renal failure, sepsis, anemia, and spinal cord compression require prompt recognition and intervention. Pain control is essential, with opioid analgesics preferred, as NSAIDs may worsen renal dysfunction. Pathologic fractures should be splinted, and spinal fractures immobilized.
Definitive treatment involves hematology and oncology consultation. Early or asymptomatic disease may not require immediate therapy, as chemotherapy has not shown benefit in early stages. Standard treatment regimens include melphalan and prednisone, which provide symptom relief and reduction of monoclonal protein levels in many patients. Alternative therapies include cyclophosphamide-based regimens, combination chemotherapy, and high-dose chemotherapy with stem cell transplantation. Novel agents such as thalidomide may be used in refractory cases.
Hospital admission is indicated for patients with uncontrolled pain, acute renal failure, severe hypercalcemia, sepsis, spinal cord compression, hyperviscosity syndromes, or other life-threatening complications. Patients whose pain is controlled with oral medications and who have no acute complications may be discharged with close follow-up. All patients should be referred to oncology regardless of disease stage, and neurosurgical or orthopedic consultation is warranted for persistent vertebral pain or instability that may benefit from vertebroplasty or kyphoplasty.
A key clinical pitfall is failure to recognize infectious complications, which remain the leading cause of mortality in multiple myeloma. Febrile illness in these patients should prompt early empiric antimicrobial therapy. Persistent bone pain, unexplained anemia, renal dysfunction, or neurologic symptoms in elderly patients should raise suspicion for multiple myeloma and prompt appropriate evaluation.
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Emergency and Acute Medicine – Necrotizing Ulcerative Gingivitis
Necrotizing ulcerative gingivitis (NUG) is an acute periodontal disease characterized by painful ulceration and necrosis of the gingival papillae, producing the classic “punched-out” appearance. It is also known as acute necrotizing ulcerative gingivitis, trench mouth, Vincent disease, or fusospirochetal gingivitis. The condition is not contagious and most commonly affects children and young adults, particularly in developing regions such as sub-Saharan Africa. In developed countries it is rare and is typically seen in severely immunocompromised individuals. Males are affected more often than females. If untreated, NUG can progress to more severe disease, including necrotizing stomatitis, necrotizing ulcerative periodontitis with alveolar bone involvement, or orofacial gangrene (noma).
The disease is caused by an overgrowth of normal oral flora, most notably Prevotella intermedia and spirochetes. While predisposing factors are not required for diagnosis, they are commonly present and include poor oral hygiene, gingivitis, malnutrition, smoking, emotional or physical stress, and immunodeficiency states such as HIV infection or other causes of immunosuppression. There is also a possible association with direct exposure to certain chemicals, including recreational drugs such as MDMA (ecstasy).
Clinically, NUG presents with acute onset of severe oral pain and bleeding gums that may occur spontaneously or with minimal manipulation. The hallmark finding on physical examination is loss of the interdental papillae, resulting in crater-like, “punched-out” ulcers that bleed easily. Necrotic debris often overlies the ulcerated areas, forming a grayish pseudomembrane that, when removed, reveals a bleeding surface. Patients frequently complain of foul breath and may have associated low-grade fever, malaise, and submandibular lymphadenopathy.
The diagnosis of necrotizing ulcerative gingivitis is primarily clinical, as laboratory tests and imaging studies are generally not helpful. Evaluation should focus on identifying underlying systemic disease, particularly immunosuppression, neutropenia, or HIV infection. It is also essential to assess for complications such as extension of lesions into the periodontal ligament and alveolar bone, progression to necrotizing stomatitis, or development of orofacial gangrene, which carries a high mortality rate if untreated.
Initial management focuses on supportive care and symptom relief. Dehydrated patients may require intravenous fluids. Pain control is achieved with topical agents such as viscous lidocaine and systemic analgesics, with narcotics rarely required. Gentle debridement of the pseudomembrane using gauze or a cotton-tipped applicator soaked in diluted hydrogen peroxide helps reduce bacterial load and improve healing. Antibiotic therapy is indicated in patients with fever, lymphadenopathy, or systemic symptoms, and in those who are immunocompromised. Common regimens include penicillin with metronidazole or clindamycin as an alternative.
Outpatient therapy is central to recovery and includes chlorhexidine gluconate mouth rinses, diluted hydrogen peroxide rinses, avoidance of oral irritants such as spicy foods and hot beverages, and reinforcement of good oral hygiene with gentle brushing and flossing. Nonsteroidal anti-inflammatory drugs or acetaminophen are usually sufficient for pain control. More extensive antimicrobial coverage, including antifungal or antiviral therapy, may be required in severely immunosuppressed patients.
Hospital admission is reserved for patients with extensive disease, significant systemic symptoms, severe dehydration with inability to tolerate oral intake, or evidence of progression to orofacial gangrene. Most patients who can maintain hydration and have no signs of advanced disease may be safely discharged with close follow-up. All patients require urgent referral to a dentist or periodontist for definitive care, including deep scaling and debridement.
Key clinical pearls include maintaining a high index of suspicion for underlying immunosuppression, particularly HIV infection, and recognizing that necrotizing ulcerative gingivitis can progress rapidly if left untreated. Early identification and prompt intervention are essential to prevent serious and potentially life-threatening complications.
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KembaraXtra – Medicine – Monoamine Oxidase Inhibitor (MAOI) Poisoning
Monoamine oxidase inhibitors are medications primarily used in the treatment of depression. Selegiline, a selective monoamine oxidase-B inhibitor, is also used in Parkinson disease and is available in oral and transdermal formulations. MAOIs disrupt the normal balance between monoamine synthesis and degradation, leading to increased neural norepinephrine levels, receptor downregulation, and irreversible inhibition of monoamine oxidase enzymes. Monoamine oxidase is the principal enzyme responsible for inactivation of bioactive amines. MAO-A is found predominantly in the gut and liver and protects against dietary amines, whereas MAO-B is present in neuronal terminals and platelets.
The toxicology of MAOI overdose is complex and incompletely understood. Many MAOIs have amphetamine-like structures and initially produce indirect sympathomimetic effects, followed later by a sympatholytic phase that may result in hypotension. A classic and dangerous complication is the MAOI hypertensive crisis syndrome, caused by impaired degradation of norepinephrine with sudden release triggered by indirect- or mixed-acting sympathomimetics. Common precipitants include tyramine-rich foods, cocaine, and amphetamines. Another major complication is serotonin syndrome, which results from excessive serotonergic activity, often due to drug interactions involving MAOIs combined with agents that increase serotonin synthesis, release, reuptake inhibition, receptor stimulation, or decrease serotonin metabolism.
Clinical presentation of MAOI overdose is often delayed, typically occurring 6–12 hours after ingestion. Early manifestations commonly include hypertension and severe headache, followed by hyperadrenergic features such as tachycardia, agitation, mydriasis, and neuromuscular excitation. Patients may develop tremor, hyperreflexia, myoclonus, rigidity, seizures, and marked hyperthermia. Severe toxicity may lead to rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, and acute respiratory distress syndrome. In hypertensive crisis syndromes, patients may present with occipital headache, altered mental status, intracranial hemorrhage, and seizures. Serotonin syndrome is characterized by neuromuscular hyperactivity, autonomic instability, and altered mental status, with rapid onset over hours, distinguishing it from neuroleptic malignant syndrome.
History should focus on timing and quantity of ingestion, access to pill bottles, intent (accidental versus intentional), and possible co-ingestants. Physical examination often reveals neuromuscular hyperactivity, autonomic instability, and changes in mental status. Continuous blood pressure, cardiac, and temperature monitoring is essential due to the risk of rapid deterioration.
Laboratory evaluation should include electrolytes, renal function, glucose, creatine kinase, urinalysis for myoglobin, coagulation studies, and arterial blood gas analysis in severe cases. Urine toxicology screening may show amphetamine positivity because of structural similarities. Imaging such as chest radiography is indicated if respiratory complications are suspected, and head CT is warranted for severe headache, focal neurologic findings, or altered mental status. Lumbar puncture may be required when meningitis or subarachnoid hemorrhage remains a concern.
Management begins with aggressive supportive care focused on airway, breathing, and circulation. Early IV access, oxygen, and cardiac monitoring are mandatory. Activated charcoal may be administered if the patient presents early and the airway is protected. Hyperthermia should be treated promptly with benzodiazepines for agitation and active cooling measures. Severe muscle rigidity and persistent hyperthermia may require paralysis with nondepolarizing neuromuscular blockers and mechanical ventilation. Hypertensive emergencies are treated with short-acting, titratable intravenous agents such as nitroprusside, while hypotension is managed initially with isotonic fluids and, if needed, norepinephrine. Seizures are treated with benzodiazepines, followed by barbiturates if refractory. Rhabdomyolysis requires aggressive IV hydration to preserve renal function.
Serotonin syndrome management centers on immediate discontinuation of offending agents and supportive care. Cyproheptadine, a nonselective serotonin antagonist, may be used in moderate to severe cases. Importantly, phentolamine is contraindicated in MAOI overdose due to the risk of unopposed beta-adrenergic stimulation.
All patients with suspected MAOI overdose require hospital admission to a monitored setting for at least 24 hours because of delayed toxicity. Intensive care admission is indicated for patients with severe hyperthermia, seizures, hemodynamic instability, or end-organ failure. Patients with resolved mild hypertensive or serotonin syndromes may be considered for discharge after prolonged emergency department observation. Intentional ingestions require psychiatric evaluation prior to discharge.
Key clinical pitfalls include underestimating the delayed onset of toxicity, failure to recognize drug-drug or food interactions, and inappropriate use of contraindicated antihypertensive agents. Linezolid and methylene blue should also be recognized as MAOI-like agents capable of precipitating similar toxic syndromes.
Monoamine oxidase inhibitors are medications primarily used in the treatment of depression. Selegiline, a selective monoamine oxidase-B inhibitor, is also used in Parkinson disease and is available in oral and transdermal formulations. MAOIs disrupt the normal balance between monoamine synthesis and degradation, leading to increased neural norepinephrine levels, receptor downregulation, and irreversible inhibition of monoamine oxidase enzymes. Monoamine oxidase is the principal enzyme responsible for inactivation of bioactive amines. MAO-A is found predominantly in the gut and liver and protects against dietary amines, whereas MAO-B is present in neuronal terminals and platelets.
The toxicology of MAOI overdose is complex and incompletely understood. Many MAOIs have amphetamine-like structures and initially produce indirect sympathomimetic effects, followed later by a sympatholytic phase that may result in hypotension. A classic and dangerous complication is the MAOI hypertensive crisis syndrome, caused by impaired degradation of norepinephrine with sudden release triggered by indirect- or mixed-acting sympathomimetics. Common precipitants include tyramine-rich foods, cocaine, and amphetamines. Another major complication is serotonin syndrome, which results from excessive serotonergic activity, often due to drug interactions involving MAOIs combined with agents that increase serotonin synthesis, release, reuptake inhibition, receptor stimulation, or decrease serotonin metabolism.
Clinical presentation of MAOI overdose is often delayed, typically occurring 6–12 hours after ingestion. Early manifestations commonly include hypertension and severe headache, followed by hyperadrenergic features such as tachycardia, agitation, mydriasis, and neuromuscular excitation. Patients may develop tremor, hyperreflexia, myoclonus, rigidity, seizures, and marked hyperthermia. Severe toxicity may lead to rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, and acute respiratory distress syndrome. In hypertensive crisis syndromes, patients may present with occipital headache, altered mental status, intracranial hemorrhage, and seizures. Serotonin syndrome is characterized by neuromuscular hyperactivity, autonomic instability, and altered mental status, with rapid onset over hours, distinguishing it from neuroleptic malignant syndrome.
History should focus on timing and quantity of ingestion, access to pill bottles, intent (accidental versus intentional), and possible co-ingestants. Physical examination often reveals neuromuscular hyperactivity, autonomic instability, and changes in mental status. Continuous blood pressure, cardiac, and temperature monitoring is essential due to the risk of rapid deterioration.
Laboratory evaluation should include electrolytes, renal function, glucose, creatine kinase, urinalysis for myoglobin, coagulation studies, and arterial blood gas analysis in severe cases. Urine toxicology screening may show amphetamine positivity because of structural similarities. Imaging such as chest radiography is indicated if respiratory complications are suspected, and head CT is warranted for severe headache, focal neurologic findings, or altered mental status. Lumbar puncture may be required when meningitis or subarachnoid hemorrhage remains a concern.
Management begins with aggressive supportive care focused on airway, breathing, and circulation. Early IV access, oxygen, and cardiac monitoring are mandatory. Activated charcoal may be administered if the patient presents early and the airway is protected. Hyperthermia should be treated promptly with benzodiazepines for agitation and active cooling measures. Severe muscle rigidity and persistent hyperthermia may require paralysis with nondepolarizing neuromuscular blockers and mechanical ventilation. Hypertensive emergencies are treated with short-acting, titratable intravenous agents such as nitroprusside, while hypotension is managed initially with isotonic fluids and, if needed, norepinephrine. Seizures are treated with benzodiazepines, followed by barbiturates if refractory. Rhabdomyolysis requires aggressive IV hydration to preserve renal function.
Serotonin syndrome management centers on immediate discontinuation of offending agents and supportive care. Cyproheptadine, a nonselective serotonin antagonist, may be used in moderate to severe cases. Importantly, phentolamine is contraindicated in MAOI overdose due to the risk of unopposed beta-adrenergic stimulation.
All patients with suspected MAOI overdose require hospital admission to a monitored setting for at least 24 hours because of delayed toxicity. Intensive care admission is indicated for patients with severe hyperthermia, seizures, hemodynamic instability, or end-organ failure. Patients with resolved mild hypertensive or serotonin syndromes may be considered for discharge after prolonged emergency department observation. Intentional ingestions require psychiatric evaluation prior to discharge.
Key clinical pitfalls include underestimating the delayed onset of toxicity, failure to recognize drug-drug or food interactions, and inappropriate use of contraindicated antihypertensive agents. Linezolid and methylene blue should also be recognized as MAOI-like agents capable of precipitating similar toxic syndromes.
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Emergency And Acute Medicine – Infectious Mononucleosis
Infectious mononucleosis most commonly results from infection with the Epstein–Barr virus, a herpesvirus transmitted primarily through close or intimate contact with saliva, giving rise to the term “kissing disease.” Viral shedding may persist intermittently for life, even in asymptomatic individuals, and transmission may also occur through blood transfusions or organ transplantation. The incubation period is typically 4–6 weeks. More than 90% of adults demonstrate serologic evidence of prior EBV infection, although most do not recall a classic illness. Non-EBV causes of a mononucleosis-like syndrome include cytomegalovirus, adenovirus, hepatitis A, HIV, rubella, toxoplasmosis, herpesvirus 6, and group A β-hemolytic streptococci.
The clinical manifestations of infectious mononucleosis are largely driven by the host immune response. T-cell activation, particularly cytotoxic CD8 cells, leads to an elevated absolute lymphocyte count and the appearance of atypical lymphocytes on peripheral smear. EBV infects B-cells, transforming them into plasmacytoid cells that secrete immunoglobulins, including IgM heterophile antibodies detected by the Monospot test. Mortality is rare but may occur due to complications such as airway edema, splenic rupture, hepatic failure, myocarditis, neurologic involvement, or secondary bacterial infection. EBV infection is also associated with certain malignancies, including African Burkitt lymphoma and nasopharyngeal carcinoma.
Presentation is often insidious, developing over days to weeks, though abrupt onset may occur. Patients typically report profound fatigue, malaise, fever, and severe sore throat, often described as the worst they have experienced. Cervical lymphadenopathy is prominent, and headache is common. Significant abdominal pain is uncommon and should prompt concern for splenic enlargement or rupture. Rashes may occur, particularly in children and adolescents, and administration of ampicillin or amoxicillin frequently results in a morbilliform rash that should not be mistaken for a penicillin allergy.
Physical examination commonly reveals fatigue, pharyngitis with tonsillar enlargement, fever, and symmetric tender lymphadenopathy. Splenomegaly is present in approximately half of cases, and hepatomegaly occurs less frequently. Eyelid edema and palatal petechiae may be seen. Complications identified on examination include airway compromise from pharyngeal edema, jaundice from hepatitis, signs of splenic rupture such as severe abdominal tenderness or referred left shoulder pain, neurologic deficits, and evidence of hematologic abnormalities such as pallor from anemia.
Laboratory evaluation typically shows a modest leukocytosis with lymphocyte predominance, often exceeding 50% lymphocytes, and more than 10% atypical lymphocytes. Liver transaminases are elevated in the majority of patients during the first two weeks of illness, and mild hyperbilirubinemia may occur. The heterophile antibody test is highly specific but moderately sensitive and may be negative early in the disease course or in children younger than four years. EBV-specific serologic testing can confirm the diagnosis when needed, particularly in atypical or severe cases. Abdominal ultrasound or CT imaging is reserved for patients with significant abdominal pain or concern for splenic rupture.
Management in the emergency and acute care setting is primarily supportive. Attention should be given to airway assessment, hydration, fever control, and analgesia. Corticosteroids may be considered in cases of significant tonsillar or pharyngeal edema with concern for airway obstruction, as well as in select severe complications such as massive splenomegaly, hemolytic anemia, myocarditis, or hemophagocytic lymphohistiocytosis, though their use remains controversial. Antibiotics are reserved for suspected bacterial superinfection, and ampicillin should be avoided due to the high likelihood of rash development.
Hospital admission is indicated for patients with airway compromise, severe neurologic, hepatic, or hematologic complications, or inability to tolerate oral intake. Most patients may be safely discharged once hydration and pain are controlled and there is no evidence of serious complications. Patients should be counseled to avoid contact sports and strenuous activity for at least three weeks due to the risk of splenic rupture, with reassessment prior to return to full activity. While infectious mononucleosis is generally self-limited, clinicians must remain vigilant for potentially life-threatening complications and ensure appropriate follow-up.
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Emergency and Acute Medicine – Community-Acquired MRSA
Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) represents a shift from the traditional healthcare-associated MRSA infections that primarily affected elderly or chronically ill patients with frequent medical exposures. Over the past decade, CA-MRSA has emerged as a common pathogen among younger, otherwise healthy individuals without recent healthcare contact. It is now the most frequent cause of skin and soft tissue infections presenting to the emergency department. Although CA-MRSA most often causes localized skin disease, it can also result in severe, life-threatening illnesses such as sepsis and necrotizing pneumonia.
Staphylococcus aureus is a gram-positive cocci that commonly colonizes the skin and nares. MRSA refers to strains that have developed resistance to methicillin and many other β-lactam antibiotics. Certain populations are at increased risk for colonization and infection, including prisoners, athletes, military personnel, children in daycare, people who inject drugs, and individuals with prior MRSA infections or close contact with colonized or infected persons. In contrast, healthcare-associated MRSA remains more prevalent among elderly patients, particularly those in long-term care facilities or with frequent healthcare exposure.
Patients with CA-MRSA most commonly present with skin and soft tissue infections characterized by increasing redness, warmth, swelling, pain, and sometimes fever or malaise. Abscesses typically appear as tender, fluctuant, raised lesions with surrounding induration, while cellulitis presents with diffuse erythema that may include lymphangitic streaking. More severe presentations include systemic illness with signs of sepsis such as hypotension, tachycardia, altered mental status, or petechiae. CA-MRSA pneumonia may manifest with fever, rigors, dyspnea, chest pain, hypoxia, and productive cough, often progressing rapidly and associated with alveolar infiltrates on chest radiographs.
Evaluation depends on the severity and type of infection. Skin abscesses generally require incision and drainage, which is both diagnostic and therapeutic, with cultures often obtained to guide antibiotic selection due to evolving resistance patterns. In cases of suspected sepsis or pneumonia, prompt source identification, blood and urine cultures, chest imaging, and laboratory studies such as CBC and metabolic panels are indicated as resuscitation begins. Bedside ultrasound can be helpful in differentiating abscesses, which appear as anechoic fluid collections, from cellulitis, which demonstrates a “cobblestoning” pattern of subcutaneous edema.
Management in the emergency setting focuses on early recognition and appropriate treatment. Abscesses require incision and drainage, and antibiotics may be unnecessary in otherwise healthy patients without surrounding cellulitis or systemic signs. Cellulitis in stable patients can often be managed with oral antibiotics that provide coverage for CA-MRSA and streptococcal species, while ill-appearing patients or those with comorbidities require intravenous therapy. Patients with suspected sepsis, necrotizing infection, or pneumonia should receive early broad-spectrum antibiotics with MRSA coverage along with aggressive supportive care.
Antibiotic selection must take into account local resistance patterns, as CA-MRSA susceptibility varies by region. Commonly used agents include trimethoprim-sulfamethoxazole, clindamycin, doxycycline, vancomycin, linezolid, and rifampin (the latter never as monotherapy). Tetracyclines should be avoided during pregnancy, and prolonged use in children requires caution. Close follow-up is essential, with re-evaluation within 24–48 hours to ensure clinical improvement.
Hospital admission is warranted for patients with systemic illness, rapidly progressive infection, bacteremia, significant comorbidities such as diabetes or immunodeficiency, or failure of outpatient therapy. Well-appearing patients with uncomplicated skin and soft tissue infections may be safely discharged with appropriate antibiotics and follow-up instructions. Clinicians should remember that CA-MRSA is the leading cause of skin infections in the emergency department and, while often benign, can occasionally lead to severe and rapidly fatal disease if not promptly recognized and treated.
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Emergency and Acute Medicine – Mumps
Mumps is a vaccine-preventable infectious disease characterized primarily by inflammation and swelling of the salivary glands, most notably the parotid glands. The disease is caused by a single-stranded RNA virus of the Rubulavirus genus within the Paramyxovirus family, with humans as the only known reservoir. Widespread vaccination has significantly reduced incidence, but outbreaks still occur, particularly in unvaccinated or underimmunized populations.
Transmission occurs through respiratory droplets, saliva, and contact with contaminated fomites. After replication in the nasopharynx and regional lymph nodes, the virus disseminates hematogenously to target organs, including the salivary glands, pancreas, testes, ovaries, and meninges. The incubation period is typically 14 to 18 days. Patients are contagious from approximately one week before symptom onset until about six days after symptoms begin. A history of incomplete or absent immunization is common.
Clinical illness often begins with a prodrome of low-grade fever, headache, malaise, myalgia, anorexia, otalgia, and jaw pain, which may precede glandular swelling by up to 48 hours. Up to 20 percent of infections are asymptomatic but remain contagious. Approximately half of patients may present with nonspecific upper respiratory symptoms without obvious salivary gland enlargement. Parotitis is the most common clinical manifestation and occurs in the majority of symptomatic cases, presenting as painful, tender unilateral or bilateral enlargement of the parotid glands. Swelling is bilateral in most cases, and the overlying skin remains nonerythematous. Symptoms typically peak within several days and resolve by the tenth day.
Complications are more frequent and severe in adults than in children. Orchitis is the most common complication in postpubertal males and may occur before, during, or after parotitis. It presents with abrupt onset of painful testicular swelling, fever, nausea, and vomiting. Although testicular atrophy may develop in a significant proportion of patients, infertility is rare. Oophoritis may occur in postpubertal females and can mimic appendicitis but does not impair fertility. Pancreatitis may develop with fever, nausea, vomiting, epigastric pain, and transient hyperglycemia, and in severe cases may progress to shock.
Central nervous system involvement includes aseptic meningitis, which occurs in a minority of patients and usually resolves without sequelae, and encephalitis, which is rare but serious. Other neurologic complications include sensorineural hearing loss, typically unilateral and often permanent, cerebellar ataxia, and transverse myelitis. Additional rare complications include myocarditis, glomerulonephritis, polyarthritis, thrombocytopenic purpura, thyroiditis, mastitis, and ocular involvement.
Diagnosis is primarily clinical, based on the presence of parotitis with compatible systemic symptoms and epidemiologic context. Laboratory testing is not routinely required but may be useful in atypical cases or when confirmation is necessary. Elevated serum amylase due to salivary gland inflammation can support the diagnosis. Definitive diagnosis may be obtained through detection of mumps RNA by polymerase chain reaction, viral culture, or serologic testing demonstrating mumps-specific IgM antibodies or a significant rise in IgG titers. Cerebrospinal fluid analysis is reserved for patients with neurologic symptoms.
Management in the emergency setting is supportive, as no specific antiviral therapy exists. Treatment includes antipyretics, analgesics, adequate hydration, and antiemetics when needed. Ice packs and rest may relieve parotid discomfort. Patients with orchitis benefit from scrotal support, bed rest, and pain control. Infected individuals should be placed on droplet precautions to limit transmission. Vaccination remains the cornerstone of prevention, though it is not effective once infection has occurred.
Hospital admission is reserved for patients with severe complications such as meningitis, encephalitis, significant pancreatitis, or those unable to maintain hydration. Most patients can be safely discharged with instructions regarding isolation and symptom management. Patients are considered contagious until approximately one week after symptom onset.
Key clinical pearls include recognizing that mumps is the only cause of epidemic parotitis and that vaccination provides high levels of immunity when appropriately administered. The mumps vaccine should not be given to pregnant or severely immunocompromised individuals. Despite reduced incidence in many regions, mumps remains endemic worldwide and should be considered in travelers and unvaccinated populations.
Mumps is a vaccine-preventable infectious disease characterized primarily by inflammation and swelling of the salivary glands, most notably the parotid glands. The disease is caused by a single-stranded RNA virus of the Rubulavirus genus within the Paramyxovirus family, with humans as the only known reservoir. Widespread vaccination has significantly reduced incidence, but outbreaks still occur, particularly in unvaccinated or underimmunized populations.
Transmission occurs through respiratory droplets, saliva, and contact with contaminated fomites. After replication in the nasopharynx and regional lymph nodes, the virus disseminates hematogenously to target organs, including the salivary glands, pancreas, testes, ovaries, and meninges. The incubation period is typically 14 to 18 days. Patients are contagious from approximately one week before symptom onset until about six days after symptoms begin. A history of incomplete or absent immunization is common.
Clinical illness often begins with a prodrome of low-grade fever, headache, malaise, myalgia, anorexia, otalgia, and jaw pain, which may precede glandular swelling by up to 48 hours. Up to 20 percent of infections are asymptomatic but remain contagious. Approximately half of patients may present with nonspecific upper respiratory symptoms without obvious salivary gland enlargement. Parotitis is the most common clinical manifestation and occurs in the majority of symptomatic cases, presenting as painful, tender unilateral or bilateral enlargement of the parotid glands. Swelling is bilateral in most cases, and the overlying skin remains nonerythematous. Symptoms typically peak within several days and resolve by the tenth day.
Complications are more frequent and severe in adults than in children. Orchitis is the most common complication in postpubertal males and may occur before, during, or after parotitis. It presents with abrupt onset of painful testicular swelling, fever, nausea, and vomiting. Although testicular atrophy may develop in a significant proportion of patients, infertility is rare. Oophoritis may occur in postpubertal females and can mimic appendicitis but does not impair fertility. Pancreatitis may develop with fever, nausea, vomiting, epigastric pain, and transient hyperglycemia, and in severe cases may progress to shock.
Central nervous system involvement includes aseptic meningitis, which occurs in a minority of patients and usually resolves without sequelae, and encephalitis, which is rare but serious. Other neurologic complications include sensorineural hearing loss, typically unilateral and often permanent, cerebellar ataxia, and transverse myelitis. Additional rare complications include myocarditis, glomerulonephritis, polyarthritis, thrombocytopenic purpura, thyroiditis, mastitis, and ocular involvement.
Diagnosis is primarily clinical, based on the presence of parotitis with compatible systemic symptoms and epidemiologic context. Laboratory testing is not routinely required but may be useful in atypical cases or when confirmation is necessary. Elevated serum amylase due to salivary gland inflammation can support the diagnosis. Definitive diagnosis may be obtained through detection of mumps RNA by polymerase chain reaction, viral culture, or serologic testing demonstrating mumps-specific IgM antibodies or a significant rise in IgG titers. Cerebrospinal fluid analysis is reserved for patients with neurologic symptoms.
Management in the emergency setting is supportive, as no specific antiviral therapy exists. Treatment includes antipyretics, analgesics, adequate hydration, and antiemetics when needed. Ice packs and rest may relieve parotid discomfort. Patients with orchitis benefit from scrotal support, bed rest, and pain control. Infected individuals should be placed on droplet precautions to limit transmission. Vaccination remains the cornerstone of prevention, though it is not effective once infection has occurred.
Hospital admission is reserved for patients with severe complications such as meningitis, encephalitis, significant pancreatitis, or those unable to maintain hydration. Most patients can be safely discharged with instructions regarding isolation and symptom management. Patients are considered contagious until approximately one week after symptom onset.
Key clinical pearls include recognizing that mumps is the only cause of epidemic parotitis and that vaccination provides high levels of immunity when appropriately administered. The mumps vaccine should not be given to pregnant or severely immunocompromised individuals. Despite reduced incidence in many regions, mumps remains endemic worldwide and should be considered in travelers and unvaccinated populations.
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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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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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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.
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.
