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Emergency and Acute Medicine – Pediatric Apnea
Definition and Clinical Overview
Pediatric apnea is defined as the absence of effective respiratory airflow for ≥20 seconds or a shorter pause associated with bradycardia or oxygen desaturation. It represents a medical emergency that may signal underlying neurologic, respiratory, cardiac, metabolic, infectious, or traumatic pathology. Apnea may present as an isolated event or as part of an apparent life-threatening event (ALTE), which describes a clinical presentation rather than a definitive diagnosis.
Pathophysiologic Mechanisms
Central apnea results from impaired respiratory drive due to dysfunction of the brainstem or neuromuscular pathways. Obstructive apnea occurs when respiratory effort persists but airflow is blocked because of upper airway obstruction, often accompanied by paradoxical chest wall motion. Mixed apnea combines both mechanisms. ALTEs involve apnea associated with color change, altered tone, choking, or gagging and require careful evaluation to identify the underlying cause.
Etiologic Considerations
Apnea has a broad differential diagnosis. Infectious causes include sepsis, meningitis, encephalitis, pneumonia, pertussis, chlamydia, RSV, and other viral infections. Respiratory causes include enlarged tonsils or adenoids, vocal cord dysfunction, laryngotracheomalacia, vascular rings, foreign bodies, craniofacial abnormalities, and choanal atresia or stenosis, as well as functional airway collapse in premature or ill infants. Neurologic etiologies include seizures, intracranial hemorrhage, increased intracranial pressure, tumors, congenital CNS malformations, and hypoxic injury. Cardiac causes include dysrhythmias, congenital heart disease, myocarditis, cardiomyopathy, and heart failure. Gastrointestinal causes include gastroesophageal reflux, volvulus, and intussusception. Additional considerations include ingestions or toxins, metabolic and endocrine disorders, neuromuscular disease, child abuse, transient choking episodes, laryngospasm, periodic breathing, and breath-holding spells.
Clinical Presentation
Apnea may be ongoing, reported historically, or impending. The presentation may range from brief self-limited events to prolonged respiratory arrest requiring immediate intervention.
History Assessment
Key elements include duration and frequency of apnea, state at onset (sleeping, awake, crying), relationship to feeding or positioning, degree of respiratory effort, presence and distribution of color change, eye position, abnormal movements or tone changes, and caregiver interventions. Antecedent symptoms such as fever, cough, or trauma should be elicited, along with prior medical history including prematurity, cardiopulmonary disease, neurologic disorders, gastrointestinal conditions, and prior ALTEs in the patient or family.
Physical Examination
Evaluation includes vital signs with temperature, growth trends, and continuous pulse oximetry. Airway and lung examination should assess for stridor, abnormal respiratory rates, accessory muscle use, and adventitious sounds. Cardiac examination focuses on rhythm abnormalities, murmurs, and signs of heart failure. A focused neurologic examination assesses mental status, tone, reflexes, seizure activity, signs of trauma, and funduscopic findings.
Initial Evaluation Priorities
A complete history and physical examination guide diagnostic testing and management. Immediate priorities include ensuring airway patency, clearing secretions or obstructions, and maintaining proper head and neck positioning, especially when occult trauma is a concern.
Diagnostic Studies
Laboratory evaluation is directed by clinical presentation and may include bedside glucose, CBC, urinalysis, blood, urine, and CSF cultures, CSF analysis, electrolytes including calcium, renal function tests, blood gas analysis, respiratory viral testing, pertussis and chlamydia studies, toxicology screening, liver function tests, and ammonia levels. Imaging may include chest radiography, head CT or MRI, ECG, and GI studies when indicated. EEG or polysomnography is typically reserved for follow-up evaluation. Skeletal survey should be considered when nonaccidental trauma is suspected.
Differential Diagnosis
The differential diagnosis is extensive and reflects the wide range of etiologies. Breath-holding spells are reflexive expiratory events seen in otherwise healthy children. Periodic breathing may be a normal finding in neonates. In newborns, occult infection—particularly sepsis—must always be strongly considered.
Prehospital and Emergency Management
If apnea is present, intervention must begin immediately. Management includes airway clearance, high-flow oxygen, bag-valve-mask ventilation, and endotracheal intubation if apnea persists. IV access and cardiac monitoring should be established, and empiric therapy initiated when indicated. Supportive care and caregiver counseling are essential components of management.
Disposition and Follow-Up
Most children with confirmed or suspected apnea require hospital admission for monitoring, particularly those with abnormal vital signs, concerning medical histories, or recurrent events. Intensive care is indicated for persistent instability. Discharge may be considered only in carefully selected low-risk patients who remain asymptomatic during observation and have reliable caregivers and clearly defined follow-up. Referral to primary care and appropriate subspecialists should be based on the suspected etiology.
Key Clinical Considerations and Common Pitfalls
Always maintain a high index of suspicion for hidden infection, especially neonatal sepsis. Unexplained apnea should also prompt careful evaluation for unrecognized trauma, as presentations may be subtle and easily overlooked.
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Emergency And Acute Medicine – Aphthous Ulcers
Overview:
Painful, ovoid or round ulcerations of the mucous membranes of the mouth, tongue, or genitals, commonly referred to as canker sores.
Etiology And Risk Factors:
The cause is unknown and likely multifactorial. Associations include immunologic dysfunction with altered cell-mediated immunity, infections, food hypersensitivities (e.g., gluten), vitamin deficiencies, pregnancy, menstruation, trauma, stress, ethnicity, immunodeficiency, and medications such as β-blockers and anti-inflammatory agents. Aphthous ulcers most commonly affect children and young adults, with peak onset between 10–19 years. They are the most common inflammatory ulcerative condition of the oral cavity, affecting 20–40% of the population, occur more frequently in women, and may be familial.
Clinical Features:
Minor aphthous ulcers account for 70–90% of cases and are typically <5 mm in diameter, painful, shallow, with necrotic centers, raised margins, erythematous halos, and a gray-white pseudomembrane. they affect non-keratinized mucosa of the anterior oral cavity heal within 10–14 days without scarring.< />pan>
Major aphthous ulcers (Sutton disease) are larger, deeper, more painful, last weeks to months, may scar, and are often associated with systemic disease.
Herpetiform aphthous ulcers present as clusters of numerous small ulcers that may coalesce; despite appearance, herpes simplex virus is not isolated.
History And Examination:
Patients often report a prodrome of burning or pricking 1–2 days before ulcer appearance. History should explore autoimmune disease, inflammatory bowel disease, Behçet disease, reactive arthritis, gluten sensitivity, HIV, malignancy, sexual history, and medication use. Examination focuses on oral lesions, hydration status, secondary infection, and signs of systemic disease.
Evaluation:
Diagnosis is clinical. Further workup is reserved for ulcers persisting longer than three weeks, recurrent severe disease, or associated systemic symptoms. Directed laboratory testing and biopsy may be indicated based on clinical suspicion.
Differential Considerations:
Trauma, medication reactions, viral and bacterial infections, erythema multiforme, autoimmune disease, inflammatory bowel disease, hematologic disorders, and malignancy must be considered, particularly in atypical or persistent cases.
Management Approach:
Treatment is guided by severity and duration, with the primary goal of pain control and inflammation reduction.
Therapeutic Options:
Mild to moderate disease is managed with avoidance of oral trauma and acidic foods, topical anesthetics, protective bioadhesives, topical anti-inflammatory agents, and antimicrobial mouth rinses.
Severe disease may require short courses of systemic corticosteroids or, in refractory cases, specialist-guided immunomodulatory therapy.
Disposition And Follow-Up:
Admission is reserved for patients unable to maintain oral intake, those with dehydration, or abnormal vital signs. Most patients may be discharged once pain is controlled and fluids are tolerated. Persistent lesions beyond two weeks warrant outpatient follow-up and further evaluation.
Clinical Pearls And Pitfalls:
Most aphthous ulcers are benign and self-limited, requiring only symptomatic care. Emergency clinicians should remain vigilant for underlying systemic disease in patients with severe, atypical, or persistent ulcerations.
Overview:
Painful, ovoid or round ulcerations of the mucous membranes of the mouth, tongue, or genitals, commonly referred to as canker sores.
Etiology And Risk Factors:
The cause is unknown and likely multifactorial. Associations include immunologic dysfunction with altered cell-mediated immunity, infections, food hypersensitivities (e.g., gluten), vitamin deficiencies, pregnancy, menstruation, trauma, stress, ethnicity, immunodeficiency, and medications such as β-blockers and anti-inflammatory agents. Aphthous ulcers most commonly affect children and young adults, with peak onset between 10–19 years. They are the most common inflammatory ulcerative condition of the oral cavity, affecting 20–40% of the population, occur more frequently in women, and may be familial.
Clinical Features:
Minor aphthous ulcers account for 70–90% of cases and are typically <5 mm in diameter, painful, shallow, with necrotic centers, raised margins, erythematous halos, and a gray-white pseudomembrane. they affect non-keratinized mucosa of the anterior oral cavity heal within 10–14 days without scarring.< />pan>
Major aphthous ulcers (Sutton disease) are larger, deeper, more painful, last weeks to months, may scar, and are often associated with systemic disease.
Herpetiform aphthous ulcers present as clusters of numerous small ulcers that may coalesce; despite appearance, herpes simplex virus is not isolated.
History And Examination:
Patients often report a prodrome of burning or pricking 1–2 days before ulcer appearance. History should explore autoimmune disease, inflammatory bowel disease, Behçet disease, reactive arthritis, gluten sensitivity, HIV, malignancy, sexual history, and medication use. Examination focuses on oral lesions, hydration status, secondary infection, and signs of systemic disease.
Evaluation:
Diagnosis is clinical. Further workup is reserved for ulcers persisting longer than three weeks, recurrent severe disease, or associated systemic symptoms. Directed laboratory testing and biopsy may be indicated based on clinical suspicion.
Differential Considerations:
Trauma, medication reactions, viral and bacterial infections, erythema multiforme, autoimmune disease, inflammatory bowel disease, hematologic disorders, and malignancy must be considered, particularly in atypical or persistent cases.
Management Approach:
Treatment is guided by severity and duration, with the primary goal of pain control and inflammation reduction.
Therapeutic Options:
Mild to moderate disease is managed with avoidance of oral trauma and acidic foods, topical anesthetics, protective bioadhesives, topical anti-inflammatory agents, and antimicrobial mouth rinses.
Severe disease may require short courses of systemic corticosteroids or, in refractory cases, specialist-guided immunomodulatory therapy.
Disposition And Follow-Up:
Admission is reserved for patients unable to maintain oral intake, those with dehydration, or abnormal vital signs. Most patients may be discharged once pain is controlled and fluids are tolerated. Persistent lesions beyond two weeks warrant outpatient follow-up and further evaluation.
Clinical Pearls And Pitfalls:
Most aphthous ulcers are benign and self-limited, requiring only symptomatic care. Emergency clinicians should remain vigilant for underlying systemic disease in patients with severe, atypical, or persistent ulcerations.
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Emergency And Acute Medicine – Traumatic Aortic Rupture (Traumatic Aortic Injury)
Core Overview:
Traumatic aortic rupture, also termed traumatic aortic injury (TAI), is responsible for approximately 20% of deaths from fatal motor vehicle collisions. Nearly 85% of affected patients die at the scene. Those who reach the emergency department typically have a contained rupture, with hemorrhage temporarily tamponaded by the adventitia. Without intervention, mortality remains extremely high: nearly half die within 24 hours and up to 90% within four months. The mean patient age is 33 years, with a strong male predominance. Aortic tears are most often transverse and may be partial or circumferential.
Mechanisms Of Injury:
High-speed motor vehicle collisions exceeding 30 mph are the most common cause, particularly involving unrestrained occupants, drivers impacted by the steering column, or ejected passengers. Other mechanisms include pedestrian–vehicle collisions, aviation crashes, falls greater than 10 feet, blast injuries, crush injuries, and direct chest trauma. Proposed pathophysiologic mechanisms include shear stress from rapid deceleration between the fixed descending aorta and mobile arch, bending forces at the aortic isthmus, torsional stretching of the arch, compression between osseous structures and the vertebral column, and acute intravascular pressure surges (“waterhammer” effect).
Clinical Presentation:
Despite the severity of injury, manifestations are frequently subtle or absent, especially in polytrauma patients. Up to half have no external signs of chest trauma. Substernal chest pain occurs in only about one-quarter of cases. Dyspnea, hoarseness, and stridor may result from mediastinal hematoma compressing adjacent structures. Examination findings are neither sensitive nor specific. Patients may exhibit hypertension due to sympathetic stimulation, a harsh systolic murmur, signs of distal ischemia, oliguria, paraplegia, or neck base swelling. Acute coarctation physiology may develop, producing upper-extremity hypertension with reduced lower-extremity pressures.
Initial Evaluation Priorities:
Plain chest radiography is the primary screening tool and is highly sensitive, though poorly specific. A widened mediastinum is the most sensitive radiographic sign. Because false-negative radiographs occur in up to 10% of cases, high-risk mechanisms warrant advanced imaging even with a normal chest x-ray.
Diagnostic Assessment:
Laboratory studies include CBC, chemistry panel, coagulation studies, and type and crossmatch.
Chest radiography findings may include mediastinal widening, obscured aortic knob, left apical cap, abnormal paratracheal stripes, or displaced nasogastric tube.
CT angiography of the chest is the preferred confirmatory test in hemodynamically stable patients, with near-perfect sensitivity and specificity, and has largely replaced aortography.
Transesophageal echocardiography can be performed rapidly in the ED and is useful when CT is not immediately available. MRI and intravascular ultrasound are accurate but limited by availability and monitoring constraints.
Important Diagnostic Alternatives:
False-positive mediastinal widening on supine films, mediastinal hematoma from non-aortic sources, mediastinal tumors or lymphadenopathy, and age-related or hypertensive aortic tortuosity.
Prehospital Considerations:
Key scene details include collision speed, restraint use, steering column damage, and whether the patient was ejected.
Early Stabilization Strategy:
Follow standard trauma protocols with priority given to life-threatening intracranial, intra-abdominal, or retroperitoneal injuries. Establish IV access and initiate monitoring promptly.
Definitive Emergency Management:
Immediate trauma and cardiothoracic or vascular surgery consultation is mandatory. Avoid actions that increase intrathoracic pressure. Aggressive control of heart rate and blood pressure is critical to minimize shearing forces and prevent rupture progression. Target heart rate is approximately 60 bpm with systolic blood pressure between 100–120 mm Hg. β-blockers are first-line agents, with calcium-channel blockers as alternatives when β-blockade is contraindicated. Vasodilators may be added only after adequate negative inotropy is achieved. Hypotension should be treated with blood products and vasopressors as needed.
Disposition Planning:
All patients with traumatic aortic injury require ICU admission or immediate operative management.
Clinical Pearls And Pitfalls:
Maintain a high index of suspicion for traumatic aortic injury in any patient exposed to rapid deceleration mechanisms, even when symptoms are minimal or absent. Physical findings are unreliable, making imaging essential for diagnosis. Careful evaluation of the mediastinum on chest radiography is critical, but a normal x-ray does not exclude injury. Early, controlled reduction of heart rate and blood pressure significantly lowers the risk of sudden rupture and improves outcomes once the diagnosis is established.
Core Overview:
Traumatic aortic rupture, also termed traumatic aortic injury (TAI), is responsible for approximately 20% of deaths from fatal motor vehicle collisions. Nearly 85% of affected patients die at the scene. Those who reach the emergency department typically have a contained rupture, with hemorrhage temporarily tamponaded by the adventitia. Without intervention, mortality remains extremely high: nearly half die within 24 hours and up to 90% within four months. The mean patient age is 33 years, with a strong male predominance. Aortic tears are most often transverse and may be partial or circumferential.
Mechanisms Of Injury:
High-speed motor vehicle collisions exceeding 30 mph are the most common cause, particularly involving unrestrained occupants, drivers impacted by the steering column, or ejected passengers. Other mechanisms include pedestrian–vehicle collisions, aviation crashes, falls greater than 10 feet, blast injuries, crush injuries, and direct chest trauma. Proposed pathophysiologic mechanisms include shear stress from rapid deceleration between the fixed descending aorta and mobile arch, bending forces at the aortic isthmus, torsional stretching of the arch, compression between osseous structures and the vertebral column, and acute intravascular pressure surges (“waterhammer” effect).
Clinical Presentation:
Despite the severity of injury, manifestations are frequently subtle or absent, especially in polytrauma patients. Up to half have no external signs of chest trauma. Substernal chest pain occurs in only about one-quarter of cases. Dyspnea, hoarseness, and stridor may result from mediastinal hematoma compressing adjacent structures. Examination findings are neither sensitive nor specific. Patients may exhibit hypertension due to sympathetic stimulation, a harsh systolic murmur, signs of distal ischemia, oliguria, paraplegia, or neck base swelling. Acute coarctation physiology may develop, producing upper-extremity hypertension with reduced lower-extremity pressures.
Initial Evaluation Priorities:
Plain chest radiography is the primary screening tool and is highly sensitive, though poorly specific. A widened mediastinum is the most sensitive radiographic sign. Because false-negative radiographs occur in up to 10% of cases, high-risk mechanisms warrant advanced imaging even with a normal chest x-ray.
Diagnostic Assessment:
Laboratory studies include CBC, chemistry panel, coagulation studies, and type and crossmatch.
Chest radiography findings may include mediastinal widening, obscured aortic knob, left apical cap, abnormal paratracheal stripes, or displaced nasogastric tube.
CT angiography of the chest is the preferred confirmatory test in hemodynamically stable patients, with near-perfect sensitivity and specificity, and has largely replaced aortography.
Transesophageal echocardiography can be performed rapidly in the ED and is useful when CT is not immediately available. MRI and intravascular ultrasound are accurate but limited by availability and monitoring constraints.
Important Diagnostic Alternatives:
False-positive mediastinal widening on supine films, mediastinal hematoma from non-aortic sources, mediastinal tumors or lymphadenopathy, and age-related or hypertensive aortic tortuosity.
Prehospital Considerations:
Key scene details include collision speed, restraint use, steering column damage, and whether the patient was ejected.
Early Stabilization Strategy:
Follow standard trauma protocols with priority given to life-threatening intracranial, intra-abdominal, or retroperitoneal injuries. Establish IV access and initiate monitoring promptly.
Definitive Emergency Management:
Immediate trauma and cardiothoracic or vascular surgery consultation is mandatory. Avoid actions that increase intrathoracic pressure. Aggressive control of heart rate and blood pressure is critical to minimize shearing forces and prevent rupture progression. Target heart rate is approximately 60 bpm with systolic blood pressure between 100–120 mm Hg. β-blockers are first-line agents, with calcium-channel blockers as alternatives when β-blockade is contraindicated. Vasodilators may be added only after adequate negative inotropy is achieved. Hypotension should be treated with blood products and vasopressors as needed.
Disposition Planning:
All patients with traumatic aortic injury require ICU admission or immediate operative management.
Clinical Pearls And Pitfalls:
Maintain a high index of suspicion for traumatic aortic injury in any patient exposed to rapid deceleration mechanisms, even when symptoms are minimal or absent. Physical findings are unreliable, making imaging essential for diagnosis. Careful evaluation of the mediastinum on chest radiography is critical, but a normal x-ray does not exclude injury. Early, controlled reduction of heart rate and blood pressure significantly lowers the risk of sudden rupture and improves outcomes once the diagnosis is established.
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Emergency And Acute Medicine – Thoracic Aortic Dissection
Foundational Overview: Thoracic aortic dissection begins with an intimal tear, allowing blood to enter and propagate through the aortic media under systolic pressure. Systemic hypertension is the dominant precipitating factor. Dissection may extend distally to involve carotid, subclavian, or visceral branches, or proximally to affect the aortic root, coronary ostia, and pericardium. Proximal extension may result in coronary artery occlusion, acute aortic regurgitation, or cardiac tamponade.
Anatomic Classification:
Stanford system: Type A involves the ascending aorta; Type B originates distal to the ascending aorta.
DeBakey system: Type I begins at the aortic root or arch, Type II is confined to the ascending aorta, and Type III originates distal to the left subclavian artery.
Peak incidence occurs at 50–55 years for proximal dissections and 60–70 years for distal dissections. Pregnancy markedly increases risk; in women younger than 40 years, up to half of dissections occur during pregnancy.
Predisposing Causes:
Any condition that weakens aortic wall integrity may lead to dissection. Common factors include chronic hypertension, congenital heart disease (bicuspid aortic valve, coarctation), cystic medial degeneration, connective tissue disorders (Marfan syndrome, Ehlers–Danlos), pregnancy, vasculitides (e.g., lupus, syphilis, giant cell arteritis, Takayasu arteritis), prior cardiac surgery (CABG or valve repair), and tobacco use.
Clinical Presentation:
Pain is classically abrupt, severe, and sharp, though absent in up to 15% of patients. Ascending dissections often cause substernal pain, descending dissections interscapular pain, and abdominal involvement lumbar pain. Combined chest, back, and abdominal pain is common. Neurologic manifestations may include visual changes or focal deficits. Atypical symptoms—syncope, fever, nausea, vomiting, leg pain, or altered mental status—may delay diagnosis. Older adults are less likely to report sudden pain, pulse deficits, or aortic regurgitation and have higher mortality.
Examination Findings:
Hypertension is common, though 35–40% may be normotensive. Pulse or blood pressure differentials between limbs suggest branch vessel involvement. A murmur of acute aortic regurgitation (often musical or vibrating) is heard in up to one-third of patients. Shock may occur from tamponade or myocardial infarction due to coronary artery involvement. Presentations may mimic heart failure, limb ischemia, or stroke.
Immediate Assessment Priorities:
Electrocardiography helps evaluate ischemia or infarction; inferior MI may result from right coronary artery involvement. A normal ECG in the setting of sudden, severe chest or back pain should heighten suspicion for dissection rather than ischemia.
Diagnostic Evaluation:
Laboratory findings are nonspecific and may include leukocytosis, hematuria, elevated creatinine, increased amylase from bowel ischemia, or elevated cardiac enzymes. A D-dimer below 500 ng/mL reduces likelihood but is insufficient as a sole screening test.
Chest radiography may show mediastinal widening, abnormal aortic contour, or cardiomegaly from hemopericardium, though up to 18% of films are normal.
Echocardiography identifies complications; transesophageal echocardiography is useful in unstable patients.
CT angiography is the diagnostic modality of choice in most centers due to high sensitivity and rapid availability. MRI offers excellent accuracy but limited emergency access. Aortography and cardiac catheterization are now rarely first-line but may reveal an intimal flap during evaluation for ischemia.
Key Diagnostic Alternatives:
Acute coronary syndrome, unstable angina, pneumothorax, esophageal rupture, pulmonary embolism, pericarditis, pneumonia, and musculoskeletal pain.
Prehospital Care:
Provide oxygen, establish IV access, and initiate monitoring.
Early Stabilization:
Secure two large-bore IV lines, apply continuous cardiac monitoring and pulse oximetry, administer oxygen, and prepare blood for crossmatching.
Definitive Emergency Management:
Rapid blood pressure and heart rate control are essential to reduce aortic shear stress. Initiate IV β-blockade (esmolol or labetalol) before vasodilators. Nitroprusside may be added once adequate β-blockade is established.
Type A dissections require emergent cardiothoracic surgery. Stable Type B dissections are managed medically unless complications develop.
Pharmacologic Therapy:
Esmolol IV bolus followed by infusion or labetalol IV bolus and drip for rate and pressure control. Nitroprusside infusion may be titrated carefully in conjunction with β-blockade.
Disposition Planning:
All patients with acute thoracic aortic dissection require ICU admission and immediate cardiothoracic surgical consultation. There are no discharge candidates from the ED.
Follow-Up Strategy:
Long-term management requires close cardiology and cardiothoracic surgery follow-up.
Clinical Pearls And Pitfalls:
Ascending aortic dissection carries an untreated mortality approaching 75% within two weeks, with death rates of 1–3% per hour during the first 48 hours. Most patients experience sudden-onset, severe pain, but atypical presentations are common. Thrombolytics and anticoagulants may be fatal if dissection is misdiagnosed as myocardial infarction or pulmonary embolism. Maintain a high index of suspicion in patients with refractory chest pain or chest pain accompanied by neurologic, back, abdominal, or limb symptoms, particularly in the presence of hypertension, male sex, advanced age, pregnancy, cocaine use, connective tissue disease, bicuspid aortic valve, or prior cardiac surgery.
Foundational Overview: Thoracic aortic dissection begins with an intimal tear, allowing blood to enter and propagate through the aortic media under systolic pressure. Systemic hypertension is the dominant precipitating factor. Dissection may extend distally to involve carotid, subclavian, or visceral branches, or proximally to affect the aortic root, coronary ostia, and pericardium. Proximal extension may result in coronary artery occlusion, acute aortic regurgitation, or cardiac tamponade.
Anatomic Classification:
Stanford system: Type A involves the ascending aorta; Type B originates distal to the ascending aorta.
DeBakey system: Type I begins at the aortic root or arch, Type II is confined to the ascending aorta, and Type III originates distal to the left subclavian artery.
Peak incidence occurs at 50–55 years for proximal dissections and 60–70 years for distal dissections. Pregnancy markedly increases risk; in women younger than 40 years, up to half of dissections occur during pregnancy.
Predisposing Causes:
Any condition that weakens aortic wall integrity may lead to dissection. Common factors include chronic hypertension, congenital heart disease (bicuspid aortic valve, coarctation), cystic medial degeneration, connective tissue disorders (Marfan syndrome, Ehlers–Danlos), pregnancy, vasculitides (e.g., lupus, syphilis, giant cell arteritis, Takayasu arteritis), prior cardiac surgery (CABG or valve repair), and tobacco use.
Clinical Presentation:
Pain is classically abrupt, severe, and sharp, though absent in up to 15% of patients. Ascending dissections often cause substernal pain, descending dissections interscapular pain, and abdominal involvement lumbar pain. Combined chest, back, and abdominal pain is common. Neurologic manifestations may include visual changes or focal deficits. Atypical symptoms—syncope, fever, nausea, vomiting, leg pain, or altered mental status—may delay diagnosis. Older adults are less likely to report sudden pain, pulse deficits, or aortic regurgitation and have higher mortality.
Examination Findings:
Hypertension is common, though 35–40% may be normotensive. Pulse or blood pressure differentials between limbs suggest branch vessel involvement. A murmur of acute aortic regurgitation (often musical or vibrating) is heard in up to one-third of patients. Shock may occur from tamponade or myocardial infarction due to coronary artery involvement. Presentations may mimic heart failure, limb ischemia, or stroke.
Immediate Assessment Priorities:
Electrocardiography helps evaluate ischemia or infarction; inferior MI may result from right coronary artery involvement. A normal ECG in the setting of sudden, severe chest or back pain should heighten suspicion for dissection rather than ischemia.
Diagnostic Evaluation:
Laboratory findings are nonspecific and may include leukocytosis, hematuria, elevated creatinine, increased amylase from bowel ischemia, or elevated cardiac enzymes. A D-dimer below 500 ng/mL reduces likelihood but is insufficient as a sole screening test.
Chest radiography may show mediastinal widening, abnormal aortic contour, or cardiomegaly from hemopericardium, though up to 18% of films are normal.
Echocardiography identifies complications; transesophageal echocardiography is useful in unstable patients.
CT angiography is the diagnostic modality of choice in most centers due to high sensitivity and rapid availability. MRI offers excellent accuracy but limited emergency access. Aortography and cardiac catheterization are now rarely first-line but may reveal an intimal flap during evaluation for ischemia.
Key Diagnostic Alternatives:
Acute coronary syndrome, unstable angina, pneumothorax, esophageal rupture, pulmonary embolism, pericarditis, pneumonia, and musculoskeletal pain.
Prehospital Care:
Provide oxygen, establish IV access, and initiate monitoring.
Early Stabilization:
Secure two large-bore IV lines, apply continuous cardiac monitoring and pulse oximetry, administer oxygen, and prepare blood for crossmatching.
Definitive Emergency Management:
Rapid blood pressure and heart rate control are essential to reduce aortic shear stress. Initiate IV β-blockade (esmolol or labetalol) before vasodilators. Nitroprusside may be added once adequate β-blockade is established.
Type A dissections require emergent cardiothoracic surgery. Stable Type B dissections are managed medically unless complications develop.
Pharmacologic Therapy:
Esmolol IV bolus followed by infusion or labetalol IV bolus and drip for rate and pressure control. Nitroprusside infusion may be titrated carefully in conjunction with β-blockade.
Disposition Planning:
All patients with acute thoracic aortic dissection require ICU admission and immediate cardiothoracic surgical consultation. There are no discharge candidates from the ED.
Follow-Up Strategy:
Long-term management requires close cardiology and cardiothoracic surgery follow-up.
Clinical Pearls And Pitfalls:
Ascending aortic dissection carries an untreated mortality approaching 75% within two weeks, with death rates of 1–3% per hour during the first 48 hours. Most patients experience sudden-onset, severe pain, but atypical presentations are common. Thrombolytics and anticoagulants may be fatal if dissection is misdiagnosed as myocardial infarction or pulmonary embolism. Maintain a high index of suspicion in patients with refractory chest pain or chest pain accompanied by neurologic, back, abdominal, or limb symptoms, particularly in the presence of hypertension, male sex, advanced age, pregnancy, cocaine use, connective tissue disease, bicuspid aortic valve, or prior cardiac surgery.
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Emergency And Acute Medicine – Antidepressant Poisoning
Core Overview: Antidepressants are among the most commonly prescribed psychiatric medications in the United States. Overdose presentations often involve selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), or atypical antidepressants, frequently in combination with atypical antipsychotics or mood stabilizers. These agents are also prescribed for chronic pain, anxiety disorders, eating disorders, substance use disorders, and sleep disturbances. Tricyclic antidepressants are discussed separately.
Mechanisms And Causes:
SSRIs increase synaptic serotonin by inhibiting presynaptic reuptake (e.g., fluoxetine, paroxetine, sertraline, citalopram, escitalopram).
SNRIs inhibit reuptake of both serotonin and norepinephrine (e.g., venlafaxine, desvenlafaxine, duloxetine) and may be more toxic in overdose than initially assumed.
Atypical antidepressants have variable effects on serotonin, norepinephrine, and dopamine and include bupropion, trazodone, and mirtazapine.
Atypical antipsychotics act primarily on dopamine receptors with additional serotonergic, α-adrenergic, histaminic, and muscarinic effects. Many psychiatric medications can block potassium and sodium channels, resulting in QT or QRS prolongation and cardiotoxicity.
Clinical Features:
SSRIs commonly cause sedation and serotonin syndrome; most are benign in single-agent overdose, except citalopram and escitalopram, which may cause QTc prolongation, seizures, and delayed toxicity up to 12 hours.
SNRIs may cause somnolence, vomiting, tachycardia, seizures, and QTc prolongation, especially with venlafaxine and desvenlafaxine.
Atypical antidepressants: bupropion is associated with seizures and QRS/QTc prolongation; trazodone causes sedation, hypotension, QTc prolongation, and priapism; mirtazapine causes sedation and QTc prolongation, with rare neutropenia in chronic use.
Atypical antipsychotics typically cause sedation, tachycardia, and miosis, with drug-specific risks such as agranulocytosis and cardiomyopathy (clozapine), anticholinergic delirium (olanzapine, quetiapine), hypotension (quetiapine), QTc prolongation (ziprasidone), or prolonged CNS effects (aripiprazole).
Initial Assessment: Determine the specific agents, dose, timing, and possible coingestants. Check bedside glucose in patients with altered mental status.
Diagnostic Evaluation:
Laboratory drug levels are rarely helpful acutely. Obtain ECG to assess QRS and QTc intervals. Order electrolytes, renal function, glucose, urine pregnancy test when appropriate, urine drug screen (limited impact on management), acetaminophen and salicylate levels, and serum ethanol. CT brain imaging is reserved for unexplained depressed mental status; chest radiograph is indicated if intubated or hypoxic.
Key Differentials: TCA toxicity, ethanol or sedative–hypnotic overdose, isoniazid toxicity, hypoglycemia, hypoxemia, electrolyte disturbances, withdrawal syndromes, serotonin syndrome, head trauma, opioid intoxication, mood stabilizer or antiepileptic overdose, and diabetic ketoacidosis.
Prehospital Priorities: Transport all medication containers with the patient. Support airway, breathing, and circulation. Administer IV fluids for hypotension and benzodiazepines for seizures.
Early Stabilization: Provide oxygen, continuous cardiac monitoring, IV access, and pulse oximetry. Intubate if airway protection is needed. Check rapid glucose; administer naloxone or dextrose as clinically indicated. Flumazenil is not recommended in mixed or unknown overdoses or in patients with seizure risk. Treat extrapyramidal symptoms with diphenhydramine or benztropine.
Emergency Department Management: Avoid GI decontamination if the airway is unprotected; do not intubate solely for charcoal. Activated charcoal may be considered early after ingestion. Treat QRS widening with IV sodium bicarbonate boluses (continuous infusions are ineffective). Manage hypotension refractory to fluids with norepinephrine rather than dopamine. Treat seizures with benzodiazepines, escalating to barbiturates if refractory. Address serotonin syndrome with benzodiazepines and active cooling.
Medication Options: Activated charcoal 50–75 g PO (up to 100 g); benzodiazepines (diazepam or lorazepam) for seizures/agitation; diphenhydramine or benztropine for EPS; naloxone as indicated; norepinephrine infusion for hypotension; phenobarbital for refractory seizures; sodium bicarbonate 1 mEq/kg IV bolus for QRS widening.
Disposition Planning:
Admit for 24-hour telemetry after ingestion of citalopram, escitalopram, venlafaxine, desvenlafaxine, or bupropion, even if initially asymptomatic. Admit patients with coma, persistent altered mental status, ECG abnormalities, hemodynamic instability, or neuroleptic malignant syndrome. Suicidal patients require 1:1 observation.
Asymptomatic patients more than 6 hours after ingestion of less toxic antidepressants may be medically cleared for psychiatric admission if not suicidal.
Follow-Up Care: Psychiatry referral is required for intentional overdoses.
Clinical Pearls And Pitfalls: Administer IV sodium bicarbonate promptly for QRS widening. Overdoses involving citalopram, venlafaxine, and bupropion are more likely to cause severe toxicity and delayed complications, warranting medical observation before psychiatric clearance.
Core Overview: Antidepressants are among the most commonly prescribed psychiatric medications in the United States. Overdose presentations often involve selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), or atypical antidepressants, frequently in combination with atypical antipsychotics or mood stabilizers. These agents are also prescribed for chronic pain, anxiety disorders, eating disorders, substance use disorders, and sleep disturbances. Tricyclic antidepressants are discussed separately.
Mechanisms And Causes:
SSRIs increase synaptic serotonin by inhibiting presynaptic reuptake (e.g., fluoxetine, paroxetine, sertraline, citalopram, escitalopram).
SNRIs inhibit reuptake of both serotonin and norepinephrine (e.g., venlafaxine, desvenlafaxine, duloxetine) and may be more toxic in overdose than initially assumed.
Atypical antidepressants have variable effects on serotonin, norepinephrine, and dopamine and include bupropion, trazodone, and mirtazapine.
Atypical antipsychotics act primarily on dopamine receptors with additional serotonergic, α-adrenergic, histaminic, and muscarinic effects. Many psychiatric medications can block potassium and sodium channels, resulting in QT or QRS prolongation and cardiotoxicity.
Clinical Features:
SSRIs commonly cause sedation and serotonin syndrome; most are benign in single-agent overdose, except citalopram and escitalopram, which may cause QTc prolongation, seizures, and delayed toxicity up to 12 hours.
SNRIs may cause somnolence, vomiting, tachycardia, seizures, and QTc prolongation, especially with venlafaxine and desvenlafaxine.
Atypical antidepressants: bupropion is associated with seizures and QRS/QTc prolongation; trazodone causes sedation, hypotension, QTc prolongation, and priapism; mirtazapine causes sedation and QTc prolongation, with rare neutropenia in chronic use.
Atypical antipsychotics typically cause sedation, tachycardia, and miosis, with drug-specific risks such as agranulocytosis and cardiomyopathy (clozapine), anticholinergic delirium (olanzapine, quetiapine), hypotension (quetiapine), QTc prolongation (ziprasidone), or prolonged CNS effects (aripiprazole).
Initial Assessment: Determine the specific agents, dose, timing, and possible coingestants. Check bedside glucose in patients with altered mental status.
Diagnostic Evaluation:
Laboratory drug levels are rarely helpful acutely. Obtain ECG to assess QRS and QTc intervals. Order electrolytes, renal function, glucose, urine pregnancy test when appropriate, urine drug screen (limited impact on management), acetaminophen and salicylate levels, and serum ethanol. CT brain imaging is reserved for unexplained depressed mental status; chest radiograph is indicated if intubated or hypoxic.
Key Differentials: TCA toxicity, ethanol or sedative–hypnotic overdose, isoniazid toxicity, hypoglycemia, hypoxemia, electrolyte disturbances, withdrawal syndromes, serotonin syndrome, head trauma, opioid intoxication, mood stabilizer or antiepileptic overdose, and diabetic ketoacidosis.
Prehospital Priorities: Transport all medication containers with the patient. Support airway, breathing, and circulation. Administer IV fluids for hypotension and benzodiazepines for seizures.
Early Stabilization: Provide oxygen, continuous cardiac monitoring, IV access, and pulse oximetry. Intubate if airway protection is needed. Check rapid glucose; administer naloxone or dextrose as clinically indicated. Flumazenil is not recommended in mixed or unknown overdoses or in patients with seizure risk. Treat extrapyramidal symptoms with diphenhydramine or benztropine.
Emergency Department Management: Avoid GI decontamination if the airway is unprotected; do not intubate solely for charcoal. Activated charcoal may be considered early after ingestion. Treat QRS widening with IV sodium bicarbonate boluses (continuous infusions are ineffective). Manage hypotension refractory to fluids with norepinephrine rather than dopamine. Treat seizures with benzodiazepines, escalating to barbiturates if refractory. Address serotonin syndrome with benzodiazepines and active cooling.
Medication Options: Activated charcoal 50–75 g PO (up to 100 g); benzodiazepines (diazepam or lorazepam) for seizures/agitation; diphenhydramine or benztropine for EPS; naloxone as indicated; norepinephrine infusion for hypotension; phenobarbital for refractory seizures; sodium bicarbonate 1 mEq/kg IV bolus for QRS widening.
Disposition Planning:
Admit for 24-hour telemetry after ingestion of citalopram, escitalopram, venlafaxine, desvenlafaxine, or bupropion, even if initially asymptomatic. Admit patients with coma, persistent altered mental status, ECG abnormalities, hemodynamic instability, or neuroleptic malignant syndrome. Suicidal patients require 1:1 observation.
Asymptomatic patients more than 6 hours after ingestion of less toxic antidepressants may be medically cleared for psychiatric admission if not suicidal.
Follow-Up Care: Psychiatry referral is required for intentional overdoses.
Clinical Pearls And Pitfalls: Administer IV sodium bicarbonate promptly for QRS widening. Overdoses involving citalopram, venlafaxine, and bupropion are more likely to cause severe toxicity and delayed complications, warranting medical observation before psychiatric clearance.
- Published on
Emergency And Acute Medicine - Anticholinergic Poisoning
Core Overview: Anticholinergic poisoning is caused by central and peripheral cholinergic blockade. Depending on the agent, antagonism may occur at muscarinic receptors (most common), nicotinic receptors, or both. Symptoms typically begin 15–30 minutes after ingestion, with effects lasting about 2–24 hours.
Common Causes: Many medications have anticholinergic properties that are usually mild at therapeutic doses but can become life-threatening in overdose. Frequent culprits include antihistamines, belladonna alkaloids and related compounds, antiparkinsonian agents, cyclic antidepressants, antipsychotics (neuroleptics), mydriatic eye drops, skeletal muscle relaxants (e.g., orphenadrine, cyclobenzaprine), antispasmodics, and certain mushrooms/plants (Amanita muscaria, Amanita pantherina, deadly nightshade, mandrake, henbane). Jimson weed may be smoked or ingested.
How It Presents: Clarify timing, dose, and exposure route. The classic toxidrome is often remembered as: “mad as a hatter” (delirium/AMS), “hot as a hare” (hyperthermia), “red as a beet” (flushed skin), “dry as a bone” (dry skin/mucosa), and “blind as a bat” (mydriasis with blurry vision). Findings may include hyperthermia and altered mental status; fixed mydriasis with loss of accommodation; sinus tachycardia, occasional dysrhythmias (typically only in massive ingestions), hypo/HTN, and rarely cardiogenic pulmonary edema; tachypnea or respiratory failure; decreased/absent bowel sounds, dysphagia, decreased GI motility, and reduced salivation; urinary retention; decreased sweating with dry, flushed skin; hallucinations, coma, or seizures.
Essential Evaluation: Diagnosis is clinical, based on toxidrome and a reliable exposure history when possible.
Recommended Tests: Obtain a urine toxicology screen if helpful for context; electrolytes, BUN/creatinine, glucose; CBC; CPK if rhabdomyolysis is a concern; urinalysis; and acetaminophen/salicylate levels to detect occult coingestions (e.g., combination nighttime products). ECG commonly shows sinus tachycardia; may reveal QRS prolongation, AV block, bundle branch block patterns, or dysrhythmias.
Key Differentials: Sympathomimetic intoxication, withdrawal syndromes, acute psychiatric conditions, sepsis, and thyroid disease.
Prehospital Actions: Bring all pills, bottles, and packaging to support accurate identification in the ED.
Immediate Stabilization: Prioritize ABCs—airway control can be critical. Provide supplemental oxygen, establish IV access, initiate cardiac monitoring and pulse oximetry, and consider naloxone, thiamine, and dextrose (D50 or bedside glucose-guided) when altered mental status is present.
Emergency Department Care: Management is largely supportive: IV rehydration with 0.9% NS and aggressive external cooling for hyperthermia. Use benzodiazepines to control agitation and seizures; avoid phenothiazines because they can worsen anticholinergic effects. Treat seizures with benzodiazepines and barbiturates if needed. Manage dysrhythmias with standard agents, but avoid class Ia antiarrhythmics due to quinidine-like effects seen with many anticholinergic drugs; sodium bicarbonate boluses may reverse these sodium-channel blockade effects. For decontamination, give activated charcoal for oral ingestions within about 1 hour when appropriate, and use ocular irrigation for eyedrop exposure.
Antidote Considerations: Physostigmine (Antilirium) is a reversible acetylcholinesterase inhibitor that crosses the blood–brain barrier and can temporarily reverse both central and peripheral effects. Consider it when peripheral anticholinergic signs are present plus severe features such as uncontrolled agitation or seizures not responding to conventional therapy. Use with caution if QRS is prolonged due to risks of dysrhythmias (including asystole), seizures, and cholinergic crises—continuous monitoring is required. Avoid physostigmine in cyclic antidepressant overdose and use caution/avoid in cardiovascular disease, asthma/bronchospasm, intestinal obstruction, heart block, peripheral vascular disease, or bladder obstruction.
Medication Options: Activated charcoal 1 g/kg PO; dextrose 50–100 mL D50 (peds: D25 2 mL/kg over 1 minute) IV and repeat if needed; diazepam 5–10 mg IV (peds 0.2–0.5 mg/kg) q10–15 min; lorazepam 2–4 mg IV (peds 0.03–0.05 mg/kg) q10–15 min; dopamine 2–20 μg/kg/min IV titrated for hypotension; phenobarbital 10–20 mg/kg IV loading dose (monitor respiration); thiamine 100 mg IV/IM (peds 50 mg). For physostigmine, 0.5–2.0 mg IV over 5 min (peds 0.02 mg/kg), repeat in 30–60 min if needed. First-line for agitation/seizures is lorazepam or diazepam; second-line is physostigmine with caution and toxicology input when available.
Disposition Guidance: ICU admission is appropriate for moderate-to-severe toxicity (temperature control, agitation control, seizure/dysrhythmia monitoring) and for any patient receiving physostigmine. Discharge may be reasonable for mild, improving symptoms after 6–8 hours of ED observation.
Referral And Follow-Up: Arrange substance use referral for recreational misuse, poison-prevention counseling for accidental exposures, and psychiatric evaluation for intentional ingestion. Ensure appropriate psychiatric follow-up for intentional overdoses.
Clinical Tips And Common Traps: Treat hyperthermia aggressively—antipyretics do not work for toxic hyperthermia. If physostigmine is considered, use it carefully with continuous monitoring and toxicology consultation when possible.
Core Overview: Anticholinergic poisoning is caused by central and peripheral cholinergic blockade. Depending on the agent, antagonism may occur at muscarinic receptors (most common), nicotinic receptors, or both. Symptoms typically begin 15–30 minutes after ingestion, with effects lasting about 2–24 hours.
Common Causes: Many medications have anticholinergic properties that are usually mild at therapeutic doses but can become life-threatening in overdose. Frequent culprits include antihistamines, belladonna alkaloids and related compounds, antiparkinsonian agents, cyclic antidepressants, antipsychotics (neuroleptics), mydriatic eye drops, skeletal muscle relaxants (e.g., orphenadrine, cyclobenzaprine), antispasmodics, and certain mushrooms/plants (Amanita muscaria, Amanita pantherina, deadly nightshade, mandrake, henbane). Jimson weed may be smoked or ingested.
How It Presents: Clarify timing, dose, and exposure route. The classic toxidrome is often remembered as: “mad as a hatter” (delirium/AMS), “hot as a hare” (hyperthermia), “red as a beet” (flushed skin), “dry as a bone” (dry skin/mucosa), and “blind as a bat” (mydriasis with blurry vision). Findings may include hyperthermia and altered mental status; fixed mydriasis with loss of accommodation; sinus tachycardia, occasional dysrhythmias (typically only in massive ingestions), hypo/HTN, and rarely cardiogenic pulmonary edema; tachypnea or respiratory failure; decreased/absent bowel sounds, dysphagia, decreased GI motility, and reduced salivation; urinary retention; decreased sweating with dry, flushed skin; hallucinations, coma, or seizures.
Essential Evaluation: Diagnosis is clinical, based on toxidrome and a reliable exposure history when possible.
Recommended Tests: Obtain a urine toxicology screen if helpful for context; electrolytes, BUN/creatinine, glucose; CBC; CPK if rhabdomyolysis is a concern; urinalysis; and acetaminophen/salicylate levels to detect occult coingestions (e.g., combination nighttime products). ECG commonly shows sinus tachycardia; may reveal QRS prolongation, AV block, bundle branch block patterns, or dysrhythmias.
Key Differentials: Sympathomimetic intoxication, withdrawal syndromes, acute psychiatric conditions, sepsis, and thyroid disease.
Prehospital Actions: Bring all pills, bottles, and packaging to support accurate identification in the ED.
Immediate Stabilization: Prioritize ABCs—airway control can be critical. Provide supplemental oxygen, establish IV access, initiate cardiac monitoring and pulse oximetry, and consider naloxone, thiamine, and dextrose (D50 or bedside glucose-guided) when altered mental status is present.
Emergency Department Care: Management is largely supportive: IV rehydration with 0.9% NS and aggressive external cooling for hyperthermia. Use benzodiazepines to control agitation and seizures; avoid phenothiazines because they can worsen anticholinergic effects. Treat seizures with benzodiazepines and barbiturates if needed. Manage dysrhythmias with standard agents, but avoid class Ia antiarrhythmics due to quinidine-like effects seen with many anticholinergic drugs; sodium bicarbonate boluses may reverse these sodium-channel blockade effects. For decontamination, give activated charcoal for oral ingestions within about 1 hour when appropriate, and use ocular irrigation for eyedrop exposure.
Antidote Considerations: Physostigmine (Antilirium) is a reversible acetylcholinesterase inhibitor that crosses the blood–brain barrier and can temporarily reverse both central and peripheral effects. Consider it when peripheral anticholinergic signs are present plus severe features such as uncontrolled agitation or seizures not responding to conventional therapy. Use with caution if QRS is prolonged due to risks of dysrhythmias (including asystole), seizures, and cholinergic crises—continuous monitoring is required. Avoid physostigmine in cyclic antidepressant overdose and use caution/avoid in cardiovascular disease, asthma/bronchospasm, intestinal obstruction, heart block, peripheral vascular disease, or bladder obstruction.
Medication Options: Activated charcoal 1 g/kg PO; dextrose 50–100 mL D50 (peds: D25 2 mL/kg over 1 minute) IV and repeat if needed; diazepam 5–10 mg IV (peds 0.2–0.5 mg/kg) q10–15 min; lorazepam 2–4 mg IV (peds 0.03–0.05 mg/kg) q10–15 min; dopamine 2–20 μg/kg/min IV titrated for hypotension; phenobarbital 10–20 mg/kg IV loading dose (monitor respiration); thiamine 100 mg IV/IM (peds 50 mg). For physostigmine, 0.5–2.0 mg IV over 5 min (peds 0.02 mg/kg), repeat in 30–60 min if needed. First-line for agitation/seizures is lorazepam or diazepam; second-line is physostigmine with caution and toxicology input when available.
Disposition Guidance: ICU admission is appropriate for moderate-to-severe toxicity (temperature control, agitation control, seizure/dysrhythmia monitoring) and for any patient receiving physostigmine. Discharge may be reasonable for mild, improving symptoms after 6–8 hours of ED observation.
Referral And Follow-Up: Arrange substance use referral for recreational misuse, poison-prevention counseling for accidental exposures, and psychiatric evaluation for intentional ingestion. Ensure appropriate psychiatric follow-up for intentional overdoses.
Clinical Tips And Common Traps: Treat hyperthermia aggressively—antipyretics do not work for toxic hyperthermia. If physostigmine is considered, use it carefully with continuous monitoring and toxicology consultation when possible.
- Published on
Emergency And Acute Medicine - Ankylosing Spondylitis
Core Overview: Ankylosing spondylitis (AS) is a chronic inflammatory condition that primarily targets the axial skeleton, with a strong predilection for the sacroiliac (SI) joints and spine (SI joints ~100%, cervical ~75%, thoracic ~70%, lumbosacral ~50%; hips and shoulders each ~30%). Inflammation begins at vertebral entheses (outer annulus fibrosus insertions); progressive ossification with syndesmophyte formation can lead to fusion (ankylosis) and the classic brittle “bamboo spine” appearance on imaging. Typical onset is age 15–35 years, with a male predominance (about 2–3:1). ALERT: Patients with AS have markedly increased risk of spinal fracture and paralysis—serious injury can occur after relatively minor trauma.
Risk Profile: Genetics are strongly associated with AS; HLA-B27 is present in roughly 80–90% of affected patients.
Likely Cause: AS is thought to be triggered by environmental factors (often presumed infectious exposures) in genetically predisposed individuals.
Clinical Presentation: The most common presentation is inflammatory low back pain with sacroiliitis—often worse with rest and improved with movement/exercise, and may wake the patient in the second half of the night. Because the spine may be rigid and brittle, patients are at higher risk for major injury from low-energy mechanisms. Extraspinal inflammatory manifestations may occur and sometimes precede spinal symptoms, including uveitis (common; often acute, unilateral, alternating), mild increased CAD risk and valvular disease over time, restrictive lung disease from limited chest expansion and fibrosis, GI associations (notably inflammatory bowel disease in a minority), and renal risks (IgA nephropathy/amyloidosis and NSAID-related nephropathy). Enthesitis is common, frequently presenting as Achilles tendinopathy or plantar fasciitis.
History And Examination: History often features insidious back pain for >3 months in patients <40 years, radiating into the gluteal region from si area and gradually involving more of spine; ask about prior uveitis, ibd, pulmonary restriction, enthesitis, or migrating />olyarthritis. On exam, SI joint tenderness may be reproduced with direct pressure over both ASIS simultaneously; additional findings can include enthesitis or dactylitis, loss of lumbar lordosis, increased thoracic kyphosis, reduced spinal mobility, and decreased chest expansion. Pediatric Note: Juvenile AS (often boys, late childhood/adolescence) may be mistaken for recurrent sprains; it more commonly involves extraspinal joints and lower-extremity entheses—look for asymmetric pauciarthritis and ankle/knee/tarsal enthesitis, plantar fasciitis, and Achilles tendinopathy.
Key Emergency Evaluation: In any patient with known or suspected AS who develops new spinal pain (even without clear trauma), prioritize exclusion of fracture and neurologic injury; also exclude sepsis or septic joint when clinically suspected. Sacroiliitis can be assessed with pelvic compression (“pelvic rock”) or Patrick/FABER-type maneuvers that stress the SI region.
Investigations And Interpretation: CBC may show mild leukocytosis, mild–moderate anemia, and thrombocytosis; BMP can help assess renal involvement, and ESR/CRP may be elevated but are not reliably decisive in the ED. HLA-B27 testing is typically arranged by specialists and a negative result does not exclude AS. Pelvic radiographs are appropriate when undiagnosed AS is suspected; early sacroiliitis may appear as iliac-side subchondral erosions that later progress to sclerosis and bony proliferation—if plain films are unrevealing and suspicion remains, MRI should be considered. For any new spinal pain, obtain spine imaging to exclude fracture; CT is often needed to further evaluate suspected fractures, and MRI is urgent when neurologic deficits are present. CXR may show apical fibrosis or patchy inflammatory changes. ECG is reasonable with ACS symptoms or arrhythmia concerns (including AV block), and echocardiography is indicated for a new murmur or new heart-failure evidence given the increased risk of aortic insufficiency over time.
Conditions To Distinguish From AS: Consider juvenile AS (onset <20 with more enthesitis />xtraspinal involvement), reactive arthritis, enteropathic arthritis (Crohn/UC-associated), psoriatic arthritis (rash; dactylitis), septic arthritis (arthrocentesis if suspected monoarthritis), mechanical low back pain (improves with rest; worsens with exertion; lacks systemic inflammatory features), spinal epidural abscess (often constant, severe, may have fever/IVDA/immunosuppression), and neoplastic back pain (older age, night pain, persistent/unremitting).
Prehospital Priorities: ALERT: Because minor trauma can cause unstable spinal injury, immobilization should avoid forcing the spine into a neutral position; cushioning and transport in the position of comfort (e.g., scoop stretcher with padding) may be safer than rigid collar/backboard alone. Anticipate difficult airway management due to cervical/TMJ limitation—fiberoptic techniques are often preferred; consider temporizing strategies (e.g., LMA or BVM with airway adjunct) until a definitive airway can be secured safely. Ventilation may be challenging due to chest-wall restriction and fibrosis, and CPR may carry higher rib-fracture risk.
Emergency Department Management: If cord compression is suspected, obtain MRI urgently. For any new spinal pain, aggressively evaluate for fracture—CT may be required even when initial radiographs are unrevealing. If infection is a concern, pursue labs and arthrocentesis as indicated. Treat pain and inflammation, typically starting with NSAIDs when appropriate.
Medications: Use nonselective NSAIDs such as ibuprofen, indomethacin (often limited by GI/CNS adverse effects), or naproxen; COX-2 inhibitors (e.g., celecoxib) can be considered, especially when GI bleeding risk is elevated. TNF-α inhibitors (e.g., adalimumab, etanercept) are disease-modifying options typically initiated in specialist care. In pregnancy, avoid NSAIDs when possible—use acetaminophen first-line and opioids second-line if needed. In older adults, weigh NSAID risks (CV, GI bleed, renal injury, hypertension) and consider gastroprotection (H2 blocker/PPI) or COX-2 selection when appropriate. If NSAIDs/acetaminophen are ineffective at appropriate doses, second-line options may include opioid analgesics, muscle relaxants, or short courses of low-dose steroids in select cases.
Disposition Planning: Admit for acute neurologic deficits, uncontrolled pain, or when sepsis/septic joint cannot be excluded. Discharge may be reasonable when serious injury and neurologic deficit have been ruled out and pain is controlled to a safe level.
Referral And Follow-Up: Encourage a medical alert bracelet due to high trauma risk. Arrange rheumatology referral for suspected new AS or for escalation to immunomodulating therapy, and consider physical medicine/rehab for splints and orthoses (e.g., heel cushioning to unload Achilles enthesis). Advise primary care reassessment within 1–2 weeks to gauge response, with earlier review for patients at higher risk of NSAID complications (elderly, hypertensive, high GI-bleed risk).
Clinical Tips And Common Traps: Anticipate a difficult airway and avoid neck repositioning because cervical instability and severe rigidity can make standard techniques hazardous—use airway adjuncts and pursue fiberoptic intubation when feasible. Immobilization should prioritize the patient’s position of comfort with padding rather than forcing standard collar/backboard alignment. Maintain high suspicion for fracture and cord injury after even low-energy trauma, as seemingly minor mechanisms can cause catastrophic spinal injury in AS.
Core Overview: Ankylosing spondylitis (AS) is a chronic inflammatory condition that primarily targets the axial skeleton, with a strong predilection for the sacroiliac (SI) joints and spine (SI joints ~100%, cervical ~75%, thoracic ~70%, lumbosacral ~50%; hips and shoulders each ~30%). Inflammation begins at vertebral entheses (outer annulus fibrosus insertions); progressive ossification with syndesmophyte formation can lead to fusion (ankylosis) and the classic brittle “bamboo spine” appearance on imaging. Typical onset is age 15–35 years, with a male predominance (about 2–3:1). ALERT: Patients with AS have markedly increased risk of spinal fracture and paralysis—serious injury can occur after relatively minor trauma.
Risk Profile: Genetics are strongly associated with AS; HLA-B27 is present in roughly 80–90% of affected patients.
Likely Cause: AS is thought to be triggered by environmental factors (often presumed infectious exposures) in genetically predisposed individuals.
Clinical Presentation: The most common presentation is inflammatory low back pain with sacroiliitis—often worse with rest and improved with movement/exercise, and may wake the patient in the second half of the night. Because the spine may be rigid and brittle, patients are at higher risk for major injury from low-energy mechanisms. Extraspinal inflammatory manifestations may occur and sometimes precede spinal symptoms, including uveitis (common; often acute, unilateral, alternating), mild increased CAD risk and valvular disease over time, restrictive lung disease from limited chest expansion and fibrosis, GI associations (notably inflammatory bowel disease in a minority), and renal risks (IgA nephropathy/amyloidosis and NSAID-related nephropathy). Enthesitis is common, frequently presenting as Achilles tendinopathy or plantar fasciitis.
History And Examination: History often features insidious back pain for >3 months in patients <40 years, radiating into the gluteal region from si area and gradually involving more of spine; ask about prior uveitis, ibd, pulmonary restriction, enthesitis, or migrating />olyarthritis. On exam, SI joint tenderness may be reproduced with direct pressure over both ASIS simultaneously; additional findings can include enthesitis or dactylitis, loss of lumbar lordosis, increased thoracic kyphosis, reduced spinal mobility, and decreased chest expansion. Pediatric Note: Juvenile AS (often boys, late childhood/adolescence) may be mistaken for recurrent sprains; it more commonly involves extraspinal joints and lower-extremity entheses—look for asymmetric pauciarthritis and ankle/knee/tarsal enthesitis, plantar fasciitis, and Achilles tendinopathy.
Key Emergency Evaluation: In any patient with known or suspected AS who develops new spinal pain (even without clear trauma), prioritize exclusion of fracture and neurologic injury; also exclude sepsis or septic joint when clinically suspected. Sacroiliitis can be assessed with pelvic compression (“pelvic rock”) or Patrick/FABER-type maneuvers that stress the SI region.
Investigations And Interpretation: CBC may show mild leukocytosis, mild–moderate anemia, and thrombocytosis; BMP can help assess renal involvement, and ESR/CRP may be elevated but are not reliably decisive in the ED. HLA-B27 testing is typically arranged by specialists and a negative result does not exclude AS. Pelvic radiographs are appropriate when undiagnosed AS is suspected; early sacroiliitis may appear as iliac-side subchondral erosions that later progress to sclerosis and bony proliferation—if plain films are unrevealing and suspicion remains, MRI should be considered. For any new spinal pain, obtain spine imaging to exclude fracture; CT is often needed to further evaluate suspected fractures, and MRI is urgent when neurologic deficits are present. CXR may show apical fibrosis or patchy inflammatory changes. ECG is reasonable with ACS symptoms or arrhythmia concerns (including AV block), and echocardiography is indicated for a new murmur or new heart-failure evidence given the increased risk of aortic insufficiency over time.
Conditions To Distinguish From AS: Consider juvenile AS (onset <20 with more enthesitis />xtraspinal involvement), reactive arthritis, enteropathic arthritis (Crohn/UC-associated), psoriatic arthritis (rash; dactylitis), septic arthritis (arthrocentesis if suspected monoarthritis), mechanical low back pain (improves with rest; worsens with exertion; lacks systemic inflammatory features), spinal epidural abscess (often constant, severe, may have fever/IVDA/immunosuppression), and neoplastic back pain (older age, night pain, persistent/unremitting).
Prehospital Priorities: ALERT: Because minor trauma can cause unstable spinal injury, immobilization should avoid forcing the spine into a neutral position; cushioning and transport in the position of comfort (e.g., scoop stretcher with padding) may be safer than rigid collar/backboard alone. Anticipate difficult airway management due to cervical/TMJ limitation—fiberoptic techniques are often preferred; consider temporizing strategies (e.g., LMA or BVM with airway adjunct) until a definitive airway can be secured safely. Ventilation may be challenging due to chest-wall restriction and fibrosis, and CPR may carry higher rib-fracture risk.
Emergency Department Management: If cord compression is suspected, obtain MRI urgently. For any new spinal pain, aggressively evaluate for fracture—CT may be required even when initial radiographs are unrevealing. If infection is a concern, pursue labs and arthrocentesis as indicated. Treat pain and inflammation, typically starting with NSAIDs when appropriate.
Medications: Use nonselective NSAIDs such as ibuprofen, indomethacin (often limited by GI/CNS adverse effects), or naproxen; COX-2 inhibitors (e.g., celecoxib) can be considered, especially when GI bleeding risk is elevated. TNF-α inhibitors (e.g., adalimumab, etanercept) are disease-modifying options typically initiated in specialist care. In pregnancy, avoid NSAIDs when possible—use acetaminophen first-line and opioids second-line if needed. In older adults, weigh NSAID risks (CV, GI bleed, renal injury, hypertension) and consider gastroprotection (H2 blocker/PPI) or COX-2 selection when appropriate. If NSAIDs/acetaminophen are ineffective at appropriate doses, second-line options may include opioid analgesics, muscle relaxants, or short courses of low-dose steroids in select cases.
Disposition Planning: Admit for acute neurologic deficits, uncontrolled pain, or when sepsis/septic joint cannot be excluded. Discharge may be reasonable when serious injury and neurologic deficit have been ruled out and pain is controlled to a safe level.
Referral And Follow-Up: Encourage a medical alert bracelet due to high trauma risk. Arrange rheumatology referral for suspected new AS or for escalation to immunomodulating therapy, and consider physical medicine/rehab for splints and orthoses (e.g., heel cushioning to unload Achilles enthesis). Advise primary care reassessment within 1–2 weeks to gauge response, with earlier review for patients at higher risk of NSAID complications (elderly, hypertensive, high GI-bleed risk).
Clinical Tips And Common Traps: Anticipate a difficult airway and avoid neck repositioning because cervical instability and severe rigidity can make standard techniques hazardous—use airway adjuncts and pursue fiberoptic intubation when feasible. Immobilization should prioritize the patient’s position of comfort with padding rather than forcing standard collar/backboard alignment. Maintain high suspicion for fracture and cord injury after even low-energy trauma, as seemingly minor mechanisms can cause catastrophic spinal injury in AS.
- Published on
Emergency and Acute Medicine – Ankle Sprain
Core Description
Ankle sprains involve injury to the ligamentous stabilizers of the ankle joint, a hinge joint formed by the tibia, fibula, and talus. Injury severity ranges from ligament stretching with microscopic damage (grade I), to partial tearing (grade II), to complete ligament rupture (grade III).
Mechanisms And Causes
Ankle sprains most often result from forced inversion or eversion, frequently during sports or collisions. Approximately 85–90% involve the lateral ligament complex, including the anterior talofibular, posterior talofibular, and calcaneofibular ligaments. Inversion injury most commonly affects the anterior talofibular ligament; calcaneofibular ligament injury is more likely when the ankle is in neutral position, while isolated posterior talofibular ligament injury is rare. Deltoid ligament injuries typically result from eversion and are often associated with medial malleolar avulsion or talar insertion injury; isolated deltoid injuries are uncommon and should raise concern for associated lateral malleolus or proximal fibular (Maisonneuve) fracture. Syndesmotic sprains involve the distal tibiofibular ligaments, occur frequently in collision sports, and carry higher morbidity with risk of long-term complications. In children younger than 10 years, traumatic ankle pain with normal radiographs most commonly represents a Salter–Harris type I fracture, as the physis is weaker than surrounding ligaments.
Clinical Presentation
Patients usually present with ankle pain, swelling, and difficulty bearing weight. History should include time and mechanism of injury, presence of a pop or crack, prior ankle trauma, relevant medical conditions, treatments attempted before arrival, and ability to bear weight at the scene and in the emergency department. Physical examination focuses on detecting instability and associated injury, including bony tenderness along the posterior edges of the medial and lateral malleoli and the base of the fifth metatarsal, distal neurovascular status, and comparison of range of motion with the uninjured side. Stress testing is often limited by pain. The squeeze test helps identify syndesmotic injury when compression of the tibia and fibula at the midcalf reproduces ankle pain.
Imaging Decision Strategy
The Ottawa Ankle Rules provide a validated approach for determining the need for radiographs. Imaging is recommended for bony tenderness at the posterior edge or distal 6 cm of either malleolus, tenderness at the base of the fifth metatarsal or navicular, or inability to bear weight for four unassisted steps both immediately after injury and in the emergency department.
Diagnostic Evaluation
Radiographs should be obtained when fracture is suspected. Stress radiographs are rarely useful acutely and should not be routinely ordered unless requested by a consultant.
Differential Considerations
Ankle fracture or dislocation, Achilles tendon rupture, Maisonneuve fracture, os trigonum fracture, fifth metatarsal fracture, talar dome lesion, and peroneal tendon injury should be considered.
Initial Management
Prehospital care includes immobilization as needed to reduce pain and prevent further injury.
Emergency Department Care
Initial therapy focuses on preventing further injury and avoiding painful weight bearing using rest, ice, compression, and elevation. Treatment aims to reduce pain and restore function without chronic instability. Evidence supports early mobilization with functional treatment. Grade I and II sprains are managed with elastic bandaging combined with an air-stirrup or gel splint and weight bearing as tolerated. Grade III sprains or those with severe pain may benefit from brief immobilization followed by early functional rehabilitation and orthopedic referral. Crutches may be used initially for comfort. Once swelling and pain resolve, strengthening and proprioceptive exercises improve recovery and reduce reinjury. Return to sports should occur only when running and directional changes are pain free. Bracing or taping reduces recurrence in high-risk sports.
Pharmacologic Therapy
NSAIDs are effective for acute pain control, including oral ibuprofen or topical diclofenac gel. Opioid analgesics may be required for severe pain.
Disposition And Follow-Up
Isolated ankle sprains do not require admission and may be discharged with appropriate treatment, prescriptions, and aftercare instructions. Copies of radiographs may assist early follow-up. Grade I and II sprains should follow up with primary care within 1–2 weeks, while grade III sprains and syndesmotic injuries require orthopedic or sports medicine evaluation within 7–10 days.
Clinical Pearls And Common Errors
Appropriate application of the Ottawa Ankle Rules reduces unnecessary imaging. Functional treatment with early mobilization shortens recovery time, while prolonged immobilization increases the risk of chronic pain and recurrent instability.
Core Description
Ankle sprains involve injury to the ligamentous stabilizers of the ankle joint, a hinge joint formed by the tibia, fibula, and talus. Injury severity ranges from ligament stretching with microscopic damage (grade I), to partial tearing (grade II), to complete ligament rupture (grade III).
Mechanisms And Causes
Ankle sprains most often result from forced inversion or eversion, frequently during sports or collisions. Approximately 85–90% involve the lateral ligament complex, including the anterior talofibular, posterior talofibular, and calcaneofibular ligaments. Inversion injury most commonly affects the anterior talofibular ligament; calcaneofibular ligament injury is more likely when the ankle is in neutral position, while isolated posterior talofibular ligament injury is rare. Deltoid ligament injuries typically result from eversion and are often associated with medial malleolar avulsion or talar insertion injury; isolated deltoid injuries are uncommon and should raise concern for associated lateral malleolus or proximal fibular (Maisonneuve) fracture. Syndesmotic sprains involve the distal tibiofibular ligaments, occur frequently in collision sports, and carry higher morbidity with risk of long-term complications. In children younger than 10 years, traumatic ankle pain with normal radiographs most commonly represents a Salter–Harris type I fracture, as the physis is weaker than surrounding ligaments.
Clinical Presentation
Patients usually present with ankle pain, swelling, and difficulty bearing weight. History should include time and mechanism of injury, presence of a pop or crack, prior ankle trauma, relevant medical conditions, treatments attempted before arrival, and ability to bear weight at the scene and in the emergency department. Physical examination focuses on detecting instability and associated injury, including bony tenderness along the posterior edges of the medial and lateral malleoli and the base of the fifth metatarsal, distal neurovascular status, and comparison of range of motion with the uninjured side. Stress testing is often limited by pain. The squeeze test helps identify syndesmotic injury when compression of the tibia and fibula at the midcalf reproduces ankle pain.
Imaging Decision Strategy
The Ottawa Ankle Rules provide a validated approach for determining the need for radiographs. Imaging is recommended for bony tenderness at the posterior edge or distal 6 cm of either malleolus, tenderness at the base of the fifth metatarsal or navicular, or inability to bear weight for four unassisted steps both immediately after injury and in the emergency department.
Diagnostic Evaluation
Radiographs should be obtained when fracture is suspected. Stress radiographs are rarely useful acutely and should not be routinely ordered unless requested by a consultant.
Differential Considerations
Ankle fracture or dislocation, Achilles tendon rupture, Maisonneuve fracture, os trigonum fracture, fifth metatarsal fracture, talar dome lesion, and peroneal tendon injury should be considered.
Initial Management
Prehospital care includes immobilization as needed to reduce pain and prevent further injury.
Emergency Department Care
Initial therapy focuses on preventing further injury and avoiding painful weight bearing using rest, ice, compression, and elevation. Treatment aims to reduce pain and restore function without chronic instability. Evidence supports early mobilization with functional treatment. Grade I and II sprains are managed with elastic bandaging combined with an air-stirrup or gel splint and weight bearing as tolerated. Grade III sprains or those with severe pain may benefit from brief immobilization followed by early functional rehabilitation and orthopedic referral. Crutches may be used initially for comfort. Once swelling and pain resolve, strengthening and proprioceptive exercises improve recovery and reduce reinjury. Return to sports should occur only when running and directional changes are pain free. Bracing or taping reduces recurrence in high-risk sports.
Pharmacologic Therapy
NSAIDs are effective for acute pain control, including oral ibuprofen or topical diclofenac gel. Opioid analgesics may be required for severe pain.
Disposition And Follow-Up
Isolated ankle sprains do not require admission and may be discharged with appropriate treatment, prescriptions, and aftercare instructions. Copies of radiographs may assist early follow-up. Grade I and II sprains should follow up with primary care within 1–2 weeks, while grade III sprains and syndesmotic injuries require orthopedic or sports medicine evaluation within 7–10 days.
Clinical Pearls And Common Errors
Appropriate application of the Ottawa Ankle Rules reduces unnecessary imaging. Functional treatment with early mobilization shortens recovery time, while prolonged immobilization increases the risk of chronic pain and recurrent instability.
- Published on
Emergency and Acute Medicine – Ataxia
Clinical Definition
Ataxia is the inability to perform coordinated voluntary movements and most commonly results from dysfunction of the cerebellum or its neural connections. Lesions of the lateral cerebellar hemispheres produce ipsilateral limb findings, whereas midline lesions result in truncal ataxia.
Etiology And Pathophysiology
Although typically cerebellar in origin, ataxia may also arise from sensory, motor, or vestibular system dysfunction. Causes include trauma, intracranial mass lesions, vascular disorders, infections and postinfectious processes, toxins or medications, metabolic and endocrine derangements, demyelinating disease, congenital malformations, hereditary disorders such as inborn errors of metabolism and progressive degenerative ataxias, as well as nutritional deficiencies.
Clinical Presentation
Gait disturbance is the most common presenting feature and often begins as a subjective sense of imbalance or insecurity while walking. Patients may report difficulty with activities requiring coordination such as bicycling, skiing, or climbing. Examination often reveals a wide-based stance and staggering gait; tandem gait testing is useful for detecting subtle abnormalities. Limb ataxia manifests as incoordination, intention tremor, clumsiness with fine motor tasks, dysmetria on finger-to-nose or heel-to-shin testing, and dysdiadochokinesis during rapid alternating movements. Truncal ataxia may present with head tremor, truncal instability, titubation, and difficulty maintaining posture while seated or standing. Speech abnormalities include slurred, scanning, or staccato dysarthria and bulbar symptoms such as choking from impaired swallowing coordination. Visual complaints may include blurred vision or vertigo; central vertigo must be distinguished from peripheral causes, which are typically severe, positional, and associated with ear symptoms. Nystagmus may be gaze-evoked or rebound in nature. Cerebellar disease rarely causes true muscle weakness or hypotonia, though isometrataxia may be demonstrated by inability to sustain constant force. Sensory ataxia presents with paresthesias, numbness, a cautious steppage gait, loss of position or vibration sense, and marked worsening with eye closure, producing a positive Romberg sign.
History And Examination
A careful history is essential, as gait disturbance may reflect pain, weakness, lightheadedness, vertigo, or incoordination rather than true ataxia. Determine onset and progression, distinguishing acute (hours to days), subacute (weeks to months), and chronic (months to years) presentations. Assess for symmetry or focality of symptoms, associated fever, altered mental status, weakness, sensory loss, urinary incontinence, recent infections or immunizations, trauma, toxic exposures, and family history of movement disorders. Physical examination should include a complete neurologic and gait assessment, with careful evaluation for life-threatening conditions such as stroke, hemorrhage, CNS infection, or elevated intracranial pressure manifested by headache, papilledema, bradycardia, hypertension, abnormal respirations, bulging fontanelles, nausea, vomiting, or meningismus. Ear examination and provocative testing for nystagmus may help identify vestibular pathology. Intoxication and toxidromes should be considered when ingestion is suspected.
Diagnostic Evaluation
Workup is guided by history and examination. Basic laboratory testing includes blood glucose, serum electrolytes, thyroid function tests, and targeted toxicology screening, recognizing that standard panels may miss relevant agents. Imaging is critical when central causes are suspected. Head CT can identify hemorrhage, mass lesions, hydrocephalus, or subacute infarction, though sensitivity for posterior fossa pathology is limited. CT with contrast or CT angiography may be indicated when mass or vascular disease is suspected. MRI is superior for evaluating posterior fossa lesions, acute ischemia, demyelination, and vascular abnormalities, and MR angiography may be required for suspected vascular etiologies. Lumbar puncture is indicated when infection or Guillain–Barré syndrome is suspected. Electrocardiography is not routinely required but may assist in evaluating nonspecific dizziness.
Differential Diagnosis
Acute symmetric ataxia includes head trauma, drug or toxin exposure such as alcohol, lithium, phenytoin, barbiturates, carbamazepine, phenobarbital, valproic acid, benzodiazepines, diphenhydramine, or dextromethorphan, acute viral cerebellitis, meningitis or encephalitis, hydrocephalus, postinfectious syndromes, hypoglycemia, hyponatremia, and severe heat stroke. Acute focal ataxia suggests posterior circulation infarction, vertebrobasilar insufficiency, cerebellar hemorrhage, subdural hematoma, cerebellar abscess, acute disseminated encephalomyelitis, complicated migraine, or atypical seizure. Subacute symmetric ataxia may result from heavy metals, hydrocarbons, chemotherapy, organophosphates, vitamin B1 or B12 deficiency, paraneoplastic syndromes, Lyme disease, toxoplasmosis, or Creutzfeldt–Jakob disease. Subacute focal ataxia includes cerebellar glioma, metastases, lymphoma, multiple sclerosis, Guillain–Barré syndrome, AIDS-related progressive multifocal leukoencephalopathy, syringomyelia, or cervical spondylosis. Chronic ataxia may reflect alcohol-related cerebellar degeneration, inherited disorders such as spinocerebellar ataxias, Friedreich ataxia, ataxia telangiectasia, Niemann–Pick disease, hypothyroidism, vitamin E deficiency, tabes dorsalis, or congenital malformations including Arnold–Chiari and Dandy–Walker syndromes. Peripheral vestibular disorders may mimic ataxic gait.
Special Populations
Children may present with refusal to walk. Acute pediatric ataxia is often benign and self-limited, most commonly due to acute cerebellar ataxia or drug ingestion. Postinfectious acute cerebellar ataxia typically affects children aged 2–5 years, occurs 1–3 weeks after illness or immunization, features normal mental status, and resolves within three months. Toxic ingestions often produce mental status changes. Guillain–Barré syndrome may present with sensory ataxia, particularly in the Miller–Fisher variant. Brain tumors frequently involve the cerebellum or brainstem, and opsoclonus–myoclonus–ataxia syndrome is strongly associated with neuroblastoma. Stroke is rare in children but occurs in those with sickle cell disease or hypercoagulable states. In elderly patients, gait disorders are frequently multifactorial, and posterior circulation stroke or vertebrobasilar insufficiency may present with vague symptoms such as dizziness.
Emergency Management
Acute onset ataxia should prompt concern for stroke or hemorrhage. Initial stabilization includes airway, breathing, and circulation, IV access, supplemental oxygen, cardiac monitoring, and immediate blood glucose assessment with dextrose administration for hypoglycemia. Thiamine should be given to malnourished or alcoholic patients. Fall precautions are essential. Management is directed at the underlying cause; cerebellar infarction may cause rapid edema with mass effect and require urgent neurosurgical consultation for decompression.
Medications
Administer dextrose for hypoglycemia and thiamine when indicated. Additional therapies are etiology-specific.
Disposition
Admission is indicated for acute or subacute ataxia when a benign cause cannot be confidently established, inability to ambulate safely, or evidence of cerebellar hemorrhage or mass effect, which requires ICU care. Discharge may be considered for patients with mild or reversible symptoms, normal mental status, and safe ambulation.
Follow-Up
Arrange follow-up with primary care or neurology based on the suspected etiology.
Clinical Lessons And Safety Points
Common errors include failing to distinguish true ataxia from other gait disturbances, overlooking trauma in intoxicated patients, overreliance on CT for posterior fossa evaluation, and underestimating the risk of herniation from cerebellar lesions such as stroke.
Clinical Definition
Ataxia is the inability to perform coordinated voluntary movements and most commonly results from dysfunction of the cerebellum or its neural connections. Lesions of the lateral cerebellar hemispheres produce ipsilateral limb findings, whereas midline lesions result in truncal ataxia.
Etiology And Pathophysiology
Although typically cerebellar in origin, ataxia may also arise from sensory, motor, or vestibular system dysfunction. Causes include trauma, intracranial mass lesions, vascular disorders, infections and postinfectious processes, toxins or medications, metabolic and endocrine derangements, demyelinating disease, congenital malformations, hereditary disorders such as inborn errors of metabolism and progressive degenerative ataxias, as well as nutritional deficiencies.
Clinical Presentation
Gait disturbance is the most common presenting feature and often begins as a subjective sense of imbalance or insecurity while walking. Patients may report difficulty with activities requiring coordination such as bicycling, skiing, or climbing. Examination often reveals a wide-based stance and staggering gait; tandem gait testing is useful for detecting subtle abnormalities. Limb ataxia manifests as incoordination, intention tremor, clumsiness with fine motor tasks, dysmetria on finger-to-nose or heel-to-shin testing, and dysdiadochokinesis during rapid alternating movements. Truncal ataxia may present with head tremor, truncal instability, titubation, and difficulty maintaining posture while seated or standing. Speech abnormalities include slurred, scanning, or staccato dysarthria and bulbar symptoms such as choking from impaired swallowing coordination. Visual complaints may include blurred vision or vertigo; central vertigo must be distinguished from peripheral causes, which are typically severe, positional, and associated with ear symptoms. Nystagmus may be gaze-evoked or rebound in nature. Cerebellar disease rarely causes true muscle weakness or hypotonia, though isometrataxia may be demonstrated by inability to sustain constant force. Sensory ataxia presents with paresthesias, numbness, a cautious steppage gait, loss of position or vibration sense, and marked worsening with eye closure, producing a positive Romberg sign.
History And Examination
A careful history is essential, as gait disturbance may reflect pain, weakness, lightheadedness, vertigo, or incoordination rather than true ataxia. Determine onset and progression, distinguishing acute (hours to days), subacute (weeks to months), and chronic (months to years) presentations. Assess for symmetry or focality of symptoms, associated fever, altered mental status, weakness, sensory loss, urinary incontinence, recent infections or immunizations, trauma, toxic exposures, and family history of movement disorders. Physical examination should include a complete neurologic and gait assessment, with careful evaluation for life-threatening conditions such as stroke, hemorrhage, CNS infection, or elevated intracranial pressure manifested by headache, papilledema, bradycardia, hypertension, abnormal respirations, bulging fontanelles, nausea, vomiting, or meningismus. Ear examination and provocative testing for nystagmus may help identify vestibular pathology. Intoxication and toxidromes should be considered when ingestion is suspected.
Diagnostic Evaluation
Workup is guided by history and examination. Basic laboratory testing includes blood glucose, serum electrolytes, thyroid function tests, and targeted toxicology screening, recognizing that standard panels may miss relevant agents. Imaging is critical when central causes are suspected. Head CT can identify hemorrhage, mass lesions, hydrocephalus, or subacute infarction, though sensitivity for posterior fossa pathology is limited. CT with contrast or CT angiography may be indicated when mass or vascular disease is suspected. MRI is superior for evaluating posterior fossa lesions, acute ischemia, demyelination, and vascular abnormalities, and MR angiography may be required for suspected vascular etiologies. Lumbar puncture is indicated when infection or Guillain–Barré syndrome is suspected. Electrocardiography is not routinely required but may assist in evaluating nonspecific dizziness.
Differential Diagnosis
Acute symmetric ataxia includes head trauma, drug or toxin exposure such as alcohol, lithium, phenytoin, barbiturates, carbamazepine, phenobarbital, valproic acid, benzodiazepines, diphenhydramine, or dextromethorphan, acute viral cerebellitis, meningitis or encephalitis, hydrocephalus, postinfectious syndromes, hypoglycemia, hyponatremia, and severe heat stroke. Acute focal ataxia suggests posterior circulation infarction, vertebrobasilar insufficiency, cerebellar hemorrhage, subdural hematoma, cerebellar abscess, acute disseminated encephalomyelitis, complicated migraine, or atypical seizure. Subacute symmetric ataxia may result from heavy metals, hydrocarbons, chemotherapy, organophosphates, vitamin B1 or B12 deficiency, paraneoplastic syndromes, Lyme disease, toxoplasmosis, or Creutzfeldt–Jakob disease. Subacute focal ataxia includes cerebellar glioma, metastases, lymphoma, multiple sclerosis, Guillain–Barré syndrome, AIDS-related progressive multifocal leukoencephalopathy, syringomyelia, or cervical spondylosis. Chronic ataxia may reflect alcohol-related cerebellar degeneration, inherited disorders such as spinocerebellar ataxias, Friedreich ataxia, ataxia telangiectasia, Niemann–Pick disease, hypothyroidism, vitamin E deficiency, tabes dorsalis, or congenital malformations including Arnold–Chiari and Dandy–Walker syndromes. Peripheral vestibular disorders may mimic ataxic gait.
Special Populations
Children may present with refusal to walk. Acute pediatric ataxia is often benign and self-limited, most commonly due to acute cerebellar ataxia or drug ingestion. Postinfectious acute cerebellar ataxia typically affects children aged 2–5 years, occurs 1–3 weeks after illness or immunization, features normal mental status, and resolves within three months. Toxic ingestions often produce mental status changes. Guillain–Barré syndrome may present with sensory ataxia, particularly in the Miller–Fisher variant. Brain tumors frequently involve the cerebellum or brainstem, and opsoclonus–myoclonus–ataxia syndrome is strongly associated with neuroblastoma. Stroke is rare in children but occurs in those with sickle cell disease or hypercoagulable states. In elderly patients, gait disorders are frequently multifactorial, and posterior circulation stroke or vertebrobasilar insufficiency may present with vague symptoms such as dizziness.
Emergency Management
Acute onset ataxia should prompt concern for stroke or hemorrhage. Initial stabilization includes airway, breathing, and circulation, IV access, supplemental oxygen, cardiac monitoring, and immediate blood glucose assessment with dextrose administration for hypoglycemia. Thiamine should be given to malnourished or alcoholic patients. Fall precautions are essential. Management is directed at the underlying cause; cerebellar infarction may cause rapid edema with mass effect and require urgent neurosurgical consultation for decompression.
Medications
Administer dextrose for hypoglycemia and thiamine when indicated. Additional therapies are etiology-specific.
Disposition
Admission is indicated for acute or subacute ataxia when a benign cause cannot be confidently established, inability to ambulate safely, or evidence of cerebellar hemorrhage or mass effect, which requires ICU care. Discharge may be considered for patients with mild or reversible symptoms, normal mental status, and safe ambulation.
Follow-Up
Arrange follow-up with primary care or neurology based on the suspected etiology.
Clinical Lessons And Safety Points
Common errors include failing to distinguish true ataxia from other gait disturbances, overlooking trauma in intoxicated patients, overreliance on CT for posterior fossa evaluation, and underestimating the risk of herniation from cerebellar lesions such as stroke.
- Published on
Emergency and Acute Medicine – Asystole
Clinical Definition
Asystole is the complete absence of ventricular electrical activity.
Causes And Pathophysiology
Asystole is typically a terminal rhythm and may evolve from prolonged bradycardia, prolonged ventricular fibrillation, or prolonged pulseless electrical activity. Survival is extremely unlikely when asystole occurs out of hospital; roughly 40% may achieve return of spontaneous circulation and survive to hospital admission, but fewer than 15% survive to hospital discharge. Prognosis is similarly poor when asystole develops after countershock for ventricular tachycardia or ventricular fibrillation, with fewer than 10% surviving to hospital discharge. Potentially reversible causes include hypoxia, hypovolemia from blood loss, acidosis, hyperkalemia, hypokalemia, drug overdose, hypothermia, pulmonary embolism, myocardial infarction, tension pneumothorax, and cardiac tamponade.
Clinical Presentation
Patients are unresponsive, pulseless, and may have agonal respirations or no spontaneous breathing.
Immediate Assessment Priorities
Confirm true asystole in two limb leads to avoid mistaking fine ventricular fibrillation for asystole. Check lead and cable connections, ensure the monitor is powered on, and verify the gain is adequately increased. Actively look for reversible causes while resuscitation is ongoing.
Investigations In The ED
Arterial blood gas analysis may assist, particularly for potassium and hemoglobin assessment. Bedside cardiac ultrasound is useful to evaluate for pericardial tamponade.
Key Alternative Diagnosis
Fine ventricular fibrillation can mimic asystole and must be excluded.
Prehospital Considerations
No intervention should be performed if a valid Do Not Resuscitate order is present. Resuscitation should not be initiated when death is verifiable by rigor mortis, dependent livedo, or injuries incompatible with life such as decapitation.
Resuscitation Approach
Begin CPR immediately with emphasis on high-quality chest compressions with minimal interruptions. Confirm asystole on the cardiac monitor. Secure the airway using an endotracheal tube when feasible, though bag-valve-mask ventilation is acceptable, then confirm placement and provide 100% inspired oxygen while ventilating slowly at 6–12 breaths per minute. Limit pauses in compressions during airway placement. Establish IV or intraosseous access. Use continuous waveform capnography to guide and optimize compression quality; end-tidal CO₂ correlates with cardiac output and myocardial blood flow during CPR. Administer epinephrine every 3–5 minutes. Search for and treat reversible causes without delay. Sodium bicarbonate is reserved for suspected hyperkalemia or drug overdose. There is no proven benefit to giving an empiric single countershock, and no proven benefit to electrical pacing in asystole. If the rhythm converts to ventricular fibrillation or ventricular tachycardia, defibrillate immediately without delay.
Post-ROSC Care And ED Management
If return of spontaneous circulation occurs and the patient remains comatose, initiate induced hypothermia as part of post–cardiac arrest care. Consider termination of resuscitation only when high-quality compressions have been delivered for an adequate period, the trachea has been intubated to ensure oxygenation, fine ventricular fibrillation has been excluded, reversible causes have been corrected or ruled out, bedside ultrasound shows no pericardial effusion, and there is no clinical evidence of tension pneumothorax.
Medications
Epinephrine is given as 1 mg IV every 3–5 minutes in adults, and 0.01 mg/kg IV every 3–5 minutes in children. Sodium bicarbonate is dosed at 1 mEq/kg IV and should be used only when there is pre-existing acidosis, suspected hyperkalemia, or suspected tricyclic antidepressant overdose.
Disposition And Monitoring
Any patient with return of spontaneous circulation requires admission, and there are no discharge pathways from the ED after asystolic arrest. Post-arrest care should occur in an ICU with cardiac monitoring and induced hypothermia when indicated.
Follow-Up Planning
A permanent pacemaker may be considered only when asystole is determined to be due to primary heart block.
Clinical Lessons And Safety Points
Outcomes depend heavily on immediate, minimally interrupted, high-quality chest compressions while aggressively searching for reversible causes. Successful resuscitation is most likely only when a reversible cause is identified and corrected promptly.
Clinical Definition
Asystole is the complete absence of ventricular electrical activity.
Causes And Pathophysiology
Asystole is typically a terminal rhythm and may evolve from prolonged bradycardia, prolonged ventricular fibrillation, or prolonged pulseless electrical activity. Survival is extremely unlikely when asystole occurs out of hospital; roughly 40% may achieve return of spontaneous circulation and survive to hospital admission, but fewer than 15% survive to hospital discharge. Prognosis is similarly poor when asystole develops after countershock for ventricular tachycardia or ventricular fibrillation, with fewer than 10% surviving to hospital discharge. Potentially reversible causes include hypoxia, hypovolemia from blood loss, acidosis, hyperkalemia, hypokalemia, drug overdose, hypothermia, pulmonary embolism, myocardial infarction, tension pneumothorax, and cardiac tamponade.
Clinical Presentation
Patients are unresponsive, pulseless, and may have agonal respirations or no spontaneous breathing.
Immediate Assessment Priorities
Confirm true asystole in two limb leads to avoid mistaking fine ventricular fibrillation for asystole. Check lead and cable connections, ensure the monitor is powered on, and verify the gain is adequately increased. Actively look for reversible causes while resuscitation is ongoing.
Investigations In The ED
Arterial blood gas analysis may assist, particularly for potassium and hemoglobin assessment. Bedside cardiac ultrasound is useful to evaluate for pericardial tamponade.
Key Alternative Diagnosis
Fine ventricular fibrillation can mimic asystole and must be excluded.
Prehospital Considerations
No intervention should be performed if a valid Do Not Resuscitate order is present. Resuscitation should not be initiated when death is verifiable by rigor mortis, dependent livedo, or injuries incompatible with life such as decapitation.
Resuscitation Approach
Begin CPR immediately with emphasis on high-quality chest compressions with minimal interruptions. Confirm asystole on the cardiac monitor. Secure the airway using an endotracheal tube when feasible, though bag-valve-mask ventilation is acceptable, then confirm placement and provide 100% inspired oxygen while ventilating slowly at 6–12 breaths per minute. Limit pauses in compressions during airway placement. Establish IV or intraosseous access. Use continuous waveform capnography to guide and optimize compression quality; end-tidal CO₂ correlates with cardiac output and myocardial blood flow during CPR. Administer epinephrine every 3–5 minutes. Search for and treat reversible causes without delay. Sodium bicarbonate is reserved for suspected hyperkalemia or drug overdose. There is no proven benefit to giving an empiric single countershock, and no proven benefit to electrical pacing in asystole. If the rhythm converts to ventricular fibrillation or ventricular tachycardia, defibrillate immediately without delay.
Post-ROSC Care And ED Management
If return of spontaneous circulation occurs and the patient remains comatose, initiate induced hypothermia as part of post–cardiac arrest care. Consider termination of resuscitation only when high-quality compressions have been delivered for an adequate period, the trachea has been intubated to ensure oxygenation, fine ventricular fibrillation has been excluded, reversible causes have been corrected or ruled out, bedside ultrasound shows no pericardial effusion, and there is no clinical evidence of tension pneumothorax.
Medications
Epinephrine is given as 1 mg IV every 3–5 minutes in adults, and 0.01 mg/kg IV every 3–5 minutes in children. Sodium bicarbonate is dosed at 1 mEq/kg IV and should be used only when there is pre-existing acidosis, suspected hyperkalemia, or suspected tricyclic antidepressant overdose.
Disposition And Monitoring
Any patient with return of spontaneous circulation requires admission, and there are no discharge pathways from the ED after asystolic arrest. Post-arrest care should occur in an ICU with cardiac monitoring and induced hypothermia when indicated.
Follow-Up Planning
A permanent pacemaker may be considered only when asystole is determined to be due to primary heart block.
Clinical Lessons And Safety Points
Outcomes depend heavily on immediate, minimally interrupted, high-quality chest compressions while aggressively searching for reversible causes. Successful resuscitation is most likely only when a reversible cause is identified and corrected promptly.
