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Emergency and Acute Medicine – Calcium Channel Blocker Poisoning
Overview and Definitions
Calcium channel blocker (CCB) poisoning is a potentially life-threatening intoxication resulting from inhibition of calcium influx into cardiac and smooth muscle cells. This leads to impaired myocardial contractility, decreased vascular tone, and conduction abnormalities. CCB toxicity is associated with significant morbidity and mortality and requires early recognition and aggressive supportive care.
Three major classes of calcium channel blockers exist. Phenylalkylamines (verapamil) primarily affect the myocardium, producing negative chronotropic and inotropic effects with hypotension and bradycardia, without reflex tachycardia. Dihydropyridines (e.g., nifedipine) predominantly cause peripheral vasodilation leading to hypotension, often accompanied by reflex tachycardia. Benzothiazepines (diltiazem) have combined cardiac and vascular effects, with initial increases in heart rate and cardiac output followed by bradycardia and hypotension.
Calcium plays a critical role in cardiac and smooth muscle contraction and in insulin secretion from pancreatic beta cells. Blockade of calcium channels results in decreased contractility, impaired conduction, and reduced insulin release, leading to hyperglycemia, which is a hallmark of severe toxicity.
Etiology and Pathophysiology
CCB toxicity occurs following intentional overdose, medication errors, or accidental pediatric ingestion. Sustained-release formulations are particularly dangerous due to delayed onset and prolonged toxicity. Inhibition of calcium entry into myocardial cells reduces cardiac output and slows atrioventricular conduction, while vascular smooth muscle relaxation causes profound hypotension. Concurrent inhibition of insulin secretion leads to myocardial energy failure due to impaired carbohydrate utilization, contributing to shock and refractory hypotension.
Diagnosis
Signs and Symptoms
Cardiovascular manifestations include hypotension, bradycardia, reflex tachycardia (particularly with dihydropyridines), conduction delays, and high-grade heart blocks. Neurologic findings include altered mental status, agitation, seizures, and coma. Metabolic abnormalities include hyperglycemia and metabolic acidosis. Patients may appear warm rather than cool despite shock.
Essential Workup
A 12-lead ECG is mandatory to evaluate for bradycardia, QRS prolongation, and heart block. Continuous cardiac and hemodynamic monitoring is required.
Diagnostic Tests and Interpretation
Laboratory evaluation includes serum electrolytes, BUN, creatinine, glucose, CBC, and ionized calcium levels when calcium therapy is administered. Digoxin levels should be obtained in patients on digoxin prior to calcium administration. Hyperglycemia in the setting of bradycardia and hypotension strongly suggests CCB poisoning. Toxicology screening should be considered if co-ingestants are suspected.
Differential Diagnosis
β-blocker toxicity, clonidine toxicity, digoxin toxicity, and acute myocardial infarction with heart block.
Management
Prehospital Care
Transport all pill bottles to the emergency department. Administer calcium in unstable patients when CCB overdose is suspected.
Initial Stabilization and Therapy
Initial management follows ABC principles with early airway protection as needed. Supplemental oxygen, IV access with isotonic fluids, and continuous cardiac monitoring are essential.
Emergency Department Management
Therapeutic goals include maintaining heart rate above 60 beats/min, systolic blood pressure above 90 mm Hg, adequate urine output, and improving mental status. Syrup of ipecac is contraindicated. Activated charcoal may be considered early, particularly in sustained-release ingestions or co-ingestants.
Calcium therapy provides transient improvement. Calcium gluconate is preferred due to reduced tissue toxicity, while calcium chloride is more potent but risks extravasation injury. Calcium is contraindicated in digoxin toxicity. IV fluids should be administered cautiously. Atropine is usually ineffective.
High-dose insulin euglycemia therapy is a cornerstone of treatment, improving myocardial carbohydrate utilization and hemodynamics. Vasopressors such as dopamine, epinephrine, or norepinephrine may be required. Amrinone may improve inotropy. Electrical pacing is reserved for refractory cases. IV lipid emulsion and hypertonic sodium bicarbonate may be considered as rescue therapies.
Disposition and Follow-Up
Patients with symptoms or sustained-release ingestion require admission to a monitored setting. Asymptomatic patients who ingest immediate-release formulations may be discharged after 8 hours of observation. Psychiatric evaluation is required for intentional overdoses. Caregiver education is essential for pediatric exposures
Clinical Pearls and Pitfalls
Consider CCB toxicity in any patient presenting with unexplained hypotension, bradycardia, and hyperglycemia. Do not rely on atropine alone. Early initiation of high-dose insulin therapy improves outcomes. Sustained-release preparations may cause delayed and prolonged toxicity.
Overview and Definitions
Calcium channel blocker (CCB) poisoning is a potentially life-threatening intoxication resulting from inhibition of calcium influx into cardiac and smooth muscle cells. This leads to impaired myocardial contractility, decreased vascular tone, and conduction abnormalities. CCB toxicity is associated with significant morbidity and mortality and requires early recognition and aggressive supportive care.
Three major classes of calcium channel blockers exist. Phenylalkylamines (verapamil) primarily affect the myocardium, producing negative chronotropic and inotropic effects with hypotension and bradycardia, without reflex tachycardia. Dihydropyridines (e.g., nifedipine) predominantly cause peripheral vasodilation leading to hypotension, often accompanied by reflex tachycardia. Benzothiazepines (diltiazem) have combined cardiac and vascular effects, with initial increases in heart rate and cardiac output followed by bradycardia and hypotension.
Calcium plays a critical role in cardiac and smooth muscle contraction and in insulin secretion from pancreatic beta cells. Blockade of calcium channels results in decreased contractility, impaired conduction, and reduced insulin release, leading to hyperglycemia, which is a hallmark of severe toxicity.
Etiology and Pathophysiology
CCB toxicity occurs following intentional overdose, medication errors, or accidental pediatric ingestion. Sustained-release formulations are particularly dangerous due to delayed onset and prolonged toxicity. Inhibition of calcium entry into myocardial cells reduces cardiac output and slows atrioventricular conduction, while vascular smooth muscle relaxation causes profound hypotension. Concurrent inhibition of insulin secretion leads to myocardial energy failure due to impaired carbohydrate utilization, contributing to shock and refractory hypotension.
Diagnosis
Signs and Symptoms
Cardiovascular manifestations include hypotension, bradycardia, reflex tachycardia (particularly with dihydropyridines), conduction delays, and high-grade heart blocks. Neurologic findings include altered mental status, agitation, seizures, and coma. Metabolic abnormalities include hyperglycemia and metabolic acidosis. Patients may appear warm rather than cool despite shock.
Essential Workup
A 12-lead ECG is mandatory to evaluate for bradycardia, QRS prolongation, and heart block. Continuous cardiac and hemodynamic monitoring is required.
Diagnostic Tests and Interpretation
Laboratory evaluation includes serum electrolytes, BUN, creatinine, glucose, CBC, and ionized calcium levels when calcium therapy is administered. Digoxin levels should be obtained in patients on digoxin prior to calcium administration. Hyperglycemia in the setting of bradycardia and hypotension strongly suggests CCB poisoning. Toxicology screening should be considered if co-ingestants are suspected.
Differential Diagnosis
β-blocker toxicity, clonidine toxicity, digoxin toxicity, and acute myocardial infarction with heart block.
Management
Prehospital Care
Transport all pill bottles to the emergency department. Administer calcium in unstable patients when CCB overdose is suspected.
Initial Stabilization and Therapy
Initial management follows ABC principles with early airway protection as needed. Supplemental oxygen, IV access with isotonic fluids, and continuous cardiac monitoring are essential.
Emergency Department Management
Therapeutic goals include maintaining heart rate above 60 beats/min, systolic blood pressure above 90 mm Hg, adequate urine output, and improving mental status. Syrup of ipecac is contraindicated. Activated charcoal may be considered early, particularly in sustained-release ingestions or co-ingestants.
Calcium therapy provides transient improvement. Calcium gluconate is preferred due to reduced tissue toxicity, while calcium chloride is more potent but risks extravasation injury. Calcium is contraindicated in digoxin toxicity. IV fluids should be administered cautiously. Atropine is usually ineffective.
High-dose insulin euglycemia therapy is a cornerstone of treatment, improving myocardial carbohydrate utilization and hemodynamics. Vasopressors such as dopamine, epinephrine, or norepinephrine may be required. Amrinone may improve inotropy. Electrical pacing is reserved for refractory cases. IV lipid emulsion and hypertonic sodium bicarbonate may be considered as rescue therapies.
Disposition and Follow-Up
Patients with symptoms or sustained-release ingestion require admission to a monitored setting. Asymptomatic patients who ingest immediate-release formulations may be discharged after 8 hours of observation. Psychiatric evaluation is required for intentional overdoses. Caregiver education is essential for pediatric exposures
Clinical Pearls and Pitfalls
Consider CCB toxicity in any patient presenting with unexplained hypotension, bradycardia, and hyperglycemia. Do not rely on atropine alone. Early initiation of high-dose insulin therapy improves outcomes. Sustained-release preparations may cause delayed and prolonged toxicity.
- Published on
Emergency and Acute Medicine – Atrial Flutter
Clinical Overview
Atrial flutter is an atrial dysrhythmia affecting approximately 200,000 new patients annually. It is most commonly caused by a macroreentrant circuit within the right atrium and is considered the atrial arrhythmia most sensitive to cardioversion. Atrial flutter rarely occurs in the absence of underlying structural or organic heart disease and is less common than supraventricular tachycardia or atrial fibrillation. Episodes are typically paroxysmal, lasting seconds to hours, and atrial flutter is present in roughly 25–35% of patients who also have atrial fibrillation. When untreated, it may contribute to the development of tachycardia-induced cardiomyopathy.
Etiology And Predisposing Conditions
Common causes include alcoholism, cardiomyopathies, myocarditis, congestive heart failure, electrolyte disturbances, ischemic heart disease, pulmonary embolism and other pulmonary diseases, valvular heart disease, postoperative states following cardiac surgery—most frequently during the first postoperative week—and thyrotoxicosis.
In pediatric patients, atrial flutter may occur and is often asymptomatic. Mortality is highest during the neonatal period. It is commonly associated with congenital heart disease or infectious causes such as rheumatic fever or myocarditis. Toxic ingestions must be considered in children presenting with new atrioventricular conduction abnormalities.
Clinical Presentation
Patients may experience palpitations, syncope or presyncope, chest pain, fatigue, dyspnea, reduced exercise tolerance, and tachycardia often exceeding 150 beats per minute. Severe presentations may include hypotension or heart failure.
Infants tolerate atrial flutter poorly because the atrioventricular node may conduct very rapidly, leading to extreme ventricular rates that can result in shock or congestive heart failure. Atrial flutter can occur in fetuses and neonates without associated cardiac defects and often does not recur beyond the neonatal period. In contrast, older children usually have structural heart disease, with higher recurrence rates and more difficult rhythm control.
Initial Evaluation
Essential evaluation includes electrocardiography, laboratory studies, and chest radiography. The ECG confirms the diagnosis and guides management. Laboratory testing should include electrolytes and mineral panels, cardiac enzymes, digoxin levels when relevant, and coagulation studies. Chest radiography may reveal cardiomyopathy or evidence of heart failure. Echocardiography is useful for identifying regional wall motion abnormalities or valvular dysfunction.
Differential Diagnosis
Important considerations include supraventricular tachycardia, sinus tachycardia, atrial fibrillation, multifocal atrial tachycardia, and ventricular tachycardia.
Prehospital And Immediate Management
Initial management includes oxygen administration, cardiac monitoring, and intravenous access. Hemodynamically unstable patients should undergo immediate synchronized cardioversion in the field, typically starting at 100 joules.
Emergency Department Management
Unstable patients require immediate synchronized cardioversion. Current guidelines recommend beginning at 150–200 joules to improve first-shock success and reduce cumulative energy exposure.
Rate control should be achieved before administering antidysrhythmic agents to prevent 1:1 atrioventricular conduction and possible hemodynamic collapse, though adequate rate control can be challenging. Anticoagulation follows the same principles as atrial fibrillation, with therapeutic anticoagulation for at least three weeks prior to cardioversion when symptom duration exceeds 48 hours or is unknown, and continuation afterward even if transesophageal echocardiography is negative. Thromboembolic risk ranges from 1.7% to 7%.
Stroke risk stratification using the CHADS₂ score guides anticoagulation decisions. Patients with valvular disease, fluctuating atrial fibrillation/flutter, left ventricular dysfunction, prior stroke or thromboembolism, or symptom duration longer than 48 hours carry higher embolic risk.
Pharmacologic And Rhythm Control Options
Adenosine rarely terminates atrial flutter but may help unmask flutter waves diagnostically. Amiodarone is useful for rate control in pre-excited atrial arrhythmias and is preferred in patients with severe ventricular dysfunction, though hypotension and bradycardia may occur with rapid infusion. Calcium channel blockers and beta-blockers are effective for rate control, with verapamil associated with higher rates of hypotension and limited to narrow-complex arrhythmias. Magnesium sulfate may assist with rate control, though evidence is limited. Digoxin is a third-line agent with delayed onset but may benefit patients with ventricular dysfunction.
For rhythm control, procainamide is preferred in patients with Wolff–Parkinson–White syndrome and preserved ventricular function, though caution is required in QT prolongation. Sotalol and ibutilide may be used for rhythm conversion when arrhythmia duration is 48 hours or less and ventricular function is preserved. Ibutilide requires correction of electrolytes prior to use and post-administration monitoring due to the risk of torsades de pointes. Electrical cardioversion remains the safest and most effective method for restoring sinus rhythm.
Maintenance of sinus rhythm is challenging due to a high recurrence rate approaching 50% at one year. Amiodarone is the most effective pharmacologic agent. Catheter ablation offers acute success rates exceeding 95% with low complication rates and is recommended for recurrent, drug-resistant atrial flutter, medication intolerance, or patient preference to avoid long-term pharmacotherapy.
Pediatric Management Considerations
Verapamil is contraindicated in infants and young children due to the risk of severe cardiovascular compromise. Digoxin is the first-line pharmacologic therapy in pediatric atrial flutter. Cardioversion is often the preferred initial treatment in neonates.
Disposition And Follow-Up
Admission is indicated for new-onset atrial flutter requiring antidysrhythmic therapy, persistent symptoms, heart failure, or need for cardioversion. Discharge may be appropriate when rhythm or rate is controlled, underlying causes are addressed, anticoagulation is initiated, and reliable follow-up is arranged. Chronic atrial flutter patients with stable control and anticoagulation may be managed as outpatients. Cardiology follow-up is recommended, with catheter ablation increasingly serving as definitive therapy.
Key Clinical Insights And Safety Considerations
Wolff–Parkinson–White syndrome must always be excluded, as adenosine, beta-blockers, calcium channel blockers, and digoxin can precipitate ventricular fibrillation in these patients. Cardioversion should never be delayed in unstable patients for intravenous access. Beta-blockers must be used cautiously in those with pulmonary disease or heart failure. Management priorities include rate control, prevention of systemic embolization, restoration of sinus rhythm, and maintenance of long-term rhythm stability.
Clinical Overview
Atrial flutter is an atrial dysrhythmia affecting approximately 200,000 new patients annually. It is most commonly caused by a macroreentrant circuit within the right atrium and is considered the atrial arrhythmia most sensitive to cardioversion. Atrial flutter rarely occurs in the absence of underlying structural or organic heart disease and is less common than supraventricular tachycardia or atrial fibrillation. Episodes are typically paroxysmal, lasting seconds to hours, and atrial flutter is present in roughly 25–35% of patients who also have atrial fibrillation. When untreated, it may contribute to the development of tachycardia-induced cardiomyopathy.
Etiology And Predisposing Conditions
Common causes include alcoholism, cardiomyopathies, myocarditis, congestive heart failure, electrolyte disturbances, ischemic heart disease, pulmonary embolism and other pulmonary diseases, valvular heart disease, postoperative states following cardiac surgery—most frequently during the first postoperative week—and thyrotoxicosis.
In pediatric patients, atrial flutter may occur and is often asymptomatic. Mortality is highest during the neonatal period. It is commonly associated with congenital heart disease or infectious causes such as rheumatic fever or myocarditis. Toxic ingestions must be considered in children presenting with new atrioventricular conduction abnormalities.
Clinical Presentation
Patients may experience palpitations, syncope or presyncope, chest pain, fatigue, dyspnea, reduced exercise tolerance, and tachycardia often exceeding 150 beats per minute. Severe presentations may include hypotension or heart failure.
Infants tolerate atrial flutter poorly because the atrioventricular node may conduct very rapidly, leading to extreme ventricular rates that can result in shock or congestive heart failure. Atrial flutter can occur in fetuses and neonates without associated cardiac defects and often does not recur beyond the neonatal period. In contrast, older children usually have structural heart disease, with higher recurrence rates and more difficult rhythm control.
Initial Evaluation
Essential evaluation includes electrocardiography, laboratory studies, and chest radiography. The ECG confirms the diagnosis and guides management. Laboratory testing should include electrolytes and mineral panels, cardiac enzymes, digoxin levels when relevant, and coagulation studies. Chest radiography may reveal cardiomyopathy or evidence of heart failure. Echocardiography is useful for identifying regional wall motion abnormalities or valvular dysfunction.
Differential Diagnosis
Important considerations include supraventricular tachycardia, sinus tachycardia, atrial fibrillation, multifocal atrial tachycardia, and ventricular tachycardia.
Prehospital And Immediate Management
Initial management includes oxygen administration, cardiac monitoring, and intravenous access. Hemodynamically unstable patients should undergo immediate synchronized cardioversion in the field, typically starting at 100 joules.
Emergency Department Management
Unstable patients require immediate synchronized cardioversion. Current guidelines recommend beginning at 150–200 joules to improve first-shock success and reduce cumulative energy exposure.
Rate control should be achieved before administering antidysrhythmic agents to prevent 1:1 atrioventricular conduction and possible hemodynamic collapse, though adequate rate control can be challenging. Anticoagulation follows the same principles as atrial fibrillation, with therapeutic anticoagulation for at least three weeks prior to cardioversion when symptom duration exceeds 48 hours or is unknown, and continuation afterward even if transesophageal echocardiography is negative. Thromboembolic risk ranges from 1.7% to 7%.
Stroke risk stratification using the CHADS₂ score guides anticoagulation decisions. Patients with valvular disease, fluctuating atrial fibrillation/flutter, left ventricular dysfunction, prior stroke or thromboembolism, or symptom duration longer than 48 hours carry higher embolic risk.
Pharmacologic And Rhythm Control Options
Adenosine rarely terminates atrial flutter but may help unmask flutter waves diagnostically. Amiodarone is useful for rate control in pre-excited atrial arrhythmias and is preferred in patients with severe ventricular dysfunction, though hypotension and bradycardia may occur with rapid infusion. Calcium channel blockers and beta-blockers are effective for rate control, with verapamil associated with higher rates of hypotension and limited to narrow-complex arrhythmias. Magnesium sulfate may assist with rate control, though evidence is limited. Digoxin is a third-line agent with delayed onset but may benefit patients with ventricular dysfunction.
For rhythm control, procainamide is preferred in patients with Wolff–Parkinson–White syndrome and preserved ventricular function, though caution is required in QT prolongation. Sotalol and ibutilide may be used for rhythm conversion when arrhythmia duration is 48 hours or less and ventricular function is preserved. Ibutilide requires correction of electrolytes prior to use and post-administration monitoring due to the risk of torsades de pointes. Electrical cardioversion remains the safest and most effective method for restoring sinus rhythm.
Maintenance of sinus rhythm is challenging due to a high recurrence rate approaching 50% at one year. Amiodarone is the most effective pharmacologic agent. Catheter ablation offers acute success rates exceeding 95% with low complication rates and is recommended for recurrent, drug-resistant atrial flutter, medication intolerance, or patient preference to avoid long-term pharmacotherapy.
Pediatric Management Considerations
Verapamil is contraindicated in infants and young children due to the risk of severe cardiovascular compromise. Digoxin is the first-line pharmacologic therapy in pediatric atrial flutter. Cardioversion is often the preferred initial treatment in neonates.
Disposition And Follow-Up
Admission is indicated for new-onset atrial flutter requiring antidysrhythmic therapy, persistent symptoms, heart failure, or need for cardioversion. Discharge may be appropriate when rhythm or rate is controlled, underlying causes are addressed, anticoagulation is initiated, and reliable follow-up is arranged. Chronic atrial flutter patients with stable control and anticoagulation may be managed as outpatients. Cardiology follow-up is recommended, with catheter ablation increasingly serving as definitive therapy.
Key Clinical Insights And Safety Considerations
Wolff–Parkinson–White syndrome must always be excluded, as adenosine, beta-blockers, calcium channel blockers, and digoxin can precipitate ventricular fibrillation in these patients. Cardioversion should never be delayed in unstable patients for intravenous access. Beta-blockers must be used cautiously in those with pulmonary disease or heart failure. Management priorities include rate control, prevention of systemic embolization, restoration of sinus rhythm, and maintenance of long-term rhythm stability.
- 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 – 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 – 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.
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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.
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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 - 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.
