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Emergency and Acute Medicine – Acetaminophen (APAP) Poisoning
Overview and Pathophysiology
Acetaminophen is widely available as a single-agent analgesic, in combination with opioid medications, and as an ingredient in more than 200 over-the-counter cold and flu products. It is among the most common causes of both intentional and accidental poisoning and is the leading cause of acute liver failure requiring transplantation in the United States.
After ingestion, most acetaminophen is safely metabolized, but a small fraction is converted by the cytochrome P-450 system into N-acetyl-p-benzoquinoneimine (NAPQI), a highly toxic metabolite. Under normal conditions, NAPQI is neutralized by glutathione. In overdose, glutathione stores are rapidly depleted, allowing NAPQI to accumulate and cause hepatocellular injury. N-acetylcysteine (NAC) restores glutathione levels and prevents or limits liver damage. Patients with malnutrition are at higher risk because of reduced baseline glutathione reserves.
Pharmacokinetics and Toxic Thresholds
The normal acetaminophen half-life is approximately 2.5–4 hours but becomes prolonged in overdose, often exceeding 4 hours and indicating hepatic dysfunction. An acute ingestion greater than 150 mg/kg is potentially toxic. At 4 hours after ingestion, a serum acetaminophen level of 140 μg/mL or higher suggests toxicity, while therapeutic levels range from 5–20 μg/mL. The Rumack–Matthew nomogram is used to guide treatment decisions following a single, acute ingestion.
Clinical Course and Symptoms
Toxicity typically progresses through four stages.
Phase I (0.5–24 hours): Nausea, vomiting, and malaise may occur, particularly with large ingestions, though symptoms can be mild or absent early.
Phase II (24–72 hours): Gastrointestinal symptoms may improve, but liver injury evolves. Patients develop right upper quadrant pain, rising transaminases, prolonged PT/INR, elevated bilirubin, and sometimes oliguria.
Phase III (72–96 hours): This is the most critical period. Liver enzyme abnormalities peak, hepatic encephalopathy may appear, and worsening coagulopathy or renal failure signals a high likelihood of requiring liver transplantation.
Phase IV (96 hours to 10 days): Patients either recover with gradual hepatic regeneration or progress to fulminant liver failure.
Essential Evaluation
A careful history must identify all acetaminophen-containing products ingested and the timing of ingestion. A serum acetaminophen level should be obtained at 4 hours post-ingestion or immediately upon presentation if more than 4 hours have elapsed. The Rumack–Matthew nomogram applies only to single, acute ingestions and should not be used for chronic or delayed presentations. Early consultation with a poison center or toxicologist is strongly recommended.
Diagnostic Testing
Laboratory evaluation includes serum acetaminophen concentration, electrolytes, blood urea nitrogen, creatinine, glucose, liver enzymes (AST typically rises first), bilirubin, and PT/INR. Severe toxicity may result in AST/ALT levels exceeding 10,000 IU/L. A pregnancy test and toxicology screen should be obtained when appropriate.
Differential Diagnosis
Acetaminophen toxicity should always be considered as a co-ingestant in overdose. Other causes of acute liver injury include viral hepatitis, Reye syndrome, Amanita mushroom poisoning, herbal or dietary supplement toxicity, and other hepatotoxic drugs.
Initial Stabilization
Management begins with airway, breathing, and circulation assessment. Supplemental oxygen should be provided as needed. In patients with altered mental status, empiric administration of naloxone, thiamine, and dextrose (or bedside glucose testing) is appropriate.
Emergency Department Management
Supportive care includes intravenous fluids and antiemetics. A single dose of activated charcoal should be administered if the patient presents soon after ingestion.
N-acetylcysteine (NAC) is the cornerstone of therapy and is nearly 100% effective at preventing hepatotoxicity if started within 8 hours of acute overdose.
NAC Administration Options
Oral NAC has an unpleasant taste and odor and should be diluted to improve tolerability; antiemetics are often required. Vomited doses within one hour should be repeated, and persistent vomiting necessitates nasogastric or intravenous administration.
Intravenous NAC is given as a 21-hour infusion protocol. Oral NAC may be administered intravenously if the IV formulation is unavailable, with toxicology guidance.
Pregnancy Considerations
NAC is not teratogenic and crosses the placenta. Treating the mother effectively protects the fetus, particularly after 14 weeks’ gestation when fetal metabolism can produce toxic metabolites.
Disposition and Follow-Up
Admission is required for patients with hepatotoxic acetaminophen levels, abnormal liver tests, chronic ingestion with liver injury, or suicide attempts requiring psychiatric care.
Asymptomatic patients with non-toxic ingestions who do not require NAC may be discharged with counseling. Early hepatology or transplant consultation is warranted when significant liver injury is present. Patients with intentional overdose require psychiatric evaluation, while those with accidental poisoning need poison-prevention counseling.
Clinical Pearls and Pitfalls
Always consider occult acetaminophen exposure in patients presenting after opioid overdose or with unexplained liver injury. The Rumack–Matthew nomogram should not be used for chronic ingestion or late presentation. NAC should not be stopped until acetaminophen levels are undetectable and clinical and laboratory evidence of hepatotoxicity has improved or resolved.
Overview and Pathophysiology
Acetaminophen is widely available as a single-agent analgesic, in combination with opioid medications, and as an ingredient in more than 200 over-the-counter cold and flu products. It is among the most common causes of both intentional and accidental poisoning and is the leading cause of acute liver failure requiring transplantation in the United States.
After ingestion, most acetaminophen is safely metabolized, but a small fraction is converted by the cytochrome P-450 system into N-acetyl-p-benzoquinoneimine (NAPQI), a highly toxic metabolite. Under normal conditions, NAPQI is neutralized by glutathione. In overdose, glutathione stores are rapidly depleted, allowing NAPQI to accumulate and cause hepatocellular injury. N-acetylcysteine (NAC) restores glutathione levels and prevents or limits liver damage. Patients with malnutrition are at higher risk because of reduced baseline glutathione reserves.
Pharmacokinetics and Toxic Thresholds
The normal acetaminophen half-life is approximately 2.5–4 hours but becomes prolonged in overdose, often exceeding 4 hours and indicating hepatic dysfunction. An acute ingestion greater than 150 mg/kg is potentially toxic. At 4 hours after ingestion, a serum acetaminophen level of 140 μg/mL or higher suggests toxicity, while therapeutic levels range from 5–20 μg/mL. The Rumack–Matthew nomogram is used to guide treatment decisions following a single, acute ingestion.
Clinical Course and Symptoms
Toxicity typically progresses through four stages.
Phase I (0.5–24 hours): Nausea, vomiting, and malaise may occur, particularly with large ingestions, though symptoms can be mild or absent early.
Phase II (24–72 hours): Gastrointestinal symptoms may improve, but liver injury evolves. Patients develop right upper quadrant pain, rising transaminases, prolonged PT/INR, elevated bilirubin, and sometimes oliguria.
Phase III (72–96 hours): This is the most critical period. Liver enzyme abnormalities peak, hepatic encephalopathy may appear, and worsening coagulopathy or renal failure signals a high likelihood of requiring liver transplantation.
Phase IV (96 hours to 10 days): Patients either recover with gradual hepatic regeneration or progress to fulminant liver failure.
Essential Evaluation
A careful history must identify all acetaminophen-containing products ingested and the timing of ingestion. A serum acetaminophen level should be obtained at 4 hours post-ingestion or immediately upon presentation if more than 4 hours have elapsed. The Rumack–Matthew nomogram applies only to single, acute ingestions and should not be used for chronic or delayed presentations. Early consultation with a poison center or toxicologist is strongly recommended.
Diagnostic Testing
Laboratory evaluation includes serum acetaminophen concentration, electrolytes, blood urea nitrogen, creatinine, glucose, liver enzymes (AST typically rises first), bilirubin, and PT/INR. Severe toxicity may result in AST/ALT levels exceeding 10,000 IU/L. A pregnancy test and toxicology screen should be obtained when appropriate.
Differential Diagnosis
Acetaminophen toxicity should always be considered as a co-ingestant in overdose. Other causes of acute liver injury include viral hepatitis, Reye syndrome, Amanita mushroom poisoning, herbal or dietary supplement toxicity, and other hepatotoxic drugs.
Initial Stabilization
Management begins with airway, breathing, and circulation assessment. Supplemental oxygen should be provided as needed. In patients with altered mental status, empiric administration of naloxone, thiamine, and dextrose (or bedside glucose testing) is appropriate.
Emergency Department Management
Supportive care includes intravenous fluids and antiemetics. A single dose of activated charcoal should be administered if the patient presents soon after ingestion.
N-acetylcysteine (NAC) is the cornerstone of therapy and is nearly 100% effective at preventing hepatotoxicity if started within 8 hours of acute overdose.
- If the acetaminophen level cannot be obtained within 8 hours and toxicity is suspected, NAC should be started empirically and stopped if levels prove non-toxic.
- For presentations ≥8 hours after ingestion, NAC should be started immediately while awaiting laboratory confirmation.
- For late (>24 hours) or chronic ingestions, NAC is indicated if ingestion exceeds 150 mg/kg, symptoms are present, or liver tests are abnormal. Therapy may be discontinued once acetaminophen is undetectable and liver enzymes remain normal.
NAC Administration Options
Oral NAC has an unpleasant taste and odor and should be diluted to improve tolerability; antiemetics are often required. Vomited doses within one hour should be repeated, and persistent vomiting necessitates nasogastric or intravenous administration.
Intravenous NAC is given as a 21-hour infusion protocol. Oral NAC may be administered intravenously if the IV formulation is unavailable, with toxicology guidance.
Pregnancy Considerations
NAC is not teratogenic and crosses the placenta. Treating the mother effectively protects the fetus, particularly after 14 weeks’ gestation when fetal metabolism can produce toxic metabolites.
Disposition and Follow-Up
Admission is required for patients with hepatotoxic acetaminophen levels, abnormal liver tests, chronic ingestion with liver injury, or suicide attempts requiring psychiatric care.
Asymptomatic patients with non-toxic ingestions who do not require NAC may be discharged with counseling. Early hepatology or transplant consultation is warranted when significant liver injury is present. Patients with intentional overdose require psychiatric evaluation, while those with accidental poisoning need poison-prevention counseling.
Clinical Pearls and Pitfalls
Always consider occult acetaminophen exposure in patients presenting after opioid overdose or with unexplained liver injury. The Rumack–Matthew nomogram should not be used for chronic ingestion or late presentation. NAC should not be stopped until acetaminophen levels are undetectable and clinical and laboratory evidence of hepatotoxicity has improved or resolved.
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Emergency and Acute Medicine – Acute Coronary Syndrome: Myocardial Infarction
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
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Emergency and Acute Medicine – Acromioclavicular (AC) Joint Injury
Anatomy and Injury Overview
The acromioclavicular (AC) joint is formed by the distal clavicle articulating with the acromion of the scapula. Stability is provided by the acromioclavicular (AC) ligament, the coracoclavicular (CC) ligament, and dynamic support from the deltoid and trapezius muscles. The AC ligament primarily maintains horizontal stability, while the CC ligament provides vertical stability. Injury occurs along a predictable spectrum, classically described by the Rockwood classification, which reflects progressive disruption of these stabilizing structures.
Rockwood Classification
Type I injuries involve a sprain of the AC ligament without rupture. The CC ligament, deltoid, and trapezius remain intact, and radiographs are normal; diagnosis is clinical, with localized AC joint tenderness.
Type II injuries feature rupture of the AC ligament with horizontal instability of the distal clavicle and a sprained but intact CC ligament. Mild deltoid and trapezius injury may be present. Imaging shows slight widening of the AC joint (normally <5 mm) with a normal cc distance (11–13 mm).< />pan>
Type III injuries include rupture of both the AC and CC ligaments, producing horizontal and vertical instability. The deltoid and trapezius are detached, and radiographs demonstrate widening of the AC joint with superior displacement of the distal clavicle, typically about 100%.
Types IV, V, and VI represent severe injuries and are best appreciated on axillary or lateral views. All require operative management and carry a higher risk of prolonged disability. Type IV involves posterior displacement of the clavicle into the trapezius; Type V shows marked superior displacement with a 100–300% increase in CC distance and dramatic shoulder droop; Type VI, usually associated with high-energy trauma, features inferior displacement of the clavicle into a subacromial or subcoracoid position and is often accompanied by neurovascular injury.
Mechanism and Epidemiology
AC joint injuries are most common in young, active males, particularly during contact sports. The typical mechanism is a direct blow to the superior or lateral shoulder with the arm adducted, such as during a fall. Less commonly, injury occurs indirectly through a fall on an outstretched hand or elbow, transmitting force to the AC joint.
Clinical Presentation
Patients usually report pain over the superior or anterior shoulder following trauma, worsened by cross-body movement, reaching behind the back, or overhead activity. The severity of symptoms correlates with the degree of ligament disruption. Associated neurovascular complaints or cervical spine symptoms should heighten concern for severe injury.
Physical Examination
Examination is best performed with the patient seated or standing, as gravity accentuates instability. Inspection may reveal swelling, ecchymosis, deformity, asymmetry, or skin tenting. A prominent distal clavicle with a sagging acromion suggests at least a Type II injury.
Palpation should proceed systematically from the sternoclavicular joint along the clavicle to the AC joint, CC ligament, coracoid process, scapula, and proximal humerus. AC joint tenderness suggests AC ligament injury, while horizontal instability indicates rupture. Tenderness or vertical instability implicates CC ligament disruption.
Provocative maneuvers include the cross-body adduction test, which compresses the AC joint and reproduces pain, and the O’Brien test, which may elicit superior shoulder pain in AC pathology. A complete distal neurovascular examination, including assessment of the brachial plexus, and a careful cervical spine evaluation are essential.
Diagnostic Evaluation
Diagnosis relies on history, examination, and targeted imaging. Dedicated AC joint radiographs with bilateral comparison are recommended when injury is suspected, as standard shoulder views may obscure subtle findings. The Zanca view (10–15° cephalic tilt) improves visualization of the AC joint, while axillary views are critical for identifying posterior or inferior clavicular displacement. Stress views are no longer routinely recommended. Advanced imaging with CT or MRI is reserved for surgical planning or complex injuries, and angiography may be indicated if vascular compromise is suspected.
Differential Diagnosis
Conditions that may mimic AC joint injury include shoulder dislocation, clavicle or acromion fractures, rotator cuff pathology, tendinitis, adhesive capsulitis, cervical radiculopathy, osteoarthritis, osteomyelitis, and—in children—distal clavicle physeal fractures.
Management in the Emergency Setting
Initial care includes ice application, sling immobilization, analgesia, and cervical spine precautions when indicated.
Type I and II injuries are managed conservatively with rest, ice, NSAIDs, brief sling use (typically 3–7 days), and early range-of-motion exercises. Most patients return to normal activity within 2–4 weeks once painless strength and motion are restored.
Type III injuries require sling immobilization, analgesia, and early orthopedic referral (within 72 hours). Management is controversial, with treatment individualized based on patient age, activity level, occupation, hand dominance, and reinjury risk.
Types IV, V, and VI injuries necessitate immediate orthopedic consultation and operative repair.
A recognized long-term complication of AC joint injury is post-traumatic arthritis.
Pediatric Considerations
In children, the clavicle is encased in a periosteal sleeve, with the CC ligament contained within and the AC ligament external and more vulnerable. True AC joint dislocations are uncommon in pediatrics and are usually Type I or II. Distal clavicle physeal fractures are more frequent. Younger children with Type III injuries are typically managed conservatively, while adolescents may require more aggressive treatment. Types IV–VI generally require surgery.
Disposition and Follow-Up
Patients with Type I or II injuries may be discharged with orthopedic follow-up in 2–4 weeks. Type III injuries require urgent orthopedic evaluation, and Types IV–VI typically warrant admission for operative management. Open injuries and pediatric cases should receive prompt specialist assessment.
Clinical Pearls and Pitfalls
Normal CC spacing distinguishes Type I and II injuries and supports conservative management. Type III injuries demonstrate complete superior displacement and require early orthopedic input. Types IV–VI share ligamentous disruption with Type III injuries but differ by clavicular position and uniformly require surgical repair.
Anatomy and Injury Overview
The acromioclavicular (AC) joint is formed by the distal clavicle articulating with the acromion of the scapula. Stability is provided by the acromioclavicular (AC) ligament, the coracoclavicular (CC) ligament, and dynamic support from the deltoid and trapezius muscles. The AC ligament primarily maintains horizontal stability, while the CC ligament provides vertical stability. Injury occurs along a predictable spectrum, classically described by the Rockwood classification, which reflects progressive disruption of these stabilizing structures.
Rockwood Classification
Type I injuries involve a sprain of the AC ligament without rupture. The CC ligament, deltoid, and trapezius remain intact, and radiographs are normal; diagnosis is clinical, with localized AC joint tenderness.
Type II injuries feature rupture of the AC ligament with horizontal instability of the distal clavicle and a sprained but intact CC ligament. Mild deltoid and trapezius injury may be present. Imaging shows slight widening of the AC joint (normally <5 mm) with a normal cc distance (11–13 mm).< />pan>
Type III injuries include rupture of both the AC and CC ligaments, producing horizontal and vertical instability. The deltoid and trapezius are detached, and radiographs demonstrate widening of the AC joint with superior displacement of the distal clavicle, typically about 100%.
Types IV, V, and VI represent severe injuries and are best appreciated on axillary or lateral views. All require operative management and carry a higher risk of prolonged disability. Type IV involves posterior displacement of the clavicle into the trapezius; Type V shows marked superior displacement with a 100–300% increase in CC distance and dramatic shoulder droop; Type VI, usually associated with high-energy trauma, features inferior displacement of the clavicle into a subacromial or subcoracoid position and is often accompanied by neurovascular injury.
Mechanism and Epidemiology
AC joint injuries are most common in young, active males, particularly during contact sports. The typical mechanism is a direct blow to the superior or lateral shoulder with the arm adducted, such as during a fall. Less commonly, injury occurs indirectly through a fall on an outstretched hand or elbow, transmitting force to the AC joint.
Clinical Presentation
Patients usually report pain over the superior or anterior shoulder following trauma, worsened by cross-body movement, reaching behind the back, or overhead activity. The severity of symptoms correlates with the degree of ligament disruption. Associated neurovascular complaints or cervical spine symptoms should heighten concern for severe injury.
Physical Examination
Examination is best performed with the patient seated or standing, as gravity accentuates instability. Inspection may reveal swelling, ecchymosis, deformity, asymmetry, or skin tenting. A prominent distal clavicle with a sagging acromion suggests at least a Type II injury.
Palpation should proceed systematically from the sternoclavicular joint along the clavicle to the AC joint, CC ligament, coracoid process, scapula, and proximal humerus. AC joint tenderness suggests AC ligament injury, while horizontal instability indicates rupture. Tenderness or vertical instability implicates CC ligament disruption.
Provocative maneuvers include the cross-body adduction test, which compresses the AC joint and reproduces pain, and the O’Brien test, which may elicit superior shoulder pain in AC pathology. A complete distal neurovascular examination, including assessment of the brachial plexus, and a careful cervical spine evaluation are essential.
Diagnostic Evaluation
Diagnosis relies on history, examination, and targeted imaging. Dedicated AC joint radiographs with bilateral comparison are recommended when injury is suspected, as standard shoulder views may obscure subtle findings. The Zanca view (10–15° cephalic tilt) improves visualization of the AC joint, while axillary views are critical for identifying posterior or inferior clavicular displacement. Stress views are no longer routinely recommended. Advanced imaging with CT or MRI is reserved for surgical planning or complex injuries, and angiography may be indicated if vascular compromise is suspected.
Differential Diagnosis
Conditions that may mimic AC joint injury include shoulder dislocation, clavicle or acromion fractures, rotator cuff pathology, tendinitis, adhesive capsulitis, cervical radiculopathy, osteoarthritis, osteomyelitis, and—in children—distal clavicle physeal fractures.
Management in the Emergency Setting
Initial care includes ice application, sling immobilization, analgesia, and cervical spine precautions when indicated.
Type I and II injuries are managed conservatively with rest, ice, NSAIDs, brief sling use (typically 3–7 days), and early range-of-motion exercises. Most patients return to normal activity within 2–4 weeks once painless strength and motion are restored.
Type III injuries require sling immobilization, analgesia, and early orthopedic referral (within 72 hours). Management is controversial, with treatment individualized based on patient age, activity level, occupation, hand dominance, and reinjury risk.
Types IV, V, and VI injuries necessitate immediate orthopedic consultation and operative repair.
A recognized long-term complication of AC joint injury is post-traumatic arthritis.
Pediatric Considerations
In children, the clavicle is encased in a periosteal sleeve, with the CC ligament contained within and the AC ligament external and more vulnerable. True AC joint dislocations are uncommon in pediatrics and are usually Type I or II. Distal clavicle physeal fractures are more frequent. Younger children with Type III injuries are typically managed conservatively, while adolescents may require more aggressive treatment. Types IV–VI generally require surgery.
Disposition and Follow-Up
Patients with Type I or II injuries may be discharged with orthopedic follow-up in 2–4 weeks. Type III injuries require urgent orthopedic evaluation, and Types IV–VI typically warrant admission for operative management. Open injuries and pediatric cases should receive prompt specialist assessment.
Clinical Pearls and Pitfalls
Normal CC spacing distinguishes Type I and II injuries and supports conservative management. Type III injuries demonstrate complete superior displacement and require early orthopedic input. Types IV–VI share ligamentous disruption with Type III injuries but differ by clavicular position and uniformly require surgical repair.
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Emergency and Acute Medicine – Acidosis
Overview and Definitions
Acidosis refers to physiologic processes that reduce blood pH and is broadly classified into respiratory acidosis and metabolic acidosis. Respiratory acidosis results from alveolar hypoventilation with retention of carbon dioxide, defined by a PaCO₂ greater than 45 mm Hg or higher than expected for appropriate respiratory compensation. Metabolic acidosis occurs when serum pH decreases due to a reduction in plasma bicarbonate, either from accumulation of acids or loss of bicarbonate from the body. Correct identification of the primary disorder and any mixed acid–base disturbances is essential in emergency care.
Respiratory Acidosis: Pathophysiology and Causes
Respiratory acidosis develops when ventilation is inadequate to eliminate carbon dioxide. Causes fall into three broad categories. The first is central nervous system depression, including sleep apnea, anesthesia, sedative or opioid overdose, CNS infections, or structural brain lesions. The second category involves impaired gas exchange at the alveolar level, such as in COPD, asthma, pneumonia, pulmonary edema, interstitial lung disease, obesity hypoventilation, or pulmonary contusion. The third category reflects failure of carbon dioxide transport from tissues to alveoli, as seen in severe heart failure or pulmonary edema. Neuromuscular disorders—including Guillain–Barré syndrome, myasthenia gravis, muscular dystrophy, spinal cord injury, or electrolyte abnormalities—may also impair ventilation. Upper airway obstruction, whether congenital, infectious, or foreign body–related, must also be considered.
Metabolic Acidosis: Classification and Mechanisms
Metabolic acidosis is classified based on the anion gap. In elevated anion gap metabolic acidosis, bicarbonate is consumed buffering excess strong acids, leaving unmeasured anions in circulation. Common causes are recalled with the mnemonic A CATPILES MUD, including lactic acidosis, ketoacidosis, renal failure (uremia), and toxic ingestions. Some causes are associated with an elevated osmolar gap, remembered by ME DIE, which suggests toxic alcohol exposure.
In normal anion gap (hyperchloremic) metabolic acidosis, bicarbonate is lost or not regenerated, without accumulation of unmeasured anions. This occurs with gastrointestinal bicarbonate losses (such as diarrhea or fistulas), renal tubular acidosis, or ingestion of substances that generate hydrochloric acid. Renal tubular acidosis is subdivided into distal (type I), proximal (type II), and type IV forms, each with characteristic bicarbonate and potassium abnormalities.
Clinical Presentation
Symptoms of acidosis are often nonspecific. Patients may present with tachypnea or deep, labored (Kussmaul) respirations in metabolic acidosis, or hypoventilation in respiratory acidosis. Additional findings include tachycardia, somnolence, confusion, altered mental status from hypercapnia, and cardiac conduction abnormalities or dysrhythmias, particularly with severe electrolyte derangements.
Essential Evaluation
Initial evaluation includes serum electrolytes, renal function, glucose, and arterial blood gases. Metabolic acidosis is suggested by a low bicarbonate level, while respiratory acidosis is characterized by carbon dioxide retention. Hyperkalemia and hypercalcemia may accompany severe metabolic acidosis. Carbon monoxide levels should be measured when exposure is suspected.
Calculation of the anion gap (Na⁺ − [Cl⁻ + HCO₃⁻]) is critical, with correction for hypoalbuminemia. The degree of compensation must be assessed by comparing expected versus observed PaCO₂ or bicarbonate levels. Failure of appropriate compensation suggests a mixed acid–base disorder.
Advanced Acid–Base Interpretation
In metabolic acidosis, expected PaCO₂ can be estimated using standard formulas. If measured PaCO₂ is higher than expected, concomitant respiratory acidosis or inadequate compensation is present. The delta gap helps identify mixed metabolic disorders by comparing changes in the anion gap with changes in bicarbonate concentration. Disproportionate changes indicate additional metabolic alkalosis or non–anion gap acidosis.
Diagnostic Testing
Arterial blood gas analysis remains the reference standard, though venous blood gas sampling may be useful in stable patients for screening. Urinalysis for glucose and ketones, serum lactate, ketone levels, and toxicology screening are obtained as indicated. Measurement of serum osmolality and calculation of the osmolar gap can suggest toxic alcohol ingestion, though a normal gap does not exclude this diagnosis. Imaging and ECG may help identify underlying cardiopulmonary or ischemic causes.
Management and Stabilization
Initial management focuses on airway, breathing, and circulation. Early intubation should be considered in severe metabolic acidosis when respiratory compensation is failing. Empiric administration of naloxone, dextrose, and thiamine is appropriate in patients with altered mental status.
Respiratory acidosis is managed by treating the underlying cause and providing ventilatory support when hypercapnia worsens. Metabolic acidosis requires identification and correction of the underlying etiology, such as diabetic ketoacidosis, lactic acidosis, or toxic ingestion, along with correction of electrolyte abnormalities and volume resuscitation. Hemodialysis may be necessary in select cases.
Disposition and Follow-Up
Patients with severe acidosis, altered mental status, respiratory failure, hemodynamic instability, significant electrolyte disturbances, or dysrhythmias generally require hospital admission, often to an intensive care setting. Discharge may be considered only when acidosis is resolving, the underlying cause is addressed, and close follow-up is ensured.
Clinical Pearls and Pitfalls
Mixed acid–base disorders are common and frequently missed. Normal pH does not exclude significant pathology if PaCO₂ and bicarbonate are both abnormal. Failure to recognize inadequate respiratory compensation in metabolic acidosis can delay lifesaving ventilatory support. Careful, systematic acid–base analysis is essential in emergency and acute care settings.
Overview and Definitions
Acidosis refers to physiologic processes that reduce blood pH and is broadly classified into respiratory acidosis and metabolic acidosis. Respiratory acidosis results from alveolar hypoventilation with retention of carbon dioxide, defined by a PaCO₂ greater than 45 mm Hg or higher than expected for appropriate respiratory compensation. Metabolic acidosis occurs when serum pH decreases due to a reduction in plasma bicarbonate, either from accumulation of acids or loss of bicarbonate from the body. Correct identification of the primary disorder and any mixed acid–base disturbances is essential in emergency care.
Respiratory Acidosis: Pathophysiology and Causes
Respiratory acidosis develops when ventilation is inadequate to eliminate carbon dioxide. Causes fall into three broad categories. The first is central nervous system depression, including sleep apnea, anesthesia, sedative or opioid overdose, CNS infections, or structural brain lesions. The second category involves impaired gas exchange at the alveolar level, such as in COPD, asthma, pneumonia, pulmonary edema, interstitial lung disease, obesity hypoventilation, or pulmonary contusion. The third category reflects failure of carbon dioxide transport from tissues to alveoli, as seen in severe heart failure or pulmonary edema. Neuromuscular disorders—including Guillain–Barré syndrome, myasthenia gravis, muscular dystrophy, spinal cord injury, or electrolyte abnormalities—may also impair ventilation. Upper airway obstruction, whether congenital, infectious, or foreign body–related, must also be considered.
Metabolic Acidosis: Classification and Mechanisms
Metabolic acidosis is classified based on the anion gap. In elevated anion gap metabolic acidosis, bicarbonate is consumed buffering excess strong acids, leaving unmeasured anions in circulation. Common causes are recalled with the mnemonic A CATPILES MUD, including lactic acidosis, ketoacidosis, renal failure (uremia), and toxic ingestions. Some causes are associated with an elevated osmolar gap, remembered by ME DIE, which suggests toxic alcohol exposure.
In normal anion gap (hyperchloremic) metabolic acidosis, bicarbonate is lost or not regenerated, without accumulation of unmeasured anions. This occurs with gastrointestinal bicarbonate losses (such as diarrhea or fistulas), renal tubular acidosis, or ingestion of substances that generate hydrochloric acid. Renal tubular acidosis is subdivided into distal (type I), proximal (type II), and type IV forms, each with characteristic bicarbonate and potassium abnormalities.
Clinical Presentation
Symptoms of acidosis are often nonspecific. Patients may present with tachypnea or deep, labored (Kussmaul) respirations in metabolic acidosis, or hypoventilation in respiratory acidosis. Additional findings include tachycardia, somnolence, confusion, altered mental status from hypercapnia, and cardiac conduction abnormalities or dysrhythmias, particularly with severe electrolyte derangements.
Essential Evaluation
Initial evaluation includes serum electrolytes, renal function, glucose, and arterial blood gases. Metabolic acidosis is suggested by a low bicarbonate level, while respiratory acidosis is characterized by carbon dioxide retention. Hyperkalemia and hypercalcemia may accompany severe metabolic acidosis. Carbon monoxide levels should be measured when exposure is suspected.
Calculation of the anion gap (Na⁺ − [Cl⁻ + HCO₃⁻]) is critical, with correction for hypoalbuminemia. The degree of compensation must be assessed by comparing expected versus observed PaCO₂ or bicarbonate levels. Failure of appropriate compensation suggests a mixed acid–base disorder.
Advanced Acid–Base Interpretation
In metabolic acidosis, expected PaCO₂ can be estimated using standard formulas. If measured PaCO₂ is higher than expected, concomitant respiratory acidosis or inadequate compensation is present. The delta gap helps identify mixed metabolic disorders by comparing changes in the anion gap with changes in bicarbonate concentration. Disproportionate changes indicate additional metabolic alkalosis or non–anion gap acidosis.
Diagnostic Testing
Arterial blood gas analysis remains the reference standard, though venous blood gas sampling may be useful in stable patients for screening. Urinalysis for glucose and ketones, serum lactate, ketone levels, and toxicology screening are obtained as indicated. Measurement of serum osmolality and calculation of the osmolar gap can suggest toxic alcohol ingestion, though a normal gap does not exclude this diagnosis. Imaging and ECG may help identify underlying cardiopulmonary or ischemic causes.
Management and Stabilization
Initial management focuses on airway, breathing, and circulation. Early intubation should be considered in severe metabolic acidosis when respiratory compensation is failing. Empiric administration of naloxone, dextrose, and thiamine is appropriate in patients with altered mental status.
Respiratory acidosis is managed by treating the underlying cause and providing ventilatory support when hypercapnia worsens. Metabolic acidosis requires identification and correction of the underlying etiology, such as diabetic ketoacidosis, lactic acidosis, or toxic ingestion, along with correction of electrolyte abnormalities and volume resuscitation. Hemodialysis may be necessary in select cases.
Disposition and Follow-Up
Patients with severe acidosis, altered mental status, respiratory failure, hemodynamic instability, significant electrolyte disturbances, or dysrhythmias generally require hospital admission, often to an intensive care setting. Discharge may be considered only when acidosis is resolving, the underlying cause is addressed, and close follow-up is ensured.
Clinical Pearls and Pitfalls
Mixed acid–base disorders are common and frequently missed. Normal pH does not exclude significant pathology if PaCO₂ and bicarbonate are both abnormal. Failure to recognize inadequate respiratory compensation in metabolic acidosis can delay lifesaving ventilatory support. Careful, systematic acid–base analysis is essential in emergency and acute care settings.
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Emergency and Acute Medicine – Acute Coronary Syndrome: Myocardial Infarction
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
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Diagnostic Test – Herpes Simplex PCR
1. What is this?
Herpes simplex PCR is a molecular diagnostic test performed on cerebrospinal fluid (CSF).
It detects HSV DNA and is the single most accurate diagnostic test for herpes simplex encephalitis.
2. When is this the correct choice?
Select HSV PCR of the CSF when the clinical scenario includes:
- Fever
- Headache
- Altered mental status or confusion
- Symptom duration less than 2 weeks
Key test-taking point:
- CSF HSV PCR is more accurate than:
- EEG
- Head CT
- Brain MRI
- Even brain biopsy
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Diagnostic Test – Gallium Scanning
1. How does this test work?
Gallium scanning is a nuclear medicine imaging study used to detect infection and certain malignancies.
Mechanism:
2. When is a gallium scan the appropriate choice?
Choose a gallium scan when the clinical picture includes:
1. How does this test work?
Gallium scanning is a nuclear medicine imaging study used to detect infection and certain malignancies.
Mechanism:
- Gallium localizes to areas with:
- Increased white blood cell activity
- Increased iron metabolism
- It is transported in the blood bound to transferrin
- Areas of inflammation, infection, or malignancy show increased gallium uptake
2. When is a gallium scan the appropriate choice?
Choose a gallium scan when the clinical picture includes:
- Persistent fever without localizing symptoms
- Negative initial evaluation, including:
- Blood cultures
- Chest X-ray
- Urinalysis
- Fever of unknown origin (FUO)
- Lymphoma
- Occult abscesses
- A biopsy is the most definitive test following an abnormal gallium scan
- Malignancy → requires histologic confirmation
- Infection → requires culture confirmation
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Diagnostic Test – Darkfield Microscopy
1. What is this?
Darkfield microscopy is the most accurate diagnostic test for primary syphilis.
It allows direct visualization of Treponema pallidum, the causative organism, from an active lesion.
2. How is it done?
- A scraping or swab is obtained from a syphilitic chancre
- The specimen is placed on a glass slide
- The slide is examined using darkfield illumination
- Motile spirochetes can be seen directly if T. pallidum is present
3. When do you select darkfield microscopy?
Choose darkfield microscopy when:
- The clinical scenario suggests primary syphilis
- The question asks for the most accurate diagnostic test
- There is a painless genital ulcer (chancre)
- In primary syphilis, RPR and VDRL have a false-negative rate of ~25%
- Darkfield microscopy is more sensitive than RPR or VDRL in this stage
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Diagnostic Test – Indium-Labeled Leukocyte Scan
1. How does this test work?
The indium-labeled leukocyte scan is a nuclear medicine study used to detect occult infection or evaluate fever of unknown origin (FUO).
Mechanism:
- A sample of the patient’s blood is drawn.
- White blood cells (leukocytes) are isolated and tagged with radioactive indium.
- The labeled blood is re-injected into the patient.
- The indium-tagged leukocytes migrate and localize to areas of active infection or inflammation.
- Nuclear imaging detects areas of increased uptake, identifying the site of infection.
2. When is an indium scan the right text?
Answer indium-labeled leukocyte scan when you see:
- Occult infection or fever of unknown origin
- Routine studies are negative, such as:
- Blood cultures
- Chest X-ray
- Urinalysis
- Suspicion of infection that is difficult to localize
- Situations where gallium scans are inaccurate, particularly:
- Intra-abdominal infections
3. What is the most accurate test?
- A biopsy of the suspected site of infection is more accurate than an indium-labeled leukocyte scan.
- The indium scan is best used as a localizing tool, guiding further definitive testing.
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Emergency and Acute Medicine – Penetrating Abdominal Trauma
Overview and Mechanism of Injury
Penetrating abdominal trauma results from injury caused by knives, gunshots, or other foreign objects breaching the abdominal wall. Damage to solid organs most often leads to significant hemorrhage, whereas hollow viscus injuries may cause leakage of bowel contents with subsequent peritonitis and sepsis. Injuries are frequently complex, and combined thoracic and abdominal involvement occurs in approximately one-quarter of cases.
Etiology and Injury Patterns
Penetrating trauma carries a high risk of intra-abdominal injury. Approximately 80% of gunshot wounds and 20–30% of stab wounds result in significant abdominal pathology. Commonly injured structures include the liver, small bowel, stomach, colon, major vascular structures, retroperitoneum, and mesentery or omentum. Less frequently affected organs include the spleen, diaphragm, kidneys, pancreas, duodenum, and biliary system.
Clinical Presentation
Patients present with an obvious penetrating wound and may range from having localized pain to overt peritoneal signs and hemodynamic instability. High-velocity projectiles can cause extensive tissue destruction through direct injury, secondary missiles (bone or bullet fragments), and temporary cavitation. Exit wounds may be larger than entrance wounds, but small or inconspicuous entry and exit sites can mask severe internal injury.
Clinicians must remember the full anatomic boundaries of the abdomen, which extend from the nipples anteriorly and the inferior scapular tips posteriorly down to the inferior gluteal folds.
Initial Evaluation and Essential Workup
Gunshot wounds to the abdomen are generally assumed to have caused intra-abdominal injury and are typically managed with operative exploration.
For stab wounds to the anterior abdomen, local wound exploration is essential. If the anterior fascia is violated, further evaluation with diagnostic peritoneal lavage or bedside ultrasonography is indicated.
Diagnostic laparoscopy is particularly useful for identifying diaphragmatic injuries and selected liver or splenic lacerations and may help avoid unnecessary laparotomy in stable patients.
CT imaging is valuable for evaluating suspected retroperitoneal injuries in stable patients but is unreliable for detecting hollow viscus or diaphragmatic injuries.
Diagnostic peritoneal lavage remains useful in select cases. A red blood cell count of 10,000/mm³ or greater is an indication for laparotomy. Patients with lower counts should be closely observed for 8–24 hours for evolving peritoneal signs.
Diagnostic Tests and Interpretation
Laboratory evaluation includes serial hemoglobin or hematocrit measurements to assess ongoing blood loss, urinalysis to screen for genitourinary injury, arterial blood gas analysis to evaluate hypovolemia, and blood typing with cross-matching for patients with suspected significant injury.
Imaging studies may include plain radiographs with external markers to localize foreign bodies, identify fractures, or detect free air. Intravenous pyelography may be used when renal injury is suspected. Focused abdominal sonography for trauma (FAST) can rapidly identify intraperitoneal fluid, while CT with intravenous contrast is reserved for stable patients in experienced centers.
Differential Diagnosis
Upper abdominal penetrating wounds may involve intrathoracic structures, while lower thoracic injuries can extend into the abdominal cavity. Both possibilities should always be considered during evaluation.
Prehospital Management
Fluid resuscitation should be carefully titrated to clinical response. Military antishock trousers are not recommended. Open wounds should be covered with sterile dressings, and eviscerated bowel should be protected with moist sterile dressings. Impaled objects must be stabilized in place and never removed in the field.
Initial Stabilization and Therapy
Management begins with high-flow oxygen and placement of two large-bore intravenous lines for crystalloid infusion. If there is no response after 2 liters of crystalloid, transfusion of packed red blood cells is indicated, using O-negative blood initially if the patient is unstable. Type-specific and cross-matched blood should be administered as soon as available.
Pediatric Considerations
Children in hypovolemic shock should receive crystalloid boluses of 20 mL/kg. Severe shock requires transfusion of packed red blood cells at 1 mL/kg. Diagnostic peritoneal lavage is relatively contraindicated in children younger than 8 years.
Emergency Department Procedures
A nasogastric tube should be placed to reduce aspiration risk and decompress the stomach prior to diagnostic peritoneal lavage. This may also relieve respiratory distress caused by diaphragmatic injury with herniation of abdominal contents.
A Foley catheter should be inserted after excluding urethral injury to assist in detecting genitourinary trauma and monitoring urine output. Tetanus prophylaxis should be administered when indicated.
Medications
Broad-spectrum intravenous antibiotics with gram-negative and anaerobic coverage are required due to the high risk of contamination. Acceptable regimens include second-generation cephalosporins, beta-lactam/beta-lactamase inhibitor combinations, or combination therapy with aminoglycosides and anaerobic agents. Tetanus toxoid and tetanus immunoglobulin should be given as appropriate.
Disposition and Follow-Up
Patients requiring operative intervention must be admitted. Those with negative diagnostic studies should be observed for at least 8 hours with serial abdominal examinations and repeated hematocrit measurements.
Patients with stab wounds that do not penetrate the fascia may be discharged after a period of observation in the emergency department.
Clinical Pearls and Pitfalls
Permissive hypotension is increasingly supported during resuscitation to limit bleeding. Overaggressive crystalloid administration should be avoided. Complete exposure of the patient is essential to avoid missed injuries. Routine spinal immobilization is unnecessary unless there is clear evidence of spinal cord injury.
Overview and Mechanism of Injury
Penetrating abdominal trauma results from injury caused by knives, gunshots, or other foreign objects breaching the abdominal wall. Damage to solid organs most often leads to significant hemorrhage, whereas hollow viscus injuries may cause leakage of bowel contents with subsequent peritonitis and sepsis. Injuries are frequently complex, and combined thoracic and abdominal involvement occurs in approximately one-quarter of cases.
Etiology and Injury Patterns
Penetrating trauma carries a high risk of intra-abdominal injury. Approximately 80% of gunshot wounds and 20–30% of stab wounds result in significant abdominal pathology. Commonly injured structures include the liver, small bowel, stomach, colon, major vascular structures, retroperitoneum, and mesentery or omentum. Less frequently affected organs include the spleen, diaphragm, kidneys, pancreas, duodenum, and biliary system.
Clinical Presentation
Patients present with an obvious penetrating wound and may range from having localized pain to overt peritoneal signs and hemodynamic instability. High-velocity projectiles can cause extensive tissue destruction through direct injury, secondary missiles (bone or bullet fragments), and temporary cavitation. Exit wounds may be larger than entrance wounds, but small or inconspicuous entry and exit sites can mask severe internal injury.
Clinicians must remember the full anatomic boundaries of the abdomen, which extend from the nipples anteriorly and the inferior scapular tips posteriorly down to the inferior gluteal folds.
Initial Evaluation and Essential Workup
Gunshot wounds to the abdomen are generally assumed to have caused intra-abdominal injury and are typically managed with operative exploration.
For stab wounds to the anterior abdomen, local wound exploration is essential. If the anterior fascia is violated, further evaluation with diagnostic peritoneal lavage or bedside ultrasonography is indicated.
Diagnostic laparoscopy is particularly useful for identifying diaphragmatic injuries and selected liver or splenic lacerations and may help avoid unnecessary laparotomy in stable patients.
CT imaging is valuable for evaluating suspected retroperitoneal injuries in stable patients but is unreliable for detecting hollow viscus or diaphragmatic injuries.
Diagnostic peritoneal lavage remains useful in select cases. A red blood cell count of 10,000/mm³ or greater is an indication for laparotomy. Patients with lower counts should be closely observed for 8–24 hours for evolving peritoneal signs.
Diagnostic Tests and Interpretation
Laboratory evaluation includes serial hemoglobin or hematocrit measurements to assess ongoing blood loss, urinalysis to screen for genitourinary injury, arterial blood gas analysis to evaluate hypovolemia, and blood typing with cross-matching for patients with suspected significant injury.
Imaging studies may include plain radiographs with external markers to localize foreign bodies, identify fractures, or detect free air. Intravenous pyelography may be used when renal injury is suspected. Focused abdominal sonography for trauma (FAST) can rapidly identify intraperitoneal fluid, while CT with intravenous contrast is reserved for stable patients in experienced centers.
Differential Diagnosis
Upper abdominal penetrating wounds may involve intrathoracic structures, while lower thoracic injuries can extend into the abdominal cavity. Both possibilities should always be considered during evaluation.
Prehospital Management
Fluid resuscitation should be carefully titrated to clinical response. Military antishock trousers are not recommended. Open wounds should be covered with sterile dressings, and eviscerated bowel should be protected with moist sterile dressings. Impaled objects must be stabilized in place and never removed in the field.
Initial Stabilization and Therapy
Management begins with high-flow oxygen and placement of two large-bore intravenous lines for crystalloid infusion. If there is no response after 2 liters of crystalloid, transfusion of packed red blood cells is indicated, using O-negative blood initially if the patient is unstable. Type-specific and cross-matched blood should be administered as soon as available.
Pediatric Considerations
Children in hypovolemic shock should receive crystalloid boluses of 20 mL/kg. Severe shock requires transfusion of packed red blood cells at 1 mL/kg. Diagnostic peritoneal lavage is relatively contraindicated in children younger than 8 years.
Emergency Department Procedures
A nasogastric tube should be placed to reduce aspiration risk and decompress the stomach prior to diagnostic peritoneal lavage. This may also relieve respiratory distress caused by diaphragmatic injury with herniation of abdominal contents.
A Foley catheter should be inserted after excluding urethral injury to assist in detecting genitourinary trauma and monitoring urine output. Tetanus prophylaxis should be administered when indicated.
Medications
Broad-spectrum intravenous antibiotics with gram-negative and anaerobic coverage are required due to the high risk of contamination. Acceptable regimens include second-generation cephalosporins, beta-lactam/beta-lactamase inhibitor combinations, or combination therapy with aminoglycosides and anaerobic agents. Tetanus toxoid and tetanus immunoglobulin should be given as appropriate.
Disposition and Follow-Up
Patients requiring operative intervention must be admitted. Those with negative diagnostic studies should be observed for at least 8 hours with serial abdominal examinations and repeated hematocrit measurements.
Patients with stab wounds that do not penetrate the fascia may be discharged after a period of observation in the emergency department.
Clinical Pearls and Pitfalls
Permissive hypotension is increasingly supported during resuscitation to limit bleeding. Overaggressive crystalloid administration should be avoided. Complete exposure of the patient is essential to avoid missed injuries. Routine spinal immobilization is unnecessary unless there is clear evidence of spinal cord injury.
