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Emergency and Acute Medicine - Subdural Hematoma
Subdural hematoma (SDH) is bleeding between the dura and arachnoid mater, most commonly due to tearing of bridging veins. It is classified based on timing into acute (within 3 days), subacute (3 days to 3 weeks), and chronic (after 3 weeks). On CT imaging, SDH typically appears as a crescent-shaped collection that crosses suture lines but does not cross the midline, often with irregular inner margins. Acute SDH is most commonly caused by acceleration–deceleration forces that stretch and tear parasagittal bridging veins, though bleeding may also arise from cortical arteries, dural lacerations, or venous sinuses. Nontraumatic causes include aneurysm rupture, arteriovenous malformations, coagulopathy, hypertension, and substance abuse. Chronic SDH develops from repeated small venous bleeds and becomes encapsulated over time.
Acute SDH is the most common intracranial hematoma, accounting for 66–70% of cases and frequently associated with blunt head trauma, particularly motor vehicle accidents, falls, and assaults. There is a bimodal age distribution, affecting young adults and the elderly, with higher risk in older patients, those with brain atrophy, alcohol use, or seizure disorders. Chronic SDH is more common in older adults and infants, often with minimal or no clear history of trauma. Coagulopathy significantly increases the risk and severity of bleeding, particularly with elevated INR levels.
Clinically, acute SDH often presents with headache and altered mental status, and up to half of patients may be unconscious at presentation. It is frequently misdiagnosed as intoxication or stroke. Focal neurologic deficits such as hemiparesis or hemiplegia are common, and pupillary abnormalities may indicate ipsilateral mass effect. Seizures can occur early. Subacute and chronic SDH present more insidiously, with symptoms such as headache, nausea, vomiting, seizures, fluctuating mental status, gait instability, and progressive neurologic deficits. In children, especially infants, symptoms may include irritability, lethargy, vomiting, seizures, or bulging fontanelles.
Diagnosis relies on urgent neuroimaging, with noncontrast CT scan as the first-line modality. Acute SDH appears as a hyperdense crescent-shaped lesion over the cerebral convexity, often associated with other intracranial injuries. Mixed densities may suggest ongoing bleeding. Chronic SDH may appear hypodense on CT after several weeks, and MRI is more sensitive in subacute or chronic stages when lesions may be isodense. The volume of hematoma and degree of midline shift are important prognostic indicators.
Management focuses on rapid stabilization and prevention of secondary brain injury. Airway protection is critical, with rapid-sequence intubation indicated for patients with a Glasgow Coma Scale (GCS) score less than 9 or signs of increased intracranial pressure. Oxygenation should be maintained with saturation above 95%, and hypotension must be avoided, as even a single episode significantly worsens outcomes. Controlled ventilation is used to maintain normocapnia, and routine hyperventilation is no longer recommended except in impending herniation. Head elevation to 20–30° can help reduce intracranial pressure once hemodynamically stable.
Early neurosurgical consultation is essential. Surgical evacuation, often via burr holes or craniotomy, is indicated in patients with significant hematomas, neurologic deficits, or clinical deterioration. Early intervention within 4 hours in comatose patients improves survival. Small, stable hematomas without mass effect may be managed conservatively with close neurologic monitoring, although a subset will require delayed surgery. Intracranial pressure management includes sedation, neuromuscular blockade if intubated, and osmotic therapy such as mannitol once euvolemia is achieved. Blood pressure control, correction of coagulopathy, and management of seizures are also critical components of care.
All patients with acute SDH require admission to an intensive care unit or operating room under neurosurgical care. Subacute cases are admitted for monitoring, while selected chronic SDH patients may be managed as outpatients with appropriate follow-up. Prognosis depends on several key factors, including initial GCS score, time to treatment, pupillary abnormalities, hematoma size, and degree of midline shift. A major pitfall is delayed recognition, especially in elderly patients or those with subtle symptoms, where SDH may mimic other conditions such as stroke, dementia, or intoxication.
Subdural hematoma (SDH) is bleeding between the dura and arachnoid mater, most commonly due to tearing of bridging veins. It is classified based on timing into acute (within 3 days), subacute (3 days to 3 weeks), and chronic (after 3 weeks). On CT imaging, SDH typically appears as a crescent-shaped collection that crosses suture lines but does not cross the midline, often with irregular inner margins. Acute SDH is most commonly caused by acceleration–deceleration forces that stretch and tear parasagittal bridging veins, though bleeding may also arise from cortical arteries, dural lacerations, or venous sinuses. Nontraumatic causes include aneurysm rupture, arteriovenous malformations, coagulopathy, hypertension, and substance abuse. Chronic SDH develops from repeated small venous bleeds and becomes encapsulated over time.
Acute SDH is the most common intracranial hematoma, accounting for 66–70% of cases and frequently associated with blunt head trauma, particularly motor vehicle accidents, falls, and assaults. There is a bimodal age distribution, affecting young adults and the elderly, with higher risk in older patients, those with brain atrophy, alcohol use, or seizure disorders. Chronic SDH is more common in older adults and infants, often with minimal or no clear history of trauma. Coagulopathy significantly increases the risk and severity of bleeding, particularly with elevated INR levels.
Clinically, acute SDH often presents with headache and altered mental status, and up to half of patients may be unconscious at presentation. It is frequently misdiagnosed as intoxication or stroke. Focal neurologic deficits such as hemiparesis or hemiplegia are common, and pupillary abnormalities may indicate ipsilateral mass effect. Seizures can occur early. Subacute and chronic SDH present more insidiously, with symptoms such as headache, nausea, vomiting, seizures, fluctuating mental status, gait instability, and progressive neurologic deficits. In children, especially infants, symptoms may include irritability, lethargy, vomiting, seizures, or bulging fontanelles.
Diagnosis relies on urgent neuroimaging, with noncontrast CT scan as the first-line modality. Acute SDH appears as a hyperdense crescent-shaped lesion over the cerebral convexity, often associated with other intracranial injuries. Mixed densities may suggest ongoing bleeding. Chronic SDH may appear hypodense on CT after several weeks, and MRI is more sensitive in subacute or chronic stages when lesions may be isodense. The volume of hematoma and degree of midline shift are important prognostic indicators.
Management focuses on rapid stabilization and prevention of secondary brain injury. Airway protection is critical, with rapid-sequence intubation indicated for patients with a Glasgow Coma Scale (GCS) score less than 9 or signs of increased intracranial pressure. Oxygenation should be maintained with saturation above 95%, and hypotension must be avoided, as even a single episode significantly worsens outcomes. Controlled ventilation is used to maintain normocapnia, and routine hyperventilation is no longer recommended except in impending herniation. Head elevation to 20–30° can help reduce intracranial pressure once hemodynamically stable.
Early neurosurgical consultation is essential. Surgical evacuation, often via burr holes or craniotomy, is indicated in patients with significant hematomas, neurologic deficits, or clinical deterioration. Early intervention within 4 hours in comatose patients improves survival. Small, stable hematomas without mass effect may be managed conservatively with close neurologic monitoring, although a subset will require delayed surgery. Intracranial pressure management includes sedation, neuromuscular blockade if intubated, and osmotic therapy such as mannitol once euvolemia is achieved. Blood pressure control, correction of coagulopathy, and management of seizures are also critical components of care.
All patients with acute SDH require admission to an intensive care unit or operating room under neurosurgical care. Subacute cases are admitted for monitoring, while selected chronic SDH patients may be managed as outpatients with appropriate follow-up. Prognosis depends on several key factors, including initial GCS score, time to treatment, pupillary abnormalities, hematoma size, and degree of midline shift. A major pitfall is delayed recognition, especially in elderly patients or those with subtle symptoms, where SDH may mimic other conditions such as stroke, dementia, or intoxication.
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Emergency and Acute Medicine - Sudden Infant Death Syndrome (SIDS)
Sudden infant death syndrome (SIDS) is defined as the sudden, unexpected death of an infant younger than 1 year of age that remains unexplained after thorough investigation, including autopsy, examination of the death scene, and review of medical and family history. It is a diagnosis of exclusion and remains the leading cause of death in infants between 1 month and 1 year of age. The peak incidence occurs between 1 and 4 months of age, with 90% of cases occurring before 6 months. The incidence has declined significantly following public health campaigns promoting supine sleeping, such as the “Back to Sleep” initiative.
The etiology of SIDS is thought to be multifactorial, involving a vulnerable infant exposed to internal and external stressors during a critical developmental period. Potential contributing factors include underlying abnormalities such as cardiac dysrhythmias, metabolic disorders, infections, neurologic immaturity, or impaired arousal mechanisms. Maternal risk factors include smoking, alcohol or drug use, poor prenatal care, young maternal age, and short interpregnancy intervals. Infant-related risk factors include prematurity, low birth weight, male gender, exposure to secondhand smoke, overheating, soft bedding, and bed sharing. Protective factors include placing infants in a supine sleeping position, breastfeeding, and pacifier use. Home monitoring has not been shown to prevent SIDS.
Clinically, SIDS is typically silent and unpredictable. Infants are usually found unresponsive during sleep, having appeared healthy when last placed to bed. There are no preceding warning signs. A related entity, known as an apparent life-threatening event (ALTE), involves episodes of apnea, color change, altered muscle tone, or choking and may be associated with an increased risk of SIDS. Infants who experience such events often appear normal upon evaluation but require careful monitoring.
The evaluation of suspected SIDS cases focuses on excluding other causes of death. This includes a detailed investigation of the death scene, including sleep position, bedding, environmental conditions, and possible bed sharing. A thorough review of prenatal, perinatal, and postnatal history, as well as family medical and social history, is essential. Autopsy is mandatory in most jurisdictions and plays a critical role in identifying alternative causes such as congenital heart disease, infections, metabolic disorders, or nonaccidental trauma. Additional investigations may include laboratory studies, toxicology screening, imaging, and assessment for familial conditions such as prolonged QT syndrome.
Management in the emergency setting involves immediate resuscitation according to pediatric advanced life support protocols. Airway, breathing, and circulation should be assessed and supported, with medications administered as indicated. If resuscitation is unsuccessful and no clear cause is identified, clinicians should avoid prematurely labeling the death as SIDS until a full investigation is complete. Equally important is providing compassionate support to the family, who may experience profound grief, guilt, and confusion. Allowing family presence during resuscitation and offering opportunities to spend time with the infant afterward can be beneficial.
All surviving infants who experience ALTE should be admitted for observation and further evaluation, particularly if episodes are recurrent or associated with concerning features. Follow-up with pediatric specialists is recommended. A key aspect of care is family education on safe sleep practices, including placing infants on their backs, using a firm sleep surface, avoiding soft bedding, and preventing overheating. A major pitfall is failure to conduct a thorough investigation, as SIDS cannot be diagnosed without excluding other potentially preventable or treatable causes.
Sudden infant death syndrome (SIDS) is defined as the sudden, unexpected death of an infant younger than 1 year of age that remains unexplained after thorough investigation, including autopsy, examination of the death scene, and review of medical and family history. It is a diagnosis of exclusion and remains the leading cause of death in infants between 1 month and 1 year of age. The peak incidence occurs between 1 and 4 months of age, with 90% of cases occurring before 6 months. The incidence has declined significantly following public health campaigns promoting supine sleeping, such as the “Back to Sleep” initiative.
The etiology of SIDS is thought to be multifactorial, involving a vulnerable infant exposed to internal and external stressors during a critical developmental period. Potential contributing factors include underlying abnormalities such as cardiac dysrhythmias, metabolic disorders, infections, neurologic immaturity, or impaired arousal mechanisms. Maternal risk factors include smoking, alcohol or drug use, poor prenatal care, young maternal age, and short interpregnancy intervals. Infant-related risk factors include prematurity, low birth weight, male gender, exposure to secondhand smoke, overheating, soft bedding, and bed sharing. Protective factors include placing infants in a supine sleeping position, breastfeeding, and pacifier use. Home monitoring has not been shown to prevent SIDS.
Clinically, SIDS is typically silent and unpredictable. Infants are usually found unresponsive during sleep, having appeared healthy when last placed to bed. There are no preceding warning signs. A related entity, known as an apparent life-threatening event (ALTE), involves episodes of apnea, color change, altered muscle tone, or choking and may be associated with an increased risk of SIDS. Infants who experience such events often appear normal upon evaluation but require careful monitoring.
The evaluation of suspected SIDS cases focuses on excluding other causes of death. This includes a detailed investigation of the death scene, including sleep position, bedding, environmental conditions, and possible bed sharing. A thorough review of prenatal, perinatal, and postnatal history, as well as family medical and social history, is essential. Autopsy is mandatory in most jurisdictions and plays a critical role in identifying alternative causes such as congenital heart disease, infections, metabolic disorders, or nonaccidental trauma. Additional investigations may include laboratory studies, toxicology screening, imaging, and assessment for familial conditions such as prolonged QT syndrome.
Management in the emergency setting involves immediate resuscitation according to pediatric advanced life support protocols. Airway, breathing, and circulation should be assessed and supported, with medications administered as indicated. If resuscitation is unsuccessful and no clear cause is identified, clinicians should avoid prematurely labeling the death as SIDS until a full investigation is complete. Equally important is providing compassionate support to the family, who may experience profound grief, guilt, and confusion. Allowing family presence during resuscitation and offering opportunities to spend time with the infant afterward can be beneficial.
All surviving infants who experience ALTE should be admitted for observation and further evaluation, particularly if episodes are recurrent or associated with concerning features. Follow-up with pediatric specialists is recommended. A key aspect of care is family education on safe sleep practices, including placing infants on their backs, using a firm sleep surface, avoiding soft bedding, and preventing overheating. A major pitfall is failure to conduct a thorough investigation, as SIDS cannot be diagnosed without excluding other potentially preventable or treatable causes.
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Emergency and Acute Medicine - Supraventricular Tachycardia
Supraventricular tachycardia (SVT) refers to a tachyarrhythmia that originates above the His bundle and produces a heart rate of 100 beats per minute or greater. It may present as a regular narrow-complex rhythm, an irregular narrow-complex rhythm, or a wide-complex rhythm if conduction occurs outside the normal His-Purkinje system. Irregular narrow-complex SVT includes atrial fibrillation, atrial flutter with variable block, and multifocal atrial tachycardia. Regular narrow-complex SVT includes atrioventricular nodal re-entry tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), atrial tachycardia, and atrial flutter. A wide-complex SVT may occur when an accessory pathway or bundle branch block is present, but any wide-complex tachycardia should be assumed to be ventricular tachycardia unless there is strong evidence otherwise.
The causes of SVT vary by rhythm type. Atrial tachycardias may be triggered by premature beats, hypoxia, electrolyte abnormalities, theophylline toxicity, or increased atrial pressure. Junctional tachycardias may result from AV nodal re-entry, myocardial ischemia, structural heart disease, or pre-excitation syndromes. Wolff-Parkinson-White syndrome involves an accessory pathway and can predispose to dangerous tachyarrhythmias. Atrial fibrillation is associated with hypertension, coronary disease, thyroid abnormalities, alcohol use, mitral valve disease, chronic lung disease, pulmonary embolism, digoxin toxicity, sepsis, and pericardial disease. Atrial flutter is often linked to ischemic heart disease, valvular disease, heart failure, myocarditis, cardiomyopathy, or pulmonary disease.
Patients commonly present with palpitations, which are the most frequent symptom. They may also report lightheadedness, dyspnea, diaphoresis, dizziness, weakness, chest discomfort, or syncope. Some patients describe abrupt onset palpitations and head pressure, while others present more gradually with fatigue, malaise, or exercise intolerance. Prominent neck vein pulsations, the so-called “frog sign,” may be seen. Signs of instability include altered mental status, ischemic chest pain, acute pulmonary edema, and hypotension.
Evaluation begins with assessment of airway, breathing, and circulation, followed by rapid determination of whether the patient is stable or unstable. History should focus on onset, prior episodes, cardiac history, medication use, stimulants, decongestants, and illicit drug exposure. Physical examination should assess heart rhythm regularity, blood pressure, respiratory status, and evidence of heart failure such as jugular venous distention or pulmonary rales. An ECG is essential for diagnosis. Atrial fibrillation typically shows an irregularly irregular rhythm without discernible P waves. Atrial flutter demonstrates sawtooth flutter waves, often with 2:1 block. Multifocal atrial tachycardia shows at least three different P-wave morphologies. Atrial tachycardia usually has abnormal but visible P waves before each QRS. Junctional tachycardia often has absent or retrograde P waves. In adults, ventricular rates over 200 beats per minute strongly suggest an accessory pathway such as WPW.
Laboratory evaluation may include CBC, electrolytes, cardiac enzymes, BNP, and occasionally thyroid studies. Chest radiography is more useful in atrial fibrillation or flutter to assess cardiac size or pulmonary pathology. The main diagnostic challenge is distinguishing SVT with aberrancy from ventricular tachycardia. If there is uncertainty, the rhythm should be treated as ventricular tachycardia.
Management depends on the rhythm type and the patient’s hemodynamic status. Unstable patients require immediate synchronized cardioversion. In stable atrial fibrillation or atrial flutter, rate control is the priority, typically with beta-blockers or calcium channel blockers, while amiodarone or digoxin may be used in selected cases. Cardioversion should generally be avoided in stable atrial fibrillation of more than 48 hours or uncertain duration because of embolic risk. In WPW with atrial fibrillation, AV nodal blocking drugs such as adenosine, beta-blockers, calcium channel blockers, and digoxin should be avoided, and agents such as procainamide or amiodarone, or direct current cardioversion, are preferred.
For regular narrow-complex SVT, vagal maneuvers should be attempted first. Valsalva is most effective when performed with the patient lying flat. Carotid massage may be considered in selected patients, and the diving reflex with ice to the face may be used in children. If vagal maneuvers fail, adenosine is the first-line medication and successfully terminates many episodes. If adenosine transiently slows but does not terminate the rhythm, escalating the dose further is usually not useful and another agent should be chosen. In wide-complex tachycardia of uncertain origin, treatment should proceed as for ventricular tachycardia, usually with amiodarone and sometimes procainamide if an accessory pathway is suspected. Verapamil should not be used in uncertain wide-complex tachycardia.
In children, SVT is the most common arrhythmia seen without structural heart disease. Initial treatment again includes vagal maneuvers, with ice to the forehead in infants or blowing through a straw in older children. Synchronized cardioversion is used for unstable patients. In pregnancy, adenosine is considered safe, and cardioversion is also safe if needed.
Patients may be admitted if there is concern for ischemia, persistent SVT, pre-excitation syndrome, or an underlying metabolic abnormality. Those whose rhythm is successfully terminated and who have no signs of organ hypoperfusion or serious underlying disease may often be discharged with outpatient follow-up. They should be advised to return for faintness, neurologic symptoms, trouble speaking or seeing, or recurrent episodes, and to avoid high-risk activities such as swimming, diving, or piloting until further evaluation. A key pitfall is misidentifying atrial fibrillation in WPW or any wide-complex tachycardia as benign SVT. When in doubt, treat the rhythm as ventricular tachycardia.
Supraventricular tachycardia (SVT) refers to a tachyarrhythmia that originates above the His bundle and produces a heart rate of 100 beats per minute or greater. It may present as a regular narrow-complex rhythm, an irregular narrow-complex rhythm, or a wide-complex rhythm if conduction occurs outside the normal His-Purkinje system. Irregular narrow-complex SVT includes atrial fibrillation, atrial flutter with variable block, and multifocal atrial tachycardia. Regular narrow-complex SVT includes atrioventricular nodal re-entry tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), atrial tachycardia, and atrial flutter. A wide-complex SVT may occur when an accessory pathway or bundle branch block is present, but any wide-complex tachycardia should be assumed to be ventricular tachycardia unless there is strong evidence otherwise.
The causes of SVT vary by rhythm type. Atrial tachycardias may be triggered by premature beats, hypoxia, electrolyte abnormalities, theophylline toxicity, or increased atrial pressure. Junctional tachycardias may result from AV nodal re-entry, myocardial ischemia, structural heart disease, or pre-excitation syndromes. Wolff-Parkinson-White syndrome involves an accessory pathway and can predispose to dangerous tachyarrhythmias. Atrial fibrillation is associated with hypertension, coronary disease, thyroid abnormalities, alcohol use, mitral valve disease, chronic lung disease, pulmonary embolism, digoxin toxicity, sepsis, and pericardial disease. Atrial flutter is often linked to ischemic heart disease, valvular disease, heart failure, myocarditis, cardiomyopathy, or pulmonary disease.
Patients commonly present with palpitations, which are the most frequent symptom. They may also report lightheadedness, dyspnea, diaphoresis, dizziness, weakness, chest discomfort, or syncope. Some patients describe abrupt onset palpitations and head pressure, while others present more gradually with fatigue, malaise, or exercise intolerance. Prominent neck vein pulsations, the so-called “frog sign,” may be seen. Signs of instability include altered mental status, ischemic chest pain, acute pulmonary edema, and hypotension.
Evaluation begins with assessment of airway, breathing, and circulation, followed by rapid determination of whether the patient is stable or unstable. History should focus on onset, prior episodes, cardiac history, medication use, stimulants, decongestants, and illicit drug exposure. Physical examination should assess heart rhythm regularity, blood pressure, respiratory status, and evidence of heart failure such as jugular venous distention or pulmonary rales. An ECG is essential for diagnosis. Atrial fibrillation typically shows an irregularly irregular rhythm without discernible P waves. Atrial flutter demonstrates sawtooth flutter waves, often with 2:1 block. Multifocal atrial tachycardia shows at least three different P-wave morphologies. Atrial tachycardia usually has abnormal but visible P waves before each QRS. Junctional tachycardia often has absent or retrograde P waves. In adults, ventricular rates over 200 beats per minute strongly suggest an accessory pathway such as WPW.
Laboratory evaluation may include CBC, electrolytes, cardiac enzymes, BNP, and occasionally thyroid studies. Chest radiography is more useful in atrial fibrillation or flutter to assess cardiac size or pulmonary pathology. The main diagnostic challenge is distinguishing SVT with aberrancy from ventricular tachycardia. If there is uncertainty, the rhythm should be treated as ventricular tachycardia.
Management depends on the rhythm type and the patient’s hemodynamic status. Unstable patients require immediate synchronized cardioversion. In stable atrial fibrillation or atrial flutter, rate control is the priority, typically with beta-blockers or calcium channel blockers, while amiodarone or digoxin may be used in selected cases. Cardioversion should generally be avoided in stable atrial fibrillation of more than 48 hours or uncertain duration because of embolic risk. In WPW with atrial fibrillation, AV nodal blocking drugs such as adenosine, beta-blockers, calcium channel blockers, and digoxin should be avoided, and agents such as procainamide or amiodarone, or direct current cardioversion, are preferred.
For regular narrow-complex SVT, vagal maneuvers should be attempted first. Valsalva is most effective when performed with the patient lying flat. Carotid massage may be considered in selected patients, and the diving reflex with ice to the face may be used in children. If vagal maneuvers fail, adenosine is the first-line medication and successfully terminates many episodes. If adenosine transiently slows but does not terminate the rhythm, escalating the dose further is usually not useful and another agent should be chosen. In wide-complex tachycardia of uncertain origin, treatment should proceed as for ventricular tachycardia, usually with amiodarone and sometimes procainamide if an accessory pathway is suspected. Verapamil should not be used in uncertain wide-complex tachycardia.
In children, SVT is the most common arrhythmia seen without structural heart disease. Initial treatment again includes vagal maneuvers, with ice to the forehead in infants or blowing through a straw in older children. Synchronized cardioversion is used for unstable patients. In pregnancy, adenosine is considered safe, and cardioversion is also safe if needed.
Patients may be admitted if there is concern for ischemia, persistent SVT, pre-excitation syndrome, or an underlying metabolic abnormality. Those whose rhythm is successfully terminated and who have no signs of organ hypoperfusion or serious underlying disease may often be discharged with outpatient follow-up. They should be advised to return for faintness, neurologic symptoms, trouble speaking or seeing, or recurrent episodes, and to avoid high-risk activities such as swimming, diving, or piloting until further evaluation. A key pitfall is misidentifying atrial fibrillation in WPW or any wide-complex tachycardia as benign SVT. When in doubt, treat the rhythm as ventricular tachycardia.
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Sympathomimetic poisoning is caused by excessive stimulation of adrenergic receptors in the central and peripheral nervous systems, either through direct receptor activation or indirect mechanisms such as increased catecholamine release. The severity of toxicity does not always correlate with the amount ingested. Certain substances, particularly cocaine, can also block sodium channels in cardiac myocytes, leading to dysrhythmias similar to those seen in tricyclic antidepressant toxicity.
Sympathomimetic toxicity can result from exposure to a wide variety of substances, including amphetamines, methamphetamines, MDMA (ecstasy), cocaine, synthetic cathinones (“bath salts”), phencyclidine (PCP), lysergic acid diethylamide (LSD), and occasionally decongestants. These substances may be administered via inhalation, injection, ingestion, or insufflation. In pediatric patients, presentation may mimic serious systemic illness such as meningitis, and diagnosis may only become apparent through toxicology screening. Medications used for attention deficit hyperactivity disorder, such as methylphenidate, may also contribute to this toxidrome.
Patients with sympathomimetic poisoning typically present with a recognizable toxidrome characterized by tachycardia, hypertension, tachypnea, and hyperthermia, although late hypotension may occur in severe cases. Neurologic manifestations include agitation, anxiety, altered mental status, seizures, and headache, while cardiovascular effects include palpitations, chest pain, myocardial ischemia, and tachydysrhythmias. Additional findings commonly include diaphoresis, which helps distinguish this condition from anticholinergic toxicity, as well as mydriasis and possible urinary retention. In severe toxicity, patients may develop agitated delirium, profound hyperthermia, seizures, and cardiovascular collapse.
Evaluation focuses on rapid assessment and monitoring for complications. Continuous monitoring of vital signs is essential, particularly core temperature due to the risk of life-threatening hyperthermia. An electrocardiogram should be obtained to assess for ischemia and arrhythmias. Laboratory investigations typically include electrolytes, renal function, glucose, creatine kinase to evaluate for rhabdomyolysis, and coagulation studies. Urine toxicology screening may be useful, although some substances may not be detected. Imaging such as CT of the brain may be indicated in patients with altered mental status or focal neurologic deficits. Careful assessment for associated trauma, infection, pneumothorax, or end-organ injury is also important.
Management begins with standard resuscitation principles, including ensuring airway, breathing, and circulation, establishing intravenous access, and initiating cardiac monitoring. In patients with altered mental status, administration of dextrose, naloxone, and thiamine should be considered. The cornerstone of treatment is sedation with benzodiazepines, which effectively reduce agitation, hypertension, and seizure risk. Hyperthermia must be treated aggressively with sedation and active cooling measures such as evaporative cooling, and paralysis may be required in refractory cases. Hypertension is initially managed with benzodiazepines, followed by vasodilators such as nicardipine or nitroglycerin if necessary, while β-blockers should be avoided due to the risk of unopposed α-adrenergic activity. Dysrhythmias associated with sodium channel blockade are treated with sodium bicarbonate, and lidocaine may be used if refractory. Seizures are treated with benzodiazepines, with phenobarbital as second-line therapy. Rhabdomyolysis requires aggressive intravenous fluid resuscitation to maintain adequate urine output, and dialysis may be necessary if renal failure or severe hyperkalemia develops. Decontamination has a limited role and is generally reserved for selected cases such as early ingestion or body packers.
Patients with severe manifestations such as seizures, dysrhythmias, hyperthermia, rhabdomyolysis, altered mental status, or significant hypertension should be admitted to a monitored setting. Mildly intoxicated patients who improve with treatment may be observed in the emergency department until symptoms resolve and then discharged safely. Referral for substance use treatment and rehabilitation should be considered when appropriate.
Benzodiazepines remain the first-line therapy for most manifestations of sympathomimetic poisoning and should be administered early. Hyperthermia above 40°C is a critical, life-threatening condition requiring immediate intervention. β-blockers should be avoided because they may worsen hypertension through unopposed α-adrenergic stimulation. Early recognition and management of complications such as rhabdomyolysis and hyperkalemia are essential to prevent morbidity and mortality. Clinicians must also remain vigilant for concurrent emergencies, including acute coronary syndrome, trauma, and infection, which may coexist in these patients.
Sympathomimetic toxicity can result from exposure to a wide variety of substances, including amphetamines, methamphetamines, MDMA (ecstasy), cocaine, synthetic cathinones (“bath salts”), phencyclidine (PCP), lysergic acid diethylamide (LSD), and occasionally decongestants. These substances may be administered via inhalation, injection, ingestion, or insufflation. In pediatric patients, presentation may mimic serious systemic illness such as meningitis, and diagnosis may only become apparent through toxicology screening. Medications used for attention deficit hyperactivity disorder, such as methylphenidate, may also contribute to this toxidrome.
Patients with sympathomimetic poisoning typically present with a recognizable toxidrome characterized by tachycardia, hypertension, tachypnea, and hyperthermia, although late hypotension may occur in severe cases. Neurologic manifestations include agitation, anxiety, altered mental status, seizures, and headache, while cardiovascular effects include palpitations, chest pain, myocardial ischemia, and tachydysrhythmias. Additional findings commonly include diaphoresis, which helps distinguish this condition from anticholinergic toxicity, as well as mydriasis and possible urinary retention. In severe toxicity, patients may develop agitated delirium, profound hyperthermia, seizures, and cardiovascular collapse.
Evaluation focuses on rapid assessment and monitoring for complications. Continuous monitoring of vital signs is essential, particularly core temperature due to the risk of life-threatening hyperthermia. An electrocardiogram should be obtained to assess for ischemia and arrhythmias. Laboratory investigations typically include electrolytes, renal function, glucose, creatine kinase to evaluate for rhabdomyolysis, and coagulation studies. Urine toxicology screening may be useful, although some substances may not be detected. Imaging such as CT of the brain may be indicated in patients with altered mental status or focal neurologic deficits. Careful assessment for associated trauma, infection, pneumothorax, or end-organ injury is also important.
Management begins with standard resuscitation principles, including ensuring airway, breathing, and circulation, establishing intravenous access, and initiating cardiac monitoring. In patients with altered mental status, administration of dextrose, naloxone, and thiamine should be considered. The cornerstone of treatment is sedation with benzodiazepines, which effectively reduce agitation, hypertension, and seizure risk. Hyperthermia must be treated aggressively with sedation and active cooling measures such as evaporative cooling, and paralysis may be required in refractory cases. Hypertension is initially managed with benzodiazepines, followed by vasodilators such as nicardipine or nitroglycerin if necessary, while β-blockers should be avoided due to the risk of unopposed α-adrenergic activity. Dysrhythmias associated with sodium channel blockade are treated with sodium bicarbonate, and lidocaine may be used if refractory. Seizures are treated with benzodiazepines, with phenobarbital as second-line therapy. Rhabdomyolysis requires aggressive intravenous fluid resuscitation to maintain adequate urine output, and dialysis may be necessary if renal failure or severe hyperkalemia develops. Decontamination has a limited role and is generally reserved for selected cases such as early ingestion or body packers.
Patients with severe manifestations such as seizures, dysrhythmias, hyperthermia, rhabdomyolysis, altered mental status, or significant hypertension should be admitted to a monitored setting. Mildly intoxicated patients who improve with treatment may be observed in the emergency department until symptoms resolve and then discharged safely. Referral for substance use treatment and rehabilitation should be considered when appropriate.
Benzodiazepines remain the first-line therapy for most manifestations of sympathomimetic poisoning and should be administered early. Hyperthermia above 40°C is a critical, life-threatening condition requiring immediate intervention. β-blockers should be avoided because they may worsen hypertension through unopposed α-adrenergic stimulation. Early recognition and management of complications such as rhabdomyolysis and hyperkalemia are essential to prevent morbidity and mortality. Clinicians must also remain vigilant for concurrent emergencies, including acute coronary syndrome, trauma, and infection, which may coexist in these patients.
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Emergency and Acute Medicine - Subarachnoid Hemorrhage
Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space and cerebrospinal fluid, most commonly due to rupture of a cerebral aneurysm. It is a life-threatening neurologic emergency with high mortality, ranging from 30–50%. It typically affects adults, with peak incidence in the sixth decade, and is rare before the third decade. Important risk factors include hypertension, smoking, alcohol abuse, stimulant drug use such as cocaine, female sex, and a family history of SAH. Certain genetic conditions, including polycystic kidney disease and connective tissue disorders, further increase risk.
The most common cause of spontaneous SAH is rupture of a saccular (berry) aneurysm, accounting for 80–90% of cases, usually occurring at arterial bifurcations within the circle of Willis. Other causes include arteriovenous malformations, arterial dissections, intracranial tumors, and mycotic aneurysms. Traumatic SAH is also seen in severe head injuries.
Patients classically present with a sudden, severe headache often described as a “thunderclap headache” or the “worst headache of life,” reaching maximal intensity within seconds. This headache is typically different from prior headaches. Associated features include vomiting, transient loss of consciousness, seizures, neck stiffness, and focal neurologic deficits. A “sentinel headache,” representing a minor bleed, may occur days to weeks before the major event in up to half of patients.
On examination, patients may have nuchal rigidity, altered mental status, and focal neurologic deficits. Cranial nerve involvement, particularly third nerve palsy presenting as a “down and out” eye, may be seen. Retinal hemorrhage can occasionally be the only clue, especially in comatose patients.
Diagnosis begins with an emergent noncontrast CT scan of the head, which detects SAH in up to 98% of cases if performed within 12 hours of symptom onset. If the CT scan is negative but clinical suspicion remains high, a lumbar puncture must be performed. The presence of red blood cells in the cerebrospinal fluid or xanthochromia confirms the diagnosis. Further imaging, such as CT angiography or digital subtraction angiography, is used to identify the source of bleeding, while transcranial Doppler may be used to monitor for vasospasm.
Management is focused on rapid stabilization and prevention of complications. Initial priorities include airway protection, oxygenation, cardiac monitoring, and establishing intravenous access. Blood pressure must be carefully controlled to reduce the risk of rebleeding while maintaining adequate cerebral perfusion, with a target systolic pressure below 160 mmHg. Measures to reduce intracranial pressure include head elevation, avoidance of straining, and use of antiemetics and stool softeners. In selected cases, mannitol and controlled ventilation may be required.
All patients should receive Nimodipine to reduce the risk of delayed cerebral vasospasm and improve neurologic outcomes. Seizures should be treated promptly with benzodiazepines, and metabolic abnormalities should be corrected. Definitive management involves urgent neurosurgical intervention, either by surgical clipping or endovascular coiling of the aneurysm.
All patients with confirmed or suspected SAH require admission to an intensive care unit. Early recognition and treatment are critical, as mortality is high and many patients deteriorate rapidly. A key pitfall is failure to consider SAH in patients presenting with acute severe headache, or stopping evaluation after a negative CT scan without proceeding to lumbar puncture when indicated.
Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space and cerebrospinal fluid, most commonly due to rupture of a cerebral aneurysm. It is a life-threatening neurologic emergency with high mortality, ranging from 30–50%. It typically affects adults, with peak incidence in the sixth decade, and is rare before the third decade. Important risk factors include hypertension, smoking, alcohol abuse, stimulant drug use such as cocaine, female sex, and a family history of SAH. Certain genetic conditions, including polycystic kidney disease and connective tissue disorders, further increase risk.
The most common cause of spontaneous SAH is rupture of a saccular (berry) aneurysm, accounting for 80–90% of cases, usually occurring at arterial bifurcations within the circle of Willis. Other causes include arteriovenous malformations, arterial dissections, intracranial tumors, and mycotic aneurysms. Traumatic SAH is also seen in severe head injuries.
Patients classically present with a sudden, severe headache often described as a “thunderclap headache” or the “worst headache of life,” reaching maximal intensity within seconds. This headache is typically different from prior headaches. Associated features include vomiting, transient loss of consciousness, seizures, neck stiffness, and focal neurologic deficits. A “sentinel headache,” representing a minor bleed, may occur days to weeks before the major event in up to half of patients.
On examination, patients may have nuchal rigidity, altered mental status, and focal neurologic deficits. Cranial nerve involvement, particularly third nerve palsy presenting as a “down and out” eye, may be seen. Retinal hemorrhage can occasionally be the only clue, especially in comatose patients.
Diagnosis begins with an emergent noncontrast CT scan of the head, which detects SAH in up to 98% of cases if performed within 12 hours of symptom onset. If the CT scan is negative but clinical suspicion remains high, a lumbar puncture must be performed. The presence of red blood cells in the cerebrospinal fluid or xanthochromia confirms the diagnosis. Further imaging, such as CT angiography or digital subtraction angiography, is used to identify the source of bleeding, while transcranial Doppler may be used to monitor for vasospasm.
Management is focused on rapid stabilization and prevention of complications. Initial priorities include airway protection, oxygenation, cardiac monitoring, and establishing intravenous access. Blood pressure must be carefully controlled to reduce the risk of rebleeding while maintaining adequate cerebral perfusion, with a target systolic pressure below 160 mmHg. Measures to reduce intracranial pressure include head elevation, avoidance of straining, and use of antiemetics and stool softeners. In selected cases, mannitol and controlled ventilation may be required.
All patients should receive Nimodipine to reduce the risk of delayed cerebral vasospasm and improve neurologic outcomes. Seizures should be treated promptly with benzodiazepines, and metabolic abnormalities should be corrected. Definitive management involves urgent neurosurgical intervention, either by surgical clipping or endovascular coiling of the aneurysm.
All patients with confirmed or suspected SAH require admission to an intensive care unit. Early recognition and treatment are critical, as mortality is high and many patients deteriorate rapidly. A key pitfall is failure to consider SAH in patients presenting with acute severe headache, or stopping evaluation after a negative CT scan without proceeding to lumbar puncture when indicated.
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Emergency and Acute Medicine – Smoke Inhalation
Smoke inhalation should be suspected in any patient exposed to fire in an enclosed space or with a history of loss of consciousness. It can cause injury through three main mechanisms: direct thermal injury to the upper airway, chemical irritation of the lower airway, and systemic toxicity from inhaled substances such as carbon monoxide and hydrogen cyanide. Notably, steam inhalation is especially dangerous due to its extremely high heat-carrying capacity, which can rapidly cause severe airway edema and obstruction.
Thermal injury is typically limited to supraglottic structures because the upper airway dissipates heat effectively. However, inhaled irritants can damage lower airway structures, leading to bronchospasm, inflammation, and impaired gas exchange. Systemic toxicity occurs when gases like carbon monoxide impair oxygen delivery or cyanide disrupts cellular respiration.
Patients often present with a history of smoke exposure, especially in confined spaces. Early symptoms may be mild or even absent, with deterioration occurring over the next 24 hours. Upper airway findings include hoarseness, stridor, cough, and nasopharyngeal irritation. Lower airway involvement may present with chest discomfort, hemoptysis, bronchospasm, and excessive secretions. Classic warning signs of significant inhalation injury include facial burns, singed nasal hairs, and carbonaceous sputum.
Evaluation includes pulse oximetry, though it may be falsely normal in carbon monoxide poisoning. Arterial blood gas analysis may reveal hypoxia or metabolic acidosis, particularly in cases of carbon monoxide or cyanide toxicity. Chest radiographs are often initially normal but may show pulmonary changes later. Laboratory testing should include carboxyhemoglobin levels for suspected carbon monoxide exposure and lactate as a marker for cyanide toxicity. Cyanide levels can be measured but treatment should not be delayed while awaiting results.
Management begins with immediate administration of 100% oxygen via face mask. Early intubation is critical in patients with signs of airway compromise such as stridor, drooling, respiratory distress, or altered mental status. Bronchospasm can be treated with nebulized bronchodilators such as albuterol, and corticosteroids may be considered in patients with underlying asthma or COPD.
For carbon monoxide toxicity, treatment includes high-flow oxygen and, in selected cases, hyperbaric oxygen therapy. Cyanide toxicity should be treated promptly with hydroxocobalamin (preferred), or with sodium thiosulfate if necessary. Care must be taken with nitrite-based antidotes in patients with concurrent carbon monoxide exposure.
Patients requiring intubation, those with significant burns, persistent respiratory symptoms, or evidence of toxic exposure should be admitted. Patients with minimal exposure who remain asymptomatic after a period of observation (typically 4–6 hours) may be discharged with clear return precautions.
Key points include maintaining a high index of suspicion even with initially normal findings, recognizing that pulse oximetry can be misleading, initiating early oxygen therapy, and not delaying treatment for suspected cyanide toxicity.
Smoke inhalation should be suspected in any patient exposed to fire in an enclosed space or with a history of loss of consciousness. It can cause injury through three main mechanisms: direct thermal injury to the upper airway, chemical irritation of the lower airway, and systemic toxicity from inhaled substances such as carbon monoxide and hydrogen cyanide. Notably, steam inhalation is especially dangerous due to its extremely high heat-carrying capacity, which can rapidly cause severe airway edema and obstruction.
Thermal injury is typically limited to supraglottic structures because the upper airway dissipates heat effectively. However, inhaled irritants can damage lower airway structures, leading to bronchospasm, inflammation, and impaired gas exchange. Systemic toxicity occurs when gases like carbon monoxide impair oxygen delivery or cyanide disrupts cellular respiration.
Patients often present with a history of smoke exposure, especially in confined spaces. Early symptoms may be mild or even absent, with deterioration occurring over the next 24 hours. Upper airway findings include hoarseness, stridor, cough, and nasopharyngeal irritation. Lower airway involvement may present with chest discomfort, hemoptysis, bronchospasm, and excessive secretions. Classic warning signs of significant inhalation injury include facial burns, singed nasal hairs, and carbonaceous sputum.
Evaluation includes pulse oximetry, though it may be falsely normal in carbon monoxide poisoning. Arterial blood gas analysis may reveal hypoxia or metabolic acidosis, particularly in cases of carbon monoxide or cyanide toxicity. Chest radiographs are often initially normal but may show pulmonary changes later. Laboratory testing should include carboxyhemoglobin levels for suspected carbon monoxide exposure and lactate as a marker for cyanide toxicity. Cyanide levels can be measured but treatment should not be delayed while awaiting results.
Management begins with immediate administration of 100% oxygen via face mask. Early intubation is critical in patients with signs of airway compromise such as stridor, drooling, respiratory distress, or altered mental status. Bronchospasm can be treated with nebulized bronchodilators such as albuterol, and corticosteroids may be considered in patients with underlying asthma or COPD.
For carbon monoxide toxicity, treatment includes high-flow oxygen and, in selected cases, hyperbaric oxygen therapy. Cyanide toxicity should be treated promptly with hydroxocobalamin (preferred), or with sodium thiosulfate if necessary. Care must be taken with nitrite-based antidotes in patients with concurrent carbon monoxide exposure.
Patients requiring intubation, those with significant burns, persistent respiratory symptoms, or evidence of toxic exposure should be admitted. Patients with minimal exposure who remain asymptomatic after a period of observation (typically 4–6 hours) may be discharged with clear return precautions.
Key points include maintaining a high index of suspicion even with initially normal findings, recognizing that pulse oximetry can be misleading, initiating early oxygen therapy, and not delaying treatment for suspected cyanide toxicity.
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Emergency and Acute Medicine: Cervical Spine Injury (Adult)
Cervical spine injury refers to trauma involving the vertebrae, spinal cord, or supporting ligaments of the neck, and may result from one or multiple mechanisms acting simultaneously. These injuries range from stable fractures to highly unstable patterns associated with spinal cord damage. Common mechanisms include flexion, extension, rotation, and axial loading forces, each producing characteristic injury patterns. Flexion injuries may cause wedge fractures, ligamentous disruption, or severe unstable injuries such as flexion teardrop fractures and bilateral facet dislocations. Extension injuries can result in fractures of the posterior elements, including the atlas or axis, and classic injuries such as the hangman fracture. Axial loading may lead to burst fractures or Jefferson fractures of C1, both of which can be highly unstable.
Blunt trauma is the leading cause of cervical spine injuries, with motor vehicle accidents accounting for the majority, followed by falls and sports-related injuries. Patients with pre-existing spinal conditions such as ankylosing spondylitis, osteoporosis, or metastatic disease are particularly vulnerable, as even minor trauma can result in significant injury. Penetrating trauma may also cause cervical spine damage, especially when associated with neurologic deficits.
Patients typically present with neck pain and tenderness, often accompanied by neurologic symptoms such as numbness, weakness, or paresthesias in the upper or lower extremities. However, a cervical spine injury must be assumed in any trauma patient with altered mental status, intoxication, inability to communicate, distracting injuries, or significant head and neck trauma, even in the absence of pain. Physical examination should include careful inspection for deformity or bruising, palpation of the cervical spine, and a thorough neurologic assessment of motor, sensory, and reflex function. Associated incomplete spinal cord syndromes such as anterior cord, Brown-Séquard, or central cord syndromes may be present and should be recognized.
Evaluation requires a complete clinical assessment combined with appropriate imaging. Standard imaging traditionally includes three-view cervical spine radiographs (lateral, anteroposterior, and odontoid views), ensuring visualization from C1 to T1. However, CT scanning has become the preferred initial imaging modality, especially in high-risk or obtunded patients, due to its superior sensitivity for detecting fractures and alignment abnormalities. MRI is indicated in patients with neurologic deficits, suspected ligamentous injury, or persistent symptoms despite normal CT, as it is the best modality for evaluating spinal cord and soft tissue injury. Flexion–extension views may be used selectively in alert patients with persistent pain to assess ligamentous stability.
Clinical decision tools such as the NEXUS criteria can help determine which patients require imaging. Patients who are alert, not intoxicated, without midline cervical tenderness, neurologic deficits, or distracting injuries may be safely cleared clinically without imaging. However, strict adherence to all criteria is essential to avoid missed injuries.
Initial management begins with strict spinal immobilization using a rigid cervical collar, backboard, and supportive padding. Airway management must be performed with in-line spinal stabilization, typically using rapid sequence intubation, with alternative airway techniques available if needed. Intravenous access should be established, and circulation supported. In cases of hypotension, clinicians must differentiate between hypovolemic shock and neurogenic shock, the latter characterized by hypotension with bradycardia due to loss of sympathetic tone.
In the emergency department, patients should be evaluated for associated injuries, as cervical spine trauma often occurs in the context of multisystem trauma. If imaging reveals fractures, dislocations, or instability, or if neurologic deficits are present, urgent consultation with neurosurgery or orthopedic spine specialists is required. Patients with persistent pain despite normal imaging may require further evaluation with MRI or dynamic studies. Historically, high-dose corticosteroids such as methylprednisolone were used in spinal cord injury, but current evidence does not support routine use, and their role remains controversial.
All patients with confirmed cervical spine fractures, dislocations, or neurologic deficits require hospital admission, often to an intensive care or monitored setting. Stable injuries without neurologic compromise may still require admission for observation and specialist management. Patients with minor soft tissue injuries such as whiplash and normal imaging may be discharged with appropriate follow-up and instructions to return if symptoms worsen.
A key pitfall is underestimating injury severity, particularly in patients with underlying spinal disease, where seemingly minor trauma can result in significant instability or cord injury. Strict application of clinical decision rules and a high index of suspicion are essential. Careful neurologic assessment, appropriate imaging, and early specialist involvement are critical to optimizing outcomes and preventing long-term disability.
Cervical spine injury refers to trauma involving the vertebrae, spinal cord, or supporting ligaments of the neck, and may result from one or multiple mechanisms acting simultaneously. These injuries range from stable fractures to highly unstable patterns associated with spinal cord damage. Common mechanisms include flexion, extension, rotation, and axial loading forces, each producing characteristic injury patterns. Flexion injuries may cause wedge fractures, ligamentous disruption, or severe unstable injuries such as flexion teardrop fractures and bilateral facet dislocations. Extension injuries can result in fractures of the posterior elements, including the atlas or axis, and classic injuries such as the hangman fracture. Axial loading may lead to burst fractures or Jefferson fractures of C1, both of which can be highly unstable.
Blunt trauma is the leading cause of cervical spine injuries, with motor vehicle accidents accounting for the majority, followed by falls and sports-related injuries. Patients with pre-existing spinal conditions such as ankylosing spondylitis, osteoporosis, or metastatic disease are particularly vulnerable, as even minor trauma can result in significant injury. Penetrating trauma may also cause cervical spine damage, especially when associated with neurologic deficits.
Patients typically present with neck pain and tenderness, often accompanied by neurologic symptoms such as numbness, weakness, or paresthesias in the upper or lower extremities. However, a cervical spine injury must be assumed in any trauma patient with altered mental status, intoxication, inability to communicate, distracting injuries, or significant head and neck trauma, even in the absence of pain. Physical examination should include careful inspection for deformity or bruising, palpation of the cervical spine, and a thorough neurologic assessment of motor, sensory, and reflex function. Associated incomplete spinal cord syndromes such as anterior cord, Brown-Séquard, or central cord syndromes may be present and should be recognized.
Evaluation requires a complete clinical assessment combined with appropriate imaging. Standard imaging traditionally includes three-view cervical spine radiographs (lateral, anteroposterior, and odontoid views), ensuring visualization from C1 to T1. However, CT scanning has become the preferred initial imaging modality, especially in high-risk or obtunded patients, due to its superior sensitivity for detecting fractures and alignment abnormalities. MRI is indicated in patients with neurologic deficits, suspected ligamentous injury, or persistent symptoms despite normal CT, as it is the best modality for evaluating spinal cord and soft tissue injury. Flexion–extension views may be used selectively in alert patients with persistent pain to assess ligamentous stability.
Clinical decision tools such as the NEXUS criteria can help determine which patients require imaging. Patients who are alert, not intoxicated, without midline cervical tenderness, neurologic deficits, or distracting injuries may be safely cleared clinically without imaging. However, strict adherence to all criteria is essential to avoid missed injuries.
Initial management begins with strict spinal immobilization using a rigid cervical collar, backboard, and supportive padding. Airway management must be performed with in-line spinal stabilization, typically using rapid sequence intubation, with alternative airway techniques available if needed. Intravenous access should be established, and circulation supported. In cases of hypotension, clinicians must differentiate between hypovolemic shock and neurogenic shock, the latter characterized by hypotension with bradycardia due to loss of sympathetic tone.
In the emergency department, patients should be evaluated for associated injuries, as cervical spine trauma often occurs in the context of multisystem trauma. If imaging reveals fractures, dislocations, or instability, or if neurologic deficits are present, urgent consultation with neurosurgery or orthopedic spine specialists is required. Patients with persistent pain despite normal imaging may require further evaluation with MRI or dynamic studies. Historically, high-dose corticosteroids such as methylprednisolone were used in spinal cord injury, but current evidence does not support routine use, and their role remains controversial.
All patients with confirmed cervical spine fractures, dislocations, or neurologic deficits require hospital admission, often to an intensive care or monitored setting. Stable injuries without neurologic compromise may still require admission for observation and specialist management. Patients with minor soft tissue injuries such as whiplash and normal imaging may be discharged with appropriate follow-up and instructions to return if symptoms worsen.
A key pitfall is underestimating injury severity, particularly in patients with underlying spinal disease, where seemingly minor trauma can result in significant instability or cord injury. Strict application of clinical decision rules and a high index of suspicion are essential. Careful neurologic assessment, appropriate imaging, and early specialist involvement are critical to optimizing outcomes and preventing long-term disability.
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Emergency and Acute Medicine: Spinal Cord Syndromes
Spinal cord syndromes represent patterns of neurologic deficits caused by localized disruption of spinal cord pathways, most commonly due to trauma. These injuries produce characteristic combinations of motor and sensory loss depending on the portion of the cord affected. While high-energy trauma is the most frequent cause, patients with underlying spinal disease such as arthritis, osteoporosis, or metastatic lesions are at increased risk of cord injury even after minor trauma.
Several classic syndromes are recognized. Anterior cord syndrome typically results from flexion or axial loading injuries, or from direct compression by fractures, discs, tumors, or abscesses, and occasionally from compromise of the anterior spinal artery. It presents with bilateral motor paralysis and loss of pain and temperature sensation below the lesion, while dorsal column functions (proprioception and vibration) are preserved. Brown-Séquard syndrome results from hemisection of the cord, most often due to penetrating trauma, and produces ipsilateral motor weakness and loss of proprioception, with contralateral loss of pain and temperature, usually beginning a few levels below the injury. Central cord syndrome, commonly seen in elderly patients with cervical spondylosis, follows hyperextension injuries and leads to greater motor weakness in the upper extremities than the lower, with variable sensory deficits. Dorsal cord syndrome involves loss of proprioception, position sense, and coordination, while complete cord syndrome represents total disruption of the cord, resulting in complete motor and sensory loss below the lesion, often accompanied by neurogenic shock characterized by hypotension, bradycardia, warm skin, and sometimes priapism. Deficits that persist beyond 24 hours are usually permanent.
Patients typically present with an acute loss of motor and/or sensory function following trauma. A detailed neurologic examination is essential to determine the level of injury, using known sensory and motor landmarks such as the clavicles (C4), nipples (T4), umbilicus (T10), and perianal region (S5), as well as key motor functions like elbow flexion (C5), finger movement (C8–T1), and ankle motion (L4–S1). Accurate documentation of these findings is critical for diagnosis, monitoring progression, and guiding management.
Evaluation begins with a thorough neurologic assessment and urgent neurosurgical consultation if any deficit is present. Imaging should include plain radiographs of suspected areas, though CT scanning is often preferred, especially in older patients or when radiographs are inconclusive, as it better visualizes bony injury and canal compromise. MRI is the imaging modality of choice for assessing spinal cord injury, particularly when neurologic deficits are unexplained, progressing, or when surgical intervention is being considered. If MRI is unavailable, CT myelography may be used. Additional studies such as lumbar puncture may be considered when alternative diagnoses like demyelinating or inflammatory conditions are suspected.
The differential diagnosis includes peripheral nerve injuries, dorsal root lesions, Guillain–Barré syndrome, multiple sclerosis, transverse myelitis, epidural abscess, and stroke, all of which may mimic spinal cord pathology and must be carefully distinguished.
Management begins in the prehospital setting with strict spinal immobilization and rapid transport to a trauma center. In the emergency department, immobilization must be maintained at all times, including during airway management with in-line stabilization. Intravenous fluids should be administered, particularly in cases of hypotension, though other causes such as hemorrhage must be excluded. Neurogenic shock should be suspected when hypotension is accompanied by bradycardia, and if unresponsive to fluids, vasopressors (preferably alpha-agonists) may be required.
Early involvement of neurosurgery is critical, as timely decompression or stabilization may improve outcomes. Associated injuries should be treated concurrently, and patients with penetrating trauma require antibiotics and tetanus prophylaxis. The routine use of high-dose corticosteroids is no longer recommended, as evidence has not demonstrated clear benefit and may increase complications.
All patients with suspected spinal cord syndromes require hospital admission, typically to an intensive care unit, for close monitoring and management. No patient with signs of spinal cord injury should be discharged from the emergency department. Early recognition, accurate neurologic assessment, and prompt specialist involvement are key factors influencing prognosis and long-term outcomes.
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Emergency and Acute Medicine: Spider Bite – Brown Recluse (Loxoscelism)
Brown recluse spider envenomation causes a spectrum of illness ranging from localized skin injury to systemic toxicity, a condition known as loxoscelism. Most patients develop a cutaneous lesion, but in some cases—particularly in children—the venom can produce significant systemic effects such as hemolysis, renal failure, or coagulopathy. The disease results from the toxic effects of enzymes within the venom that trigger inflammation, tissue destruction, and vascular injury.
The brown recluse, also known as the fiddleback spider, is a small tan-to-brown spider with a distinctive violin-shaped marking on its back and three pairs of eyes. It typically inhabits warm, dry environments such as woodpiles, attics, closets, and storage areas. Bites usually occur when the spider is trapped against the skin, making them defensive in nature. The venom contains enzymes that bind to red blood cells causing hemolysis, activate inflammatory pathways through complement, and induce tissue necrosis by lipolysis. It also promotes platelet aggregation and thrombosis, and in severe cases may lead to disseminated intravascular coagulation or shock. The severity of toxicity depends on the amount of venom, the size of the patient, and the location of the bite, with children being more susceptible to severe outcomes.
Clinically, diagnosis relies on a combination of presentation and history, although a confirmed spider bite is often difficult to establish. Most patients present with a single skin lesion, commonly in areas where clothing traps the spider. The bite is often initially painless, but within hours patients may develop burning, itching, or aching at the site. Over time, the lesion evolves into a characteristic pattern with a red outer zone, a pale ischemic ring, and a central area of bluish or purple discoloration indicating necrosis. Blisters may form within 24 to 72 hours, followed by the development of a necrotic eschar over several days. The eschar eventually sloughs, leaving an ulcer that heals slowly over weeks and may result in scarring. The extent of local tissue damage does not reliably predict systemic toxicity.
Systemic manifestations are uncommon but more likely in children and typically develop within one to three days after envenomation. Patients may experience fever, malaise, nausea, vomiting, muscle pain, and jaundice due to hemolysis. A generalized rash, dark urine, and signs of hemoglobinuria may also occur. Severe cases can progress to acute kidney injury, disseminated intravascular coagulation, and shock.
Evaluation is primarily clinical, and laboratory testing is not required in mild cases. However, if systemic toxicity is suspected, investigations may reveal hemolytic anemia, thrombocytopenia, leukocytosis, and abnormalities in coagulation consistent with DIC. Renal function tests may indicate impairment, and urinalysis may show hemoglobinuria or proteinuria. Imaging is generally reserved for complications.
It is important to consider alternative diagnoses, as brown recluse bites are frequently overdiagnosed. Conditions such as bacterial skin infections (including MRSA), necrotizing fasciitis, diabetic ulcers, vasculitis, fungal infections, and other dermatologic or vascular disorders can mimic the presentation. In the absence of a clear history of a spider bite, these alternatives should be strongly considered.
Management is largely supportive. Prehospital care includes immobilizing and elevating the affected limb and applying cool compresses. Harmful measures such as incision, suction, or tourniquets should be avoided. In the emergency setting, treatment involves wound cleansing, tetanus prophylaxis, and adequate analgesia. Antibiotics are indicated only if there is evidence of secondary infection. Early surgical excision is contraindicated, as it may worsen tissue injury.
In cases with systemic involvement, management includes intravenous fluids, monitoring of renal and hematologic parameters, and supportive care such as blood transfusions for severe hemolysis or coagulopathy. Dialysis may be required for renal failure, and vasopressors may be needed in cases of shock. The use of dapsone is controversial and should only be considered in severe cases after screening for G6PD deficiency due to the risk of hemolysis and methemoglobinemia. There is no widely available antivenom.
Patients with significant local progression, systemic toxicity, or high-risk features—especially children—should be admitted for monitoring and treatment. Those with mild, stable lesions may be discharged with close follow-up and reassessment over the next several days. Patients should be counseled about the prolonged healing process and the possibility of scarring, with surgical intervention typically delayed until the acute phase has resolved.
Brown recluse bites are relatively uncommon, and overdiagnosis is a frequent pitfall. Many suspected cases are actually due to infections or other causes of necrotic skin lesions. Careful clinical evaluation, avoidance of unnecessary interventions, and appropriate monitoring are essential to achieving good outcomes.
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Emergency and Acute Medicine – Black Widow Spider Bite
Black widow spider envenomation is a neurotoxic syndrome caused primarily by the female spider, whose venom contains α-latrotoxin. This toxin triggers massive neurotransmitter release at nerve terminals, leading to widespread neurologic, muscular, and autonomic effects. Although rarely fatal, severity depends on factors such as patient age, comorbidities (especially cardiovascular disease), number of bites, and location of envenomation. Children and elderly patients are at higher risk for severe complications.
Black widow spiders are glossy black with a characteristic red hourglass marking on the underside of the abdomen. They are commonly found in dark, sheltered environments such as garages, woodpiles, and barns, and bites often occur during warmer months.
The bite itself may feel like a mild pinprick or go unnoticed. Within minutes, local pain develops, often described as sharp or burning, and may spread proximally. Systemic symptoms typically begin within 15–60 minutes and include severe muscle cramps and spasms, which may involve the abdomen, chest, or limbs depending on the bite location. Patients may also experience headache, dizziness, diaphoresis, nausea, vomiting, chest pain, shortness of breath, and anxiety or a sense of impending doom. In severe cases, complications include hypertension, cardiac dysrhythmias, pulmonary edema, respiratory failure, seizures, and priapism.
On examination, vital signs may show hypertension, tachycardia, or fever. A classic local finding is a “target lesion” with two puncture marks, surrounding erythema, and localized sweating. Neuromuscular findings include muscle rigidity, fasciculations, and tetanic contractions. Abdominal rigidity may mimic an acute surgical abdomen, making diagnosis challenging.
Diagnosis is primarily clinical, based on symptoms and history, as laboratory tests are nonspecific. Labs may show mild leukocytosis or elevated creatine kinase due to muscle injury. ECG monitoring is recommended in patients with cardiac symptoms or risk factors. Imaging may be needed to exclude other causes of abdominal or chest pain.
Management begins with supportive care. The wound should be cleaned, and tetanus prophylaxis administered. Pain control is essential, typically with opioids, and muscle spasms are treated with benzodiazepines. Antiemetics and antihistamines may be used for associated symptoms. Severe hypertension may require antihypertensive therapy.
Antivenin is reserved for moderate to severe cases that do not respond to supportive treatment or for high-risk patients, including pregnant individuals. Indications include severe pain, hypertension, respiratory distress, seizures, or persistent symptoms. The antivenin is effective and usually produces rapid improvement but carries a risk of hypersensitivity reactions, particularly because it is derived from horse serum. Patients must be monitored closely for anaphylaxis, and pretreatment with antihistamines or epinephrine may be considered.
Admission is recommended for patients with significant symptoms, high-risk groups (children, elderly, pregnant), or those requiring antivenin. Asymptomatic patients may be observed for several hours and discharged if no symptoms develop. Most symptoms peak within a few hours and resolve within 2–3 days, though some patients may experience prolonged fatigue, weakness, or neurologic symptoms.
Key points include recognizing the characteristic muscle cramps and autonomic symptoms, distinguishing the condition from surgical emergencies, providing aggressive symptomatic treatment, and using antivenin appropriately in severe cases.
Black widow spider envenomation is a neurotoxic syndrome caused primarily by the female spider, whose venom contains α-latrotoxin. This toxin triggers massive neurotransmitter release at nerve terminals, leading to widespread neurologic, muscular, and autonomic effects. Although rarely fatal, severity depends on factors such as patient age, comorbidities (especially cardiovascular disease), number of bites, and location of envenomation. Children and elderly patients are at higher risk for severe complications.
Black widow spiders are glossy black with a characteristic red hourglass marking on the underside of the abdomen. They are commonly found in dark, sheltered environments such as garages, woodpiles, and barns, and bites often occur during warmer months.
The bite itself may feel like a mild pinprick or go unnoticed. Within minutes, local pain develops, often described as sharp or burning, and may spread proximally. Systemic symptoms typically begin within 15–60 minutes and include severe muscle cramps and spasms, which may involve the abdomen, chest, or limbs depending on the bite location. Patients may also experience headache, dizziness, diaphoresis, nausea, vomiting, chest pain, shortness of breath, and anxiety or a sense of impending doom. In severe cases, complications include hypertension, cardiac dysrhythmias, pulmonary edema, respiratory failure, seizures, and priapism.
On examination, vital signs may show hypertension, tachycardia, or fever. A classic local finding is a “target lesion” with two puncture marks, surrounding erythema, and localized sweating. Neuromuscular findings include muscle rigidity, fasciculations, and tetanic contractions. Abdominal rigidity may mimic an acute surgical abdomen, making diagnosis challenging.
Diagnosis is primarily clinical, based on symptoms and history, as laboratory tests are nonspecific. Labs may show mild leukocytosis or elevated creatine kinase due to muscle injury. ECG monitoring is recommended in patients with cardiac symptoms or risk factors. Imaging may be needed to exclude other causes of abdominal or chest pain.
Management begins with supportive care. The wound should be cleaned, and tetanus prophylaxis administered. Pain control is essential, typically with opioids, and muscle spasms are treated with benzodiazepines. Antiemetics and antihistamines may be used for associated symptoms. Severe hypertension may require antihypertensive therapy.
Antivenin is reserved for moderate to severe cases that do not respond to supportive treatment or for high-risk patients, including pregnant individuals. Indications include severe pain, hypertension, respiratory distress, seizures, or persistent symptoms. The antivenin is effective and usually produces rapid improvement but carries a risk of hypersensitivity reactions, particularly because it is derived from horse serum. Patients must be monitored closely for anaphylaxis, and pretreatment with antihistamines or epinephrine may be considered.
Admission is recommended for patients with significant symptoms, high-risk groups (children, elderly, pregnant), or those requiring antivenin. Asymptomatic patients may be observed for several hours and discharged if no symptoms develop. Most symptoms peak within a few hours and resolve within 2–3 days, though some patients may experience prolonged fatigue, weakness, or neurologic symptoms.
Key points include recognizing the characteristic muscle cramps and autonomic symptoms, distinguishing the condition from surgical emergencies, providing aggressive symptomatic treatment, and using antivenin appropriately in severe cases.
