- Published on
Emergency and Acute Medicine - Sick Sinus Syndrome
Sick sinus syndrome (SSS) is a collective term describing dysfunction of the sinoatrial (SA) node, resulting in impaired automaticity and abnormal impulse generation. It is most commonly caused by progressive degenerative fibrosis of the sinus node and typically affects older adults, with a mean age over 65 years. The condition is characterized by intermittent or persistent bradyarrhythmias, often without appropriate escape rhythms, and may include a combination of sinus pauses, SA block, and alternating tachyarrhythmias (tachy–brady syndrome). It may also present with delayed recovery of sinus node activity following cardioversion.
Etiologies can be intrinsic or extrinsic. Intrinsic causes include idiopathic fibrosis (most common), ischemic heart disease affecting the SA node, cardiomyopathy, infiltrative diseases such as amyloidosis, inflammatory conditions, and surgical trauma. Extrinsic causes—while not true SSS—can mimic the condition and include medications (e.g., β-blockers, calcium channel blockers, digoxin, amiodarone), electrolyte abnormalities, hypothyroidism, hypothermia, hypoglycemia, and systemic infections such as sepsis. In pediatric patients, SSS may be associated with congenital heart disease or post-surgical complications.
Clinical presentation varies widely. Some patients are asymptomatic, while others experience symptoms due to cerebral hypoperfusion, such as syncope, presyncope, dizziness, fatigue, or altered mental status. Cardiovascular symptoms may include palpitations, chest pain, dyspnea, and exercise intolerance. Physical findings often reveal bradycardia or alternating bradycardia and tachycardia. In severe cases, patients may present with transient ischemic attacks or stroke.
Diagnosis begins with a 12-lead ECG, which may show sinus bradycardia, sinus pauses, SA block, atrial fibrillation with slow ventricular response, or tachy–brady patterns. However, ECG findings may be intermittent, so Holter monitoring or rhythm strips may be necessary. Laboratory evaluation should include electrolytes, thyroid function tests, cardiac markers, and drug levels when appropriate. Imaging such as chest radiography may assist in identifying underlying causes.
Management depends on symptom severity and hemodynamic stability. In unstable patients with symptomatic bradycardia (e.g., hypotension, altered mental status, chest pain), initial treatment includes atropine. If ineffective, transcutaneous pacing should be initiated, followed by transvenous pacing if needed. In patients with tachy–brady syndrome, unstable tachyarrhythmias require cardioversion, but clinicians must anticipate significant post-conversion bradycardia.
Stable patients should be monitored closely, with correction of reversible causes such as medication effects, electrolyte disturbances, hypoxia, or hypothermia. Use of AV nodal blocking agents (e.g., β-blockers, calcium channel blockers, digoxin) should be approached cautiously, as they may worsen bradycardia.
The definitive treatment for symptomatic SSS is placement of a permanent pacemaker, which provides a baseline heart rate and prevents symptomatic bradyarrhythmias. Patients with concurrent atrial fibrillation may require anticoagulation and additional rate or rhythm control strategies.
Patients with new-onset or symptomatic SSS should be admitted for monitoring and cardiology evaluation. Asymptomatic patients may be managed as outpatients with further rhythm monitoring.
Key pitfalls include missing intermittent arrhythmias on ECG and precipitating severe bradycardia with nodal-blocking medications without pacing backup.
Sick sinus syndrome (SSS) is a collective term describing dysfunction of the sinoatrial (SA) node, resulting in impaired automaticity and abnormal impulse generation. It is most commonly caused by progressive degenerative fibrosis of the sinus node and typically affects older adults, with a mean age over 65 years. The condition is characterized by intermittent or persistent bradyarrhythmias, often without appropriate escape rhythms, and may include a combination of sinus pauses, SA block, and alternating tachyarrhythmias (tachy–brady syndrome). It may also present with delayed recovery of sinus node activity following cardioversion.
Etiologies can be intrinsic or extrinsic. Intrinsic causes include idiopathic fibrosis (most common), ischemic heart disease affecting the SA node, cardiomyopathy, infiltrative diseases such as amyloidosis, inflammatory conditions, and surgical trauma. Extrinsic causes—while not true SSS—can mimic the condition and include medications (e.g., β-blockers, calcium channel blockers, digoxin, amiodarone), electrolyte abnormalities, hypothyroidism, hypothermia, hypoglycemia, and systemic infections such as sepsis. In pediatric patients, SSS may be associated with congenital heart disease or post-surgical complications.
Clinical presentation varies widely. Some patients are asymptomatic, while others experience symptoms due to cerebral hypoperfusion, such as syncope, presyncope, dizziness, fatigue, or altered mental status. Cardiovascular symptoms may include palpitations, chest pain, dyspnea, and exercise intolerance. Physical findings often reveal bradycardia or alternating bradycardia and tachycardia. In severe cases, patients may present with transient ischemic attacks or stroke.
Diagnosis begins with a 12-lead ECG, which may show sinus bradycardia, sinus pauses, SA block, atrial fibrillation with slow ventricular response, or tachy–brady patterns. However, ECG findings may be intermittent, so Holter monitoring or rhythm strips may be necessary. Laboratory evaluation should include electrolytes, thyroid function tests, cardiac markers, and drug levels when appropriate. Imaging such as chest radiography may assist in identifying underlying causes.
Management depends on symptom severity and hemodynamic stability. In unstable patients with symptomatic bradycardia (e.g., hypotension, altered mental status, chest pain), initial treatment includes atropine. If ineffective, transcutaneous pacing should be initiated, followed by transvenous pacing if needed. In patients with tachy–brady syndrome, unstable tachyarrhythmias require cardioversion, but clinicians must anticipate significant post-conversion bradycardia.
Stable patients should be monitored closely, with correction of reversible causes such as medication effects, electrolyte disturbances, hypoxia, or hypothermia. Use of AV nodal blocking agents (e.g., β-blockers, calcium channel blockers, digoxin) should be approached cautiously, as they may worsen bradycardia.
The definitive treatment for symptomatic SSS is placement of a permanent pacemaker, which provides a baseline heart rate and prevents symptomatic bradyarrhythmias. Patients with concurrent atrial fibrillation may require anticoagulation and additional rate or rhythm control strategies.
Patients with new-onset or symptomatic SSS should be admitted for monitoring and cardiology evaluation. Asymptomatic patients may be managed as outpatients with further rhythm monitoring.
Key pitfalls include missing intermittent arrhythmias on ECG and precipitating severe bradycardia with nodal-blocking medications without pacing backup.
- Published on
Emergency and Acute Medicine - Shoulder Dislocation
Shoulder dislocation is a common injury due to the highly mobile and inherently unstable nature of the glenohumeral joint. The majority are anterior dislocations (90–96%), typically caused by forces applied to an abducted and externally rotated arm. Posterior dislocations are less common and frequently missed; they occur when force is applied to an adducted, internally rotated arm, often during seizures, electrocution, or trauma. Inferior dislocations (luxatio erecta) are rare and result from hyperabduction, often associated with falls from height and frequently accompanied by neurovascular injury. In children, true dislocations are uncommon and fractures should be suspected, while in older adults, associated fractures are more frequent.
Patients typically present with severe shoulder pain and limited movement. In anterior dislocation, the shoulder appears “squared off,” with a prominent acromion and anterior fullness, and the arm is held slightly abducted and externally rotated. Posterior dislocation presents with the arm adducted and internally rotated, a prominent coracoid process, and a posterior bulge. Inferior dislocation is distinctive, with the arm fixed overhead and the humeral head sometimes palpable along the chest wall.
Evaluation must always include careful assessment of neurovascular status, especially the axillary nerve, both before and after any manipulation. Imaging is essential prior to reduction unless delay would be harmful. Standard radiographs should include anteroposterior and either axillary or scapular Y views. Associated findings may include Hill–Sachs lesions, Bankart lesions, or fractures of the greater tuberosity. Posterior dislocations may show the classic “light bulb” sign on X-ray and are often missed without appropriate imaging views.
Management requires prompt reduction to minimize complications such as post-traumatic arthritis. Adequate analgesia and muscle relaxation are critical, using procedural sedation (e.g., opioids and benzodiazepines, or agents like etomidate or propofol) or intra-articular local anesthetic. Several reduction techniques can be used for anterior dislocations, including scapular manipulation, Stimson technique, traction-countertraction, and slow external rotation. Posterior and inferior dislocations require modified reduction approaches, often involving traction and directed manipulation.
After successful reduction, confirm alignment with repeat imaging and reassess neurovascular status. Immobilize the shoulder in a sling or immobilizer. Younger patients typically require immobilization for 2–3 weeks, while shorter durations are recommended in older patients to prevent stiffness and frozen shoulder.
Admission is indicated if reduction fails, if general anesthesia is required, or if there is neurovascular compromise. Most patients with successful reduction can be discharged with immobilization and arranged orthopedic follow-up. Recurrent dislocations may require surgical intervention.
A key clinical point is to always document axillary nerve function prior to reduction. Missing posterior dislocations and failing to identify associated fractures or nerve injury are common pitfalls.
Shoulder dislocation is a common injury due to the highly mobile and inherently unstable nature of the glenohumeral joint. The majority are anterior dislocations (90–96%), typically caused by forces applied to an abducted and externally rotated arm. Posterior dislocations are less common and frequently missed; they occur when force is applied to an adducted, internally rotated arm, often during seizures, electrocution, or trauma. Inferior dislocations (luxatio erecta) are rare and result from hyperabduction, often associated with falls from height and frequently accompanied by neurovascular injury. In children, true dislocations are uncommon and fractures should be suspected, while in older adults, associated fractures are more frequent.
Patients typically present with severe shoulder pain and limited movement. In anterior dislocation, the shoulder appears “squared off,” with a prominent acromion and anterior fullness, and the arm is held slightly abducted and externally rotated. Posterior dislocation presents with the arm adducted and internally rotated, a prominent coracoid process, and a posterior bulge. Inferior dislocation is distinctive, with the arm fixed overhead and the humeral head sometimes palpable along the chest wall.
Evaluation must always include careful assessment of neurovascular status, especially the axillary nerve, both before and after any manipulation. Imaging is essential prior to reduction unless delay would be harmful. Standard radiographs should include anteroposterior and either axillary or scapular Y views. Associated findings may include Hill–Sachs lesions, Bankart lesions, or fractures of the greater tuberosity. Posterior dislocations may show the classic “light bulb” sign on X-ray and are often missed without appropriate imaging views.
Management requires prompt reduction to minimize complications such as post-traumatic arthritis. Adequate analgesia and muscle relaxation are critical, using procedural sedation (e.g., opioids and benzodiazepines, or agents like etomidate or propofol) or intra-articular local anesthetic. Several reduction techniques can be used for anterior dislocations, including scapular manipulation, Stimson technique, traction-countertraction, and slow external rotation. Posterior and inferior dislocations require modified reduction approaches, often involving traction and directed manipulation.
After successful reduction, confirm alignment with repeat imaging and reassess neurovascular status. Immobilize the shoulder in a sling or immobilizer. Younger patients typically require immobilization for 2–3 weeks, while shorter durations are recommended in older patients to prevent stiffness and frozen shoulder.
Admission is indicated if reduction fails, if general anesthesia is required, or if there is neurovascular compromise. Most patients with successful reduction can be discharged with immobilization and arranged orthopedic follow-up. Recurrent dislocations may require surgical intervention.
A key clinical point is to always document axillary nerve function prior to reduction. Missing posterior dislocations and failing to identify associated fractures or nerve injury are common pitfalls.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
Febrile seizure is a seizure occurring in children between 6 months and 5 years of age associated with fever, without evidence of intracranial infection or another primary central nervous system cause. The average age of onset is around 18–22 months. It is the most common pediatric convulsive disorder, affecting approximately 2–4% of children, and typically occurs in otherwise healthy children during a systemic illness, most often viral. Febrile seizures are classified into simple and complex types. Simple febrile seizures are generalized, brief (less than 10–15 minutes), self-limited, and occur only once within a 24-hour period. Complex febrile seizures are longer than 15 minutes, may have focal features, or recur within 24 hours. Risk factors include a family history of febrile seizures, delayed neurologic development, and male sex.
The condition is usually triggered by common childhood infections, particularly viral illnesses. Frequent causes include upper respiratory infections, otitis media, gastroenteritis, and Roseola. The seizure often occurs early in the illness, sometimes coinciding with the initial rapid rise in temperature rather than the peak fever.
Clinically, children present with fever and a seizure, most commonly a generalized tonic–clonic event. The seizure may involve an initial phase of muscle rigidity followed by rhythmic jerking movements and may be associated with apnea or urinary incontinence. Most episodes are brief and resolve spontaneously within a few minutes. Other possible manifestations include staring spells, limpness, or isolated jerking movements. After the seizure, a short postictal phase with drowsiness or confusion is common. A thorough history should include the duration and characteristics of the seizure, symptoms of infection, recent immunizations, medication exposure, trauma, developmental history, and family history of seizures. Physical examination should focus on identifying the source of fever and excluding serious conditions such as meningitis, looking for signs like nuchal rigidity, bulging fontanelle, or persistent altered mental status.
Evaluation is generally minimal for simple febrile seizures. Routine laboratory testing is not required unless there is concern for a serious bacterial infection, in which case tests such as complete blood count, urinalysis, and cultures may be performed. Lumbar puncture is not routinely indicated but should be considered in certain situations, such as in children aged 12–18 months with concerning symptoms (e.g., irritability, lethargy, poor feeding), incomplete immunization status, or signs suggestive of central nervous system infection. It is also indicated in older children if there are clear signs of meningitis or persistent altered mental status. Neuroimaging and EEG are not routinely required and are reserved for atypical presentations, such as focal seizures or underlying neurologic abnormalities.
Management is primarily supportive because most febrile seizures are self-limited. Initial priorities include maintaining airway, breathing, and circulation, and protecting the child from injury during the seizure. Oxygen and supportive care should be provided as needed. Pharmacologic treatment is rarely required, but benzodiazepines such as lorazepam, diazepam, or midazolam may be used for prolonged seizures or if the child is compromised. Rectal diazepam or intranasal midazolam can be effective in emergency settings. If seizures persist despite benzodiazepines, second-line agents such as phenytoin, fosphenytoin, or phenobarbital may be used. Antipyretics such as acetaminophen or ibuprofen are recommended to improve comfort, although they do not prevent recurrence of seizures. If a bacterial infection is identified, appropriate antibiotic therapy should be initiated.
The prognosis is generally excellent. About one-third of children will experience recurrence, especially those with early onset, a family history of seizures, or lower fever at the time of the initial episode. The risk of developing epilepsy later in life is only slightly increased compared to the general population, particularly in children with simple febrile seizures and normal neurologic development. Most children can be safely discharged if they return to baseline, have a normal neurologic examination, and the source of fever is identified and manageable. Parental reassurance and education are essential, as febrile seizures are typically benign. Aggressive fever control does not prevent recurrence, and long-term anticonvulsant prophylaxis is generally not recommended.
The condition is usually triggered by common childhood infections, particularly viral illnesses. Frequent causes include upper respiratory infections, otitis media, gastroenteritis, and Roseola. The seizure often occurs early in the illness, sometimes coinciding with the initial rapid rise in temperature rather than the peak fever.
Clinically, children present with fever and a seizure, most commonly a generalized tonic–clonic event. The seizure may involve an initial phase of muscle rigidity followed by rhythmic jerking movements and may be associated with apnea or urinary incontinence. Most episodes are brief and resolve spontaneously within a few minutes. Other possible manifestations include staring spells, limpness, or isolated jerking movements. After the seizure, a short postictal phase with drowsiness or confusion is common. A thorough history should include the duration and characteristics of the seizure, symptoms of infection, recent immunizations, medication exposure, trauma, developmental history, and family history of seizures. Physical examination should focus on identifying the source of fever and excluding serious conditions such as meningitis, looking for signs like nuchal rigidity, bulging fontanelle, or persistent altered mental status.
Evaluation is generally minimal for simple febrile seizures. Routine laboratory testing is not required unless there is concern for a serious bacterial infection, in which case tests such as complete blood count, urinalysis, and cultures may be performed. Lumbar puncture is not routinely indicated but should be considered in certain situations, such as in children aged 12–18 months with concerning symptoms (e.g., irritability, lethargy, poor feeding), incomplete immunization status, or signs suggestive of central nervous system infection. It is also indicated in older children if there are clear signs of meningitis or persistent altered mental status. Neuroimaging and EEG are not routinely required and are reserved for atypical presentations, such as focal seizures or underlying neurologic abnormalities.
Management is primarily supportive because most febrile seizures are self-limited. Initial priorities include maintaining airway, breathing, and circulation, and protecting the child from injury during the seizure. Oxygen and supportive care should be provided as needed. Pharmacologic treatment is rarely required, but benzodiazepines such as lorazepam, diazepam, or midazolam may be used for prolonged seizures or if the child is compromised. Rectal diazepam or intranasal midazolam can be effective in emergency settings. If seizures persist despite benzodiazepines, second-line agents such as phenytoin, fosphenytoin, or phenobarbital may be used. Antipyretics such as acetaminophen or ibuprofen are recommended to improve comfort, although they do not prevent recurrence of seizures. If a bacterial infection is identified, appropriate antibiotic therapy should be initiated.
The prognosis is generally excellent. About one-third of children will experience recurrence, especially those with early onset, a family history of seizures, or lower fever at the time of the initial episode. The risk of developing epilepsy later in life is only slightly increased compared to the general population, particularly in children with simple febrile seizures and normal neurologic development. Most children can be safely discharged if they return to baseline, have a normal neurologic examination, and the source of fever is identified and manageable. Parental reassurance and education are essential, as febrile seizures are typically benign. Aggressive fever control does not prevent recurrence, and long-term anticonvulsant prophylaxis is generally not recommended.
- Published on
Emergency and Acute Medicine - Seizure (Adult)
Overview
A seizure is a transient episode of abnormal, excessive neuronal activity in the brain, leading to changes in consciousness, behavior, sensation, or motor activity. Seizures are broadly classified into generalized and partial (focal) types. Generalized seizures typically involve both hemispheres and often present as tonic–clonic (grand mal) activity, beginning with myoclonic jerks followed by loss of consciousness and sustained muscle contractions. Nonconvulsive generalized seizures, such as absence seizures, manifest as brief alterations in awareness without major motor activity. Partial seizures may be simple (without loss of consciousness) or complex (with impaired consciousness and features such as confusion, automatisms, or hallucinations).
Status epilepticus is a life-threatening emergency defined as a seizure lasting more than 5–10 minutes or recurrent seizures without recovery between episodes. It carries a mortality rate of approximately 10–12%. Notably, many patients presenting with status epilepticus have no prior history of seizures. Alcohol withdrawal seizures typically occur within 24 hours of cessation and rarely progress to status. A single seizure carries about a 35% risk of recurrence within five years.
Etiology
Seizures may result from a wide range of causes. Common etiologies include hypoxia, hypertensive encephalopathy, and eclampsia. Infectious causes include meningitis, encephalitis, and brain abscess. Vascular causes such as ischemic or hemorrhagic stroke, subarachnoid hemorrhage, and intracranial hematomas are important considerations. Structural abnormalities include brain tumors, prior trauma, or degenerative diseases such as multiple sclerosis. Metabolic disturbances such as hypoglycemia, hyperglycemia, hyponatremia, hypernatremia, and hypocalcemia are frequent reversible causes.
Toxins and drugs are also significant contributors, including cocaine, tricyclic antidepressants, salicylates, and withdrawal states (alcohol or benzodiazepines). Other causes include congenital abnormalities, idiopathic epilepsy, and trauma.
Clinical Features
Patients typically present with an abrupt onset of altered consciousness and involuntary motor activity, including tonic stiffening or clonic jerking. Some patients experience an aura preceding focal seizures. Seizures usually last 90–120 seconds and are followed by a postictal state, characterized by confusion, somnolence, and temporary memory impairment.
Signs suggesting recent seizure activity include intraoral injuries, urinary incontinence, and transient focal deficits such as Todd paralysis. Additional findings may point to the underlying cause, such as fever and neck stiffness in central nervous system infections, needle marks in substance abuse, or focal neurologic deficits in structural brain lesions.
Evaluation
A detailed history, especially from witnesses, is critical. Important elements include prior seizure history, medication compliance, recent illness, trauma, and substance use. Physical examination should include a complete neurologic assessment and evaluation for trauma.
In patients with known epilepsy and a typical presentation, minimal testing such as serum glucose and anticonvulsant levels may suffice. However, new-onset seizures require a full workup, including electrolytes, calcium, toxicology screening, and neuroimaging (typically noncontrast CT). Lumbar puncture is indicated in patients with fever, suspected infection, immunocompromise, or persistent altered mental status. MRI may be arranged later for more detailed evaluation. EEG is useful, particularly in suspected nonconvulsive status epilepticus.
Management
Initial management focuses on airway, breathing, and circulation (ABCs). Oxygen, suction, and airway protection are essential, with rapid-sequence intubation if the patient cannot protect the airway. Intravenous access should be established, and serum glucose checked immediately; hypoglycemia should be treated with IV dextrose.
Active seizures are treated promptly with benzodiazepines such as lorazepam or diazepam, which are first-line agents. If seizures persist, second-line agents include fosphenytoin, levetiracetam, phenobarbital, or valproate. Refractory cases may require propofol infusion and intensive care management. Naloxone should be administered if opioid overdose is suspected.
Management also depends on the clinical scenario. First-time seizures with normal evaluation and return to baseline may be discharged with close follow-up. Patients with structural lesions, recurrent seizures, or subtherapeutic antiepileptic drug levels require initiation or adjustment of therapy in consultation with neurology. In pregnant patients, eclampsia must be considered and treated with magnesium and obstetric consultation. Alcohol withdrawal seizures are treated with benzodiazepines.
Disposition and Follow-Up
Patients with status epilepticus, underlying serious conditions (e.g., meningitis, intracranial lesions), or recurrent uncontrolled seizures require hospital admission, often to the ICU. Patients with uncomplicated seizures, normal evaluation, and reliable follow-up may be discharged. Driving restrictions should be advised until seizures are controlled.
Key Points
The most common cause of recurrent seizures is subtherapeutic anticonvulsant levels. Benzodiazepines are the first-line treatment for acute seizures. Any seizure lasting longer than 5–10 minutes should be treated as status epilepticus. Identifying and treating the underlying cause is essential for long-term management.
