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Emergency and Acute Medicine - Shock
Shock is a state of inadequate tissue perfusion in which blood flow is insufficient to meet cellular metabolic demands. As a result, tissues do not receive enough oxygen and are unable to clear toxic metabolic byproducts. If untreated, shock progresses from impaired perfusion to organ dysfunction and ultimately death. Major categories include hypovolemic shock, cardiogenic or obstructive shock, septic shock, neurogenic shock, anaphylactic shock, and pharmacologic shock. Although the mechanisms differ, all forms lead to impaired oxygen delivery and end-organ injury.
Hypovolemic shock results from decreased intravascular volume, most commonly from hemorrhage or severe fluid loss. Acute onset should raise concern for bleeding, while a more progressive course with elevated hematocrit, blood urea nitrogen, and creatinine may suggest dehydration. Common causes include trauma, gastrointestinal bleeding, ruptured ectopic pregnancy, postpartum hemorrhage, vomiting, diarrhea, burns, ruptured aneurysm, and retroperitoneal bleeding. Cardiogenic or obstructive shock occurs when cardiac output is inadequate despite sufficient intravascular volume. It may result from myocardial infarction, cardiomyopathy, arrhythmias, myocarditis, valvular disease, tamponade, pulmonary embolism, or tension pneumothorax. Septic shock begins with overwhelming infection that triggers release of inflammatory mediators, producing vasodilation, capillary leak, and reduced systemic vascular resistance, later followed by myocardial depression. Neurogenic shock occurs when spinal cord injury disrupts sympathetic tone, leading to vasodilation and sometimes bradycardia, especially with lesions above T4. Anaphylactic shock results from massive mast cell degranulation after allergen exposure, leading to vasodilation, capillary leak, and airway compromise. Pharmacologic shock may result from drug-induced vasodilation or myocardial depression.
Patients in shock commonly present with hypotension, weak peripheral pulses, tachycardia, tachypnea, decreased urine output, diaphoresis, lethargy, or obtundation. History should focus on identifying the likely cause, including trauma, infection, allergic exposure, medication use, cardiac symptoms, or fluid loss. Physical examination should be targeted to the likely type of shock. In hypovolemic shock, neck veins are typically flat, mucous membranes are dry, and extremities are cold. In cardiogenic shock, jugular venous distention is often present, mucous membranes are moist, and extremities are cold. Early septic shock may show flat neck veins, dry mucous membranes, and warm extremities, though later patients can become cold and mottled. Additional findings such as wounds, urticaria, cellulitis, cardiac murmurs, or pelvic instability may help establish the diagnosis.
The workup of shock aims to identify both the type of shock and its underlying cause. Laboratory studies usually include hemoglobin and hematocrit, white blood cell count, electrolytes, glucose, coagulation studies, cardiac enzymes, urinalysis, pregnancy testing when appropriate, and serum lactate, which is a useful marker of tissue hypoperfusion. Imaging often includes chest radiograph, electrocardiogram, abdominal ultrasound, and sometimes computed tomography once the patient is stabilized. Electrocardiography may reveal ischemia, tamponade with electrical alternans or low voltage, or right-heart strain with pulmonary embolism.
Initial management centers on aggressive stabilization of airway, breathing, and circulation. Large-bore IV access is essential, and central venous access may be needed in severe cases. Oxygen should be administered, and fluid resuscitation should begin promptly in most noncardiogenic forms of shock. Active bleeding should be controlled immediately, including the use of direct pressure and pelvic stabilization when indicated. Hypovolemic shock requires rapid crystalloid resuscitation, typically 2 to 3 liters initially, followed by blood products if blood pressure does not improve. Definitive control of bleeding is crucial. Cardiogenic shock requires treatment of the specific cause, such as reperfusion for myocardial infarction, pericardiocentesis for tamponade, or treatment of dysrhythmias, with vasopressors such as norepinephrine or dopamine as needed. Septic shock requires aggressive crystalloid administration, early antibiotics, maintenance of urine output above 30 mL/hour, and vasopressor support, with norepinephrine preferred as first-line therapy. Anaphylactic shock requires prompt airway management, epinephrine, antihistamines, corticosteroids, and bronchodilators if bronchospasm is present. Pharmacologic shock may require decontamination, antidotes, and inotropic support. Neurogenic shock is treated supportively, with spinal stabilization and hemodynamic support.
All patients with shock require admission, and most with persistent shock need ICU-level monitoring. A small number whose shock is completely and definitively reversed in the emergency department may be managed outside the ICU, but no patient actively in shock should be discharged home. Important clinical priorities are to identify the cause quickly, begin aggressive fluid resuscitation early, and add vasopressors when indicated to minimize prolonged tissue hypoxia.
Shock is a state of inadequate tissue perfusion in which blood flow is insufficient to meet cellular metabolic demands. As a result, tissues do not receive enough oxygen and are unable to clear toxic metabolic byproducts. If untreated, shock progresses from impaired perfusion to organ dysfunction and ultimately death. Major categories include hypovolemic shock, cardiogenic or obstructive shock, septic shock, neurogenic shock, anaphylactic shock, and pharmacologic shock. Although the mechanisms differ, all forms lead to impaired oxygen delivery and end-organ injury.
Hypovolemic shock results from decreased intravascular volume, most commonly from hemorrhage or severe fluid loss. Acute onset should raise concern for bleeding, while a more progressive course with elevated hematocrit, blood urea nitrogen, and creatinine may suggest dehydration. Common causes include trauma, gastrointestinal bleeding, ruptured ectopic pregnancy, postpartum hemorrhage, vomiting, diarrhea, burns, ruptured aneurysm, and retroperitoneal bleeding. Cardiogenic or obstructive shock occurs when cardiac output is inadequate despite sufficient intravascular volume. It may result from myocardial infarction, cardiomyopathy, arrhythmias, myocarditis, valvular disease, tamponade, pulmonary embolism, or tension pneumothorax. Septic shock begins with overwhelming infection that triggers release of inflammatory mediators, producing vasodilation, capillary leak, and reduced systemic vascular resistance, later followed by myocardial depression. Neurogenic shock occurs when spinal cord injury disrupts sympathetic tone, leading to vasodilation and sometimes bradycardia, especially with lesions above T4. Anaphylactic shock results from massive mast cell degranulation after allergen exposure, leading to vasodilation, capillary leak, and airway compromise. Pharmacologic shock may result from drug-induced vasodilation or myocardial depression.
Patients in shock commonly present with hypotension, weak peripheral pulses, tachycardia, tachypnea, decreased urine output, diaphoresis, lethargy, or obtundation. History should focus on identifying the likely cause, including trauma, infection, allergic exposure, medication use, cardiac symptoms, or fluid loss. Physical examination should be targeted to the likely type of shock. In hypovolemic shock, neck veins are typically flat, mucous membranes are dry, and extremities are cold. In cardiogenic shock, jugular venous distention is often present, mucous membranes are moist, and extremities are cold. Early septic shock may show flat neck veins, dry mucous membranes, and warm extremities, though later patients can become cold and mottled. Additional findings such as wounds, urticaria, cellulitis, cardiac murmurs, or pelvic instability may help establish the diagnosis.
The workup of shock aims to identify both the type of shock and its underlying cause. Laboratory studies usually include hemoglobin and hematocrit, white blood cell count, electrolytes, glucose, coagulation studies, cardiac enzymes, urinalysis, pregnancy testing when appropriate, and serum lactate, which is a useful marker of tissue hypoperfusion. Imaging often includes chest radiograph, electrocardiogram, abdominal ultrasound, and sometimes computed tomography once the patient is stabilized. Electrocardiography may reveal ischemia, tamponade with electrical alternans or low voltage, or right-heart strain with pulmonary embolism.
Initial management centers on aggressive stabilization of airway, breathing, and circulation. Large-bore IV access is essential, and central venous access may be needed in severe cases. Oxygen should be administered, and fluid resuscitation should begin promptly in most noncardiogenic forms of shock. Active bleeding should be controlled immediately, including the use of direct pressure and pelvic stabilization when indicated. Hypovolemic shock requires rapid crystalloid resuscitation, typically 2 to 3 liters initially, followed by blood products if blood pressure does not improve. Definitive control of bleeding is crucial. Cardiogenic shock requires treatment of the specific cause, such as reperfusion for myocardial infarction, pericardiocentesis for tamponade, or treatment of dysrhythmias, with vasopressors such as norepinephrine or dopamine as needed. Septic shock requires aggressive crystalloid administration, early antibiotics, maintenance of urine output above 30 mL/hour, and vasopressor support, with norepinephrine preferred as first-line therapy. Anaphylactic shock requires prompt airway management, epinephrine, antihistamines, corticosteroids, and bronchodilators if bronchospasm is present. Pharmacologic shock may require decontamination, antidotes, and inotropic support. Neurogenic shock is treated supportively, with spinal stabilization and hemodynamic support.
All patients with shock require admission, and most with persistent shock need ICU-level monitoring. A small number whose shock is completely and definitively reversed in the emergency department may be managed outside the ICU, but no patient actively in shock should be discharged home. Important clinical priorities are to identify the cause quickly, begin aggressive fluid resuscitation early, and add vasopressors when indicated to minimize prolonged tissue hypoxia.
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Emergency and Acute Medicine - Seizure (Pediatric)
Seizures in children are defined as sudden, abnormal discharges of neurons that result in a change in behavior or neurologic function. They can occur across all pediatric age groups, from neonates to adolescents, and have a wide range of causes. Common etiologies include febrile seizures, infections, trauma, metabolic disturbances such as hypoglycemia or electrolyte abnormalities, toxicologic causes including drug ingestion or withdrawal, congenital or structural brain abnormalities, perinatal hypoxia, intracranial hemorrhage, degenerative diseases, and psychogenic causes.
Clinical presentation varies by age. In neonates, seizures may be subtle and difficult to recognize, often presenting as repetitive facial movements, eye deviation, eyelid fluttering, lip smacking, sucking motions, or respiratory changes such as apnea. Seizures in this group may be focal or generalized and can include tonic, clonic, or myoclonic movements. Interestingly, generalized systemic problems such as metabolic disturbances or infections may still present with focal seizure activity in neonates.
In older infants and children, seizures are more recognizable and can be classified as generalized or focal. Generalized seizures include tonic–clonic, tonic, clonic, myoclonic, atonic (“drop attacks”), and absence seizures. Focal (partial) seizures may be simple, where consciousness is preserved, or complex, where consciousness is impaired. Simple focal seizures may involve motor, sensory, or cognitive symptoms such as localized jerking, paresthesias, or hallucinations. Complex focal seizures often begin with an aura followed by altered consciousness and may progress to generalized seizures. Status epilepticus, defined as prolonged or recurrent seizures without recovery, is most commonly generalized but may also be focal or present as persistent altered mental status.
A thorough history is critical and should determine whether the seizure was febrile or afebrile, the type and duration of seizure, associated features such as aura, cyanosis, or eye deviation, and the presence of a postictal state. Family history and predisposing conditions should also be explored. Physical examination must include vital signs, especially temperature, and a detailed neurologic assessment, including mental status. Examination of the eyes and skin is important to identify underlying conditions such as neurocutaneous syndromes (e.g., tuberous sclerosis).
Evaluation begins with a bedside glucose measurement, especially in infants and in status epilepticus. Additional laboratory studies such as electrolytes, renal function, calcium, magnesium, complete blood count, and toxicology screening should be guided by clinical findings. In children already on anticonvulsants, drug levels should be checked. Imaging with head CT is indicated in cases of focal seizures, new neurologic deficits, suspected intracranial hemorrhage, or new-onset status epilepticus without a clear cause. Lumbar puncture is indicated if meningitis or encephalitis is suspected, but neuroimaging should precede it if there are signs of increased intracranial pressure. MRI is rarely required emergently. EEG is generally useful in afebrile seizures to help classify seizure type and assess recurrence risk but is not typically helpful in the acute setting.
Management focuses first on stabilization of airway, breathing, and circulation. Oxygen should be administered, and pulse oximetry monitoring initiated. A nasopharyngeal airway is preferred over an oral airway, and bag-valve-mask ventilation should be used if the child is hypoventilating or hypoxic. Intubation may be required if seizures are refractory or ventilation is inadequate. Intravenous access should be established, and hypoglycemia corrected promptly with dextrose. Spine precautions should be maintained if trauma is suspected.
Active seizures, particularly status epilepticus, require prompt pharmacologic treatment. Benzodiazepines such as lorazepam are first-line due to their rapid onset and longer duration of action. If intravenous access is not available, alternatives include buccal midazolam, intranasal lorazepam, or rectal diazepam. If seizures persist, second-line agents such as phenytoin or fosphenytoin are used for longer-term control. Phenobarbital may be administered if seizures are refractory, although there is an increased risk of respiratory depression, especially when combined with benzodiazepines. In refractory status epilepticus, advanced therapies such as barbiturate coma or general anesthesia may be required, with continuous EEG monitoring to confirm seizure suppression. In neonates, phenobarbital is often the preferred first-line and maintenance therapy.
Disposition depends on the clinical scenario. Children with ongoing status epilepticus, persistent altered mental status, or requiring intubation should be admitted to the intensive care unit. Those with resolved status epilepticus but unclear or serious underlying causes should be admitted for further evaluation. Discharge may be appropriate if the child has returned to baseline mental status, has a normal neurologic examination, no serious underlying cause is identified, and reliable caregivers are available.
Follow-up includes providing seizure precautions, education for caregivers, and arranging evaluation with a primary care physician or pediatric neurologist. Important clinical points include recognizing that many conditions can mimic seizures, ensuring early treatment of prolonged seizures to reduce morbidity, and considering alternative routes of benzodiazepine administration when intravenous access is not available.
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Emergency and Acute Medicine - Sepsis
Sepsis is defined as the presence of an infection accompanied by a systemic inflammatory response. This response is classically described by systemic inflammatory response syndrome (SIRS), which includes abnormalities in temperature (>38°C or <36°C), heart rate (>90 bpm), respiratory rate (>20/min or PaCO₂ <32 mm Hg), and white blood cell count (>12,000/mm³, <4,000/mm³, or >10% band forms). Sepsis occurs when infection is associated with at least two of these criteria. The condition results from the release of inflammatory mediators, leading to macrocirculatory failure (reduced cardiac output or perfusion pressure), microcirculatory dysfunction with impaired oxygen delivery, and cellular metabolic failure due to mitochondrial dysfunction.
Hemodynamic changes in sepsis initially include increased cardiac output due to vasodilation, followed later by myocardial depression. As the disease progresses, patients may develop multiple organ dysfunction syndrome (MODS), which can involve acute respiratory distress syndrome, acute kidney injury, hepatic failure, and disseminated intravascular coagulation. Sepsis exists on a continuum: severe sepsis involves sepsis with organ dysfunction such as acidosis, renal impairment, altered mental status, pulmonary dysfunction, hypotension, thrombocytopenia, or liver dysfunction, while septic shock is defined as persistent hypotension despite adequate fluid resuscitation. Sepsis remains a major cause of mortality, with septic shock carrying an in-hospital mortality of about 30%.
The most common causes of sepsis are bacterial infections. Gram-negative organisms such as Escherichia coli, Pseudomonas aeruginosa, Rickettsiae, and Legionella species are frequent causes, while gram-positive organisms include Enterococcus species, Staphylococcus aureus, and Streptococcus pneumoniae. Fungal infections, particularly Candida species, and viral infections may also contribute. In pediatric patients, important pathogens include Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae, although children with minor infections may still meet SIRS criteria.
Patients commonly present with nonspecific symptoms such as fever, dyspnea, nausea, vomiting, and altered mental status including confusion or delirium. Identifying the source of infection is essential and may involve respiratory symptoms (cough, shortness of breath), gastrointestinal complaints (abdominal pain, diarrhea), or urinary symptoms (dysuria, frequency). Risk factors include immunosuppression, malignancy, recent chemotherapy, HIV, diabetes, splenectomy, and residence in nursing facilities. On examination, tachypnea is often an early sign, while blood pressure may initially remain normal before progressing to hypotension in septic shock. Patients may appear warm and flushed due to vasodilation. Physical examination should focus on identifying infection sources, including lungs, abdomen, skin, indwelling catheters, and central nervous system signs such as neck stiffness or coma.
Early diagnostic evaluation is critical. Serum lactate should be measured promptly, as levels >4 mmol/L indicate severe sepsis, although normal levels do not exclude shock. Blood cultures should be obtained prior to antibiotic administration. Laboratory investigations include complete blood count, electrolytes, renal and liver function tests, coagulation studies, and blood gas analysis, often revealing mixed acid–base disorders such as respiratory alkalosis with metabolic acidosis. Imaging studies such as chest radiography, abdominal CT, or ultrasound help identify the infection source. Lumbar puncture is indicated if meningitis is suspected, and central venous access may be required for monitoring and therapy.
Management begins with rapid stabilization of airway, breathing, and circulation. Supplemental oxygen should be provided to maintain adequate oxygenation, and mechanical ventilation may be required in cases of respiratory failure. Aggressive fluid resuscitation with isotonic crystalloids is essential, typically using repeated boluses. Early goal-directed therapy includes targeting adequate central venous pressure, mean arterial pressure, and central venous oxygen saturation.
If hypotension persists despite adequate fluid resuscitation, vasopressors should be initiated. Norepinephrine is the preferred first-line agent, especially in patients with tachyarrhythmias, while dopamine may be used in selected cases. Epinephrine may be considered in refractory shock. If oxygen delivery remains inadequate, blood transfusion and inotropic support such as dobutamine may be required. Broad-spectrum antibiotics must be administered as early as possible and tailored to the suspected source of infection, with coverage for resistant organisms such as MRSA, VRE, and Pseudomonas when indicated. Source control, such as drainage of abscesses or removal of infected devices, is crucial. Corticosteroids like hydrocortisone may be considered in refractory shock or suspected adrenal insufficiency.
Most patients with sepsis require hospital admission, often to an intensive care unit, particularly if there is evidence of organ dysfunction or shock. Only patients with mild infections and stable vital signs may be considered for discharge. Early recognition, prompt antibiotic administration, and aggressive fluid resuscitation are essential to improving outcomes. Failure to recognize multiorgan dysfunction or delays in treatment remain major pitfalls in the management of sepsis.
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Emergency and Acute Medicine - Serotonin Syndrome (Drug-Induced)
Serotonin syndrome is a clinical condition caused by excessive stimulation of central and peripheral serotonergic receptors. It presents as a spectrum ranging from mild symptoms to severe, life-threatening toxicity. The condition typically results from the use of serotonergic medications, either alone, in overdose, or more commonly through drug interactions. The classic triad includes autonomic dysfunction (such as hyperthermia, diaphoresis, tachycardia, and hypertension), cognitive or behavioral changes (including agitation, confusion, hallucinations, or decreased responsiveness), and neuromuscular hyperactivity (such as hyperreflexia, clonus, tremor, and myoclonus).
Serotonin syndrome is most frequently associated with psychiatric medications, particularly selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). Other implicated agents include monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants, opioids (e.g., fentanyl, tramadol, methadone), antiemetics like ondansetron, and substances such as cocaine and MDMA (ecstasy). Herbal supplements like St. John’s wort may also contribute. The condition is more common in young adults and has a higher incidence in females, although fatalities are more common in males. Most severe cases result from drug interactions or recreational drug use.
Diagnosis is clinical and relies heavily on history and physical examination. The Hunter criteria are the most sensitive and specific diagnostic tool and require recent exposure to a serotonergic agent along with features such as clonus (spontaneous, inducible, or ocular), agitation, diaphoresis, tremor with hyperreflexia, or hypertonia with hyperthermia. Patients may present with hyperthermia, tachycardia, hypertension or hypotension, diaphoresis, and gastrointestinal symptoms such as diarrhea. Neurologically, agitation, delirium, hallucinations, and characteristic findings like clonus and hyperreflexia—especially in the lower extremities—are key diagnostic clues.
Laboratory testing is not diagnostic but helps assess severity and exclude other conditions. Tests may include electrolytes, renal function, creatine kinase, lactate, and toxicology screens. Imaging such as CT of the head may be considered if alternative diagnoses like trauma or intracranial pathology are suspected. Electrocardiography is useful to evaluate for arrhythmias or conduction abnormalities. Differential diagnoses include neuroleptic malignant syndrome, malignant hyperthermia, anticholinergic toxicity, sympathomimetic toxicity, and central nervous system infections such as meningitis or encephalitis.
Management focuses on supportive care and prompt recognition. Initial stabilization includes airway management, oxygen, IV access, and continuous monitoring of vital signs and temperature. All serotonergic agents must be discontinued immediately. Benzodiazepines such as lorazepam or diazepam are first-line treatments to control agitation and neuromuscular symptoms. Aggressive cooling measures are essential in cases of hyperthermia, which results from increased muscle activity rather than hypothalamic set-point changes, making antipyretics ineffective.
In severe cases, especially with uncontrollable hyperthermia or significant rigidity, intubation and paralysis may be required. Cyproheptadine, a serotonin antagonist, may be considered in severe cases, although evidence of its benefit is limited and it is only available in oral form. Consultation with a poison control center or toxicologist is recommended.
All patients with suspected serotonin syndrome should be admitted for monitoring, even if symptoms appear mild. Severe cases with instability, significant hyperthermia, or altered mental status require ICU care. Patients may be discharged once symptoms have completely resolved, with careful review of medications and education to prevent recurrence. Early recognition, discontinuation of offending agents, and supportive management are key to favorable outcomes.
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Emergency and Acute Medicine - Serum Sickness
Serum sickness is a type III hypersensitivity reaction that occurs when the immune system forms antigen–antibody complexes in response to a foreign protein or drug. These immune complexes deposit in tissues and activate the complement system, leading to inflammation and tissue damage. Complement components such as C3a and C5a act as anaphylatoxins, with C5a strongly attracting neutrophils. These neutrophils infiltrate vessel walls and release enzymes like collagenase and elastase, resulting in vascular injury. Symptoms typically develop 6–21 days after initial exposure to the antigen, but may occur sooner (1–4 days) if there has been prior sensitization. The condition is usually self-limited, resolving within 1–2 weeks.
Serum sickness can be triggered by exposure to foreign proteins such as vaccines (e.g., pneumococcal or rabies vaccines), antivenoms, and tetanus immunizations derived from animal serum. It may also occur with monoclonal antibodies. A related condition, serum sickness–like reaction, is more commonly caused by nonprotein drugs, especially antibiotics such as penicillins, amoxicillin, cephalosporins (e.g., cefaclor), and sulfonamides. Other implicated medications include thiazides, aspirin, gold, thiouracils, hydantoins, and certain antimicrobials.
The classic clinical presentation includes fever, rash, arthralgias, and lymphadenopathy. Patients may also report myalgias, facial or neck edema, chest pain, and shortness of breath. The rash is often urticarial, morbilliform, or scarlatiniform. On examination, findings may include fever, lymphadenopathy, arthritis, edema, splenomegaly, and, in severe cases, peripheral neuritis, myocarditis, pericarditis, or even anaphylaxis. A key diagnostic clue is the timing of symptoms following exposure to a potential offending agent.
Diagnosis is primarily clinical, based on history and physical findings. Laboratory studies may support the diagnosis and include decreased complement levels, elevated erythrocyte sedimentation rate (ESR), hypergammaglobulinemia, and possible eosinophilia. Urinalysis may reveal proteinuria or hematuria, indicating renal involvement. Imaging such as chest radiography may be considered in selected cases. A biopsy can confirm the diagnosis but is rarely required in routine practice.
The differential diagnosis includes other vasculitides such as polyarteritis nodosa, Goodpasture syndrome, and granulomatosis with polyangiitis, as well as dermatologic conditions like erythema multiforme or toxic epidermal necrolysis. Immunologic diseases such as systemic lupus erythematosus and infectious conditions like tick-borne illnesses or mononucleosis should also be considered.
Management is largely supportive, as the condition is usually self-limited. The most important step is identification and discontinuation of the offending agent. Treatment focuses on symptom relief using antihistamines, antipyretics, and nonsteroidal anti-inflammatory drugs. Corticosteroids such as prednisone may be used in more severe cases, although their use remains somewhat controversial. In cases involving airway compromise or anaphylaxis, standard emergency management with airway support and resuscitation is required.
Most patients can be discharged once stable, as symptoms typically resolve spontaneously. Hospital admission may be necessary for patients with severe systemic involvement, airway compromise, immunosuppression, or significant comorbid conditions. Follow-up with a primary care physician is recommended, and future exposure to the offending antigen should be avoided. Early recognition and removal of the causative agent are essential to prevent complications and ensure recovery.
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Emergency and Acute Medicine - Sexual Assault
Sexual assault refers to a range of nonconsensual sexual acts, including attempted or completed penetration (vaginal, anal, or oral), penetration with objects, and intentional touching of genital or intimate areas. Legal definitions vary by jurisdiction, but all forms involve lack of consent. Sexual assault is a significant public health issue, with a lifetime prevalence of approximately 18% in women and 5% in men. Most female victims know their assailant, whereas male victims are more often assaulted by strangers or acquaintances. Risk is higher among vulnerable populations, including individuals with disabilities, those experiencing intimate partner violence, and certain high-risk groups such as prisoners or individuals seeking mental health care.
Victims may present with a wide range of physical and psychological symptoms, and many do not initially disclose the assault unless directly asked. Common complaints include headaches, nausea, abdominal pain, sleep disturbances, anxiety, and breathing difficulties. Physical injuries may be absent in up to 70% of cases, but when present, may include genital trauma, lacerations, contusions, abrasions, bite marks, or more severe injuries such as fractures or burns. In pediatric cases, most physical examinations are normal, and evaluation must follow legal child protection requirements. Pregnancy increases vulnerability to assault, and special considerations apply.
A thorough and sensitive history is essential and should be obtained even if the patient does not wish to involve law enforcement. Important details include timing and location of the assault, number and description of assailants, type of contact or penetration, use of force or substances, and activities since the assault (e.g., bathing, changing clothes). A complete medical and gynecologic history should also be obtained. The physical examination should be conducted with informed consent, respecting the patient’s comfort and pace, and ideally performed by a trained sexual assault examiner (SANE) if available. Documentation should include the patient’s emotional state, clothing condition, and any physical injuries. Forensic evidence collection may include clothing, swabs, hair samples, and fingernail scrapings, following strict protocols to preserve evidence.
Laboratory evaluation may include testing for sexually transmitted infections such as gonorrhea, chlamydia, syphilis, hepatitis B and C, and HIV, as well as pregnancy testing. Drug screening may be considered if drug-facilitated assault is suspected. Imaging and additional procedures are guided by the presence of injuries.
Management begins with ensuring patient safety, privacy, and a supportive, nonjudgmental environment. Life-threatening injuries must be addressed first. Patients should be placed in a quiet setting and offered access to an advocate or support person. Confidentiality should be emphasized, and the patient’s autonomy respected regarding reporting to law enforcement, unless mandated by local laws.
Preventive treatment is a key component of care. Emergency contraception should be offered within 72 hours if there is a risk of pregnancy. Prophylactic treatment for sexually transmitted infections is recommended, typically including antibiotics for gonorrhea, chlamydia, and trichomonas. Hepatitis B vaccination should be initiated if the patient is not immunized, and HIV post-exposure prophylaxis should be considered within 72 hours for high-risk exposures. Baseline laboratory tests should be obtained if HIV prophylaxis is started.
Disposition depends on the patient’s physical and psychological condition. Admission is required for serious injuries, while most patients can be discharged with appropriate follow-up. Follow-up care includes repeat HIV testing at 6 weeks, 3 months, and 6 months, as well as monitoring for medication side effects. Referral for mental health support and counseling is essential. Pediatric cases require involvement of child protective services.
A key challenge in managing sexual assault is underreporting, as many victims do not disclose the event unless directly asked. Extragenital injuries are often more common than genital findings, and normal examination does not exclude assault. The use of specialized forensic examiners improves the quality of care, evidence collection, and patient outcomes.
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Emergency and Acute Medicine – Sciatica / Herniated Disc
Sciatica, most commonly caused by a herniated lumbar disc, refers to radicular pain radiating from the lower back into the buttock and down the leg (typically below the knee). It is highly suggestive of nerve root compression, with about 95% of cases involving the L5 or S1 nerve roots. The condition has a 3–5% lifetime prevalence, most commonly affecting individuals in their 40s to 50s, and accounts for a subset of low back pain presentations. Fortunately, ~90% of patients improve with conservative treatment, and symptoms usually resolve within 6 weeks, though a small percentage require surgery.
The underlying mechanism involves herniation of the nucleus pulposus through the annulus fibrosus, leading to compression and inflammation of adjacent nerve roots. Common risk factors include smoking, obesity, repetitive lifting or twisting, prolonged vibration exposure (e.g., driving machinery), and sedentary lifestyle. Symptoms often begin with low back pain, followed by progressively dominant leg pain that is sharp, well localized, and radiates distally.
Patients typically report worsening pain with activities that increase intradiscal pressure, such as coughing, sneezing, or straining (Valsalva maneuver), as well as prolonged sitting or leg elevation. Pain is often relieved by lying supine or walking. The most common sensory symptom is paresthesia. On examination, a detailed neurologic assessment is essential. Findings depend on the affected nerve root:
- L4 (L3–L4 disc): Knee extension weakness, reduced patellar reflex, sensory loss over medial leg
- L5 (L4–L5 disc): Weakness in great toe dorsiflexion, sensory loss in 1st web space
- S1 (L5–S1 disc): Weak plantarflexion, reduced Achilles reflex, sensory loss over lateral foot
The straight leg raise (SLR) test is a key bedside maneuver—raising the affected leg to 30–60° reproducing radicular pain is highly sensitive. A crossed SLR test (pain in the affected leg when lifting the opposite leg) is less sensitive but highly specific.
Diagnosis is primarily clinical. Imaging is not routinely required unless red flags are present (e.g., trauma, fever, cancer history, severe or progressive neurologic deficits). MRI is the gold standard when indicated—especially in cases of suspected infection, severe deficits, or failure of conservative therapy after 6 weeks. Importantly, imaging findings must be correlated clinically, as many asymptomatic individuals have disc abnormalities.
Emergency management focuses on excluding neurosurgical emergencies, particularly cauda equina syndrome (e.g., urinary retention, saddle anesthesia, decreased rectal tone). In uncomplicated cases, treatment is conservative, including:
- NSAIDs (first-line) for pain relief
- Short-term use of muscle relaxants or opioids if needed
- Early mobilization (avoid prolonged bed rest—max 1–2 days)
Patients should be advised to gradually resume activity while avoiding heavy lifting, bending, twisting, and vibration exposure.
Admission is required for severe or progressive neurologic deficits, inability to ambulate, suspected infection, malignancy, or cauda equina syndrome. Most patients can be safely discharged with follow-up within 1 week and a plan for conservative therapy over 4–6 weeks.
A critical clinical pearl is to always assess for red flags and neurologic deficits, as missing serious causes (e.g., epidural abscess or cauda equina syndrome) can lead to permanent disability. Conversely, overuse of imaging should be avoided in uncomplicated cases, as most patients improve without intervention.
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Emergency and Acute Medicine – Scaphoid Fractures
A scaphoid fracture is the most common fracture of the carpal bones and typically occurs after a fall on an outstretched hand (FOOSH). The scaphoid plays a key stabilizing role between the proximal and distal carpal rows, so injury to this bone can lead to significant long-term complications such as arthritis, malunion, or avascular necrosis (AVN). Fractures most commonly occur at the waist (middle third, 70–80%), followed by the proximal and distal thirds. Because the blood supply enters distally, fractures closer to the proximal pole have a much higher risk of AVN.
Clinically, patients usually present with wrist pain after trauma, especially after FOOSH. The most important physical finding is tenderness in the anatomic snuffbox, which is highly sensitive (≈90%) but not very specific. Additional findings include pain with axial loading of the thumb, tenderness over the scaphoid tubercle, and reduced wrist or thumb range of motion. Despite these signs, diagnosis can be tricky because 10–15% of fractures are not visible on initial X-rays, making clinical suspicion crucial.
Initial imaging includes wrist radiographs (PA, lateral, oblique, and scaphoid views), but a normal X-ray does not exclude a fracture. If suspicion remains high, the injury should be treated as a fracture, and repeat imaging in 7–10 days or advanced imaging (MRI or bone scan) should be arranged. MRI is particularly useful as it can detect fractures within a few days of injury.
Management in the emergency setting focuses on immobilization and prevention of complications. Any patient with snuffbox tenderness should be placed in a thumb spica splint, even if imaging is negative. Nondisplaced fractures are typically managed conservatively with immobilization, while displaced fractures (>1 mm) have a high risk of nonunion (up to 50%) and usually require surgical fixation. All suspected or confirmed cases should have orthopedic follow-up within 7–10 days.
A key clinical pitfall is missing the diagnosis—patients presenting with what seems like a simple wrist sprain may actually have a scaphoid fracture. Failure to immobilize can result in avascular necrosis, chronic pain, and long-term disability. Therefore, when in doubt, always treat as a fracture until proven otherwise.
Emergency and Acute Medicine – Scaphoid Fractures
A scaphoid fracture is the most common fracture of the carpal bones and typically occurs after a fall on an outstretched hand (FOOSH). The scaphoid plays a key stabilizing role between the proximal and distal carpal rows, so injury to this bone can lead to significant long-term complications such as arthritis, malunion, or avascular necrosis (AVN). Fractures most commonly occur at the waist (middle third, 70–80%), followed by the proximal and distal thirds. Because the blood supply enters distally, fractures closer to the proximal pole have a much higher risk of AVN.
Clinically, patients usually present with wrist pain after trauma, especially after FOOSH. The most important physical finding is tenderness in the anatomic snuffbox, which is highly sensitive (≈90%) but not very specific. Additional findings include pain with axial loading of the thumb, tenderness over the scaphoid tubercle, and reduced wrist or thumb range of motion. Despite these signs, diagnosis can be tricky because 10–15% of fractures are not visible on initial X-rays, making clinical suspicion crucial.
Initial imaging includes wrist radiographs (PA, lateral, oblique, and scaphoid views), but a normal X-ray does not exclude a fracture. If suspicion remains high, the injury should be treated as a fracture, and repeat imaging in 7–10 days or advanced imaging (MRI or bone scan) should be arranged. MRI is particularly useful as it can detect fractures within a few days of injury.
Management in the emergency setting focuses on immobilization and prevention of complications. Any patient with snuffbox tenderness should be placed in a thumb spica splint, even if imaging is negative. Nondisplaced fractures are typically managed conservatively with immobilization, while displaced fractures (>1 mm) have a high risk of nonunion (up to 50%) and usually require surgical fixation. All suspected or confirmed cases should have orthopedic follow-up within 7–10 days.
A key clinical pitfall is missing the diagnosis—patients presenting with what seems like a simple wrist sprain may actually have a scaphoid fracture. Failure to immobilize can result in avascular necrosis, chronic pain, and long-term disability. Therefore, when in doubt, always treat as a fracture until proven otherwise.
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Emergency and Acute Medicine – Schizophrenia
Schizophrenia is a chronic psychotic disorder characterized by delusions, hallucinations, disorganized thinking and behavior, negative symptoms, and cognitive impairment. The illness typically progresses through three phases: a premorbid phase with social withdrawal and decline in functioning, an active phase with prominent psychotic symptoms, and a residual phase marked by persistent cognitive and social deficits. Onset is usually in early adulthood (before age 30), and comorbid substance use—especially alcohol, cannabis, and stimulants—is common. Patients have a reduced life expectancy (by 12–25 years), largely due to cardiovascular disease, suicide (5–10%), and barriers to accessing medical care.
The exact cause remains unclear, but dysfunction in dopamine pathways is strongly implicated. There is a significant genetic component, with higher concordance in identical twins, and associations with conditions such as 22q11.2 deletion syndrome. Environmental and developmental factors—including prenatal infections, advanced paternal age, and cannabis use—may contribute. Schizophrenia is best understood as a multifactorial neurodevelopmental disorder with both biological and environmental influences.
Diagnosis is clinical and based on criteria (e.g., DSM) requiring at least two core symptoms for more than 6 months, including delusions, hallucinations, disorganized speech, disorganized/catatonic behavior, or negative symptoms (e.g., flat affect, apathy, social withdrawal). Patients often present to the emergency setting with acute psychosis, agitation, or behavioral disturbance, frequently related to medication noncompliance. A thorough evaluation must include screening for danger to self or others, substance use, and medical causes of psychosis (e.g., delirium, metabolic disturbances, neurologic disease), as schizophrenia does not typically impair orientation.
Emergency management prioritizes safety. Patients may be unpredictable or agitated, requiring a calm environment, verbal de-escalation, and sometimes physical or chemical restraints. First-line pharmacologic treatment for acute agitation includes antipsychotics such as haloperidol, often combined with benzodiazepines like lorazepam. Alternative agents include olanzapine, ziprasidone, and aripiprazole, though caution is required (e.g., avoid combining IM olanzapine with IV benzodiazepines due to risk of cardiopulmonary collapse). Continuous monitoring and a structured environment are essential.
Long-term treatment centers on antipsychotic medications. First-generation (typical) agents are effective but carry higher risk of extrapyramidal side effects, while second-generation (atypical) agents are better tolerated but associated with metabolic syndrome and weight gain. Clozapine is the most effective for treatment-resistant cases and reducing suicide risk but requires strict monitoring due to risk of agranulocytosis. Long-acting injectable formulations improve adherence in patients with frequent relapse due to noncompliance.
Disposition depends on patient safety and functional status. Hospital admission is indicated if the patient poses a danger to self or others, is unable to care for themselves, or has new-onset psychosis requiring evaluation. Stable patients with support and follow-up may be discharged with close psychiatric follow-up within 1 week.
Key clinical pearls include maintaining a high index of suspicion for medical causes of atypical psychosis, recognizing neuroleptic malignant syndrome in patients on antipsychotics, and understanding that early treatment improves long-term outcomes. Management is not only pharmacologic but also involves psychosocial support, therapy, and addressing comorbid conditions, especially substance use and cardiovascular risk factors.
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Emergency and Acute Medicine - Seborrheic Dermatitis
Seborrheic dermatitis is a common, chronic papulosquamous inflammatory skin disorder that affects individuals of all ages. It ranges in severity from mild dandruff to extensive, greasy, scaling plaques that are typically yellow to red or brown in color. The condition most often involves areas rich in sebaceous glands, such as the scalp, face, chest, and skin folds. It follows a relapsing and remitting course, with exacerbations frequently triggered by physical stress, emotional stress, or intercurrent illness.
The exact cause of seborrheic dermatitis is not fully understood, but it is considered multifactorial. Environmental, genetic, hormonal, immunologic, and microbial influences all play a role. A strong association exists with the yeast Malassezia, which thrives in sebaceous areas and contributes to inflammation. The disease involves a complex interaction of immune responses, inflammation, and increased epidermal turnover. Certain conditions predispose individuals to more severe or refractory disease, including neurologic disorders such as Parkinson disease, immunosuppression such as HIV/AIDS, mood disorders, and chronic systemic illness. Various medications, including lithium and interferon, may also exacerbate the condition.
Clinical presentation varies by age group. In infants, seborrheic dermatitis commonly appears within the first few weeks of life and is usually self-limited, resolving by 12 months. The classic manifestation is cradle cap, characterized by thick, greasy scales on the scalp, sometimes accompanied by inflammation or secondary infection. It may also involve flexural areas, presenting similarly to diaper dermatitis. In children, seborrheic dermatitis may present as blepharitis with scaling along the eyelid margins and can be persistent or resistant to treatment.
In adolescents and adults, seborrheic dermatitis typically presents with mild itching and greasy, fine scaling over erythematous skin. The distribution is usually bilateral and symmetrical, affecting the scalp, eyebrows, eyelids, nasolabial folds, ears, posterior neck, and presternal area, as well as body folds such as the axillae and groin. In individuals with darker skin tones, affected areas may show hypopigmentation. The condition is often exacerbated by infrequent washing and environmental stressors.
Diagnosis is primarily clinical, based on history and physical examination. Laboratory testing is rarely required but may include potassium hydroxide preparation to assess for yeast or fungal cultures to exclude dermatophyte infections. Skin biopsy is seldom necessary and is reserved for unclear or treatment-resistant cases.
Management focuses on controlling symptoms rather than curing the disease, as seborrheic dermatitis is chronic. General measures include patient education, regular cleansing, and the use of emollients such as mineral oil to soften scales before removal. Gentle brushing after washing can help remove adherent scales. Moderate exposure to sunlight may also be beneficial due to its inhibitory effect on yeast growth.
Pharmacologic treatment is typically multifaceted. First-line therapy includes topical antifungal agents such as ketoconazole, which target Malassezia species, along with low-potency topical corticosteroids like hydrocortisone for short-term control of inflammation. Medicated shampoos containing pyrithione zinc, selenium sulfide, coal tar, or salicylic acid are commonly used, especially for scalp involvement. In more resistant cases, second-line treatments include ciclopirox and topical calcineurin inhibitors such as tacrolimus or pimecrolimus, which provide anti-inflammatory effects without the long-term risks of corticosteroids.
In infants, treatment is generally gentle and supportive, using emollients, mild shampoos, and low-potency topical steroids if needed. Blepharitis associated with seborrheic dermatitis is managed with warm compresses and careful cleansing of the eyelid margins. Severe cases, particularly those involving extensive scaling or secondary infection, may require more intensive therapy.
The prognosis is generally good, although seborrheic dermatitis tends to be chronic with recurrent flares. Symptoms often improve within 7 to 10 days of treatment, but complete resolution may take longer, and recurrence is common. Patients should be advised about the chronic nature of the condition and the importance of maintenance therapy.
Important clinical considerations include recognizing that sudden or severe seborrheic dermatitis may be a sign of underlying immunosuppression, particularly HIV infection. Overuse of topical corticosteroids should be avoided due to the risk of skin atrophy and rebound flares. Clinicians should also remain vigilant for signs of secondary bacterial or fungal infection, such as increased erythema, tenderness, or systemic symptoms, which may require additional treatment.
