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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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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 - 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 - 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: Stridor
Stridor is a high-pitched, harsh, vibratory sound predominantly heard during inspiration and indicates obstruction of airflow through the upper airway. It reflects narrowing at the level of the larynx or trachea and is a clinical sign of potentially serious airway compromise. Because it signifies upper airway obstruction, stridor must always be approached as an emergency, especially in children where deterioration can be rapid.
The causes of stridor are diverse and can be broadly divided into congenital, infectious, structural, and obstructive categories. Congenital causes include conditions such as laryngomalacia, vocal cord abnormalities, and subglottic stenosis. Infectious causes are particularly important in acute presentations and include viral croup, epiglottitis, bacterial tracheitis, and deep neck space infections like peritonsillar or retropharyngeal abscesses. Extrinsic compression from trauma, hematoma, or vascular anomalies may also compromise the airway. Intraluminal obstruction can occur due to foreign bodies, tumors, cysts, or tracheomalacia, while conditions like angioedema can cause rapid airway swelling.
Patients typically present with breathing difficulty and audible noisy respiration that worsens with agitation, crying, feeding, or lying supine. Associated symptoms may include hoarseness, a muffled “hot potato” voice, drooling, sore throat, cough, and dysphagia. Infants may have feeding difficulties, apnea, or cyanotic episodes. On examination, signs of respiratory distress are common, including tachypnea, nasal flaring, intercostal and subcostal retractions, and use of accessory muscles. Cyanosis and paradoxical breathing are late and concerning findings. Certain features, such as trismus, may suggest deep neck infections.
Diagnosis is primarily clinical, and unnecessary investigations should be avoided if they risk agitating the patient, particularly children. Imaging is reserved for very mild or unclear cases. Definitive evaluation is achieved through direct visualization of the airway, typically with laryngoscopy. However, this must only be performed in a controlled setting, such as an operating room, with immediate availability of a surgical airway, as manipulation can precipitate complete obstruction.
Management focuses first on airway stabilization. In prehospital and early care, the patient—especially a child—should be kept calm, given oxygen, and monitored closely. Agitation must be minimized as it can worsen airway obstruction. In the emergency setting, stridor is treated as a difficult airway, and clinicians must be prepared for rapid deterioration.
If intubation is required, it should ideally be performed in a controlled environment with experienced personnel. A smaller endotracheal tube is recommended due to airway narrowing. Ketamine is often preferred for induction because it preserves spontaneous breathing. Blind nasotracheal intubation should be avoided. If intubation fails or the airway is lost, an emergency surgical airway such as cricothyrotomy or tracheostomy is required.
Adjunctive treatments depend on the underlying cause. Nebulized epinephrine and corticosteroids such as dexamethasone are commonly used in conditions like croup. Antibiotics, such as ceftriaxone, are indicated when a bacterial infection is suspected. Sedation and paralysis may be required after securing the airway.
All patients with unresolved stridor require hospital admission for monitoring and further evaluation. Discharge is only appropriate when symptoms have completely resolved and a non-threatening cause is identified. Early involvement of specialists such as otolaryngologists or pediatric surgeons is essential.
A key clinical pitfall is attempting airway examination without adequate preparation for emergency airway intervention. Stridor should always prompt urgent evaluation and careful airway management, as delay or improper handling can lead to sudden and catastrophic airway obstruction.
Stridor is a high-pitched, harsh, vibratory sound predominantly heard during inspiration and indicates obstruction of airflow through the upper airway. It reflects narrowing at the level of the larynx or trachea and is a clinical sign of potentially serious airway compromise. Because it signifies upper airway obstruction, stridor must always be approached as an emergency, especially in children where deterioration can be rapid.
The causes of stridor are diverse and can be broadly divided into congenital, infectious, structural, and obstructive categories. Congenital causes include conditions such as laryngomalacia, vocal cord abnormalities, and subglottic stenosis. Infectious causes are particularly important in acute presentations and include viral croup, epiglottitis, bacterial tracheitis, and deep neck space infections like peritonsillar or retropharyngeal abscesses. Extrinsic compression from trauma, hematoma, or vascular anomalies may also compromise the airway. Intraluminal obstruction can occur due to foreign bodies, tumors, cysts, or tracheomalacia, while conditions like angioedema can cause rapid airway swelling.
Patients typically present with breathing difficulty and audible noisy respiration that worsens with agitation, crying, feeding, or lying supine. Associated symptoms may include hoarseness, a muffled “hot potato” voice, drooling, sore throat, cough, and dysphagia. Infants may have feeding difficulties, apnea, or cyanotic episodes. On examination, signs of respiratory distress are common, including tachypnea, nasal flaring, intercostal and subcostal retractions, and use of accessory muscles. Cyanosis and paradoxical breathing are late and concerning findings. Certain features, such as trismus, may suggest deep neck infections.
Diagnosis is primarily clinical, and unnecessary investigations should be avoided if they risk agitating the patient, particularly children. Imaging is reserved for very mild or unclear cases. Definitive evaluation is achieved through direct visualization of the airway, typically with laryngoscopy. However, this must only be performed in a controlled setting, such as an operating room, with immediate availability of a surgical airway, as manipulation can precipitate complete obstruction.
Management focuses first on airway stabilization. In prehospital and early care, the patient—especially a child—should be kept calm, given oxygen, and monitored closely. Agitation must be minimized as it can worsen airway obstruction. In the emergency setting, stridor is treated as a difficult airway, and clinicians must be prepared for rapid deterioration.
If intubation is required, it should ideally be performed in a controlled environment with experienced personnel. A smaller endotracheal tube is recommended due to airway narrowing. Ketamine is often preferred for induction because it preserves spontaneous breathing. Blind nasotracheal intubation should be avoided. If intubation fails or the airway is lost, an emergency surgical airway such as cricothyrotomy or tracheostomy is required.
Adjunctive treatments depend on the underlying cause. Nebulized epinephrine and corticosteroids such as dexamethasone are commonly used in conditions like croup. Antibiotics, such as ceftriaxone, are indicated when a bacterial infection is suspected. Sedation and paralysis may be required after securing the airway.
All patients with unresolved stridor require hospital admission for monitoring and further evaluation. Discharge is only appropriate when symptoms have completely resolved and a non-threatening cause is identified. Early involvement of specialists such as otolaryngologists or pediatric surgeons is essential.
A key clinical pitfall is attempting airway examination without adequate preparation for emergency airway intervention. Stridor should always prompt urgent evaluation and careful airway management, as delay or improper handling can lead to sudden and catastrophic airway obstruction.
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Emergency and Acute Medicine: Scorpion Sting (Envenomation)
Scorpion envenomation is a potentially serious condition caused by injection of neurotoxic venom, which affects sodium channels and leads to prolonged neuronal firing. This results in widespread stimulation of autonomic, somatic, and cranial nerves. Symptoms typically begin within minutes of the sting and can last from several hours up to 72 hours. The severity of illness varies depending on the species and the patient, with children at significantly higher risk of severe toxicity and complications.
The most clinically significant species in North America is Centruroides sculpturatus (bark scorpion), found in parts of the southern United States, Mexico, and Central America. Globally, many dangerous species exist across Asia, Africa, the Middle East, and South America. Pediatric patients are especially vulnerable due to lower body mass and may present with symptoms that mimic seizures, poisoning, or central nervous system infections.
Clinical manifestations develop rapidly, usually peaking within 1–2 hours. Local findings are often minimal, typically limited to pain and heightened sensitivity without significant redness or swelling. Systemic toxicity is more prominent and includes autonomic disturbances such as tachycardia, hypertension, sweating, agitation, and hyperthermia from sympathetic activation, as well as bradycardia, hypotension, and excessive salivation from parasympathetic effects. Neuromuscular symptoms include restlessness, involuntary muscle jerking, and severe agitation. Cranial nerve involvement may lead to abnormal eye movements, blurred vision, tongue fasciculations, and impaired swallowing or airway control.
Severity is classified into four grades. Mild cases (grades I and II) involve only local or regional symptoms, while severe envenomation (grades III and IV) includes neuromuscular dysfunction and combined autonomic and cranial nerve involvement. Severe cases may progress to respiratory compromise, requiring urgent intervention.
Diagnosis is clinical and based on symptom recognition, especially in endemic areas. Identification of the scorpion is not necessary. Laboratory tests are generally not required for mild cases but may be indicated in severe envenomation to assess complications such as electrolyte imbalance, renal injury, or rhabdomyolysis. Imaging and ECG may be used when cardiopulmonary symptoms are present.
Management begins with stabilization of airway, breathing, and circulation. Oxygen and intravenous access should be established early. Mild envenomations are treated with supportive care, including oral analgesics and tetanus prophylaxis. Severe envenomations require close monitoring and may necessitate airway protection, sedation (e.g., midazolam for agitation), and cardiovascular support.
Antivenom (Anascorp) is the definitive treatment for severe cases and works rapidly to reverse neurologic symptoms. It is administered intravenously, with initial dosing followed by reassessment and additional doses if needed. Importantly, the same dosing is used in both adults and children, as it is based on venom load rather than body weight.
Patients with severe envenomation should be admitted to an intensive care setting. Those who respond well to antivenom and remain stable after observation may be discharged with instructions regarding delayed reactions such as serum sickness. Mild cases can be safely discharged after a short observation period if symptoms do not progress.
A critical clinical point is maintaining a high index of suspicion in endemic regions, especially in children presenting with unexplained neurologic or autonomic symptoms. Early recognition and timely administration of antivenom can significantly reduce morbidity and prevent life-threatening complications.
Scorpion envenomation is a potentially serious condition caused by injection of neurotoxic venom, which affects sodium channels and leads to prolonged neuronal firing. This results in widespread stimulation of autonomic, somatic, and cranial nerves. Symptoms typically begin within minutes of the sting and can last from several hours up to 72 hours. The severity of illness varies depending on the species and the patient, with children at significantly higher risk of severe toxicity and complications.
The most clinically significant species in North America is Centruroides sculpturatus (bark scorpion), found in parts of the southern United States, Mexico, and Central America. Globally, many dangerous species exist across Asia, Africa, the Middle East, and South America. Pediatric patients are especially vulnerable due to lower body mass and may present with symptoms that mimic seizures, poisoning, or central nervous system infections.
Clinical manifestations develop rapidly, usually peaking within 1–2 hours. Local findings are often minimal, typically limited to pain and heightened sensitivity without significant redness or swelling. Systemic toxicity is more prominent and includes autonomic disturbances such as tachycardia, hypertension, sweating, agitation, and hyperthermia from sympathetic activation, as well as bradycardia, hypotension, and excessive salivation from parasympathetic effects. Neuromuscular symptoms include restlessness, involuntary muscle jerking, and severe agitation. Cranial nerve involvement may lead to abnormal eye movements, blurred vision, tongue fasciculations, and impaired swallowing or airway control.
Severity is classified into four grades. Mild cases (grades I and II) involve only local or regional symptoms, while severe envenomation (grades III and IV) includes neuromuscular dysfunction and combined autonomic and cranial nerve involvement. Severe cases may progress to respiratory compromise, requiring urgent intervention.
Diagnosis is clinical and based on symptom recognition, especially in endemic areas. Identification of the scorpion is not necessary. Laboratory tests are generally not required for mild cases but may be indicated in severe envenomation to assess complications such as electrolyte imbalance, renal injury, or rhabdomyolysis. Imaging and ECG may be used when cardiopulmonary symptoms are present.
Management begins with stabilization of airway, breathing, and circulation. Oxygen and intravenous access should be established early. Mild envenomations are treated with supportive care, including oral analgesics and tetanus prophylaxis. Severe envenomations require close monitoring and may necessitate airway protection, sedation (e.g., midazolam for agitation), and cardiovascular support.
Antivenom (Anascorp) is the definitive treatment for severe cases and works rapidly to reverse neurologic symptoms. It is administered intravenously, with initial dosing followed by reassessment and additional doses if needed. Importantly, the same dosing is used in both adults and children, as it is based on venom load rather than body weight.
Patients with severe envenomation should be admitted to an intensive care setting. Those who respond well to antivenom and remain stable after observation may be discharged with instructions regarding delayed reactions such as serum sickness. Mild cases can be safely discharged after a short observation period if symptoms do not progress.
A critical clinical point is maintaining a high index of suspicion in endemic regions, especially in children presenting with unexplained neurologic or autonomic symptoms. Early recognition and timely administration of antivenom can significantly reduce morbidity and prevent life-threatening complications.
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Emergency and Acute Medicine: Bee Sting (Hymenoptera Envenomation)
Bee stings are a common form of envenomation caused by insects from the order Hymenoptera, which includes bees, wasps, hornets, and fire ants. Their venom triggers the release of biologically active substances that can produce a range of reactions, from mild local irritation to life-threatening systemic responses. Most reactions are IgE-mediated type I hypersensitivity reactions, although less commonly, delayed immune responses such as type III (Arthus) reactions may occur.
Clinical presentation varies widely depending on the individual’s immune response and the amount of venom delivered. The most common reaction is a localized response, characterized by immediate pain, redness, and swelling at the sting site, typically resolving within a few hours. Larger local reactions may involve an entire limb, peak within 48 hours, and persist for several days, sometimes accompanied by mild fever.
Systemic reactions represent true allergic responses and can progress to anaphylaxis, which is potentially fatal. Symptoms usually develop within 15–20 minutes and may include respiratory distress (wheezing, stridor, shortness of breath), cardiovascular instability (hypotension, tachycardia, shock), gastrointestinal symptoms (nausea, vomiting, diarrhea), and skin manifestations such as urticaria, flushing, and angioedema. Toxic reactions can occur after multiple stings due to a large venom load and may mimic anaphylaxis. Rare delayed or unusual immune-mediated complications include vasculitis, nephropathy, serum sickness, and neurologic involvement.
Diagnosis is primarily clinical, based on history and physical examination. There are no specific laboratory or imaging tests required for uncomplicated cases. However, investigations such as blood tests or ECG may be warranted in patients with significant systemic involvement, particularly those with underlying cardiovascular disease.
Management depends on the severity of the reaction. Immediate priorities in severe systemic reactions include airway stabilization, oxygen administration, intravenous access, and prompt use of epinephrine, which is the first-line treatment for anaphylaxis. Antihistamines (both H1 and H2 blockers), corticosteroids, and inhaled β-agonists are used as adjunct therapies. Persistent hypotension requires aggressive fluid resuscitation and possibly vasopressor support.
For local reactions, treatment is supportive and includes removal of the stinger (preferably by scraping rather than squeezing to avoid further venom release), application of cold compresses, limb elevation, and use of oral or topical antihistamines or corticosteroids. Pain control and avoidance of constrictive items such as rings or tight clothing are also important.
Patients with systemic reactions should be observed for at least 6 hours, while those with severe or life-threatening reactions may require admission and prolonged monitoring. Discharge is appropriate for patients with mild local reactions or resolved systemic symptoms after observation. Importantly, individuals who experience systemic reactions should be prescribed an epinephrine auto-injector and referred to an allergist for further evaluation and possible immunotherapy.
A key clinical point is that most fatal outcomes occur within the first hour due to airway compromise or circulatory collapse. Rapid recognition and early administration of epinephrine are critical. Patients with a history of severe reactions must be educated on avoidance strategies and emergency self-treatment to reduce the risk of recurrence.
Bee stings are a common form of envenomation caused by insects from the order Hymenoptera, which includes bees, wasps, hornets, and fire ants. Their venom triggers the release of biologically active substances that can produce a range of reactions, from mild local irritation to life-threatening systemic responses. Most reactions are IgE-mediated type I hypersensitivity reactions, although less commonly, delayed immune responses such as type III (Arthus) reactions may occur.
Clinical presentation varies widely depending on the individual’s immune response and the amount of venom delivered. The most common reaction is a localized response, characterized by immediate pain, redness, and swelling at the sting site, typically resolving within a few hours. Larger local reactions may involve an entire limb, peak within 48 hours, and persist for several days, sometimes accompanied by mild fever.
Systemic reactions represent true allergic responses and can progress to anaphylaxis, which is potentially fatal. Symptoms usually develop within 15–20 minutes and may include respiratory distress (wheezing, stridor, shortness of breath), cardiovascular instability (hypotension, tachycardia, shock), gastrointestinal symptoms (nausea, vomiting, diarrhea), and skin manifestations such as urticaria, flushing, and angioedema. Toxic reactions can occur after multiple stings due to a large venom load and may mimic anaphylaxis. Rare delayed or unusual immune-mediated complications include vasculitis, nephropathy, serum sickness, and neurologic involvement.
Diagnosis is primarily clinical, based on history and physical examination. There are no specific laboratory or imaging tests required for uncomplicated cases. However, investigations such as blood tests or ECG may be warranted in patients with significant systemic involvement, particularly those with underlying cardiovascular disease.
Management depends on the severity of the reaction. Immediate priorities in severe systemic reactions include airway stabilization, oxygen administration, intravenous access, and prompt use of epinephrine, which is the first-line treatment for anaphylaxis. Antihistamines (both H1 and H2 blockers), corticosteroids, and inhaled β-agonists are used as adjunct therapies. Persistent hypotension requires aggressive fluid resuscitation and possibly vasopressor support.
For local reactions, treatment is supportive and includes removal of the stinger (preferably by scraping rather than squeezing to avoid further venom release), application of cold compresses, limb elevation, and use of oral or topical antihistamines or corticosteroids. Pain control and avoidance of constrictive items such as rings or tight clothing are also important.
Patients with systemic reactions should be observed for at least 6 hours, while those with severe or life-threatening reactions may require admission and prolonged monitoring. Discharge is appropriate for patients with mild local reactions or resolved systemic symptoms after observation. Importantly, individuals who experience systemic reactions should be prescribed an epinephrine auto-injector and referred to an allergist for further evaluation and possible immunotherapy.
A key clinical point is that most fatal outcomes occur within the first hour due to airway compromise or circulatory collapse. Rapid recognition and early administration of epinephrine are critical. Patients with a history of severe reactions must be educated on avoidance strategies and emergency self-treatment to reduce the risk of recurrence.
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Emergency and Acute Medicine: Stevens–Johnson Syndrome
Stevens–Johnson syndrome (SJS) is a rare but severe mucocutaneous disorder characterized by widespread skin and mucosal injury. It involves blistering and epidermal detachment affecting less than 10% of the body surface area, distinguishing it from more extensive conditions such as toxic epidermal necrolysis. The disease almost always involves mucous membranes, typically affecting at least two sites such as the oral cavity, eyes, or genitalia. Skin lesions often begin on the face, neck, and trunk and may rapidly become confluent over hours to days. Although part of a spectrum with toxic epidermal necrolysis, SJS is considered a distinct clinical entity.
The condition is most commonly triggered by medications or infections. Drugs such as antibiotics (especially sulfonamides and penicillins), anticonvulsants, nonsteroidal anti-inflammatory drugs, and allopurinol are frequent culprits. Infectious causes include Mycoplasma pneumoniae and herpes simplex virus. The underlying mechanism involves an immune-mediated process in which cytotoxic T cells target keratinocytes expressing drug-related antigens, leading to widespread apoptosis of skin cells and systemic inflammation.
Patients typically present with a prodrome resembling a viral illness, occurring one to three days before the rash. Symptoms include fever, malaise, headache, upper respiratory symptoms, and sometimes joint or muscle pain. This is followed by skin tenderness, burning, and the development of erythematous or purpuric macules that may evolve into target-like lesions or flaccid blisters. These lesions can detach with slight pressure, demonstrating the Nikolsky sign. Painful mucosal involvement is a hallmark feature, leading to symptoms such as difficulty swallowing, urination discomfort, and eye irritation or conjunctivitis. Ocular involvement is common and may progress to serious complications such as corneal damage.
Diagnosis is primarily clinical and based on history, examination, and the extent of skin involvement. A careful medication history is crucial, as symptoms typically develop within two weeks of drug exposure, or more rapidly upon re-exposure. Laboratory tests may reveal nonspecific findings such as anemia or lymphopenia, while skin biopsy can confirm the diagnosis by showing full-thickness epidermal necrosis and subepidermal separation.
Management focuses on early recognition, withdrawal of the offending agent, and supportive care. Patients should be treated similarly to burn victims, especially those with significant skin involvement. Fluid resuscitation is essential due to fluid losses from denuded skin. Pain control is critical, as mucosal lesions can be extremely painful. Monitoring and treatment of secondary infections are vital, as sepsis—particularly from gram-negative organisms—is the leading cause of death. Advanced therapies such as intravenous immunoglobulin or corticosteroids may be considered, although their use remains controversial.
All patients with SJS require hospital admission, and those with extensive skin involvement should be managed in a burn unit or intensive care setting. Airway protection and ventilatory support may be necessary in severe cases. Long-term follow-up is important, particularly for ocular and dermatologic complications. Patients must be clearly educated about the causative drug and advised to avoid it permanently, as re-exposure can lead to rapid and more severe recurrence.
A key challenge is early recognition, as SJS often begins with nonspecific flu-like symptoms. Clinicians must maintain a high index of suspicion in patients presenting with mucocutaneous lesions and recent drug exposure. Prompt diagnosis and aggressive supportive care significantly improve outcomes.
Stevens–Johnson syndrome (SJS) is a rare but severe mucocutaneous disorder characterized by widespread skin and mucosal injury. It involves blistering and epidermal detachment affecting less than 10% of the body surface area, distinguishing it from more extensive conditions such as toxic epidermal necrolysis. The disease almost always involves mucous membranes, typically affecting at least two sites such as the oral cavity, eyes, or genitalia. Skin lesions often begin on the face, neck, and trunk and may rapidly become confluent over hours to days. Although part of a spectrum with toxic epidermal necrolysis, SJS is considered a distinct clinical entity.
The condition is most commonly triggered by medications or infections. Drugs such as antibiotics (especially sulfonamides and penicillins), anticonvulsants, nonsteroidal anti-inflammatory drugs, and allopurinol are frequent culprits. Infectious causes include Mycoplasma pneumoniae and herpes simplex virus. The underlying mechanism involves an immune-mediated process in which cytotoxic T cells target keratinocytes expressing drug-related antigens, leading to widespread apoptosis of skin cells and systemic inflammation.
Patients typically present with a prodrome resembling a viral illness, occurring one to three days before the rash. Symptoms include fever, malaise, headache, upper respiratory symptoms, and sometimes joint or muscle pain. This is followed by skin tenderness, burning, and the development of erythematous or purpuric macules that may evolve into target-like lesions or flaccid blisters. These lesions can detach with slight pressure, demonstrating the Nikolsky sign. Painful mucosal involvement is a hallmark feature, leading to symptoms such as difficulty swallowing, urination discomfort, and eye irritation or conjunctivitis. Ocular involvement is common and may progress to serious complications such as corneal damage.
Diagnosis is primarily clinical and based on history, examination, and the extent of skin involvement. A careful medication history is crucial, as symptoms typically develop within two weeks of drug exposure, or more rapidly upon re-exposure. Laboratory tests may reveal nonspecific findings such as anemia or lymphopenia, while skin biopsy can confirm the diagnosis by showing full-thickness epidermal necrosis and subepidermal separation.
Management focuses on early recognition, withdrawal of the offending agent, and supportive care. Patients should be treated similarly to burn victims, especially those with significant skin involvement. Fluid resuscitation is essential due to fluid losses from denuded skin. Pain control is critical, as mucosal lesions can be extremely painful. Monitoring and treatment of secondary infections are vital, as sepsis—particularly from gram-negative organisms—is the leading cause of death. Advanced therapies such as intravenous immunoglobulin or corticosteroids may be considered, although their use remains controversial.
All patients with SJS require hospital admission, and those with extensive skin involvement should be managed in a burn unit or intensive care setting. Airway protection and ventilatory support may be necessary in severe cases. Long-term follow-up is important, particularly for ocular and dermatologic complications. Patients must be clearly educated about the causative drug and advised to avoid it permanently, as re-exposure can lead to rapid and more severe recurrence.
A key challenge is early recognition, as SJS often begins with nonspecific flu-like symptoms. Clinicians must maintain a high index of suspicion in patients presenting with mucocutaneous lesions and recent drug exposure. Prompt diagnosis and aggressive supportive care significantly improve outcomes.
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Emergency and Acute Medicine: Sporotrichosis
Sporotrichosis is a subacute or chronic fungal infection caused by Sporothrix schenckii, a dimorphic organism found in soil, decaying vegetation, and organic matter. Infection typically occurs through traumatic inoculation into the skin, such as via thorns or splinters, or through animal scratches—particularly from cats. Less commonly, inhalation of fungal spores can lead to pulmonary disease. The condition is classically associated with occupational exposure among farmers, gardeners, and forestry workers, and is more severe in immunocompromised individuals.
The most common form is lymphocutaneous sporotrichosis, which begins as a painless papule at the site of inoculation that gradually enlarges into a nodule and may ulcerate. Over time, additional nodular lesions develop along the draining lymphatic channels, forming a characteristic chain-like pattern. These lesions are typically nonpurulent and only mildly painful, and systemic symptoms are usually absent. A fixed cutaneous form may also occur, presenting as a localized plaque or verrucous lesion without lymphatic spread.
More severe disease occurs in extracutaneous forms, particularly in immunocompromised patients. Osteoarticular sporotrichosis presents as a chronic, indolent infection involving joints such as the knee, wrist, or elbow, often mimicking other causes of arthritis. Pulmonary sporotrichosis resembles tuberculosis, with symptoms including cough, fever, weight loss, and hemoptysis, and can be fatal if untreated. Disseminated disease may involve multiple organ systems, including skin, bones, central nervous system, and eyes, and is associated with significant morbidity and mortality.
Diagnosis relies on isolating the organism from clinical specimens such as tissue biopsy, aspirate, sputum, or synovial fluid. Histologic examination may reveal characteristic “cigar-shaped” yeast forms, although cultures remain the gold standard. Routine blood tests are not particularly helpful in cutaneous disease but may assist in evaluating systemic involvement. Imaging studies are guided by clinical presentation, such as chest radiographs in pulmonary disease or bone scans in suspected disseminated infection.
Treatment depends on the severity and extent of disease. For cutaneous and lymphocutaneous forms, oral itraconazole is the treatment of choice and is continued for several weeks after lesion resolution. Alternatives include terbinafine or saturated potassium iodide solution, although the latter is less well tolerated. Local heat therapy may be used in selected patients who cannot tolerate medications. More severe infections, including pulmonary, osteoarticular, and disseminated forms, require prolonged antifungal therapy, often starting with amphotericin B followed by itraconazole. Immunocompromised patients, particularly those with HIV, may require long-term suppressive therapy.
Patients with localized cutaneous disease can usually be managed as outpatients, whereas those with systemic involvement or immunosuppression require hospital admission and specialist care. Early recognition is important, as delayed diagnosis—especially in disseminated disease—can lead to poor outcomes. A key clinical clue is a history of exposure to soil, plant material, or cats in combination with nodular skin lesions tracking along lymphatics.
Sporotrichosis is a subacute or chronic fungal infection caused by Sporothrix schenckii, a dimorphic organism found in soil, decaying vegetation, and organic matter. Infection typically occurs through traumatic inoculation into the skin, such as via thorns or splinters, or through animal scratches—particularly from cats. Less commonly, inhalation of fungal spores can lead to pulmonary disease. The condition is classically associated with occupational exposure among farmers, gardeners, and forestry workers, and is more severe in immunocompromised individuals.
The most common form is lymphocutaneous sporotrichosis, which begins as a painless papule at the site of inoculation that gradually enlarges into a nodule and may ulcerate. Over time, additional nodular lesions develop along the draining lymphatic channels, forming a characteristic chain-like pattern. These lesions are typically nonpurulent and only mildly painful, and systemic symptoms are usually absent. A fixed cutaneous form may also occur, presenting as a localized plaque or verrucous lesion without lymphatic spread.
More severe disease occurs in extracutaneous forms, particularly in immunocompromised patients. Osteoarticular sporotrichosis presents as a chronic, indolent infection involving joints such as the knee, wrist, or elbow, often mimicking other causes of arthritis. Pulmonary sporotrichosis resembles tuberculosis, with symptoms including cough, fever, weight loss, and hemoptysis, and can be fatal if untreated. Disseminated disease may involve multiple organ systems, including skin, bones, central nervous system, and eyes, and is associated with significant morbidity and mortality.
Diagnosis relies on isolating the organism from clinical specimens such as tissue biopsy, aspirate, sputum, or synovial fluid. Histologic examination may reveal characteristic “cigar-shaped” yeast forms, although cultures remain the gold standard. Routine blood tests are not particularly helpful in cutaneous disease but may assist in evaluating systemic involvement. Imaging studies are guided by clinical presentation, such as chest radiographs in pulmonary disease or bone scans in suspected disseminated infection.
Treatment depends on the severity and extent of disease. For cutaneous and lymphocutaneous forms, oral itraconazole is the treatment of choice and is continued for several weeks after lesion resolution. Alternatives include terbinafine or saturated potassium iodide solution, although the latter is less well tolerated. Local heat therapy may be used in selected patients who cannot tolerate medications. More severe infections, including pulmonary, osteoarticular, and disseminated forms, require prolonged antifungal therapy, often starting with amphotericin B followed by itraconazole. Immunocompromised patients, particularly those with HIV, may require long-term suppressive therapy.
Patients with localized cutaneous disease can usually be managed as outpatients, whereas those with systemic involvement or immunosuppression require hospital admission and specialist care. Early recognition is important, as delayed diagnosis—especially in disseminated disease—can lead to poor outcomes. A key clinical clue is a history of exposure to soil, plant material, or cats in combination with nodular skin lesions tracking along lymphatics.
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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.
