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Emergency and Acute Medicine – Bundle Branch Blocks
Overview And Definitions
Bundle branch blocks (BBBs) result from impaired intraventricular conduction through the right or left bundle branches. In complete BBB, conduction is absent or markedly delayed in one bundle while the other conducts normally, causing the affected ventricle to depolarize via slower muscle-to-muscle transmission. This produces a widened, disorganized QRS complex ≥120 msec.
Incomplete BBB represents delayed but not fully blocked conduction, with QRS duration between 100 and 120 msec.
Right bundle branch block (RBBB) reflects delayed right ventricular depolarization, whereas left bundle branch block (LBBB) reflects delayed left ventricular depolarization. LBBB may result from delay in the main left bundle or both left fascicles and leads to early right septal activation with loss of normal septal Q waves on ECG.
Anatomic And Conduction Considerations
The left bundle divides into two fascicles. The left anterior fascicle conducts impulses inferiorly, anteriorly, and to the right; its blockage alters frontal plane axis. The left posterior fascicle activates the midseptum and inferior–posterior walls; isolated block is rare.
Bifascicular block refers to RBBB combined with either left anterior or left posterior fascicular block.
Etiology And Pathophysiology
Common causes include myocardial infarction, cardiomyopathy, chronic hypertension, valvular heart disease, age-related fibrosis of the Purkinje system, and postoperative changes after cardiac surgery. Congenital heart disease such as atrial septal defect may be associated. Exercise-induced BBBs can occur.
Certain diseases and conditions are notable, including Brugada syndrome (typically presenting with RBBB pattern and associated with sudden cardiac death) and Chagas disease, particularly in Central and South America.
Medications may contribute, including β-blockers, calcium channel blockers, tricyclic antidepressants, class Ia and Ic antiarrhythmics, and digoxin.
Clinical Presentation
Many patients are asymptomatic. RBBB may be associated with a split S2 that persists with expiration, while LBBB produces a paradoxical or reversed split S2. When symptoms occur, they may include syncope or presyncope, chest pain, or manifestations related to the underlying cardiac disease.
Initial Evaluation And Essential Workup
A 12-lead ECG is central to diagnosis. Careful clinical assessment is required to identify ischemia, syncope, or associated dysrhythmias.
Electrocardiographic Features
RBBB shows a QRS duration ≥0.12 sec when complete and 0.10–0.12 sec when incomplete, with rsrʹ, rsRʹ, or rSRʹ (“M-shaped”) complexes in V1–V2 and a wide, deep S wave in V5–V6. Brugada syndrome presents with RBBB morphology plus ST-segment elevation in V1–V3.
LBBB is characterized by broad, slurred R waves in leads V5–V6, I, and aVL; small or absent R waves with deep S waves in V1–V2; and absence of normal septal Q waves in V5–V6 and I.
Left anterior fascicular block shows a QRS <120 msec with left-axis deviation (approximately −45° to −90°), deep s waves in ii, iii, and avf, qr complexes i avl.< />pan>
Left posterior fascicular block shows QRS <120 msec with right-axis deviation (≥120°), rs complexes in i and avl, qr ii, iii, avf, after excluding other causes of deviation.< />pan>
Diagnostic Testing
Laboratory testing may include electrolytes when metabolic disturbances are suspected and cardiac enzymes if ischemia is a concern. Chest radiography can reveal cardiomegaly or congestive heart failure. Electrophysiologic testing may be indicated in patients with unexplained syncope and structural heart disease as part of inpatient evaluation.
Differential Diagnosis
Consider ventricular tachycardia, myocardial infarction, ventricular hypertrophy, hyperkalemia, and drug-induced conduction abnormalities. In patients with LBBB, myocardial infarction assessment relies on criteria such as the Sgarbossa criteria, including concordant ST elevation or depression and excessive discordant ST elevation.
Management In The Emergency Setting
Isolated bundle branch block itself does not require specific therapy. Management focuses on treating associated conditions such as ischemia, heart failure, or syncope. Continuous monitoring is important, as BBBs can complicate rhythm interpretation and mimic ventricular tachycardia or ischemia.
Patients with symptomatic bifascicular block or high-grade atrioventricular block should have transcutaneous pacing pads applied, with sedation and analgesia as needed. Transvenous pacing is indicated for bifascicular block with type II second-degree or third-degree AV block, or for alternating LBBB and RBBB. New BBB with symptoms suggestive of myocardial infarction warrants urgent reperfusion therapy or catheterization.
Disposition And Follow-Up
Admission is required for patients with suspected myocardial ischemia, syncope, dysrhythmias, or BBB associated with high-grade AV block. Asymptomatic patients or those with incidental findings may be discharged with appropriate counseling. Referral to a cardiologist is recommended to evaluate for underlying cardiac disease.
Clinical Pearls And Pitfalls
New conduction abnormalities should always prompt consideration of myocardial ischemia. Specific ECG criteria help identify infarction in the presence of bundle branch block. Careful rhythm interpretation is essential to avoid misdiagnosing ventricular tachycardia or missing acute ischemia.
Overview And Definitions
Bundle branch blocks (BBBs) result from impaired intraventricular conduction through the right or left bundle branches. In complete BBB, conduction is absent or markedly delayed in one bundle while the other conducts normally, causing the affected ventricle to depolarize via slower muscle-to-muscle transmission. This produces a widened, disorganized QRS complex ≥120 msec.
Incomplete BBB represents delayed but not fully blocked conduction, with QRS duration between 100 and 120 msec.
Right bundle branch block (RBBB) reflects delayed right ventricular depolarization, whereas left bundle branch block (LBBB) reflects delayed left ventricular depolarization. LBBB may result from delay in the main left bundle or both left fascicles and leads to early right septal activation with loss of normal septal Q waves on ECG.
Anatomic And Conduction Considerations
The left bundle divides into two fascicles. The left anterior fascicle conducts impulses inferiorly, anteriorly, and to the right; its blockage alters frontal plane axis. The left posterior fascicle activates the midseptum and inferior–posterior walls; isolated block is rare.
Bifascicular block refers to RBBB combined with either left anterior or left posterior fascicular block.
Etiology And Pathophysiology
Common causes include myocardial infarction, cardiomyopathy, chronic hypertension, valvular heart disease, age-related fibrosis of the Purkinje system, and postoperative changes after cardiac surgery. Congenital heart disease such as atrial septal defect may be associated. Exercise-induced BBBs can occur.
Certain diseases and conditions are notable, including Brugada syndrome (typically presenting with RBBB pattern and associated with sudden cardiac death) and Chagas disease, particularly in Central and South America.
Medications may contribute, including β-blockers, calcium channel blockers, tricyclic antidepressants, class Ia and Ic antiarrhythmics, and digoxin.
Clinical Presentation
Many patients are asymptomatic. RBBB may be associated with a split S2 that persists with expiration, while LBBB produces a paradoxical or reversed split S2. When symptoms occur, they may include syncope or presyncope, chest pain, or manifestations related to the underlying cardiac disease.
Initial Evaluation And Essential Workup
A 12-lead ECG is central to diagnosis. Careful clinical assessment is required to identify ischemia, syncope, or associated dysrhythmias.
Electrocardiographic Features
RBBB shows a QRS duration ≥0.12 sec when complete and 0.10–0.12 sec when incomplete, with rsrʹ, rsRʹ, or rSRʹ (“M-shaped”) complexes in V1–V2 and a wide, deep S wave in V5–V6. Brugada syndrome presents with RBBB morphology plus ST-segment elevation in V1–V3.
LBBB is characterized by broad, slurred R waves in leads V5–V6, I, and aVL; small or absent R waves with deep S waves in V1–V2; and absence of normal septal Q waves in V5–V6 and I.
Left anterior fascicular block shows a QRS <120 msec with left-axis deviation (approximately −45° to −90°), deep s waves in ii, iii, and avf, qr complexes i avl.< />pan>
Left posterior fascicular block shows QRS <120 msec with right-axis deviation (≥120°), rs complexes in i and avl, qr ii, iii, avf, after excluding other causes of deviation.< />pan>
Diagnostic Testing
Laboratory testing may include electrolytes when metabolic disturbances are suspected and cardiac enzymes if ischemia is a concern. Chest radiography can reveal cardiomegaly or congestive heart failure. Electrophysiologic testing may be indicated in patients with unexplained syncope and structural heart disease as part of inpatient evaluation.
Differential Diagnosis
Consider ventricular tachycardia, myocardial infarction, ventricular hypertrophy, hyperkalemia, and drug-induced conduction abnormalities. In patients with LBBB, myocardial infarction assessment relies on criteria such as the Sgarbossa criteria, including concordant ST elevation or depression and excessive discordant ST elevation.
Management In The Emergency Setting
Isolated bundle branch block itself does not require specific therapy. Management focuses on treating associated conditions such as ischemia, heart failure, or syncope. Continuous monitoring is important, as BBBs can complicate rhythm interpretation and mimic ventricular tachycardia or ischemia.
Patients with symptomatic bifascicular block or high-grade atrioventricular block should have transcutaneous pacing pads applied, with sedation and analgesia as needed. Transvenous pacing is indicated for bifascicular block with type II second-degree or third-degree AV block, or for alternating LBBB and RBBB. New BBB with symptoms suggestive of myocardial infarction warrants urgent reperfusion therapy or catheterization.
Disposition And Follow-Up
Admission is required for patients with suspected myocardial ischemia, syncope, dysrhythmias, or BBB associated with high-grade AV block. Asymptomatic patients or those with incidental findings may be discharged with appropriate counseling. Referral to a cardiologist is recommended to evaluate for underlying cardiac disease.
Clinical Pearls And Pitfalls
New conduction abnormalities should always prompt consideration of myocardial ischemia. Specific ECG criteria help identify infarction in the presence of bundle branch block. Careful rhythm interpretation is essential to avoid misdiagnosing ventricular tachycardia or missing acute ischemia.
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Emergency and Acute Medicine – Brugada Syndrome
Overview And Definitions
Brugada syndrome is an inherited cardiac channelopathy caused by mutations in cardiac sodium (Na⁺) channels, occurring in the absence of structural heart disease. It carries a very high risk of sudden cardiac death, typically due to ventricular fibrillation. Two-year mortality approaches 30% without intervention. The condition accounts for 40–60% of cases previously labeled idiopathic ventricular fibrillation. It is more prevalent in men, particularly those of Southeast Asian descent, but can affect all ages, sexes, and races.
Etiology And Pathophysiology
Brugada syndrome is inherited in an autosomal dominant pattern in approximately 50% of cases, with variable penetrance. More than 70 sodium channel mutations have been identified, most involving the SCN5A gene, which accounts for roughly 20% of cases. The abnormal sodium current predisposes to malignant ventricular dysrhythmias, especially under triggering conditions such as fever, metabolic derangements, or drug exposure.
Clinical Presentation
Patients most commonly present with syncope, near-syncope, palpitations, or sudden cardiac arrest due to polymorphic ventricular tachycardia or ventricular fibrillation. Episodes often occur at rest or during sleep. A history may reveal nocturnal agonal respirations, fever-associated symptoms, cocaine use, or exposure to tricyclic antidepressants or psychotropic drugs. Family history is critical and may include unexplained drowning, early or sudden cardiac death, or known Brugada syndrome in relatives. Physical examination is usually normal but should focus on excluding alternative causes of syncope or dysrhythmia.
Diagnostic Evaluation
A 12-lead ECG is essential. Toxicology screening and careful history and family assessment are required. Laboratory studies should evaluate electrolytes, metabolic abnormalities, and ischemia when appropriate.
Electrocardiographic Findings
Diagnosis is based on characteristic ECG patterns in the right precordial leads (V1–V3), often with right bundle branch block or incomplete right bundle branch block morphology and ST-segment elevation.
Type 1 (coved pattern) shows ≥2 mm ST elevation with a downsloping, concave ST segment and a negative symmetric T wave, without QRS duration mismatch between V1 and V6.
Type 2 (saddleback pattern) shows an r′ ≥2 mm followed by convex ST elevation and a QRS duration mismatch between V1 and V6. ST elevation may be limited to V1 and rarely extends to V3.
Additional Testing
Laboratory testing includes serum chemistries, cardiac biomarkers if ischemia is suspected, CBC in syncope evaluation, and D-dimer when pulmonary embolism is considered. Chest radiography assesses cardiomegaly, and CT angiography is used selectively. Electrophysiology testing with sodium channel blocker challenge may unmask diagnostic ECG changes. Implantable cardioverter-defibrillator (ICD) placement dramatically reduces mortality.
Differential Diagnosis
Consider other causes of syncope and dysrhythmia, including vasovagal syncope, hypovolemia, pregnancy, atrial and ventricular tachyarrhythmias, Wolff–Parkinson–White syndrome, long QT syndromes, high-grade AV block, symptomatic bradycardia, and drug overdose (especially TCAs). ECG mimics include isolated RBBB, athletic heart changes, septal hypertrophy, pectus excavatum, arrhythmogenic right ventricular cardiomyopathy, STEMI, myocarditis, pericarditis, electrolyte disorders, and pulmonary embolism.
Management And Emergency Care
Initial management follows standard airway, breathing, and circulation principles, with full ACLS protocols for arrest or unstable dysrhythmias. Continuous cardiac monitoring is required. Cardiology consultation for electrophysiology evaluation is essential. Electrolyte and metabolic abnormalities should be corrected promptly. Antiarrhythmic medications are generally ineffective. Management of asymptomatic patients remains controversial, though EP evaluation is recommended.
Disposition And Follow-Up
Patients with concerning ECG findings, unexplained syncope, ongoing dysrhythmias, or inability to obtain urgent cardiology follow-up should be admitted. Discharge may be considered only if the patient is asymptomatic, hemodynamically stable, and cleared by cardiology, including appropriate ICD interrogation if present. All patients with suspected or confirmed Brugada syndrome require electrophysiology follow-up.
Key Clinical Insights And Diagnostic Traps
Maintain suspicion for Brugada syndrome in cases of unexplained syncope or sudden cardiac death, particularly with a relevant family history. The ECG pattern—RBBB or incomplete RBBB with ST elevation isolated to V1–V3—is central to diagnosis, but several mimics exist. Fever, systemic illness, or drugs may unmask the Brugada pattern. Early cardiology involvement is critical, as ICD implantation is the only proven therapy that nearly eliminates the risk of sudden cardiac death.
Overview And Definitions
Brugada syndrome is an inherited cardiac channelopathy caused by mutations in cardiac sodium (Na⁺) channels, occurring in the absence of structural heart disease. It carries a very high risk of sudden cardiac death, typically due to ventricular fibrillation. Two-year mortality approaches 30% without intervention. The condition accounts for 40–60% of cases previously labeled idiopathic ventricular fibrillation. It is more prevalent in men, particularly those of Southeast Asian descent, but can affect all ages, sexes, and races.
Etiology And Pathophysiology
Brugada syndrome is inherited in an autosomal dominant pattern in approximately 50% of cases, with variable penetrance. More than 70 sodium channel mutations have been identified, most involving the SCN5A gene, which accounts for roughly 20% of cases. The abnormal sodium current predisposes to malignant ventricular dysrhythmias, especially under triggering conditions such as fever, metabolic derangements, or drug exposure.
Clinical Presentation
Patients most commonly present with syncope, near-syncope, palpitations, or sudden cardiac arrest due to polymorphic ventricular tachycardia or ventricular fibrillation. Episodes often occur at rest or during sleep. A history may reveal nocturnal agonal respirations, fever-associated symptoms, cocaine use, or exposure to tricyclic antidepressants or psychotropic drugs. Family history is critical and may include unexplained drowning, early or sudden cardiac death, or known Brugada syndrome in relatives. Physical examination is usually normal but should focus on excluding alternative causes of syncope or dysrhythmia.
Diagnostic Evaluation
A 12-lead ECG is essential. Toxicology screening and careful history and family assessment are required. Laboratory studies should evaluate electrolytes, metabolic abnormalities, and ischemia when appropriate.
Electrocardiographic Findings
Diagnosis is based on characteristic ECG patterns in the right precordial leads (V1–V3), often with right bundle branch block or incomplete right bundle branch block morphology and ST-segment elevation.
Type 1 (coved pattern) shows ≥2 mm ST elevation with a downsloping, concave ST segment and a negative symmetric T wave, without QRS duration mismatch between V1 and V6.
Type 2 (saddleback pattern) shows an r′ ≥2 mm followed by convex ST elevation and a QRS duration mismatch between V1 and V6. ST elevation may be limited to V1 and rarely extends to V3.
Additional Testing
Laboratory testing includes serum chemistries, cardiac biomarkers if ischemia is suspected, CBC in syncope evaluation, and D-dimer when pulmonary embolism is considered. Chest radiography assesses cardiomegaly, and CT angiography is used selectively. Electrophysiology testing with sodium channel blocker challenge may unmask diagnostic ECG changes. Implantable cardioverter-defibrillator (ICD) placement dramatically reduces mortality.
Differential Diagnosis
Consider other causes of syncope and dysrhythmia, including vasovagal syncope, hypovolemia, pregnancy, atrial and ventricular tachyarrhythmias, Wolff–Parkinson–White syndrome, long QT syndromes, high-grade AV block, symptomatic bradycardia, and drug overdose (especially TCAs). ECG mimics include isolated RBBB, athletic heart changes, septal hypertrophy, pectus excavatum, arrhythmogenic right ventricular cardiomyopathy, STEMI, myocarditis, pericarditis, electrolyte disorders, and pulmonary embolism.
Management And Emergency Care
Initial management follows standard airway, breathing, and circulation principles, with full ACLS protocols for arrest or unstable dysrhythmias. Continuous cardiac monitoring is required. Cardiology consultation for electrophysiology evaluation is essential. Electrolyte and metabolic abnormalities should be corrected promptly. Antiarrhythmic medications are generally ineffective. Management of asymptomatic patients remains controversial, though EP evaluation is recommended.
Disposition And Follow-Up
Patients with concerning ECG findings, unexplained syncope, ongoing dysrhythmias, or inability to obtain urgent cardiology follow-up should be admitted. Discharge may be considered only if the patient is asymptomatic, hemodynamically stable, and cleared by cardiology, including appropriate ICD interrogation if present. All patients with suspected or confirmed Brugada syndrome require electrophysiology follow-up.
Key Clinical Insights And Diagnostic Traps
Maintain suspicion for Brugada syndrome in cases of unexplained syncope or sudden cardiac death, particularly with a relevant family history. The ECG pattern—RBBB or incomplete RBBB with ST elevation isolated to V1–V3—is central to diagnosis, but several mimics exist. Fever, systemic illness, or drugs may unmask the Brugada pattern. Early cardiology involvement is critical, as ICD implantation is the only proven therapy that nearly eliminates the risk of sudden cardiac death.
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Emergency and Acute Medicine – Bronchiolitis
Overview and Definitions
Bronchiolitis is a lower respiratory tract infection characterized by airway inflammation, bronchoconstriction, wheezing, tachypnea, and varying degrees of respiratory distress, typically preceded by an upper respiratory prodrome.
Etiology and Pathophysiology
Respiratory syncytial virus is responsible for approximately 85–90% of cases. Other causative viruses include influenza, parainfluenza, and adenovirus. Disease incidence peaks during winter months. Viral infection leads to mucosal edema, increased mucus production, and small airway obstruction, resulting in impaired ventilation and increased work of breathing.
Clinical Presentation
Bronchiolitis primarily affects children younger than 2 years, most commonly infants under 1 year. Initial symptoms include nasal congestion with marked rhinorrhea, followed by cough that may be associated with posttussive vomiting. Wheezing, crackles, and rhonchi are common on auscultation. Respiratory distress manifests as tachypnea, nasal flaring, retractions, and grunting, often worsening over 1–3 days. Fever is usually low-grade (<39.5°c). hypoxemia is typically mild, and cyanosis rare. decreased oral intake common, though frank dehydration uncommon. apnea may occur, particularly in premature or very young infants. high-risk children receive monthly intramuscular palivizumab during rsv season to reduce infection risk.< />pan>
Essential Evaluation
Diagnosis is clinical. Assessment focuses on respiratory effort, oxygenation, and hydration status. Pulse oximetry is useful for confirming oxygenation and trending disease progression. Identification of the viral cause may assist with inpatient cohorting but rarely alters acute management.
Diagnostic Tests and Interpretation
Most patients require no laboratory testing beyond pulse oximetry. Nasopharyngeal aspirates or washes for viral studies may be considered in critically ill children, febrile infants under 3 months, those with atypical features, suspected alternative diagnoses (e.g., pertussis or chlamydia), significant comorbidities (chronic lung or cardiac disease), or prematurity. Chest radiographs typically show hyperinflation, peribronchial thickening, atelectasis, or variable infiltrates; atelectasis in young infants suggests more severe disease. Imaging is not routinely indicated and is reserved for atypical presentations, lack of improvement after 2–3 weeks, concern for alternative diagnoses, or impending respiratory failure. Septic evaluation may be required in febrile neonates, and urine testing should be considered in febrile infants 1–3 months old.
Differential Diagnosis
Asthma or recurrent virus-induced wheezing, pertussis (paroxysmal cough without wheeze between spells), bacterial pneumonia (toxic appearance, focal consolidation), foreign body aspiration (sudden onset, often afebrile), and congestive heart failure (feeding difficulty, failure to thrive).
Prehospital Care
Young infants have limited respiratory reserve and may deteriorate rapidly. Continuous cardiorespiratory monitoring and oxygen supplementation are indicated when saturations fall below 90–92% or distress is severe. Vigilance for apnea is critical, especially in infants under 7 weeks, weight <4 kg, or with marked tachypnea comorbidities. bag-mask ventilation may be required for recurrent apneas.< />pan>
Initial Stabilization in the ED
Management follows pediatric advanced life support principles with attention to airway, ventilation, and hydration. Early intubation is indicated for recurrent apnea or impending respiratory failure.
Emergency Department Management
Supplemental oxygen is provided for hypoxemia. Parenteral hydration is used when oral intake is inadequate or respiratory distress is significant. Most children do not benefit from routine pharmacotherapy. Bronchodilators may be trialed in moderate to severe disease, continued only if a clear reduction in work of breathing is observed. Corticosteroids alone generally do not alter outcomes; however, combined nebulized epinephrine with oral dexamethasone may reduce admissions in moderate to severe cases, likely due to synergistic effects. Antibiotics are not indicated unless there is evidence of bacterial infection. Ribavirin has no role in ED management.
Medications
Therapeutic trials may include nebulized albuterol or levalbuterol, nebulized epinephrine, and dexamethasone in selected patients. Most children require no medications, and bronchodilators after discharge are ineffective unless clear benefit was demonstrated prior to discharge.
Disposition
Admission is indicated for hypoxemia requiring oxygen, inability to maintain hydration, significant or persistent respiratory distress, apnea, severe comorbidities, failure to improve after therapy, or unreliable home monitoring. Discharge may be considered when feeding is adequate, oxygenation is acceptable on room air, respiratory distress has resolved, and close follow-up is assured.
Follow-Up Care
Because bronchiolitis often worsens early in its course, close outpatient follow-up within 24 hours is essential. Caregivers should be counseled regarding signs of worsening respiratory distress, dehydration, and apnea. Symptoms may persist for 2–3 weeks, and small, frequent feeds are recommended.
Key Clinical Insights and Common Errors
Infants with bronchiolitis frequently present with a combination of respiratory distress, hypoxia, dehydration, and apnea. Underestimating the potential for rapid deterioration is a common error; vigilant monitoring and early supportive care are critical to preventing adverse outcomes.
Overview and Definitions
Bronchiolitis is a lower respiratory tract infection characterized by airway inflammation, bronchoconstriction, wheezing, tachypnea, and varying degrees of respiratory distress, typically preceded by an upper respiratory prodrome.
Etiology and Pathophysiology
Respiratory syncytial virus is responsible for approximately 85–90% of cases. Other causative viruses include influenza, parainfluenza, and adenovirus. Disease incidence peaks during winter months. Viral infection leads to mucosal edema, increased mucus production, and small airway obstruction, resulting in impaired ventilation and increased work of breathing.
Clinical Presentation
Bronchiolitis primarily affects children younger than 2 years, most commonly infants under 1 year. Initial symptoms include nasal congestion with marked rhinorrhea, followed by cough that may be associated with posttussive vomiting. Wheezing, crackles, and rhonchi are common on auscultation. Respiratory distress manifests as tachypnea, nasal flaring, retractions, and grunting, often worsening over 1–3 days. Fever is usually low-grade (<39.5°c). hypoxemia is typically mild, and cyanosis rare. decreased oral intake common, though frank dehydration uncommon. apnea may occur, particularly in premature or very young infants. high-risk children receive monthly intramuscular palivizumab during rsv season to reduce infection risk.< />pan>
Essential Evaluation
Diagnosis is clinical. Assessment focuses on respiratory effort, oxygenation, and hydration status. Pulse oximetry is useful for confirming oxygenation and trending disease progression. Identification of the viral cause may assist with inpatient cohorting but rarely alters acute management.
Diagnostic Tests and Interpretation
Most patients require no laboratory testing beyond pulse oximetry. Nasopharyngeal aspirates or washes for viral studies may be considered in critically ill children, febrile infants under 3 months, those with atypical features, suspected alternative diagnoses (e.g., pertussis or chlamydia), significant comorbidities (chronic lung or cardiac disease), or prematurity. Chest radiographs typically show hyperinflation, peribronchial thickening, atelectasis, or variable infiltrates; atelectasis in young infants suggests more severe disease. Imaging is not routinely indicated and is reserved for atypical presentations, lack of improvement after 2–3 weeks, concern for alternative diagnoses, or impending respiratory failure. Septic evaluation may be required in febrile neonates, and urine testing should be considered in febrile infants 1–3 months old.
Differential Diagnosis
Asthma or recurrent virus-induced wheezing, pertussis (paroxysmal cough without wheeze between spells), bacterial pneumonia (toxic appearance, focal consolidation), foreign body aspiration (sudden onset, often afebrile), and congestive heart failure (feeding difficulty, failure to thrive).
Prehospital Care
Young infants have limited respiratory reserve and may deteriorate rapidly. Continuous cardiorespiratory monitoring and oxygen supplementation are indicated when saturations fall below 90–92% or distress is severe. Vigilance for apnea is critical, especially in infants under 7 weeks, weight <4 kg, or with marked tachypnea comorbidities. bag-mask ventilation may be required for recurrent apneas.< />pan>
Initial Stabilization in the ED
Management follows pediatric advanced life support principles with attention to airway, ventilation, and hydration. Early intubation is indicated for recurrent apnea or impending respiratory failure.
Emergency Department Management
Supplemental oxygen is provided for hypoxemia. Parenteral hydration is used when oral intake is inadequate or respiratory distress is significant. Most children do not benefit from routine pharmacotherapy. Bronchodilators may be trialed in moderate to severe disease, continued only if a clear reduction in work of breathing is observed. Corticosteroids alone generally do not alter outcomes; however, combined nebulized epinephrine with oral dexamethasone may reduce admissions in moderate to severe cases, likely due to synergistic effects. Antibiotics are not indicated unless there is evidence of bacterial infection. Ribavirin has no role in ED management.
Medications
Therapeutic trials may include nebulized albuterol or levalbuterol, nebulized epinephrine, and dexamethasone in selected patients. Most children require no medications, and bronchodilators after discharge are ineffective unless clear benefit was demonstrated prior to discharge.
Disposition
Admission is indicated for hypoxemia requiring oxygen, inability to maintain hydration, significant or persistent respiratory distress, apnea, severe comorbidities, failure to improve after therapy, or unreliable home monitoring. Discharge may be considered when feeding is adequate, oxygenation is acceptable on room air, respiratory distress has resolved, and close follow-up is assured.
Follow-Up Care
Because bronchiolitis often worsens early in its course, close outpatient follow-up within 24 hours is essential. Caregivers should be counseled regarding signs of worsening respiratory distress, dehydration, and apnea. Symptoms may persist for 2–3 weeks, and small, frequent feeds are recommended.
Key Clinical Insights and Common Errors
Infants with bronchiolitis frequently present with a combination of respiratory distress, hypoxia, dehydration, and apnea. Underestimating the potential for rapid deterioration is a common error; vigilant monitoring and early supportive care are critical to preventing adverse outcomes.
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Emergency and Acute Medicine – Bradyarrhythmias
Overview and Definitions
Bradyarrhythmias are defined as a ventricular heart rate <60 beats />in. Sinus bradycardia may be a normal physiologic variant, whereas all other bradyarrhythmias are considered pathologic. Patients may be asymptomatic or present with hypotension, altered mental status, fatigue, nausea, syncope, or cardiac arrest. Management depends on ECG findings and the patient’s clinical stability rather than heart rate alone.
Etiology and Pathophysiology
Bradyarrhythmias may be idiopathic or secondary to intrinsic or extrinsic causes. Idiopathic causes include healthy, well-conditioned athletes. Intrinsic cardiac causes include sinus node dysfunction (e.g., sick sinus syndrome with brady–tachy variants), atrioventricular (AV) block with junctional or ventricular escape rhythms, infiltrative diseases (amyloidosis, sarcoidosis, hemochromatosis), collagen vascular diseases (SLE, scleroderma, rheumatoid arthritis), congenital or acquired anatomic abnormalities (postsurgical, post-transplant, postradiation), muscular disorders (myotonic dystrophy), and myocardial contusion from trauma.
Extrinsic causes include myocardial ischemia or infarction (RCA infarction → sinus bradycardia; LAD infarction → high-grade AV block), acidemia, medications and toxins (β-blockers, calcium channel blockers, digoxin, clonidine, antiarrhythmics, lithium, organophosphates), electrolyte abnormalities (hypo-/hyperkalemia, hypoglycemia, hypo-/hypercalcemia, hypermagnesemia), hypoxia, hypothermia, hypotension or severe hypertension, endocrine disorders (hypothyroidism), infections (Lyme disease, Chagas disease, diphtheria, endocarditis, myocarditis), and neurologic conditions (increased intracranial pressure, increased vagal tone, carotid sinus hypersensitivity, spinal cord injury). Vagal triggers include micturition, defecation, coughing, vomiting, ocular pressure, and other Valsalva maneuvers.
Special Populations
In children, hypoxia is the most common cause of bradycardia. During pregnancy, maternal SLE may result in congenital complete heart block.
Clinical Presentation
Many patients are asymptomatic. Symptomatic presentations include lightheadedness, confusion, fatigue, decreased level of consciousness, dyspnea, cyanosis, pallor, chest pain or pressure, diaphoresis, hypotension, syncope, hypothermia, or cardiac arrest.
History and Physical Examination
Key historical elements include recent medication changes, urine output patterns suggesting electrolyte disturbances, trauma (intracranial injury or myocardial contusion), and activity at symptom onset suggesting increased vagal tone. Physical examination focuses on respiratory status, perfusion and pulses, rhythm regularity, mental status with full neurologic assessment, body habitus, skin/hair/nails, and temperature.
Essential Evaluation
Immediate evaluation includes ECG with continuous cardiac monitoring, pulse oximetry, blood pressure monitoring, and bedside glucose and electrolyte assessment.
Diagnostic Tests and Interpretation
Laboratory testing may include serum glucose, electrolytes, BUN/creatinine, cardiac enzymes, digoxin level, thyroid function tests, rheumatologic markers (ANA, RF), Lyme titers, and iron studies. Imaging includes chest radiograph and CT head for altered mental status.
ECG findings define the rhythm: sinus bradycardia with normal P–QRS relationship; sinoatrial block; sinus arrest; AV block (first degree, Mobitz I, Mobitz II, complete heart block); junctional rhythm; and idioventricular rhythm with wide QRS complexes.
Differential Diagnosis
Normal physiologic bradycardia, cardiac ischemia, medication or toxin effects, pacemaker malfunction, hypoxia, hypothermia, electrolyte disturbances, renal failure, hypothyroidism, infection, rheumatologic disease, neuromuscular disease, increased intracranial pressure, and myocardial contusion.
Prehospital Management
Treat the patient rather than the heart rate. Provide oxygen for all patients. In hypothermia, rewarm gently and avoid pacing; administer magnesium as indicated. Use atropine or epinephrine only for hypotension or altered mental status. Initiate transcutaneous pacing if other measures fail.
Initial Stabilization in the ED
Address ABCs, administer oxygen, apply pacing pads, establish IV access, and begin continuous cardiac monitoring.
Emergency Department Management
Asymptomatic bradycardia requires monitoring and evaluation. Symptomatic or unstable bradycardia is treated with oxygen, atropine for symptomatic sinus bradycardia and low-grade AV block, epinephrine, and pacing. High-grade AV block typically requires pacing. Definitive care targets the underlying cause.
Medications
Atropine, epinephrine, calcium gluconate, dextrose, digoxin immune Fab, glucagon, insulin, and pacing are used based on etiology and stability. First-line therapy includes atropine, epinephrine, and pacing; second-line therapy addresses the specific cause.
Disposition
ICU admission is required for hemodynamic instability, Mobitz II or complete heart block, pacing or vasopressor needs, or acute ischemia. Telemetry admission is appropriate for stable cases. Asymptomatic sinus bradycardia may be discharged.
Follow-Up and Referral
All patients except those with isolated asymptomatic sinus bradycardia require cardiology follow-up. Specialty referral is indicated for underlying systemic causes.
Key Clinical Insights and Common Errors
Sinus bradycardia without symptoms is the only potentially normal bradyarrhythmia; all others warrant evaluation or follow-up. Ensure oxygenation, IV access, ECG, and continuous monitoring in all cases. Pediatric bradycardia is most often due to hypoxia. Pacing pads should be readily available for symptomatic patients. Definitive management hinges on identifying and correcting the underlying cause rather than focusing solely on heart rate.
Overview and Definitions
Bradyarrhythmias are defined as a ventricular heart rate <60 beats />in. Sinus bradycardia may be a normal physiologic variant, whereas all other bradyarrhythmias are considered pathologic. Patients may be asymptomatic or present with hypotension, altered mental status, fatigue, nausea, syncope, or cardiac arrest. Management depends on ECG findings and the patient’s clinical stability rather than heart rate alone.
Etiology and Pathophysiology
Bradyarrhythmias may be idiopathic or secondary to intrinsic or extrinsic causes. Idiopathic causes include healthy, well-conditioned athletes. Intrinsic cardiac causes include sinus node dysfunction (e.g., sick sinus syndrome with brady–tachy variants), atrioventricular (AV) block with junctional or ventricular escape rhythms, infiltrative diseases (amyloidosis, sarcoidosis, hemochromatosis), collagen vascular diseases (SLE, scleroderma, rheumatoid arthritis), congenital or acquired anatomic abnormalities (postsurgical, post-transplant, postradiation), muscular disorders (myotonic dystrophy), and myocardial contusion from trauma.
Extrinsic causes include myocardial ischemia or infarction (RCA infarction → sinus bradycardia; LAD infarction → high-grade AV block), acidemia, medications and toxins (β-blockers, calcium channel blockers, digoxin, clonidine, antiarrhythmics, lithium, organophosphates), electrolyte abnormalities (hypo-/hyperkalemia, hypoglycemia, hypo-/hypercalcemia, hypermagnesemia), hypoxia, hypothermia, hypotension or severe hypertension, endocrine disorders (hypothyroidism), infections (Lyme disease, Chagas disease, diphtheria, endocarditis, myocarditis), and neurologic conditions (increased intracranial pressure, increased vagal tone, carotid sinus hypersensitivity, spinal cord injury). Vagal triggers include micturition, defecation, coughing, vomiting, ocular pressure, and other Valsalva maneuvers.
Special Populations
In children, hypoxia is the most common cause of bradycardia. During pregnancy, maternal SLE may result in congenital complete heart block.
Clinical Presentation
Many patients are asymptomatic. Symptomatic presentations include lightheadedness, confusion, fatigue, decreased level of consciousness, dyspnea, cyanosis, pallor, chest pain or pressure, diaphoresis, hypotension, syncope, hypothermia, or cardiac arrest.
History and Physical Examination
Key historical elements include recent medication changes, urine output patterns suggesting electrolyte disturbances, trauma (intracranial injury or myocardial contusion), and activity at symptom onset suggesting increased vagal tone. Physical examination focuses on respiratory status, perfusion and pulses, rhythm regularity, mental status with full neurologic assessment, body habitus, skin/hair/nails, and temperature.
Essential Evaluation
Immediate evaluation includes ECG with continuous cardiac monitoring, pulse oximetry, blood pressure monitoring, and bedside glucose and electrolyte assessment.
Diagnostic Tests and Interpretation
Laboratory testing may include serum glucose, electrolytes, BUN/creatinine, cardiac enzymes, digoxin level, thyroid function tests, rheumatologic markers (ANA, RF), Lyme titers, and iron studies. Imaging includes chest radiograph and CT head for altered mental status.
ECG findings define the rhythm: sinus bradycardia with normal P–QRS relationship; sinoatrial block; sinus arrest; AV block (first degree, Mobitz I, Mobitz II, complete heart block); junctional rhythm; and idioventricular rhythm with wide QRS complexes.
Differential Diagnosis
Normal physiologic bradycardia, cardiac ischemia, medication or toxin effects, pacemaker malfunction, hypoxia, hypothermia, electrolyte disturbances, renal failure, hypothyroidism, infection, rheumatologic disease, neuromuscular disease, increased intracranial pressure, and myocardial contusion.
Prehospital Management
Treat the patient rather than the heart rate. Provide oxygen for all patients. In hypothermia, rewarm gently and avoid pacing; administer magnesium as indicated. Use atropine or epinephrine only for hypotension or altered mental status. Initiate transcutaneous pacing if other measures fail.
Initial Stabilization in the ED
Address ABCs, administer oxygen, apply pacing pads, establish IV access, and begin continuous cardiac monitoring.
Emergency Department Management
Asymptomatic bradycardia requires monitoring and evaluation. Symptomatic or unstable bradycardia is treated with oxygen, atropine for symptomatic sinus bradycardia and low-grade AV block, epinephrine, and pacing. High-grade AV block typically requires pacing. Definitive care targets the underlying cause.
Medications
Atropine, epinephrine, calcium gluconate, dextrose, digoxin immune Fab, glucagon, insulin, and pacing are used based on etiology and stability. First-line therapy includes atropine, epinephrine, and pacing; second-line therapy addresses the specific cause.
Disposition
ICU admission is required for hemodynamic instability, Mobitz II or complete heart block, pacing or vasopressor needs, or acute ischemia. Telemetry admission is appropriate for stable cases. Asymptomatic sinus bradycardia may be discharged.
Follow-Up and Referral
All patients except those with isolated asymptomatic sinus bradycardia require cardiology follow-up. Specialty referral is indicated for underlying systemic causes.
Key Clinical Insights and Common Errors
Sinus bradycardia without symptoms is the only potentially normal bradyarrhythmia; all others warrant evaluation or follow-up. Ensure oxygenation, IV access, ECG, and continuous monitoring in all cases. Pediatric bradycardia is most often due to hypoxia. Pacing pads should be readily available for symptomatic patients. Definitive management hinges on identifying and correcting the underlying cause rather than focusing solely on heart rate.
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Emergency and Acute Medicine – Bowel Obstruction (Small and Large)
Overview And Definitions
Bowel obstruction is interruption of normal intestinal transit from mechanical or functional (nonmechanical) causes. Small-bowel obstruction (SBO) accounts for about 20% of acute surgical admissions. Adhesions are the leading cause (≈60%), followed by neoplasms, hernias, strictures (e.g., inflammatory bowel disease), trauma-related bowel wall hematoma, and miscellaneous causes such as ascaris infection. Large-bowel obstruction (LBO) occurs primarily in older adults and is most commonly due to carcinoma (≈60%), diverticular disease (≈20%), volvulus (≈5%), colitis (ischemic or radiation), Crohn’s disease, foreign bodies, and functional obstruction. Functional, nonmechanical etiologies include paralytic ileus (e.g., electrolyte derangements, injury) and pseudo-obstruction (Ogilvie syndrome), which represents about 11%.
Etiology And Pathophysiology
Obstruction causes proximal intestinal dilation from swallowed air and accumulated GI secretions, increasing intraluminal pressure. Retrograde peristalsis produces vomiting. Progressive bowel edema and ongoing secretions worsen distention and lead to third spacing into the lumen. Strangulated obstruction can cause bowel wall ischemia, promoting aerobic and anaerobic bacterial overgrowth with methane and hydrogen production. This can progress to peritonitis, sepsis, and death. Mortality is essentially 100% for untreated strangulated obstruction, drops to ~8% with surgery within 36 hours, and rises to ~25% if surgery is delayed beyond 36 hours.
Clinical Presentation
Key historical clues include prior abdominal surgery, malignancy, hernias, prior colonoscopy, and significant family history. Pain is often intermittent early, but becomes constant with strangulation; symptoms may be vague in elderly or altered patients. Vomiting varies with level of obstruction—bilious emesis with proximal obstruction and feculent emesis with distal obstruction. Patients may report obstipation, constipation, diarrhea, stool caliber changes, and weight loss.
Vital signs may show tachycardia and hypotension from volume depletion, fever with strangulation or perforation, and hypothermia with sepsis. Abdominal examination often reveals distention and variable, frequently diffuse tenderness. Bowel sounds may be hyperactive and high-pitched early, becoming hypoactive late. Pain out of proportion to exam should raise concern for ischemic or gangrenous bowel. Peritoneal signs suggest strangulation or perforation. Evaluate for ventral, inguinal, and femoral hernias. Digital rectal exam may reveal a rectal mass or blood (gross or occult).
Geriatric Considerations
Abdominal pain in older adults may be vague. Nausea, vomiting, and abdominal pain can also occur with acute myocardial infarction; however, abdominal distention, obstipation, and colicky pain support a GI source.
Pediatric Considerations
Intussusception is the leading cause of obstruction in infants, most commonly between 3 and 12 months. Other causes include incarcerated inguinal or umbilical hernia and malrotation with volvulus, which can occur as early as 3–7 days of life. The “double bubble” sign on plain radiograph suggests partial duodenal obstruction (air in stomach and proximal duodenum). Pyloric stenosis presents with progressive, projectile, nonbilious postprandial vomiting, typically at 2–5 weeks of age, with a male predominance (≈5:1). Additional pediatric causes include duodenal atresia, Hirschsprung disease, and imperforate anus.
Essential Evaluation
A careful history and physical examination are central.
Diagnostic Tests And Interpretation
Laboratory studies commonly include CBC (leukocytosis is common), electrolytes/BUN/creatinine/glucose (hypokalemia, hypochloremic metabolic alkalosis, prerenal azotemia), lactate, amylase/lipase, liver enzymes/function tests to exclude hepatobiliary pathology, stool heme testing, urinalysis, type and crossmatch, PT/PTT, and ECG in patients at risk for coronary disease.
Imaging begins with upright chest radiograph to assess for pulmonary pathology and free air under the diaphragm. Abdominal radiographs (supine and upright) have ~75% sensitivity and ~53% specificity. Findings include dilated bowel loops (normal small bowel <3 cm), cecal dilation>13 cm suggesting perforation risk, air–fluid levels, and the “string of pearls” sign when small bowel is nearly fluid-filled. Plain films are less helpful for detecting strangulation. CT abdomen is highly sensitive (≈90% for SBO; ≈91% for LBO), identifies neoplasms and stages malignancy, localizes the transition point, and is more useful than plain films for early strangulation when IV contrast is used; CT has reduced the need for contrast enemas. MRI can approach CT sensitivity but availability varies. Ultrasound is more sensitive and specific than plain films for SBO but generally less accurate than CT. Upper GI studies, barium enemas, and endoscopy may be used when carcinoma or a mass is suspected, though their use has declined due to CT and they may be difficult in severely ill patients.
Differential Diagnosis
Paralytic ileus, pseudo-obstruction (Ogilvie), perforated ulcer, pancreatitis, cholecystitis, colitis, and mesenteric ischemia.
Prehospital Care
Establish IV access for patients with dehydration, vomiting, or significant abdominal pain.
Initial Stabilization And ED Management
Prioritize ABCs. Provide isotonic IV fluid resuscitation with 0.9% normal saline or lactated Ringer’s, especially for volume depletion and suspected strangulation or perforation (adults: 1 L bolus; pediatrics: 20 mL/kg bolus). Correct electrolyte abnormalities, particularly hypokalemia. Place a nasogastric tube for decompression, insert a Foley catheter for urine output monitoring, and obtain early surgical consultation. Administer antibiotics when strangulation or perforation is suspected, ensuring coverage for gram-negative aerobes and anaerobes. Provide analgesics and antiemetics. Address underlying causes when appropriate (e.g., steroids for inflammatory bowel disease or radiation enteritis).
Medications
For suspected ischemia/strangulation, options include combination therapy with metronidazole (1 g IV then 500 mg IV q6h; pediatrics 7.5-30 mg/kg/day divided q6-8h) plus ciprofloxacin 400 mg IV q12h or ceftriaxone 1-2 g IV q24h (pediatrics 25-75 mg/kg/day IV up to 2 g divided q12-24h). Single-agent broad-spectrum regimens include piperacillin-tazobactam 3.375 g IV q4-6h (pediatrics 150-400 mg/kg/day divided q6-8h), ampicillin-sulbactam 1.5-3 g IV q6h (pediatrics 100-400 mg/kg/day divided q6h), meropenem 1 g IV q8h (pediatrics 60-120 mg/kg/day divided q8h), or imipenem-cilastatin 250-1,000 mg IV q6-8h (pediatrics 50-100 mg/kg/day divided q6-12h). Analgesia may include morphine 2-10 mg per dose (pediatrics 0.1-0.2 mg/kg IV/IM/SC q2-4h) q2-6h PRN. Antiemetics include ondansetron 4 mg IV (pediatrics 0.1 mg/kg IV divided q8h) q4-8h PRN or promethazine 12.5-25 mg (pediatrics >2 years: 0.25–1 mg/kg/day IV/IM/PR divided q4–6h PRN) q4h.
Disposition
All suspected or confirmed bowel obstructions require admission with early surgical consultation. Discharge is appropriate only when labs and imaging are normal, symptoms resolve, and obstruction is no longer suspected.
Follow-Up Recommendations
Discharged patients should have normal laboratory and radiologic studies, a timely re-evaluation appointment, and clear return precautions outlining symptoms that require immediate ED return.
Clinical Insights And Common Errors
Patients with vomiting should be carefully examined for incarcerated hernias. Strangulated obstruction can be missed when symptoms are subtle, particularly in very young, very old, or altered patients. Another frequent error is inadequate correction of fluid deficits and electrolyte abnormalities.
Overview And Definitions
Bowel obstruction is interruption of normal intestinal transit from mechanical or functional (nonmechanical) causes. Small-bowel obstruction (SBO) accounts for about 20% of acute surgical admissions. Adhesions are the leading cause (≈60%), followed by neoplasms, hernias, strictures (e.g., inflammatory bowel disease), trauma-related bowel wall hematoma, and miscellaneous causes such as ascaris infection. Large-bowel obstruction (LBO) occurs primarily in older adults and is most commonly due to carcinoma (≈60%), diverticular disease (≈20%), volvulus (≈5%), colitis (ischemic or radiation), Crohn’s disease, foreign bodies, and functional obstruction. Functional, nonmechanical etiologies include paralytic ileus (e.g., electrolyte derangements, injury) and pseudo-obstruction (Ogilvie syndrome), which represents about 11%.
Etiology And Pathophysiology
Obstruction causes proximal intestinal dilation from swallowed air and accumulated GI secretions, increasing intraluminal pressure. Retrograde peristalsis produces vomiting. Progressive bowel edema and ongoing secretions worsen distention and lead to third spacing into the lumen. Strangulated obstruction can cause bowel wall ischemia, promoting aerobic and anaerobic bacterial overgrowth with methane and hydrogen production. This can progress to peritonitis, sepsis, and death. Mortality is essentially 100% for untreated strangulated obstruction, drops to ~8% with surgery within 36 hours, and rises to ~25% if surgery is delayed beyond 36 hours.
Clinical Presentation
Key historical clues include prior abdominal surgery, malignancy, hernias, prior colonoscopy, and significant family history. Pain is often intermittent early, but becomes constant with strangulation; symptoms may be vague in elderly or altered patients. Vomiting varies with level of obstruction—bilious emesis with proximal obstruction and feculent emesis with distal obstruction. Patients may report obstipation, constipation, diarrhea, stool caliber changes, and weight loss.
Vital signs may show tachycardia and hypotension from volume depletion, fever with strangulation or perforation, and hypothermia with sepsis. Abdominal examination often reveals distention and variable, frequently diffuse tenderness. Bowel sounds may be hyperactive and high-pitched early, becoming hypoactive late. Pain out of proportion to exam should raise concern for ischemic or gangrenous bowel. Peritoneal signs suggest strangulation or perforation. Evaluate for ventral, inguinal, and femoral hernias. Digital rectal exam may reveal a rectal mass or blood (gross or occult).
Geriatric Considerations
Abdominal pain in older adults may be vague. Nausea, vomiting, and abdominal pain can also occur with acute myocardial infarction; however, abdominal distention, obstipation, and colicky pain support a GI source.
Pediatric Considerations
Intussusception is the leading cause of obstruction in infants, most commonly between 3 and 12 months. Other causes include incarcerated inguinal or umbilical hernia and malrotation with volvulus, which can occur as early as 3–7 days of life. The “double bubble” sign on plain radiograph suggests partial duodenal obstruction (air in stomach and proximal duodenum). Pyloric stenosis presents with progressive, projectile, nonbilious postprandial vomiting, typically at 2–5 weeks of age, with a male predominance (≈5:1). Additional pediatric causes include duodenal atresia, Hirschsprung disease, and imperforate anus.
Essential Evaluation
A careful history and physical examination are central.
Diagnostic Tests And Interpretation
Laboratory studies commonly include CBC (leukocytosis is common), electrolytes/BUN/creatinine/glucose (hypokalemia, hypochloremic metabolic alkalosis, prerenal azotemia), lactate, amylase/lipase, liver enzymes/function tests to exclude hepatobiliary pathology, stool heme testing, urinalysis, type and crossmatch, PT/PTT, and ECG in patients at risk for coronary disease.
Imaging begins with upright chest radiograph to assess for pulmonary pathology and free air under the diaphragm. Abdominal radiographs (supine and upright) have ~75% sensitivity and ~53% specificity. Findings include dilated bowel loops (normal small bowel <3 cm), cecal dilation>13 cm suggesting perforation risk, air–fluid levels, and the “string of pearls” sign when small bowel is nearly fluid-filled. Plain films are less helpful for detecting strangulation. CT abdomen is highly sensitive (≈90% for SBO; ≈91% for LBO), identifies neoplasms and stages malignancy, localizes the transition point, and is more useful than plain films for early strangulation when IV contrast is used; CT has reduced the need for contrast enemas. MRI can approach CT sensitivity but availability varies. Ultrasound is more sensitive and specific than plain films for SBO but generally less accurate than CT. Upper GI studies, barium enemas, and endoscopy may be used when carcinoma or a mass is suspected, though their use has declined due to CT and they may be difficult in severely ill patients.
Differential Diagnosis
Paralytic ileus, pseudo-obstruction (Ogilvie), perforated ulcer, pancreatitis, cholecystitis, colitis, and mesenteric ischemia.
Prehospital Care
Establish IV access for patients with dehydration, vomiting, or significant abdominal pain.
Initial Stabilization And ED Management
Prioritize ABCs. Provide isotonic IV fluid resuscitation with 0.9% normal saline or lactated Ringer’s, especially for volume depletion and suspected strangulation or perforation (adults: 1 L bolus; pediatrics: 20 mL/kg bolus). Correct electrolyte abnormalities, particularly hypokalemia. Place a nasogastric tube for decompression, insert a Foley catheter for urine output monitoring, and obtain early surgical consultation. Administer antibiotics when strangulation or perforation is suspected, ensuring coverage for gram-negative aerobes and anaerobes. Provide analgesics and antiemetics. Address underlying causes when appropriate (e.g., steroids for inflammatory bowel disease or radiation enteritis).
Medications
For suspected ischemia/strangulation, options include combination therapy with metronidazole (1 g IV then 500 mg IV q6h; pediatrics 7.5-30 mg/kg/day divided q6-8h) plus ciprofloxacin 400 mg IV q12h or ceftriaxone 1-2 g IV q24h (pediatrics 25-75 mg/kg/day IV up to 2 g divided q12-24h). Single-agent broad-spectrum regimens include piperacillin-tazobactam 3.375 g IV q4-6h (pediatrics 150-400 mg/kg/day divided q6-8h), ampicillin-sulbactam 1.5-3 g IV q6h (pediatrics 100-400 mg/kg/day divided q6h), meropenem 1 g IV q8h (pediatrics 60-120 mg/kg/day divided q8h), or imipenem-cilastatin 250-1,000 mg IV q6-8h (pediatrics 50-100 mg/kg/day divided q6-12h). Analgesia may include morphine 2-10 mg per dose (pediatrics 0.1-0.2 mg/kg IV/IM/SC q2-4h) q2-6h PRN. Antiemetics include ondansetron 4 mg IV (pediatrics 0.1 mg/kg IV divided q8h) q4-8h PRN or promethazine 12.5-25 mg (pediatrics >2 years: 0.25–1 mg/kg/day IV/IM/PR divided q4–6h PRN) q4h.
Disposition
All suspected or confirmed bowel obstructions require admission with early surgical consultation. Discharge is appropriate only when labs and imaging are normal, symptoms resolve, and obstruction is no longer suspected.
Follow-Up Recommendations
Discharged patients should have normal laboratory and radiologic studies, a timely re-evaluation appointment, and clear return precautions outlining symptoms that require immediate ED return.
Clinical Insights And Common Errors
Patients with vomiting should be carefully examined for incarcerated hernias. Strangulated obstruction can be missed when symptoms are subtle, particularly in very young, very old, or altered patients. Another frequent error is inadequate correction of fluid deficits and electrolyte abnormalities.
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Emergency and Acute Medicine – Acute Bronchitis
Overview And Definitions
Acute bronchitis is an inflammatory condition of the bronchial airways characterized by mucosal hyperemia, edema, and excess mucus production. Impairment of ciliary function and local immune defenses leads to airway obstruction caused by edema, secretions, and bronchial smooth muscle spasm. The condition is usually self-limited and most often follows an upper respiratory tract infection.
Etiology And Pathophysiology
Acute bronchitis is predominantly viral in origin. Common pathogens include parainfluenza, influenza A and B, respiratory syncytial virus, human metapneumovirus, adenovirus, coronavirus, rhinovirus, echovirus, coxsackievirus, and, less commonly, measles and herpes viruses, which may cause severe disease. Certain organisms are associated with more prolonged or severe illness, including Mycoplasma pneumoniae, Chlamydia pneumoniae, and Bordetella pertussis. Pertussis incidence is increasing even among immunized individuals due to waning immunity. Bacterial causes are otherwise uncommon except in patients with chronic lung disease.
Clinical Presentation
Patients often describe a prodrome of malaise, chills, myalgias, coryza, and sore throat, followed by cough that is initially dry and later becomes mucoid or mucopurulent. Mild dyspnea and chest discomfort or burning related to coughing are common. Symptoms typically improve after 3–5 days, though cough and fatigue may persist for 1–3 weeks. Physical examination may reveal low-grade fever, tachypnea, rhonchi or wheezing, and occasional crackles. Mild hemoptysis can occur.
Diagnostic Evaluation
Diagnosis is primarily clinical. Routine laboratory testing is generally unnecessary. Influenza A and B testing may be useful when results would alter management or reporting. Pertussis should be considered in patients with cough lasting 14 days or longer, especially with paroxysms, post-tussive vomiting, inspiratory whoop, or known outbreak exposure. Chest radiography is not routinely indicated but should be obtained in patients with hypoxia, dyspnea, chest pain, tachycardia, tachypnea, fever ≥38°C, focal lung findings, advanced age, or significant comorbid disease. Imaging typically shows no consolidation in uncomplicated bronchitis.
Differential Diagnosis
Important alternatives include pneumonia, reactive airway disease or asthma, aspiration, acute sinusitis, and, in chronic cases, gastroesophageal reflux disease, chronic bronchitis, bronchiectasis, ACE inhibitor–related cough, malignancy, heart failure, sarcoidosis, and psychogenic cough.
Management And Emergency Care
Treatment is supportive. Oxygen is administered for hypoxia, and fluids are given if dehydration is present. Bronchodilators may benefit patients with wheezing or evidence of airflow obstruction. Antitussives and antipyretics can be used for symptomatic relief. Antiviral therapy such as oseltamivir or zanamivir may be considered for early influenza-related illness, and amantadine may be used selectively during influenza A outbreaks, accounting for resistance patterns. Antibiotics are generally not recommended, even with purulent sputum, due to minimal benefit and risks of resistance and adverse effects. They may be considered if fever recurs after initial improvement or if pertussis is confirmed. Smoking cessation should be encouraged but does not alone justify antibiotic use.
Disposition And Follow-Up
Most patients can be safely discharged if there is no significant respiratory compromise. Admission is reserved for those with hypoxia, significant cardiopulmonary disease, severe illness, or diagnostic uncertainty. Patients should be advised that cough may persist for several weeks and instructed to return for worsening symptoms, new dyspnea, or lack of improvement after 2–3 weeks. Routine follow-up is unnecessary if symptoms resolve.
Key Clinical Insights And Common Errors
High fever, hypoxia, or focal pulmonary findings should prompt evaluation for pneumonia. Acute bronchitis is most often viral, and unnecessary antibiotic use is a frequent error. Immunocompromised patients may develop more severe disease and warrant closer monitoring and coordination with their primary physician.
Overview And Definitions
Acute bronchitis is an inflammatory condition of the bronchial airways characterized by mucosal hyperemia, edema, and excess mucus production. Impairment of ciliary function and local immune defenses leads to airway obstruction caused by edema, secretions, and bronchial smooth muscle spasm. The condition is usually self-limited and most often follows an upper respiratory tract infection.
Etiology And Pathophysiology
Acute bronchitis is predominantly viral in origin. Common pathogens include parainfluenza, influenza A and B, respiratory syncytial virus, human metapneumovirus, adenovirus, coronavirus, rhinovirus, echovirus, coxsackievirus, and, less commonly, measles and herpes viruses, which may cause severe disease. Certain organisms are associated with more prolonged or severe illness, including Mycoplasma pneumoniae, Chlamydia pneumoniae, and Bordetella pertussis. Pertussis incidence is increasing even among immunized individuals due to waning immunity. Bacterial causes are otherwise uncommon except in patients with chronic lung disease.
Clinical Presentation
Patients often describe a prodrome of malaise, chills, myalgias, coryza, and sore throat, followed by cough that is initially dry and later becomes mucoid or mucopurulent. Mild dyspnea and chest discomfort or burning related to coughing are common. Symptoms typically improve after 3–5 days, though cough and fatigue may persist for 1–3 weeks. Physical examination may reveal low-grade fever, tachypnea, rhonchi or wheezing, and occasional crackles. Mild hemoptysis can occur.
Diagnostic Evaluation
Diagnosis is primarily clinical. Routine laboratory testing is generally unnecessary. Influenza A and B testing may be useful when results would alter management or reporting. Pertussis should be considered in patients with cough lasting 14 days or longer, especially with paroxysms, post-tussive vomiting, inspiratory whoop, or known outbreak exposure. Chest radiography is not routinely indicated but should be obtained in patients with hypoxia, dyspnea, chest pain, tachycardia, tachypnea, fever ≥38°C, focal lung findings, advanced age, or significant comorbid disease. Imaging typically shows no consolidation in uncomplicated bronchitis.
Differential Diagnosis
Important alternatives include pneumonia, reactive airway disease or asthma, aspiration, acute sinusitis, and, in chronic cases, gastroesophageal reflux disease, chronic bronchitis, bronchiectasis, ACE inhibitor–related cough, malignancy, heart failure, sarcoidosis, and psychogenic cough.
Management And Emergency Care
Treatment is supportive. Oxygen is administered for hypoxia, and fluids are given if dehydration is present. Bronchodilators may benefit patients with wheezing or evidence of airflow obstruction. Antitussives and antipyretics can be used for symptomatic relief. Antiviral therapy such as oseltamivir or zanamivir may be considered for early influenza-related illness, and amantadine may be used selectively during influenza A outbreaks, accounting for resistance patterns. Antibiotics are generally not recommended, even with purulent sputum, due to minimal benefit and risks of resistance and adverse effects. They may be considered if fever recurs after initial improvement or if pertussis is confirmed. Smoking cessation should be encouraged but does not alone justify antibiotic use.
Disposition And Follow-Up
Most patients can be safely discharged if there is no significant respiratory compromise. Admission is reserved for those with hypoxia, significant cardiopulmonary disease, severe illness, or diagnostic uncertainty. Patients should be advised that cough may persist for several weeks and instructed to return for worsening symptoms, new dyspnea, or lack of improvement after 2–3 weeks. Routine follow-up is unnecessary if symptoms resolve.
Key Clinical Insights And Common Errors
High fever, hypoxia, or focal pulmonary findings should prompt evaluation for pneumonia. Acute bronchitis is most often viral, and unnecessary antibiotic use is a frequent error. Immunocompromised patients may develop more severe disease and warrant closer monitoring and coordination with their primary physician.
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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.
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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 – 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.
- Published on
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.
