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KembaraXtra- Medicine- Aortic Regurgitation
Aortic regurgitation (AR), also known as aortic insufficiency, is a condition characterized by abnormal retrograde flow of blood from the aorta into the left ventricle during diastole due to incomplete closure of the aortic valve. This inadequate valve closure may result from intrinsic disease of the aortic valve leaflets or from pathology involving the aortic root or ascending aorta, such as dilation. Aortic regurgitation may be acute or chronic in nature. Chronic AR is further classified into stages: Stage A refers to patients at risk for AR without even trace regurgitation (for example, those with bicuspid aortic valves, aortic valve sclerosis, aortic root disease, or a history of rheumatic heart disease or infective endocarditis); Stage B includes patients with progressive mild to moderate AR and preserved left ventricular ejection fraction (LVEF); Stage C includes asymptomatic patients with severe AR, subdivided into those with preserved LVEF (C1) and those with reduced LVEF (C2); and Stage D includes patients with symptomatic severe AR.
The epidemiology of AR varies according to severity, age, and sex. Mild AR becomes increasingly common with advancing age, while moderate to severe AR remains less frequent but rises in prevalence among older adults. In developing countries, the most common cause of AR is rheumatic heart disease. In developed countries, aortic root dilation, congenital bicuspid aortic valve, and degenerative calcific valve disease are the predominant causes. Infective endocarditis is the most common cause of acute AR. Other causes include leaflet abnormalities such as trauma with valvular rupture, myxomatous degeneration, drug-induced valve disease (e.g., fenfluramine, dexfenfluramine, pergolide, cabergoline), congenital heart disease (including bicuspid aortic valve and sinus of Valsalva aneurysm), systemic inflammatory or rheumatologic disorders (such as ankylosing spondylitis, rheumatoid arthritis, and systemic lupus erythematosus), and iatrogenic injury (e.g., following aortic balloon valvotomy). Abnormalities of the aortic root or ascending aorta, including annuloaortic ectasia, connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome), trauma, syphilitic aortitis, systemic hypertension, and aortic dissection, are also important etiologies. Postprocedural AR, most often due to paravalvular leak, occurs in a notable proportion of patients after transcatheter aortic valve replacement (TAVR) and is associated with worse outcomes when more than mild.
Clinical presentation depends on whether AR is acute or chronic. Chronic AR is often well tolerated for many years because of compensatory left ventricular dilation and hypertrophy. Symptoms typically appear when left ventricular systolic function deteriorates and include dyspnea on exertion, decreased exercise tolerance, chest pain, syncope, and signs of congestive heart failure. Acute severe AR presents dramatically, often with hypotension, pulmonary edema, and cardiogenic shock, due to the inability of the left ventricle to accommodate the sudden volume overload. In acute AR, the rapid rise in left ventricular diastolic pressure reduces coronary perfusion, further worsening hemodynamics.
Physical examination findings in chronic AR are largely related to increased stroke volume and widened pulse pressure. These include bounding or “water-hammer” pulses (Corrigan pulse), head bobbing with each heartbeat (de Musset sign), loud systolic and diastolic femoral sounds (“pistol-shot” femorals or Traube sign), capillary pulsations of the nail beds or lips (Quincke sign), and a to-and-fro femoral murmur with compression of the femoral artery (Duroziez sign). A significant increase in popliteal systolic pressure compared with brachial pressure (Hill sign) may be present. Historical signs such as uvular pulsation (Mueller sign), retinal arterial pulsations (Becker sign), diastolic blood pressure drop with arm elevation (Mayne sign), hepatic pulsations (Rosenbach sign), splenic pulsations (Gerhard sign), and pupillary changes (Landolfi sign) are neither sensitive nor specific but may be noted. Cardiac auscultation typically reveals a high-pitched, blowing, decrescendo diastolic murmur best heard along the left sternal border, an S3 at the apex, displacement of the apical impulse downward and laterally, and sometimes an Austin Flint murmur, which is a low-pitched apical diastolic rumble related to altered mitral inflow dynamics. In acute AR, these classic peripheral signs are often absent, and a short, soft diastolic murmur may be the only auscultatory finding.
The diagnostic evaluation of AR includes a careful history and physical examination, with particular attention to symptoms of exertional dyspnea, chest pain, syncope, and heart failure. Echocardiography is the cornerstone of diagnosis and is used to confirm AR, determine severity, assess valve anatomy, and evaluate left ventricular size and systolic function. Severity can be assessed qualitatively (e.g., vena contracta width) and quantitatively using effective regurgitant orifice area, regurgitant volume, and regurgitant fraction. Evidence of left ventricular dilation is required for the diagnosis of chronic severe AR. Chest radiography may demonstrate left ventricular enlargement and aortic dilation in chronic AR, while acute AR may show pulmonary edema with a relatively normal cardiac silhouette. Electrocardiography is not diagnostic but often reveals left ventricular hypertrophy in chronic AR and helps assess for associated arrhythmias. When transthoracic echocardiographic images are suboptimal or discordant with clinical findings, transesophageal echocardiography, cardiac magnetic resonance imaging, or cardiac catheterization may be used to further define AR severity, ventricular function, and aortic dimensions.
Management strategies differ between acute and chronic AR. Acute severe AR is a medical and surgical emergency. Definitive treatment is urgent aortic valve replacement or repair. Medical stabilization includes afterload reduction with vasodilators such as nitroprusside and treatment of pulmonary edema with diuretics. Beta-blockers are avoided because they prolong diastole and worsen regurgitation, and intra-aortic balloon pump support is contraindicated. Immediate surgical referral is required in cases of cardiogenic shock.
Chronic AR management depends on symptom status, severity of regurgitation, left ventricular systolic function, and ventricular dimensions. According to ACC/AHA guidelines, aortic valve replacement is indicated for symptomatic patients with severe AR regardless of LVEF and for asymptomatic patients with severe AR and LVEF less than 55%. Surgery is also indicated in patients with severe AR who are undergoing other cardiac surgery. In selected asymptomatic patients with preserved LVEF but significant left ventricular dilation, surgery may be reasonable if surgical risk is low. Medical therapy plays a supportive role and focuses on treating hypertension and heart failure symptoms. ACE inhibitors or angiotensin receptor blockers are recommended for blood pressure control, and diuretics with sodium restriction are used for congestive heart failure. Long-term vasodilator therapy has not consistently been shown to delay surgery in asymptomatic patients with severe AR but is appropriate for concomitant hypertension. Beta-blockers may be considered in patients with symptomatic severe AR or left ventricular dysfunction when surgery is not feasible, and observational studies suggest a potential survival benefit in such cases. For patients with pure aortic insufficiency who are not surgical candidates, TAVR may be considered, although it is associated with higher rates of certain complications compared with surgical valve replacement.
Referral for surgical or advanced cardiac evaluation is indicated in patients with acute severe AR, symptomatic severe AR, evidence of left ventricular systolic dysfunction, or significant ventricular dilation even in the absence of symptoms. With timely intervention and appropriate long-term follow-up, outcomes in patients with chronic AR can be significantly improved, particularly when surgery is performed before irreversible left ventricular dysfunction develops.
Aortic regurgitation (AR), also known as aortic insufficiency, is a condition characterized by abnormal retrograde flow of blood from the aorta into the left ventricle during diastole due to incomplete closure of the aortic valve. This inadequate valve closure may result from intrinsic disease of the aortic valve leaflets or from pathology involving the aortic root or ascending aorta, such as dilation. Aortic regurgitation may be acute or chronic in nature. Chronic AR is further classified into stages: Stage A refers to patients at risk for AR without even trace regurgitation (for example, those with bicuspid aortic valves, aortic valve sclerosis, aortic root disease, or a history of rheumatic heart disease or infective endocarditis); Stage B includes patients with progressive mild to moderate AR and preserved left ventricular ejection fraction (LVEF); Stage C includes asymptomatic patients with severe AR, subdivided into those with preserved LVEF (C1) and those with reduced LVEF (C2); and Stage D includes patients with symptomatic severe AR.
The epidemiology of AR varies according to severity, age, and sex. Mild AR becomes increasingly common with advancing age, while moderate to severe AR remains less frequent but rises in prevalence among older adults. In developing countries, the most common cause of AR is rheumatic heart disease. In developed countries, aortic root dilation, congenital bicuspid aortic valve, and degenerative calcific valve disease are the predominant causes. Infective endocarditis is the most common cause of acute AR. Other causes include leaflet abnormalities such as trauma with valvular rupture, myxomatous degeneration, drug-induced valve disease (e.g., fenfluramine, dexfenfluramine, pergolide, cabergoline), congenital heart disease (including bicuspid aortic valve and sinus of Valsalva aneurysm), systemic inflammatory or rheumatologic disorders (such as ankylosing spondylitis, rheumatoid arthritis, and systemic lupus erythematosus), and iatrogenic injury (e.g., following aortic balloon valvotomy). Abnormalities of the aortic root or ascending aorta, including annuloaortic ectasia, connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome), trauma, syphilitic aortitis, systemic hypertension, and aortic dissection, are also important etiologies. Postprocedural AR, most often due to paravalvular leak, occurs in a notable proportion of patients after transcatheter aortic valve replacement (TAVR) and is associated with worse outcomes when more than mild.
Clinical presentation depends on whether AR is acute or chronic. Chronic AR is often well tolerated for many years because of compensatory left ventricular dilation and hypertrophy. Symptoms typically appear when left ventricular systolic function deteriorates and include dyspnea on exertion, decreased exercise tolerance, chest pain, syncope, and signs of congestive heart failure. Acute severe AR presents dramatically, often with hypotension, pulmonary edema, and cardiogenic shock, due to the inability of the left ventricle to accommodate the sudden volume overload. In acute AR, the rapid rise in left ventricular diastolic pressure reduces coronary perfusion, further worsening hemodynamics.
Physical examination findings in chronic AR are largely related to increased stroke volume and widened pulse pressure. These include bounding or “water-hammer” pulses (Corrigan pulse), head bobbing with each heartbeat (de Musset sign), loud systolic and diastolic femoral sounds (“pistol-shot” femorals or Traube sign), capillary pulsations of the nail beds or lips (Quincke sign), and a to-and-fro femoral murmur with compression of the femoral artery (Duroziez sign). A significant increase in popliteal systolic pressure compared with brachial pressure (Hill sign) may be present. Historical signs such as uvular pulsation (Mueller sign), retinal arterial pulsations (Becker sign), diastolic blood pressure drop with arm elevation (Mayne sign), hepatic pulsations (Rosenbach sign), splenic pulsations (Gerhard sign), and pupillary changes (Landolfi sign) are neither sensitive nor specific but may be noted. Cardiac auscultation typically reveals a high-pitched, blowing, decrescendo diastolic murmur best heard along the left sternal border, an S3 at the apex, displacement of the apical impulse downward and laterally, and sometimes an Austin Flint murmur, which is a low-pitched apical diastolic rumble related to altered mitral inflow dynamics. In acute AR, these classic peripheral signs are often absent, and a short, soft diastolic murmur may be the only auscultatory finding.
The diagnostic evaluation of AR includes a careful history and physical examination, with particular attention to symptoms of exertional dyspnea, chest pain, syncope, and heart failure. Echocardiography is the cornerstone of diagnosis and is used to confirm AR, determine severity, assess valve anatomy, and evaluate left ventricular size and systolic function. Severity can be assessed qualitatively (e.g., vena contracta width) and quantitatively using effective regurgitant orifice area, regurgitant volume, and regurgitant fraction. Evidence of left ventricular dilation is required for the diagnosis of chronic severe AR. Chest radiography may demonstrate left ventricular enlargement and aortic dilation in chronic AR, while acute AR may show pulmonary edema with a relatively normal cardiac silhouette. Electrocardiography is not diagnostic but often reveals left ventricular hypertrophy in chronic AR and helps assess for associated arrhythmias. When transthoracic echocardiographic images are suboptimal or discordant with clinical findings, transesophageal echocardiography, cardiac magnetic resonance imaging, or cardiac catheterization may be used to further define AR severity, ventricular function, and aortic dimensions.
Management strategies differ between acute and chronic AR. Acute severe AR is a medical and surgical emergency. Definitive treatment is urgent aortic valve replacement or repair. Medical stabilization includes afterload reduction with vasodilators such as nitroprusside and treatment of pulmonary edema with diuretics. Beta-blockers are avoided because they prolong diastole and worsen regurgitation, and intra-aortic balloon pump support is contraindicated. Immediate surgical referral is required in cases of cardiogenic shock.
Chronic AR management depends on symptom status, severity of regurgitation, left ventricular systolic function, and ventricular dimensions. According to ACC/AHA guidelines, aortic valve replacement is indicated for symptomatic patients with severe AR regardless of LVEF and for asymptomatic patients with severe AR and LVEF less than 55%. Surgery is also indicated in patients with severe AR who are undergoing other cardiac surgery. In selected asymptomatic patients with preserved LVEF but significant left ventricular dilation, surgery may be reasonable if surgical risk is low. Medical therapy plays a supportive role and focuses on treating hypertension and heart failure symptoms. ACE inhibitors or angiotensin receptor blockers are recommended for blood pressure control, and diuretics with sodium restriction are used for congestive heart failure. Long-term vasodilator therapy has not consistently been shown to delay surgery in asymptomatic patients with severe AR but is appropriate for concomitant hypertension. Beta-blockers may be considered in patients with symptomatic severe AR or left ventricular dysfunction when surgery is not feasible, and observational studies suggest a potential survival benefit in such cases. For patients with pure aortic insufficiency who are not surgical candidates, TAVR may be considered, although it is associated with higher rates of certain complications compared with surgical valve replacement.
Referral for surgical or advanced cardiac evaluation is indicated in patients with acute severe AR, symptomatic severe AR, evidence of left ventricular systolic dysfunction, or significant ventricular dilation even in the absence of symptoms. With timely intervention and appropriate long-term follow-up, outcomes in patients with chronic AR can be significantly improved, particularly when surgery is performed before irreversible left ventricular dysfunction develops.
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Emergency And Acute Medicine – Isoniazid Poisoning
Basics Description
Isoniazid (INH) toxicity results from interference with pyridoxine (vitamin B6) metabolism. INH complexes with and inactivates pyridoxal-5-phosphate, the active form of pyridoxine, and inhibits pyridoxine phosphokinase, preventing conversion to its active form. This leads to a net decrease in γ-aminobutyric acid (GABA) production, causing cerebral excitability and seizures. INH also inhibits lactate dehydrogenase, impairing conversion of lactate to pyruvate and contributing to profound anion gap metabolic acidosis. Free effects include mitochondrial dysfunction and impaired oxidative metabolism.
Chronic toxicity interferes with nicotinic acid (niacin) synthesis and may produce a pellagra-like syndrome after months of therapy. INH has some monoamine oxidase inhibitor–like effects, with rare reports of tyramine reactions, mania, depression, obsessive–compulsive symptoms, and psychosis. Pharmacokinetically, INH is rapidly absorbed with peak levels within 1–2 hours. It has a volume of distribution of 0.6 L/kg, low protein binding, hepatic acetylation, and renal excretion within 24 hours. Half-life is less than 1 hour in fast acetylators and 2–4 hours in slow acetylators.
Etiology
High-risk populations include immigrants, individuals experiencing homelessness, people with HIV infection, alcohol use disorder, and those of lower socioeconomic status. Slow acetylators are more prone to chronic toxicity. The estimated LD50 is 80–150 mg/kg. Ingestions less than 1.5 g typically cause mild toxicity, while ingestions of 10 g or more are often fatal.
Diagnosis: Signs and Symptoms
Acute toxicity primarily affects the nervous system and presents with altered mental status, seizures refractory to standard therapy, agitation, coma, dizziness, ataxia, hyperreflexia, slurred speech, hallucinations, and psychosis. Gastrointestinal symptoms include nausea and vomiting. Renal findings may include oliguria or anuria. Cardiovascular manifestations include hypotension, tachycardia, shock, and cyanosis. Metabolically, patients develop profound anion gap metabolic acidosis with elevated lactate and may be hyperthermic.
Chronic toxicity presents with peripheral neuropathy, optic neuritis or atrophy, insomnia, vertigo, psychosis, and features of pellagra. Hepatic involvement may include hepatitis or liver failure, along with anorexia, nausea, vomiting, and constipation.
Essential Workup
In the absence of a clear ingestion history, evaluation should focus on unexplained altered mental status, seizures, and metabolic acidosis.
Diagnosis Tests and Interpretation
Laboratory evaluation typically reveals severe metabolic acidosis on arterial blood gas. Serum chemistries show elevated anion gap acidosis and possible hyperglycemia. CBC may show leukocytosis and eosinophilia in acute toxicity, or agranulocytosis, hemolysis, anemia, and eosinophilia in chronic toxicity. Chest radiography may show evidence of tuberculosis or aspiration pneumonia. CT imaging or lumbar puncture may be required if the history is unclear.
Differential Diagnosis
The differential includes other toxicologic causes such as tricyclic antidepressants, salicylates, theophylline, methanol, ethylene glycol, lithium, carbon monoxide, and cyanide. Non-toxicologic causes include stroke, intracranial hemorrhage or mass, trauma, abscess, hypoglycemia, uremia, and thyrotoxicosis.
Treatment Prehospital
All prescription bottles and medications should be collected and transported with the patient for identification.
Initial Stabilization and Therapy
Initial management prioritizes airway, breathing, and circulation. Supplemental oxygen should be provided, and intubation performed if airway protection is required. Establish IV access, initiate cardiac monitoring, and administer isotonic fluids. For altered mental status, give naloxone, thiamine, and dextrose as indicated.
ED Treatment and Procedures
Pyridoxine (vitamin B6) is the specific antidote for INH toxicity. The goal dose is 1 g of pyridoxine for each gram of INH ingested, administered IV in divided doses every 2–3 minutes. If the amount ingested is unknown, give 5 g IV. Doses may be repeated after 20 minutes for refractory seizures or persistent coma. If IV pyridoxine is unavailable, tablets may be crushed and administered via nasogastric tube.
Seizure control relies on pyridoxine replacement; benzodiazepines are synergistic and should be used as needed. Phenytoin is ineffective and should not be used. After stabilization, gastric decontamination may be considered in life-threatening ingestions presenting within one hour, provided the airway is protected. Activated charcoal may be given at a 10:1 charcoal-to-drug ratio. Hemodialysis is reserved for persistent symptoms despite adequate therapy or in patients with renal insufficiency. Metabolic acidosis usually resolves after seizure control and does not routinely require bicarbonate therapy.
Medication
Supportive medications may include IV dextrose, benzodiazepines such as diazepam or lorazepam for seizures, naloxone if indicated, pyridoxine as the antidote, and thiamine.
Follow-Up Disposition
ICU admission is required for refractory seizures, severe acidosis, coma, or persistent altered mental status. Patients with unclear ingestion history, uncontrolled vomiting, or intentional overdose also require admission and toxicology consultation. Asymptomatic patients may be discharged after at least 6 hours of observation, as symptoms typically develop within 45 minutes to 2 hours.
Follow-Up Recommendations
Psychiatric evaluation is recommended for all intentional ingestions or suicidal patients.
Pearls and Pitfalls
Refractory seizures unresponsive to standard therapy are a key clue to INH poisoning. Severe lactic acidosis in a patient with seizures and altered mental status should raise suspicion for INH toxicity. Pyridoxine dosing should be gram-for-gram relative to INH ingestion, and additional doses may be given if seizures resolve but coma persists. Never paralyze an actively seizing patient without continuous EEG monitoring.
Basics Description
Isoniazid (INH) toxicity results from interference with pyridoxine (vitamin B6) metabolism. INH complexes with and inactivates pyridoxal-5-phosphate, the active form of pyridoxine, and inhibits pyridoxine phosphokinase, preventing conversion to its active form. This leads to a net decrease in γ-aminobutyric acid (GABA) production, causing cerebral excitability and seizures. INH also inhibits lactate dehydrogenase, impairing conversion of lactate to pyruvate and contributing to profound anion gap metabolic acidosis. Free effects include mitochondrial dysfunction and impaired oxidative metabolism.
Chronic toxicity interferes with nicotinic acid (niacin) synthesis and may produce a pellagra-like syndrome after months of therapy. INH has some monoamine oxidase inhibitor–like effects, with rare reports of tyramine reactions, mania, depression, obsessive–compulsive symptoms, and psychosis. Pharmacokinetically, INH is rapidly absorbed with peak levels within 1–2 hours. It has a volume of distribution of 0.6 L/kg, low protein binding, hepatic acetylation, and renal excretion within 24 hours. Half-life is less than 1 hour in fast acetylators and 2–4 hours in slow acetylators.
Etiology
High-risk populations include immigrants, individuals experiencing homelessness, people with HIV infection, alcohol use disorder, and those of lower socioeconomic status. Slow acetylators are more prone to chronic toxicity. The estimated LD50 is 80–150 mg/kg. Ingestions less than 1.5 g typically cause mild toxicity, while ingestions of 10 g or more are often fatal.
Diagnosis: Signs and Symptoms
Acute toxicity primarily affects the nervous system and presents with altered mental status, seizures refractory to standard therapy, agitation, coma, dizziness, ataxia, hyperreflexia, slurred speech, hallucinations, and psychosis. Gastrointestinal symptoms include nausea and vomiting. Renal findings may include oliguria or anuria. Cardiovascular manifestations include hypotension, tachycardia, shock, and cyanosis. Metabolically, patients develop profound anion gap metabolic acidosis with elevated lactate and may be hyperthermic.
Chronic toxicity presents with peripheral neuropathy, optic neuritis or atrophy, insomnia, vertigo, psychosis, and features of pellagra. Hepatic involvement may include hepatitis or liver failure, along with anorexia, nausea, vomiting, and constipation.
Essential Workup
In the absence of a clear ingestion history, evaluation should focus on unexplained altered mental status, seizures, and metabolic acidosis.
Diagnosis Tests and Interpretation
Laboratory evaluation typically reveals severe metabolic acidosis on arterial blood gas. Serum chemistries show elevated anion gap acidosis and possible hyperglycemia. CBC may show leukocytosis and eosinophilia in acute toxicity, or agranulocytosis, hemolysis, anemia, and eosinophilia in chronic toxicity. Chest radiography may show evidence of tuberculosis or aspiration pneumonia. CT imaging or lumbar puncture may be required if the history is unclear.
Differential Diagnosis
The differential includes other toxicologic causes such as tricyclic antidepressants, salicylates, theophylline, methanol, ethylene glycol, lithium, carbon monoxide, and cyanide. Non-toxicologic causes include stroke, intracranial hemorrhage or mass, trauma, abscess, hypoglycemia, uremia, and thyrotoxicosis.
Treatment Prehospital
All prescription bottles and medications should be collected and transported with the patient for identification.
Initial Stabilization and Therapy
Initial management prioritizes airway, breathing, and circulation. Supplemental oxygen should be provided, and intubation performed if airway protection is required. Establish IV access, initiate cardiac monitoring, and administer isotonic fluids. For altered mental status, give naloxone, thiamine, and dextrose as indicated.
ED Treatment and Procedures
Pyridoxine (vitamin B6) is the specific antidote for INH toxicity. The goal dose is 1 g of pyridoxine for each gram of INH ingested, administered IV in divided doses every 2–3 minutes. If the amount ingested is unknown, give 5 g IV. Doses may be repeated after 20 minutes for refractory seizures or persistent coma. If IV pyridoxine is unavailable, tablets may be crushed and administered via nasogastric tube.
Seizure control relies on pyridoxine replacement; benzodiazepines are synergistic and should be used as needed. Phenytoin is ineffective and should not be used. After stabilization, gastric decontamination may be considered in life-threatening ingestions presenting within one hour, provided the airway is protected. Activated charcoal may be given at a 10:1 charcoal-to-drug ratio. Hemodialysis is reserved for persistent symptoms despite adequate therapy or in patients with renal insufficiency. Metabolic acidosis usually resolves after seizure control and does not routinely require bicarbonate therapy.
Medication
Supportive medications may include IV dextrose, benzodiazepines such as diazepam or lorazepam for seizures, naloxone if indicated, pyridoxine as the antidote, and thiamine.
Follow-Up Disposition
ICU admission is required for refractory seizures, severe acidosis, coma, or persistent altered mental status. Patients with unclear ingestion history, uncontrolled vomiting, or intentional overdose also require admission and toxicology consultation. Asymptomatic patients may be discharged after at least 6 hours of observation, as symptoms typically develop within 45 minutes to 2 hours.
Follow-Up Recommendations
Psychiatric evaluation is recommended for all intentional ingestions or suicidal patients.
Pearls and Pitfalls
Refractory seizures unresponsive to standard therapy are a key clue to INH poisoning. Severe lactic acidosis in a patient with seizures and altered mental status should raise suspicion for INH toxicity. Pyridoxine dosing should be gram-for-gram relative to INH ingestion, and additional doses may be given if seizures resolve but coma persists. Never paralyze an actively seizing patient without continuous EEG monitoring.
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Emergency and Acute Medicine – Isopropanol Poisoning
Basics Description
Isopropanol (isopropyl alcohol) is a potent central nervous system depressant, with effects that are two to three times stronger than ethanol. It is rapidly absorbed after oral ingestion and is metabolized by alcohol dehydrogenase to acetone, which itself is a CNS depressant. Unlike other toxic alcohols, isopropanol is ketogenic but does not usually cause significant metabolic acidosis. Concomitant ethanol ingestion prolongs the half-life of isopropanol but not acetone. Isopropanol has a half-life of approximately 3–16 hours, while acetone persists longer, with a half-life of 7.5–26 hours. Acetone is eliminated through the lungs and kidneys.
Etiology
Isopropanol is a clear, colorless, volatile liquid with a bitter taste and a faint odor of acetone. It is commonly available as a 70% rubbing alcohol solution, sometimes containing blue dye (“blue heaven”) to discourage abuse. It is found in many household and industrial products, including toiletries, disinfectants, window cleaners, paint removers, solvents, jewelry cleaners, detergents, antifreeze, and hand sanitizers. The typical adult patient is a chronic alcoholic who has depleted their ethanol supply and substitutes isopropanol. Systemic toxicity can also occur from dermal absorption or rectal administration.
Diagnosis: Signs and Symptoms
Symptoms usually develop within 30–60 minutes of ingestion. Neurologic manifestations include lethargy, weakness, headache, inebriation, vertigo, ataxia, apnea, and coma. Unlike ethanol, an initial excitation phase is typically absent. Gastrointestinal symptoms are common and include nausea, vomiting, abdominal pain, gastritis, and hematemesis. Cardiovascular findings may include hypotension, tachycardia, myocardial depression, and peripheral vasodilation. Pulmonary effects include respiratory depression and hemorrhagic tracheobronchitis. Dermatologic exposure can cause skin irritation or burns, and ocular exposure leads to irritation and lacrimation.
In children, accidental ingestions are common in those younger than 6 years, and rubbing alcohol sponge baths may cause inhalational toxicity. Pediatric patients are particularly prone to hypoglycemia.
Essential Workup
Diagnosis is supported by a history of ingestion and the presence of an acetone or isopropanol odor on the patient’s breath.
Diagnosis Tests and Interpretation
Laboratory evaluation should include electrolytes, BUN, creatinine, and glucose. Hypoglycemia may be present. Significant acidosis is uncommon unless there is associated hypoperfusion or a coingestant. Acetone can falsely elevate serum creatinine; when acetone levels exceed 40 mg/dL, creatinine may rise approximately 1 mg/dL for every 100 mg/dL of acetone, returning to baseline as acetone is cleared. CBC may show decreased hematocrit in cases of hemorrhagic gastritis. Arterial blood gas analysis typically shows little or no acidosis. Urinalysis and serum testing reveal ketosis.
Serum isopropanol levels correlate with severity, with coma often occurring at levels above 150 mg/dL. Serum osmolarity should be assessed, as an elevated osmolar gap (>10) is common. Each 5.9 mg/dL of isopropanol and 5.5 mg/dL of acetone increases the osmolar gap by approximately 1 mOsm/kg. Chest radiography is indicated if aspiration pneumonia is suspected, and head CT should be considered when altered mental status or head injury is possible.
Differential Diagnosis
The differential diagnosis for CNS depression with an elevated osmolar gap includes ethanol, ethylene glycol, methanol, glycerol, and mannitol.
Treatment Prehospital
All potentially ingested bottles and medications should be located and transported with the patient to the emergency department.
Initial Stabilization and Therapy
Management begins with airway, breathing, and circulation. Airway protection and ventilatory support may be required. Hypotension should initially be treated with IV 0.9% normal saline; vasopressors such as dopamine or norepinephrine may be required if hypotension persists. Patients with significant hemorrhagic gastritis may require packed red blood cell transfusion. Nasogastric tube placement and irrigation may be indicated for hematemesis. Naloxone, thiamine, and dextrose should be administered for altered mental status as indicated.
ED Treatment and Procedures
Treatment is primarily supportive, as there is no specific antidote. Skin and eye exposures should be treated with copious irrigation. Activated charcoal may be considered for coingestants and, in large doses, can adsorb some isopropanol. Ethanol infusion and fomepizole (4-methylpyrazole) are not indicated. Hemodialysis effectively removes both isopropanol and acetone but is rarely required. Indications for dialysis include persistent hemodynamic instability despite fluids and pressors or very high serum levels (>400 mg/dL), which are associated with severe hypotension and prolonged coma.
Medication
Supportive medications may include activated charcoal, IV dextrose for hypoglycemia, dopamine for refractory hypotension, naloxone if opioid exposure is suspected, and thiamine for patients at risk of deficiency.
Follow-Up Disposition
Patients with moderate to severe toxicity, including altered mental status or hypotension, should be admitted. Asymptomatic patients should be observed for 2–4 hours after ingestion before discharge. Mild intoxication that resolves within 4–6 hours may be safely discharged.
Follow-Up Recommendations
Patients with intentional ingestion should be referred for alcohol detoxification or psychiatric evaluation. Gastroenterology referral is recommended for those with recurrent hematemesis requiring endoscopic evaluation.
Pearls and Pitfalls
Supportive care is the cornerstone of treatment for isopropanol poisoning. Unlike other toxic alcohol ingestions, ethanol infusion and fomepizole should not be used.
Basics Description
Isopropanol (isopropyl alcohol) is a potent central nervous system depressant, with effects that are two to three times stronger than ethanol. It is rapidly absorbed after oral ingestion and is metabolized by alcohol dehydrogenase to acetone, which itself is a CNS depressant. Unlike other toxic alcohols, isopropanol is ketogenic but does not usually cause significant metabolic acidosis. Concomitant ethanol ingestion prolongs the half-life of isopropanol but not acetone. Isopropanol has a half-life of approximately 3–16 hours, while acetone persists longer, with a half-life of 7.5–26 hours. Acetone is eliminated through the lungs and kidneys.
Etiology
Isopropanol is a clear, colorless, volatile liquid with a bitter taste and a faint odor of acetone. It is commonly available as a 70% rubbing alcohol solution, sometimes containing blue dye (“blue heaven”) to discourage abuse. It is found in many household and industrial products, including toiletries, disinfectants, window cleaners, paint removers, solvents, jewelry cleaners, detergents, antifreeze, and hand sanitizers. The typical adult patient is a chronic alcoholic who has depleted their ethanol supply and substitutes isopropanol. Systemic toxicity can also occur from dermal absorption or rectal administration.
Diagnosis: Signs and Symptoms
Symptoms usually develop within 30–60 minutes of ingestion. Neurologic manifestations include lethargy, weakness, headache, inebriation, vertigo, ataxia, apnea, and coma. Unlike ethanol, an initial excitation phase is typically absent. Gastrointestinal symptoms are common and include nausea, vomiting, abdominal pain, gastritis, and hematemesis. Cardiovascular findings may include hypotension, tachycardia, myocardial depression, and peripheral vasodilation. Pulmonary effects include respiratory depression and hemorrhagic tracheobronchitis. Dermatologic exposure can cause skin irritation or burns, and ocular exposure leads to irritation and lacrimation.
In children, accidental ingestions are common in those younger than 6 years, and rubbing alcohol sponge baths may cause inhalational toxicity. Pediatric patients are particularly prone to hypoglycemia.
Essential Workup
Diagnosis is supported by a history of ingestion and the presence of an acetone or isopropanol odor on the patient’s breath.
Diagnosis Tests and Interpretation
Laboratory evaluation should include electrolytes, BUN, creatinine, and glucose. Hypoglycemia may be present. Significant acidosis is uncommon unless there is associated hypoperfusion or a coingestant. Acetone can falsely elevate serum creatinine; when acetone levels exceed 40 mg/dL, creatinine may rise approximately 1 mg/dL for every 100 mg/dL of acetone, returning to baseline as acetone is cleared. CBC may show decreased hematocrit in cases of hemorrhagic gastritis. Arterial blood gas analysis typically shows little or no acidosis. Urinalysis and serum testing reveal ketosis.
Serum isopropanol levels correlate with severity, with coma often occurring at levels above 150 mg/dL. Serum osmolarity should be assessed, as an elevated osmolar gap (>10) is common. Each 5.9 mg/dL of isopropanol and 5.5 mg/dL of acetone increases the osmolar gap by approximately 1 mOsm/kg. Chest radiography is indicated if aspiration pneumonia is suspected, and head CT should be considered when altered mental status or head injury is possible.
Differential Diagnosis
The differential diagnosis for CNS depression with an elevated osmolar gap includes ethanol, ethylene glycol, methanol, glycerol, and mannitol.
Treatment Prehospital
All potentially ingested bottles and medications should be located and transported with the patient to the emergency department.
Initial Stabilization and Therapy
Management begins with airway, breathing, and circulation. Airway protection and ventilatory support may be required. Hypotension should initially be treated with IV 0.9% normal saline; vasopressors such as dopamine or norepinephrine may be required if hypotension persists. Patients with significant hemorrhagic gastritis may require packed red blood cell transfusion. Nasogastric tube placement and irrigation may be indicated for hematemesis. Naloxone, thiamine, and dextrose should be administered for altered mental status as indicated.
ED Treatment and Procedures
Treatment is primarily supportive, as there is no specific antidote. Skin and eye exposures should be treated with copious irrigation. Activated charcoal may be considered for coingestants and, in large doses, can adsorb some isopropanol. Ethanol infusion and fomepizole (4-methylpyrazole) are not indicated. Hemodialysis effectively removes both isopropanol and acetone but is rarely required. Indications for dialysis include persistent hemodynamic instability despite fluids and pressors or very high serum levels (>400 mg/dL), which are associated with severe hypotension and prolonged coma.
Medication
Supportive medications may include activated charcoal, IV dextrose for hypoglycemia, dopamine for refractory hypotension, naloxone if opioid exposure is suspected, and thiamine for patients at risk of deficiency.
Follow-Up Disposition
Patients with moderate to severe toxicity, including altered mental status or hypotension, should be admitted. Asymptomatic patients should be observed for 2–4 hours after ingestion before discharge. Mild intoxication that resolves within 4–6 hours may be safely discharged.
Follow-Up Recommendations
Patients with intentional ingestion should be referred for alcohol detoxification or psychiatric evaluation. Gastroenterology referral is recommended for those with recurrent hematemesis requiring endoscopic evaluation.
Pearls and Pitfalls
Supportive care is the cornerstone of treatment for isopropanol poisoning. Unlike other toxic alcohol ingestions, ethanol infusion and fomepizole should not be used.
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Emergency and Acute Medicine – Knee Injuries: ACL, PCL, MCL, and Meniscus
Basic Description
Knee ligament and meniscal injuries are common causes of acute knee pain and instability, particularly in athletes and patients involved in high-energy trauma. Cruciate ligament injuries involve the anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL), which provide primary anteroposterior and rotational stability to the knee. The ACL runs from the posteromedial aspect of the lateral femoral condyle to the interspinous area of the tibia and prevents excessive anterior tibial translation, internal rotation, and hyperextension. The PCL is thicker and stronger than the ACL and extends from the anterolateral aspect of the medial femoral condyle to the posterior tibia, limiting posterior tibial translation.
Meniscal injuries most commonly involve the medial meniscus, which is less mobile and more firmly attached to the joint capsule than the lateral meniscus. Tears occur due to compressive or rotational forces between the femur and tibia. Displaced meniscal fragments can cause a true locked knee with inability to extend. The medial collateral ligament (MCL) extends from the medial femoral condyle to the tibia distal to the joint and is frequently injured in association with other ligamentous injuries.
Epidemiology
ACL injuries are the most common ligamentous knee injury, with approximately 200,000 cases annually in the United States. Nearly two-thirds are noncontact injuries, and females have a threefold increased risk compared with males. About half of ACL injuries are associated with meniscal tears, and chondral or subchondral damage is common. Medial meniscus injuries are significantly more frequent than lateral meniscus injuries, although true mechanical locking occurs in only about 30% of cases.
Etiology
ACL injuries typically result from deceleration combined with rotation or hyperextension, often during sports such as football or skiing, using a plant-and-pivot or stop-and-jump mechanism. PCL injuries are classically caused by a “dashboard injury,” where a posterior force is applied to the proximal tibia with the knee flexed, or from a fall onto a flexed knee. Meniscal injuries usually occur with sudden twisting motions during squatting, pivoting, or kneeling, and are common in both athletes and certain occupations. MCL injuries most often result from valgus stress applied to a flexed knee, such as from a lateral blow or ski injury.
In children, the ACL is the most frequently injured knee ligament, while isolated MCL injuries are uncommon before closure of the growth plates.
Diagnosis: Signs and Symptoms
Patients with cruciate ligament injuries often report a popping sensation, tearing feeling, or the knee “giving way,” followed by immediate dysfunction. A large effusion developing within 2–3 hours suggests hemarthrosis, most commonly from ACL injury. MCL injuries cause medial knee pain and tenderness, sometimes more pronounced in partial tears. Meniscal injuries are characterized by joint-line pain, intermittent swelling, mechanical symptoms, and difficulty fully extending the knee; patients may still complete activity at the time of injury. Degenerative meniscal tears present more insidiously and are often associated with osteoarthritis.
Physical Examination
Examination should include assessment of weight-bearing ability, palpation of bony landmarks and joint lines, evaluation of range of motion, and identification of effusion or locking. Immediate effusion suggests significant intra-articular injury, whereas delayed swelling is more typical of MCL, PCL, or meniscal injuries. A thorough neurovascular exam is essential. Stress testing should always compare the injured knee to the uninjured side.
The Lachman test is the most reliable maneuver for ACL injury in the acute setting. Anterior and posterior drawer tests assess ACL and PCL integrity, respectively, while the quadriceps active test helps confirm PCL injury. Valgus and varus stress testing evaluate MCL and LCL stability. Meniscal tests such as McMurray and Apley are best performed once acute pain is controlled.
Diagnostic Testing and Imaging
Laboratory testing is rarely required unless infection or inflammatory disease is suspected. Plain radiographs are recommended in most acute knee injuries to exclude fractures, especially in suspected ACL injuries and in children, where growth plate or tibial spine fractures may occur. MRI is highly sensitive and specific for ligamentous and meniscal injuries but is rarely needed emergently. Ottawa knee rules guide imaging decisions in adults but do not apply to children.
Essential Workup
Key priorities include careful neurovascular assessment, exclusion of fracture or infection, evaluation for multidirectional instability, and focused ligament testing, particularly the Lachman test for suspected ACL injury.
Differential Diagnosis
Consider growth plate injuries, tibial plateau fractures, transient knee or patellar dislocation, referred hip pathology, septic arthritis, gout, osteoarthritis, and inflammatory arthritides.
Treatment and Initial Management
Initial management includes immobilization, ice, elevation, and analgesia, along with documentation of neurovascular status. In the emergency department, locked knees due to meniscal injury may sometimes be reduced with gentle traction and rotation. Arthrocentesis can relieve pain from large effusions. In the absence of fracture, treatment consists of rest, ice, compression, elevation, and weight bearing as tolerated, often with crutches. Knee immobilizers may be used for comfort, but early gentle motion is encouraged.
Disposition and Follow-Up
Most isolated ligament or meniscal injuries can be managed as outpatients. Admission is rarely required unless a knee dislocation or vascular injury is suspected. Orthopedic follow-up within 1–2 weeks is recommended for confirmed or suspected significant ligamentous injury, and re-examination within 48 hours is helpful when initial assessment is limited by pain or swelling.
Pearls and Pitfalls
Always perform and document a thorough neurovascular exam. Maintain a high index of suspicion for occult knee dislocation in patients with multidirectional instability or multiple ligament injuries. Do not miss fractures, septic joints, referred hip pathology, or vascular compromise.
Basic Description
Knee ligament and meniscal injuries are common causes of acute knee pain and instability, particularly in athletes and patients involved in high-energy trauma. Cruciate ligament injuries involve the anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL), which provide primary anteroposterior and rotational stability to the knee. The ACL runs from the posteromedial aspect of the lateral femoral condyle to the interspinous area of the tibia and prevents excessive anterior tibial translation, internal rotation, and hyperextension. The PCL is thicker and stronger than the ACL and extends from the anterolateral aspect of the medial femoral condyle to the posterior tibia, limiting posterior tibial translation.
Meniscal injuries most commonly involve the medial meniscus, which is less mobile and more firmly attached to the joint capsule than the lateral meniscus. Tears occur due to compressive or rotational forces between the femur and tibia. Displaced meniscal fragments can cause a true locked knee with inability to extend. The medial collateral ligament (MCL) extends from the medial femoral condyle to the tibia distal to the joint and is frequently injured in association with other ligamentous injuries.
Epidemiology
ACL injuries are the most common ligamentous knee injury, with approximately 200,000 cases annually in the United States. Nearly two-thirds are noncontact injuries, and females have a threefold increased risk compared with males. About half of ACL injuries are associated with meniscal tears, and chondral or subchondral damage is common. Medial meniscus injuries are significantly more frequent than lateral meniscus injuries, although true mechanical locking occurs in only about 30% of cases.
Etiology
ACL injuries typically result from deceleration combined with rotation or hyperextension, often during sports such as football or skiing, using a plant-and-pivot or stop-and-jump mechanism. PCL injuries are classically caused by a “dashboard injury,” where a posterior force is applied to the proximal tibia with the knee flexed, or from a fall onto a flexed knee. Meniscal injuries usually occur with sudden twisting motions during squatting, pivoting, or kneeling, and are common in both athletes and certain occupations. MCL injuries most often result from valgus stress applied to a flexed knee, such as from a lateral blow or ski injury.
In children, the ACL is the most frequently injured knee ligament, while isolated MCL injuries are uncommon before closure of the growth plates.
Diagnosis: Signs and Symptoms
Patients with cruciate ligament injuries often report a popping sensation, tearing feeling, or the knee “giving way,” followed by immediate dysfunction. A large effusion developing within 2–3 hours suggests hemarthrosis, most commonly from ACL injury. MCL injuries cause medial knee pain and tenderness, sometimes more pronounced in partial tears. Meniscal injuries are characterized by joint-line pain, intermittent swelling, mechanical symptoms, and difficulty fully extending the knee; patients may still complete activity at the time of injury. Degenerative meniscal tears present more insidiously and are often associated with osteoarthritis.
Physical Examination
Examination should include assessment of weight-bearing ability, palpation of bony landmarks and joint lines, evaluation of range of motion, and identification of effusion or locking. Immediate effusion suggests significant intra-articular injury, whereas delayed swelling is more typical of MCL, PCL, or meniscal injuries. A thorough neurovascular exam is essential. Stress testing should always compare the injured knee to the uninjured side.
The Lachman test is the most reliable maneuver for ACL injury in the acute setting. Anterior and posterior drawer tests assess ACL and PCL integrity, respectively, while the quadriceps active test helps confirm PCL injury. Valgus and varus stress testing evaluate MCL and LCL stability. Meniscal tests such as McMurray and Apley are best performed once acute pain is controlled.
Diagnostic Testing and Imaging
Laboratory testing is rarely required unless infection or inflammatory disease is suspected. Plain radiographs are recommended in most acute knee injuries to exclude fractures, especially in suspected ACL injuries and in children, where growth plate or tibial spine fractures may occur. MRI is highly sensitive and specific for ligamentous and meniscal injuries but is rarely needed emergently. Ottawa knee rules guide imaging decisions in adults but do not apply to children.
Essential Workup
Key priorities include careful neurovascular assessment, exclusion of fracture or infection, evaluation for multidirectional instability, and focused ligament testing, particularly the Lachman test for suspected ACL injury.
Differential Diagnosis
Consider growth plate injuries, tibial plateau fractures, transient knee or patellar dislocation, referred hip pathology, septic arthritis, gout, osteoarthritis, and inflammatory arthritides.
Treatment and Initial Management
Initial management includes immobilization, ice, elevation, and analgesia, along with documentation of neurovascular status. In the emergency department, locked knees due to meniscal injury may sometimes be reduced with gentle traction and rotation. Arthrocentesis can relieve pain from large effusions. In the absence of fracture, treatment consists of rest, ice, compression, elevation, and weight bearing as tolerated, often with crutches. Knee immobilizers may be used for comfort, but early gentle motion is encouraged.
Disposition and Follow-Up
Most isolated ligament or meniscal injuries can be managed as outpatients. Admission is rarely required unless a knee dislocation or vascular injury is suspected. Orthopedic follow-up within 1–2 weeks is recommended for confirmed or suspected significant ligamentous injury, and re-examination within 48 hours is helpful when initial assessment is limited by pain or swelling.
Pearls and Pitfalls
Always perform and document a thorough neurovascular exam. Maintain a high index of suspicion for occult knee dislocation in patients with multidirectional instability or multiple ligament injuries. Do not miss fractures, septic joints, referred hip pathology, or vascular compromise.
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Emergency and Acute Medicine – Legg–Calvé–Perthes Disease
Basic description
Legg–Calvé–Perthes disease is an idiopathic avascular necrosis of the femoral head occurring exclusively in children. It is thought to result from repeated vascular insults to the developing femoral head, leading to ischemia, collapse, and subsequent remodeling. Genetic associations include increased frequency in children with factor V Leiden mutation and anticardiolipin antibodies, supporting a possible hypercoagulable contribution.
Etiology
The condition is believed to arise from successive vascular occlusions of the femoral head and is likely multifactorial. Risk factors include male sex, Caucasian race, exposure to tobacco or wood smoke, low birth weight, and short birth length. The disease progresses through four stages: an initial ischemic stage with dense femoral head and synovitis, a fragmentation stage with femoral head softening and deformation, a healing stage with reossification, and a residual stage with variable permanent deformity. It most commonly affects children aged 3–7 years, with a male predominance of approximately 4:1, and is bilateral in 10–15% of cases.
Diagnosis: signs and symptoms
Presentation is often insidious. Limping is the most common initial complaint. Pain is typically dull or aching and may localize to the hip, groin, anteromedial thigh, or knee. Pain is activity related and improves with rest. Muscle spasm is common early in the disease course. On examination, children are usually afebrile and well appearing. Early findings include limited internal rotation and abduction of the hip. Later findings may include adductor contractures, muscle atrophy, and leg-length discrepancy. Some patients may be minimally symptomatic or asymptomatic.
Essential workup
Plain radiographs of the hips are the most important initial diagnostic study in the emergency setting. Septic arthritis must be considered and excluded, particularly in children with fever, acute onset, or toxic appearance.
Diagnostic tests and interpretation
No laboratory test is diagnostic for Legg–Calvé–Perthes disease. CBC, ESR, and CRP may be obtained if infection is a concern. Imaging establishes the diagnosis. AP and frog-leg lateral radiographs of both hips should be obtained to assess disease stage and detect bilateral involvement. Early radiographs may be normal in the first 3–6 months. MRI is more sensitive and can detect early ischemic changes and assess the extent of femoral head infarction. Bone scintigraphy can identify disease before radiographic changes but is less commonly used. Ultrasound may show a hip effusion but is nonspecific. CT and arthrography are primarily used for surgical planning rather than initial diagnosis.
Differential diagnosis
Unilateral disease considerations include transient synovitis, septic arthritis, osteomyelitis, sickle cell disease, juvenile idiopathic arthritis, trauma, slipped capital femoral epiphysis, tuberculosis, and malignancy. Bilateral disease raises consideration of hypothyroidism, epiphyseal dysplasia, and Gaucher disease.
Treatment
This is not a life-threatening condition, and emergency management focuses on symptom control. Pain management with NSAIDs is the primary intervention. Activity restriction is recommended, and crutches may be required if weight bearing is painful. Clinical instability, fever, or toxic appearance should prompt evaluation for alternative diagnoses.
Medications
First-line therapy is ibuprofen at 10 mg/kg per dose orally every 6–8 hours as needed for pain. Diazepam may be used as a second-line agent for significant muscle spasm.
Disposition and follow-up
Admission is rarely required and is reserved for severe pain not controlled with oral medications or social situations where home care is not feasible. Most patients can be discharged once pain is controlled, with orthopedic follow-up arranged within 1–2 weeks. Long-term management is determined by orthopedics and may include observation, activity modification, bracing, traction, or surgical intervention depending on age at onset and disease severity.
Pearls and pitfalls
Acute onset, fever, toxic appearance, or inability to bear weight should raise concern for diagnoses other than Legg–Calvé–Perthes disease, particularly septic arthritis. Early disease may have normal radiographs, so persistent symptoms warrant close follow-up and repeat imaging.
Basic description
Legg–Calvé–Perthes disease is an idiopathic avascular necrosis of the femoral head occurring exclusively in children. It is thought to result from repeated vascular insults to the developing femoral head, leading to ischemia, collapse, and subsequent remodeling. Genetic associations include increased frequency in children with factor V Leiden mutation and anticardiolipin antibodies, supporting a possible hypercoagulable contribution.
Etiology
The condition is believed to arise from successive vascular occlusions of the femoral head and is likely multifactorial. Risk factors include male sex, Caucasian race, exposure to tobacco or wood smoke, low birth weight, and short birth length. The disease progresses through four stages: an initial ischemic stage with dense femoral head and synovitis, a fragmentation stage with femoral head softening and deformation, a healing stage with reossification, and a residual stage with variable permanent deformity. It most commonly affects children aged 3–7 years, with a male predominance of approximately 4:1, and is bilateral in 10–15% of cases.
Diagnosis: signs and symptoms
Presentation is often insidious. Limping is the most common initial complaint. Pain is typically dull or aching and may localize to the hip, groin, anteromedial thigh, or knee. Pain is activity related and improves with rest. Muscle spasm is common early in the disease course. On examination, children are usually afebrile and well appearing. Early findings include limited internal rotation and abduction of the hip. Later findings may include adductor contractures, muscle atrophy, and leg-length discrepancy. Some patients may be minimally symptomatic or asymptomatic.
Essential workup
Plain radiographs of the hips are the most important initial diagnostic study in the emergency setting. Septic arthritis must be considered and excluded, particularly in children with fever, acute onset, or toxic appearance.
Diagnostic tests and interpretation
No laboratory test is diagnostic for Legg–Calvé–Perthes disease. CBC, ESR, and CRP may be obtained if infection is a concern. Imaging establishes the diagnosis. AP and frog-leg lateral radiographs of both hips should be obtained to assess disease stage and detect bilateral involvement. Early radiographs may be normal in the first 3–6 months. MRI is more sensitive and can detect early ischemic changes and assess the extent of femoral head infarction. Bone scintigraphy can identify disease before radiographic changes but is less commonly used. Ultrasound may show a hip effusion but is nonspecific. CT and arthrography are primarily used for surgical planning rather than initial diagnosis.
Differential diagnosis
Unilateral disease considerations include transient synovitis, septic arthritis, osteomyelitis, sickle cell disease, juvenile idiopathic arthritis, trauma, slipped capital femoral epiphysis, tuberculosis, and malignancy. Bilateral disease raises consideration of hypothyroidism, epiphyseal dysplasia, and Gaucher disease.
Treatment
This is not a life-threatening condition, and emergency management focuses on symptom control. Pain management with NSAIDs is the primary intervention. Activity restriction is recommended, and crutches may be required if weight bearing is painful. Clinical instability, fever, or toxic appearance should prompt evaluation for alternative diagnoses.
Medications
First-line therapy is ibuprofen at 10 mg/kg per dose orally every 6–8 hours as needed for pain. Diazepam may be used as a second-line agent for significant muscle spasm.
Disposition and follow-up
Admission is rarely required and is reserved for severe pain not controlled with oral medications or social situations where home care is not feasible. Most patients can be discharged once pain is controlled, with orthopedic follow-up arranged within 1–2 weeks. Long-term management is determined by orthopedics and may include observation, activity modification, bracing, traction, or surgical intervention depending on age at onset and disease severity.
Pearls and pitfalls
Acute onset, fever, toxic appearance, or inability to bear weight should raise concern for diagnoses other than Legg–Calvé–Perthes disease, particularly septic arthritis. Early disease may have normal radiographs, so persistent symptoms warrant close follow-up and repeat imaging.
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Emergency and Acute Medicine – Lead Poisoning
Basic description
Lead toxicity results from multiple mechanisms. Lead binds sulfhydryl groups, disrupting numerous enzymatic processes, and mimics calcium, interfering with calcium-dependent signaling pathways. High serum lead levels compromise the blood–brain barrier, allowing lead entry into the CNS and causing neurotoxicity. After absorption, up to 99% of lead binds to erythrocytes and is later redistributed into bone, where approximately 95% of total body lead resides in adults and 70% in children. Lead commonly coexists with iron deficiency, which increases gastrointestinal absorption. It also impairs heme synthesis, resulting in elevated free erythrocyte protoporphyrin that complexes with zinc, producing increased zinc protoporphyrin levels. Blood lead levels correlate poorly with symptoms but are associated with reduced IQ and increased behavioral problems.
Etiology
Acute lead toxicity most often results from inhalation of environmental sources or ingestion of lead-containing substances such as pottery glazes, folk remedies, cosmetics, jewelry, weights, home-distilled alcohol, or lead dust from ammunition. Chronic toxicity is usually occupational, particularly in battery manufacturing or recycling, bridge painting, construction, electronic waste recycling, firing ranges, mining, smelting, pottery work, and welding. Pediatric poisoning typically arises from home exposures, including lead-based paint ingestion or inhalation, contaminated water from old pipes, lead dust carried home on clothing, imported foods, and folk medicines.
Diagnosis: signs and symptoms
Neurologic manifestations include seizures, encephalopathy, learning disabilities, psychiatric disturbances, cerebral edema, and peripheral motor neuropathy such as wrist drop, which is classic but uncommon. Gastrointestinal findings include colicky abdominal pain (lead colic), ileus, nausea, vomiting, gingival Burton lines indicating lifetime burden, and occasionally hepatitis or pancreatitis. Cardiovascular effects include hypertension, often secondary to renal disease, as well as myocarditis and conduction abnormalities. Renal involvement presents as chronic renal insufficiency with prolonged exposure. Hematologic effects include anemia from impaired globin synthesis and shortened red blood cell lifespan. Musculoskeletal effects include metaphyseal “lead lines,” reflecting altered calcium deposition rather than lead itself, along with impaired bone growth and strength.
Essential workup
The cornerstone of diagnosis is measurement of a whole blood lead level (BLL). There is no normal BLL. In children, educational and environmental interventions begin at BLL ≥10 μg/dL, while chelation therapy is recommended at ≥45 μg/dL. In adults, chelation is usually considered at ≥70 μg/dL, with levels ≥100 μg/dL associated with severe encephalopathy.
Diagnostic tests and interpretation
Laboratory evaluation includes CBC to assess for anemia, RBC indices and iron studies, renal function tests, electrolytes, glucose, liver function tests prior to chelation, and FEP or ZPP levels. Imaging may include abdominal radiographs to detect radiopaque foreign bodies and long-bone radiographs in children to identify lead lines. Cranial CT and other imaging are guided by clinical status.
Differential diagnosis
Acute presentations may mimic appendicitis, gastroenteritis, colitis, cholera, distributive shock, encephalopathy, or other toxic ingestions. Chronic toxicity may resemble Addison disease, Guillain–Barré syndrome, vitamin deficiencies (B3, B6, B12), or Wernicke–Korsakoff syndrome.
Treatment: prehospital and initial stabilization
Management begins with airway, breathing, and circulation support, cardiac monitoring, and seizure control. Skin decontamination should be performed for dermal exposure when safe. Naloxone, thiamine, and dextrose are administered as indicated for altered mental status.
Emergency department management
Whole-bowel irrigation with polyethylene glycol is indicated if radiopaque material is seen on abdominal imaging; activated charcoal is ineffective. Decisions regarding chelation therapy depend on BLL, symptom severity, acuity of exposure, and consultation with a medical toxicologist or poison center. Adults with encephalopathy or BLL >100 μg/dL typically require chelation with dimercaprol followed by calcium disodium EDTA. Asymptomatic adults with BLL 70–100 μg/dL may be treated with oral succimer, while chelation is not indicated for asymptomatic adults with BLL <70 μg/dL. Children with BLL ≥45 μg/dL require chelation, with DMSA for asymptomatic cases and BAL plus CaNa₂EDTA for symptomatic or very high levels. Pregnant patients require multidisciplinary consultation.
Medications
Chelating agents include dimercaprol (BAL), calcium disodium EDTA, and succimer (DMSA). Supportive medications include benzodiazepines for seizures, dextrose for hypoglycemia, naloxone, and thiamine. BAL is contraindicated in patients with peanut allergy.
Disposition and follow-up
Admission is required for symptomatic patients, children at risk for re-exposure, those unable to tolerate oral chelation, and pregnant patients with elevated BLL. Asymptomatic patients not requiring IV chelation may be discharged once a safe environment is ensured and outpatient follow-up is arranged. Pediatric patients must demonstrate tolerance of oral chelation prior to discharge.
Pearls and pitfalls
Heel-stick testing may falsely elevate BLL and should be confirmed with venous sampling. Environmental assessment and social support are critical to prevent re-exposure. Family members and siblings should be screened when a patient is diagnosed with lead toxicity. Avoid BAL in patients with peanut allergy.
Basic description
Lead toxicity results from multiple mechanisms. Lead binds sulfhydryl groups, disrupting numerous enzymatic processes, and mimics calcium, interfering with calcium-dependent signaling pathways. High serum lead levels compromise the blood–brain barrier, allowing lead entry into the CNS and causing neurotoxicity. After absorption, up to 99% of lead binds to erythrocytes and is later redistributed into bone, where approximately 95% of total body lead resides in adults and 70% in children. Lead commonly coexists with iron deficiency, which increases gastrointestinal absorption. It also impairs heme synthesis, resulting in elevated free erythrocyte protoporphyrin that complexes with zinc, producing increased zinc protoporphyrin levels. Blood lead levels correlate poorly with symptoms but are associated with reduced IQ and increased behavioral problems.
Etiology
Acute lead toxicity most often results from inhalation of environmental sources or ingestion of lead-containing substances such as pottery glazes, folk remedies, cosmetics, jewelry, weights, home-distilled alcohol, or lead dust from ammunition. Chronic toxicity is usually occupational, particularly in battery manufacturing or recycling, bridge painting, construction, electronic waste recycling, firing ranges, mining, smelting, pottery work, and welding. Pediatric poisoning typically arises from home exposures, including lead-based paint ingestion or inhalation, contaminated water from old pipes, lead dust carried home on clothing, imported foods, and folk medicines.
Diagnosis: signs and symptoms
Neurologic manifestations include seizures, encephalopathy, learning disabilities, psychiatric disturbances, cerebral edema, and peripheral motor neuropathy such as wrist drop, which is classic but uncommon. Gastrointestinal findings include colicky abdominal pain (lead colic), ileus, nausea, vomiting, gingival Burton lines indicating lifetime burden, and occasionally hepatitis or pancreatitis. Cardiovascular effects include hypertension, often secondary to renal disease, as well as myocarditis and conduction abnormalities. Renal involvement presents as chronic renal insufficiency with prolonged exposure. Hematologic effects include anemia from impaired globin synthesis and shortened red blood cell lifespan. Musculoskeletal effects include metaphyseal “lead lines,” reflecting altered calcium deposition rather than lead itself, along with impaired bone growth and strength.
Essential workup
The cornerstone of diagnosis is measurement of a whole blood lead level (BLL). There is no normal BLL. In children, educational and environmental interventions begin at BLL ≥10 μg/dL, while chelation therapy is recommended at ≥45 μg/dL. In adults, chelation is usually considered at ≥70 μg/dL, with levels ≥100 μg/dL associated with severe encephalopathy.
Diagnostic tests and interpretation
Laboratory evaluation includes CBC to assess for anemia, RBC indices and iron studies, renal function tests, electrolytes, glucose, liver function tests prior to chelation, and FEP or ZPP levels. Imaging may include abdominal radiographs to detect radiopaque foreign bodies and long-bone radiographs in children to identify lead lines. Cranial CT and other imaging are guided by clinical status.
Differential diagnosis
Acute presentations may mimic appendicitis, gastroenteritis, colitis, cholera, distributive shock, encephalopathy, or other toxic ingestions. Chronic toxicity may resemble Addison disease, Guillain–Barré syndrome, vitamin deficiencies (B3, B6, B12), or Wernicke–Korsakoff syndrome.
Treatment: prehospital and initial stabilization
Management begins with airway, breathing, and circulation support, cardiac monitoring, and seizure control. Skin decontamination should be performed for dermal exposure when safe. Naloxone, thiamine, and dextrose are administered as indicated for altered mental status.
Emergency department management
Whole-bowel irrigation with polyethylene glycol is indicated if radiopaque material is seen on abdominal imaging; activated charcoal is ineffective. Decisions regarding chelation therapy depend on BLL, symptom severity, acuity of exposure, and consultation with a medical toxicologist or poison center. Adults with encephalopathy or BLL >100 μg/dL typically require chelation with dimercaprol followed by calcium disodium EDTA. Asymptomatic adults with BLL 70–100 μg/dL may be treated with oral succimer, while chelation is not indicated for asymptomatic adults with BLL <70 μg/dL. Children with BLL ≥45 μg/dL require chelation, with DMSA for asymptomatic cases and BAL plus CaNa₂EDTA for symptomatic or very high levels. Pregnant patients require multidisciplinary consultation.
Medications
Chelating agents include dimercaprol (BAL), calcium disodium EDTA, and succimer (DMSA). Supportive medications include benzodiazepines for seizures, dextrose for hypoglycemia, naloxone, and thiamine. BAL is contraindicated in patients with peanut allergy.
Disposition and follow-up
Admission is required for symptomatic patients, children at risk for re-exposure, those unable to tolerate oral chelation, and pregnant patients with elevated BLL. Asymptomatic patients not requiring IV chelation may be discharged once a safe environment is ensured and outpatient follow-up is arranged. Pediatric patients must demonstrate tolerance of oral chelation prior to discharge.
Pearls and pitfalls
Heel-stick testing may falsely elevate BLL and should be confirmed with venous sampling. Environmental assessment and social support are critical to prevent re-exposure. Family members and siblings should be screened when a patient is diagnosed with lead toxicity. Avoid BAL in patients with peanut allergy.
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Emergency and Acute Medicine – Larynx Fracture
Basic description
Laryngeal fracture results from the direct transfer of severe force to the anterior neck, producing injuries that range from simple mucosal tears to fractured or comminuted laryngeal cartilages. Structures that may be involved include the epiglottis, thyroid, arytenoid, cricoid, corniculate, and cuneiform cartilages. Although rare, laryngeal fractures are life-threatening because of the risk of progressive airway compromise.
Etiology and epidemiology
Laryngeal fracture is uncommon, accounting for fewer than 1% of blunt trauma cases, with an incidence estimated at 1 in 5,000 to 1 in 42,000 emergency department visits. Mortality directly related to the injury ranges from 2% to 15%. Most cases result from blunt or penetrating trauma to the anterior neck during motor vehicle or motorcycle crashes, assaults, or recreational activities. A classic mechanism is the “clothesline” injury, in which the neck strikes a fixed object such as a wire or branch during forward motion. Hyperextension of the neck combined with a direct blow is typical. Iatrogenic injuries from intubation are increasingly recognized, particularly in older adults. In children, bicycle handlebar injuries are a common mechanism, with neck extension compressing the larynx against the cervical spine.
Diagnosis: signs and symptoms
Symptoms may be delayed for hours, making diagnosis challenging, especially in polytrauma patients or those immobilized in cervical collars. Clinical findings include anterior neck tenderness, bruising or abrasions, hoarseness or voice change, dysphonia, hemoptysis, stridor, dyspnea, and subcutaneous or mediastinal emphysema. Pneumothorax, loss of normal laryngeal landmarks, and difficulty with mechanical ventilation may also be present. Pediatric patients may initially appear minimally symptomatic but can deteriorate rapidly because of airway edema.
Essential workup
Airway evaluation is the priority. Endoscopic assessment should take precedence over plain radiography because mucosal edema may cause airway compromise even in the absence of obvious skeletal injury. Cervical spine CT is preferred over plain radiographs, which are often nondiagnostic. Chest radiography helps identify pneumothorax, pneumomediastinum, or subcutaneous emphysema. CT scan of the cervical spine with fine cuts through the larynx and IV contrast is recommended unless the patient proceeds directly to surgery, as it can identify cartilage fractures and associated vascular injury. Continuous pulse oximetry is essential. MRI is generally not useful due to time constraints and limited evaluation of cartilaginous injury.
Diagnostic tests and procedures
Arterial blood gas analysis may be helpful in patients with respiratory compromise. Flexible fiberoptic laryngoscopy is a key diagnostic tool for visualization of mucosal injuries, vocal cord mobility, and airway patency. CT angiography is preferred when vascular injury is suspected, particularly in penetrating trauma. Fiberoptic bronchoscopy and esophagoscopy may be required to evaluate associated aerodigestive injuries. Surgical exploration is indicated based on injury severity.
Differential diagnosis
Associated injuries must be considered, including intracranial injury, cervical spine injury, esophageal injury, carotid artery injury, phrenic nerve injury, aspiration pneumonitis, hypoxic cerebral injury, airway edema, air embolism, and pneumothorax. In children, massive edema and hematoma may occur without visible fractures on imaging.
Treatment: prehospital and initial stabilization
Airway protection is critical. Supplemental oxygen and gentle suctioning should be provided, with cervical spine immobilization maintained. Elective intubation is controversial and not routinely recommended, as repeated orotracheal attempts may worsen injury. In severe cases, early surgical airway management may be required.
Emergency department management
Airway control remains the highest priority. Early intubation may be necessary for impending airway compromise, but in patients with severe neck injury, formal tracheostomy under local anesthesia is often safer than endotracheal intubation. Cricothyrotomy may be used for injuries above the cricothyroid membrane but should be avoided if there is evidence of cricotracheal disruption or hematoma over the membrane. Supplemental humidified oxygen, head-of-bed elevation, strict NPO status, and voice rest are recommended. IV access should be established, and early otolaryngology consultation obtained. Mechanical ventilation strategies may be required for associated pulmonary injury.
Medications
Broad-spectrum antibiotics are indicated when subcutaneous emphysema suggests mucosal breach, commonly using ampicillin/sulbactam or clindamycin. Acid suppression with H2 blockers or proton pump inhibitors may reduce irritation of mucosal injuries. Corticosteroids are not routinely indicated but may be considered for severe laryngeal edema. In pediatric patients with stridor, nebulized racemic epinephrine may provide temporary relief.
Disposition and follow-up
All patients with confirmed or suspected laryngeal fracture require admission to a monitored setting for airway observation and serial examinations, often including repeat fiberoptic laryngoscopy. Pediatric patients should be admitted routinely because of the risk of rapid airway compromise. Discharge may be considered only after an adequate observation period, typically at least 6 hours, in patients with no evidence of airway injury, edema, or compromise. When in doubt, admission is recommended.
Pearls and pitfalls
Laryngeal fractures are rare but potentially fatal. Symptoms may be subtle or delayed, and airway deterioration can be rapid. Avoid repeated intubation attempts, and maintain a low threshold for surgical airway management. Early recognition, careful airway control, and otolaryngology involvement are key to improving outcomes.
Basic description
Laryngeal fracture results from the direct transfer of severe force to the anterior neck, producing injuries that range from simple mucosal tears to fractured or comminuted laryngeal cartilages. Structures that may be involved include the epiglottis, thyroid, arytenoid, cricoid, corniculate, and cuneiform cartilages. Although rare, laryngeal fractures are life-threatening because of the risk of progressive airway compromise.
Etiology and epidemiology
Laryngeal fracture is uncommon, accounting for fewer than 1% of blunt trauma cases, with an incidence estimated at 1 in 5,000 to 1 in 42,000 emergency department visits. Mortality directly related to the injury ranges from 2% to 15%. Most cases result from blunt or penetrating trauma to the anterior neck during motor vehicle or motorcycle crashes, assaults, or recreational activities. A classic mechanism is the “clothesline” injury, in which the neck strikes a fixed object such as a wire or branch during forward motion. Hyperextension of the neck combined with a direct blow is typical. Iatrogenic injuries from intubation are increasingly recognized, particularly in older adults. In children, bicycle handlebar injuries are a common mechanism, with neck extension compressing the larynx against the cervical spine.
Diagnosis: signs and symptoms
Symptoms may be delayed for hours, making diagnosis challenging, especially in polytrauma patients or those immobilized in cervical collars. Clinical findings include anterior neck tenderness, bruising or abrasions, hoarseness or voice change, dysphonia, hemoptysis, stridor, dyspnea, and subcutaneous or mediastinal emphysema. Pneumothorax, loss of normal laryngeal landmarks, and difficulty with mechanical ventilation may also be present. Pediatric patients may initially appear minimally symptomatic but can deteriorate rapidly because of airway edema.
Essential workup
Airway evaluation is the priority. Endoscopic assessment should take precedence over plain radiography because mucosal edema may cause airway compromise even in the absence of obvious skeletal injury. Cervical spine CT is preferred over plain radiographs, which are often nondiagnostic. Chest radiography helps identify pneumothorax, pneumomediastinum, or subcutaneous emphysema. CT scan of the cervical spine with fine cuts through the larynx and IV contrast is recommended unless the patient proceeds directly to surgery, as it can identify cartilage fractures and associated vascular injury. Continuous pulse oximetry is essential. MRI is generally not useful due to time constraints and limited evaluation of cartilaginous injury.
Diagnostic tests and procedures
Arterial blood gas analysis may be helpful in patients with respiratory compromise. Flexible fiberoptic laryngoscopy is a key diagnostic tool for visualization of mucosal injuries, vocal cord mobility, and airway patency. CT angiography is preferred when vascular injury is suspected, particularly in penetrating trauma. Fiberoptic bronchoscopy and esophagoscopy may be required to evaluate associated aerodigestive injuries. Surgical exploration is indicated based on injury severity.
Differential diagnosis
Associated injuries must be considered, including intracranial injury, cervical spine injury, esophageal injury, carotid artery injury, phrenic nerve injury, aspiration pneumonitis, hypoxic cerebral injury, airway edema, air embolism, and pneumothorax. In children, massive edema and hematoma may occur without visible fractures on imaging.
Treatment: prehospital and initial stabilization
Airway protection is critical. Supplemental oxygen and gentle suctioning should be provided, with cervical spine immobilization maintained. Elective intubation is controversial and not routinely recommended, as repeated orotracheal attempts may worsen injury. In severe cases, early surgical airway management may be required.
Emergency department management
Airway control remains the highest priority. Early intubation may be necessary for impending airway compromise, but in patients with severe neck injury, formal tracheostomy under local anesthesia is often safer than endotracheal intubation. Cricothyrotomy may be used for injuries above the cricothyroid membrane but should be avoided if there is evidence of cricotracheal disruption or hematoma over the membrane. Supplemental humidified oxygen, head-of-bed elevation, strict NPO status, and voice rest are recommended. IV access should be established, and early otolaryngology consultation obtained. Mechanical ventilation strategies may be required for associated pulmonary injury.
Medications
Broad-spectrum antibiotics are indicated when subcutaneous emphysema suggests mucosal breach, commonly using ampicillin/sulbactam or clindamycin. Acid suppression with H2 blockers or proton pump inhibitors may reduce irritation of mucosal injuries. Corticosteroids are not routinely indicated but may be considered for severe laryngeal edema. In pediatric patients with stridor, nebulized racemic epinephrine may provide temporary relief.
Disposition and follow-up
All patients with confirmed or suspected laryngeal fracture require admission to a monitored setting for airway observation and serial examinations, often including repeat fiberoptic laryngoscopy. Pediatric patients should be admitted routinely because of the risk of rapid airway compromise. Discharge may be considered only after an adequate observation period, typically at least 6 hours, in patients with no evidence of airway injury, edema, or compromise. When in doubt, admission is recommended.
Pearls and pitfalls
Laryngeal fractures are rare but potentially fatal. Symptoms may be subtle or delayed, and airway deterioration can be rapid. Avoid repeated intubation attempts, and maintain a low threshold for surgical airway management. Early recognition, careful airway control, and otolaryngology involvement are key to improving outcomes.
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Emergency and Acute Medicine – Laryngitis
Basic description
Laryngitis is inflammation of the laryngeal mucosa, most commonly caused by viral upper respiratory infection. Incidence peaks in late fall, winter, and early spring and parallels viral epidemics. Inflammation reduces normal vocal cord vibration, resulting in hoarseness and voice changes.
Etiology
Acute laryngitis is most often viral, including influenza A and B, parainfluenza, adenovirus, coronavirus, coxsackievirus, respiratory syncytial virus, measles, and rhinovirus. Bacterial causes are uncommon but include β-hemolytic streptococcus, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Bordetella pertussis, diphtheria, tuberculosis, syphilis, and leprosy. Noninfectious causes include laryngopharyngeal reflux related to GERD, fungal infection (often with inhaled steroid use or immunocompromise), allergy, voice abuse, inhalation or ingestion of irritants or caustics, autoimmune disease, trauma, and idiopathic causes. In children, acute spasmodic laryngitis (spasmodic croup) is more often infectious, and foreign body must be considered in unimmunized patients.
Diagnosis: signs and symptoms
Patients typically present with hoarseness or abnormal voice quality, throat irritation or rawness, throat swelling, frequent throat clearing, cough, malaise, fever, and occasionally dysphagia. Physical examination may reveal hoarse voice, pharyngeal erythema or edema, regional lymphadenopathy, stridor in infants, or asymmetric breath sounds if a foreign body is present.
Essential workup
Acute laryngitis is usually a clinical diagnosis based on history and throat inspection and typically resolves within 7–10 days. Increased suspicion for epiglottitis is required in unimmunized patients or those with respiratory distress. Chronic laryngitis lasting longer than 3 weeks warrants evaluation for GERD, chronic infection, neurologic disorders, or malignancy, with referral for laryngeal visualization by otolaryngology.
Diagnostic tests and interpretation
Laboratory studies are generally unnecessary, as leukocytosis does not reliably distinguish viral from bacterial disease. Throat cultures are reserved for cases with exam findings suggestive of bacterial infection. Imaging is rarely required; fiberoptic laryngoscopy is preferred when visualization is necessary. Soft-tissue neck radiographs are reserved for suspected epiglottitis or foreign body when laryngoscopy is unavailable and the patient is stable.
Differential diagnosis
Asthma, epiglottitis, GERD, vocal cord nodules, laryngeal or thyroid malignancy, croup or laryngotracheobronchitis, and foreign-body aspiration should be considered.
Treatment: prehospital care
Supportive care is usually sufficient. Stridor suggests potential airway obstruction, particularly in children, and warrants urgent evaluation. Neck trauma–associated laryngitis requires otolaryngology assessment. Caustic ingestion raises concern for esophageal injury. Suspected epiglottitis requires transport in the upright position with supplemental oxygen and avoidance of unnecessary airway manipulation.
Initial stabilization and therapy
Stabilization is required only for patients with respiratory distress. Management should follow epiglottitis protocols, including supplemental oxygen and preparation for advanced airway management in a controlled setting.
Emergency department treatment and procedures
Management is primarily supportive. Antibiotics are not recommended for routine adult acute laryngitis, as evidence shows no benefit over placebo. Vocal rest is essential, avoiding whispering; patients should use a soft, relaxed voice if speaking is necessary. Humidified air, increased oral fluids, analgesics, and smoking cessation are recommended. Symptoms typically resolve within 7–10 days if viral. Inhaled steroids are controversial and not standard therapy.
Medications
Treatment is cause-specific. Acetaminophen or NSAIDs may be used for pain and fever. Guaifenesin may help if associated with upper respiratory infection. Proton pump inhibitors are indicated for GERD-related laryngitis. Antifungal therapy is used for candidal infection. For croup, a single dose of dexamethasone is indicated. Antibiotics are reserved for confirmed bacterial infection or high-risk patients.
Follow-up and disposition
Admission is required for tuberculous laryngitis, respiratory distress, suspected epiglottitis, neck trauma, anaphylaxis, or airway compromise. Most patients with uncomplicated laryngitis can be discharged if breathing is normal and hydration is adequate. Chronic or nonresolving symptoms require otolaryngology referral.
Pearls and pitfalls
Most acute laryngitis is viral, and antibiotics provide no benefit. Always consider life-threatening causes of altered voice such as epiglottitis. Laryngitis without upper respiratory symptoms may indicate GERD. Persistent hoarseness beyond 3 weeks warrants evaluation to exclude malignancy.
Basic description
Laryngitis is inflammation of the laryngeal mucosa, most commonly caused by viral upper respiratory infection. Incidence peaks in late fall, winter, and early spring and parallels viral epidemics. Inflammation reduces normal vocal cord vibration, resulting in hoarseness and voice changes.
Etiology
Acute laryngitis is most often viral, including influenza A and B, parainfluenza, adenovirus, coronavirus, coxsackievirus, respiratory syncytial virus, measles, and rhinovirus. Bacterial causes are uncommon but include β-hemolytic streptococcus, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Bordetella pertussis, diphtheria, tuberculosis, syphilis, and leprosy. Noninfectious causes include laryngopharyngeal reflux related to GERD, fungal infection (often with inhaled steroid use or immunocompromise), allergy, voice abuse, inhalation or ingestion of irritants or caustics, autoimmune disease, trauma, and idiopathic causes. In children, acute spasmodic laryngitis (spasmodic croup) is more often infectious, and foreign body must be considered in unimmunized patients.
Diagnosis: signs and symptoms
Patients typically present with hoarseness or abnormal voice quality, throat irritation or rawness, throat swelling, frequent throat clearing, cough, malaise, fever, and occasionally dysphagia. Physical examination may reveal hoarse voice, pharyngeal erythema or edema, regional lymphadenopathy, stridor in infants, or asymmetric breath sounds if a foreign body is present.
Essential workup
Acute laryngitis is usually a clinical diagnosis based on history and throat inspection and typically resolves within 7–10 days. Increased suspicion for epiglottitis is required in unimmunized patients or those with respiratory distress. Chronic laryngitis lasting longer than 3 weeks warrants evaluation for GERD, chronic infection, neurologic disorders, or malignancy, with referral for laryngeal visualization by otolaryngology.
Diagnostic tests and interpretation
Laboratory studies are generally unnecessary, as leukocytosis does not reliably distinguish viral from bacterial disease. Throat cultures are reserved for cases with exam findings suggestive of bacterial infection. Imaging is rarely required; fiberoptic laryngoscopy is preferred when visualization is necessary. Soft-tissue neck radiographs are reserved for suspected epiglottitis or foreign body when laryngoscopy is unavailable and the patient is stable.
Differential diagnosis
Asthma, epiglottitis, GERD, vocal cord nodules, laryngeal or thyroid malignancy, croup or laryngotracheobronchitis, and foreign-body aspiration should be considered.
Treatment: prehospital care
Supportive care is usually sufficient. Stridor suggests potential airway obstruction, particularly in children, and warrants urgent evaluation. Neck trauma–associated laryngitis requires otolaryngology assessment. Caustic ingestion raises concern for esophageal injury. Suspected epiglottitis requires transport in the upright position with supplemental oxygen and avoidance of unnecessary airway manipulation.
Initial stabilization and therapy
Stabilization is required only for patients with respiratory distress. Management should follow epiglottitis protocols, including supplemental oxygen and preparation for advanced airway management in a controlled setting.
Emergency department treatment and procedures
Management is primarily supportive. Antibiotics are not recommended for routine adult acute laryngitis, as evidence shows no benefit over placebo. Vocal rest is essential, avoiding whispering; patients should use a soft, relaxed voice if speaking is necessary. Humidified air, increased oral fluids, analgesics, and smoking cessation are recommended. Symptoms typically resolve within 7–10 days if viral. Inhaled steroids are controversial and not standard therapy.
Medications
Treatment is cause-specific. Acetaminophen or NSAIDs may be used for pain and fever. Guaifenesin may help if associated with upper respiratory infection. Proton pump inhibitors are indicated for GERD-related laryngitis. Antifungal therapy is used for candidal infection. For croup, a single dose of dexamethasone is indicated. Antibiotics are reserved for confirmed bacterial infection or high-risk patients.
Follow-up and disposition
Admission is required for tuberculous laryngitis, respiratory distress, suspected epiglottitis, neck trauma, anaphylaxis, or airway compromise. Most patients with uncomplicated laryngitis can be discharged if breathing is normal and hydration is adequate. Chronic or nonresolving symptoms require otolaryngology referral.
Pearls and pitfalls
Most acute laryngitis is viral, and antibiotics provide no benefit. Always consider life-threatening causes of altered voice such as epiglottitis. Laryngitis without upper respiratory symptoms may indicate GERD. Persistent hoarseness beyond 3 weeks warrants evaluation to exclude malignancy.
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Emergency and Acute Medicine – Laceration ManagementBasic description
A laceration is a disruption in skin integrity, most commonly resulting from trauma. Lacerations may involve single or multiple tissue layers and can be associated with deeper structural injury depending on mechanism and location.
Etiology
Lacerations result from multiple mechanisms including sharp objects, blunt trauma, crushing injuries, and bites.
Diagnosis: signs and symptoms
Lacerations may present with bleeding, pain, hematoma, retained foreign bodies, tissue loss, numbness, loss of motor function, diminished pulses, or delayed capillary refill. History should include mechanism and circumstances of injury, time of injury, possible foreign body exposure (glass, wood, teeth), tetanus immunization status, and comorbidities or medications that impair wound healing. Physical examination focuses on careful assessment of neurovascular status, tendon and motor function, and evaluation for devitalized tissue, contamination, joint or bone involvement, and tendon injury. Sharp objects should not be digitally explored if there is risk of further injury.
Essential workup
Consider operative repair if safe wound management cannot be achieved in the emergency department, particularly in children requiring deep sedation. Early surgical consultation is recommended for complex wounds, especially those involving the face, eyes, hands, or joints. Pediatric patients should be assessed for possible nonaccidental trauma.
Diagnostic tests and interpretation
Imaging is used when foreign bodies are suspected. Plain radiographs may identify radiopaque objects but will not reliably detect wood or plant material. Ultrasound can identify radiolucent foreign bodies. CT or MRI may be required for deep or complex injuries, with metal precautions as appropriate.
Differential diagnosis
Skin avulsion, abrasion, contusion, and crush injury should be considered.
Treatment: prehospital care
Initial care includes bleeding control with direct pressure, gentle realignment of skin flaps to preserve perfusion, splinting when indicated, and adherence to universal precautions.
Initial stabilization and therapy
Airway, breathing, and circulation are addressed first. Hemostasis is achieved, rings and constricting jewelry are removed to prevent ischemia, and the wound is protected.
Emergency department treatment and procedures
Primary closure timing depends on wound age and location. Most wounds may be closed within 8–12 hours, facial wounds up to 24 hours if clean and well irrigated. Older or contaminated wounds may require delayed primary closure or healing by secondary intention. Adequate analgesia is essential, using topical, local, or regional anesthesia, with procedural sedation when necessary. Wounds are irrigated with copious normal saline under appropriate pressure, avoiding antiseptics inside the wound. Devitalized tissue is debrided. Foreign bodies are removed when they pose risk of infection, toxicity, or functional impairment. Closure technique is selected based on wound tension, location, and depth, with careful reapproximation of anatomic landmarks. Dressings include antibiotic ointment and nonadherent coverings, and splinting is applied when needed. Prophylactic antibiotics are not required for uncomplicated wounds but are considered for high-risk injuries such as bites or heavily contaminated wounds. Tetanus prophylaxis is updated as indicated.
Medications
Local anesthetics include lidocaine and bupivacaine, with topical agents such as LET, EMLA, or TAC when appropriate. Tetanus immunization is administered according to age and immunization status. Analgesics are provided as needed.
Follow-up and disposition
Most lacerations do not require admission unless associated with major injury, infection risk requiring IV antibiotics, or social concerns such as suspected abuse. Discharge requires clear wound care instructions, infection precautions, and follow-up planning. Wound checks are recommended within 48 hours for high-risk injuries. Suture removal timing varies by anatomic location and perfusion.
Issues for referral
Immediate referral is required for suspected tear duct injuries, complex facial wounds, tendon or nerve involvement, and wounds requiring specialized surgical repair.
Pearls and pitfalls
Careful neurovascular examination before and after repair is essential. Inadequate irrigation and missed foreign bodies increase infection risk. Always consider deeper structural injury, especially in hand and joint lacerations, and maintain a low threshold for consultation when cosmetic or functional outcomes may be compromised.
A laceration is a disruption in skin integrity, most commonly resulting from trauma. Lacerations may involve single or multiple tissue layers and can be associated with deeper structural injury depending on mechanism and location.
Etiology
Lacerations result from multiple mechanisms including sharp objects, blunt trauma, crushing injuries, and bites.
Diagnosis: signs and symptoms
Lacerations may present with bleeding, pain, hematoma, retained foreign bodies, tissue loss, numbness, loss of motor function, diminished pulses, or delayed capillary refill. History should include mechanism and circumstances of injury, time of injury, possible foreign body exposure (glass, wood, teeth), tetanus immunization status, and comorbidities or medications that impair wound healing. Physical examination focuses on careful assessment of neurovascular status, tendon and motor function, and evaluation for devitalized tissue, contamination, joint or bone involvement, and tendon injury. Sharp objects should not be digitally explored if there is risk of further injury.
Essential workup
Consider operative repair if safe wound management cannot be achieved in the emergency department, particularly in children requiring deep sedation. Early surgical consultation is recommended for complex wounds, especially those involving the face, eyes, hands, or joints. Pediatric patients should be assessed for possible nonaccidental trauma.
Diagnostic tests and interpretation
Imaging is used when foreign bodies are suspected. Plain radiographs may identify radiopaque objects but will not reliably detect wood or plant material. Ultrasound can identify radiolucent foreign bodies. CT or MRI may be required for deep or complex injuries, with metal precautions as appropriate.
Differential diagnosis
Skin avulsion, abrasion, contusion, and crush injury should be considered.
Treatment: prehospital care
Initial care includes bleeding control with direct pressure, gentle realignment of skin flaps to preserve perfusion, splinting when indicated, and adherence to universal precautions.
Initial stabilization and therapy
Airway, breathing, and circulation are addressed first. Hemostasis is achieved, rings and constricting jewelry are removed to prevent ischemia, and the wound is protected.
Emergency department treatment and procedures
Primary closure timing depends on wound age and location. Most wounds may be closed within 8–12 hours, facial wounds up to 24 hours if clean and well irrigated. Older or contaminated wounds may require delayed primary closure or healing by secondary intention. Adequate analgesia is essential, using topical, local, or regional anesthesia, with procedural sedation when necessary. Wounds are irrigated with copious normal saline under appropriate pressure, avoiding antiseptics inside the wound. Devitalized tissue is debrided. Foreign bodies are removed when they pose risk of infection, toxicity, or functional impairment. Closure technique is selected based on wound tension, location, and depth, with careful reapproximation of anatomic landmarks. Dressings include antibiotic ointment and nonadherent coverings, and splinting is applied when needed. Prophylactic antibiotics are not required for uncomplicated wounds but are considered for high-risk injuries such as bites or heavily contaminated wounds. Tetanus prophylaxis is updated as indicated.
Medications
Local anesthetics include lidocaine and bupivacaine, with topical agents such as LET, EMLA, or TAC when appropriate. Tetanus immunization is administered according to age and immunization status. Analgesics are provided as needed.
Follow-up and disposition
Most lacerations do not require admission unless associated with major injury, infection risk requiring IV antibiotics, or social concerns such as suspected abuse. Discharge requires clear wound care instructions, infection precautions, and follow-up planning. Wound checks are recommended within 48 hours for high-risk injuries. Suture removal timing varies by anatomic location and perfusion.
Issues for referral
Immediate referral is required for suspected tear duct injuries, complex facial wounds, tendon or nerve involvement, and wounds requiring specialized surgical repair.
Pearls and pitfalls
Careful neurovascular examination before and after repair is essential. Inadequate irrigation and missed foreign bodies increase infection risk. Always consider deeper structural injury, especially in hand and joint lacerations, and maintain a low threshold for consultation when cosmetic or functional outcomes may be compromised.
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Emergency and Acute Medicine – Labor
Basic description
Labor is the sequence of physiologic processes that results in transport of the fetus from the uterus through the birth canal. It is characterized by synchronous, coordinated uterine contractions that progressively increase in strength, duration, and frequency, leading to cervical effacement, dilation, and eventual delivery of the fetus and placenta.
Physiology and stages of labor
Labor produces cervical changes that allow passage of the fetus through the birth canal and is divided into three stages. Stage one extends from the onset of regular uterine contractions to complete cervical dilation and is subdivided into latent and active phases. During the latent phase, contractions are mild, irregular, and short, usually lasting less than 45 seconds, with minimal cervical change. The active phase typically begins at 3–4 cm dilation, with strong, regular contractions occurring every 2–3 minutes and lasting longer than 45 seconds. Stage two spans from complete cervical dilation to delivery of the infant. Stage three begins after delivery of the infant and ends with placental delivery.
The total duration of labor varies among patients. Nulliparous patients generally have longer labor, with an average first stage of 14.4 hours and a second stage of 1 hour. Parous patients have shorter labors, with an average first stage of 7.7 hours and a second stage of 0.2 hours. Progression of the second stage is influenced by the “three Ps”: passenger (fetal size and presentation), passageway (pelvic anatomy and soft tissues), and powers (uterine contractions). Abnormalities in any of these factors may lead to dysfunctional labor.
False labor, or Braxton Hicks contractions, consists of irregular, nonsynchronous uterine contractions occurring days to weeks before true labor and does not result in cervical dilation.
Etiology
Preterm labor occurs in approximately 8–10% of pregnancies. Uterine, cervical, or urinary tract infections account for 30–40% of cases. Premature rupture of membranes, defined as rupture of membranes at least two hours before labor onset in patients under 37 weeks’ gestation, occurs in about 3% of pregnancies but accounts for 30–40% of premature births.
Diagnosis: signs and symptoms
True labor presents with regular uterine contractions occurring at least every five minutes, lasting 30–60 seconds, and associated with progressive cervical dilation or effacement. Pain is typically intermittent, located in the lower abdomen, and may radiate to the lower back. Preterm labor produces these changes before 37 weeks’ gestation. Labor is not associated with vaginal bleeding, and bleeding in the third trimester should prompt concern for placental abruption or placenta previa. Sudden release of clear vaginal fluid or persistent perineal wetness suggests rupture of membranes, which may precede labor.
History and physical examination
Assessment should include gestational age, adequacy of prenatal care, prior obstetric history including cesarean delivery, and recent infections. Fundal height should be measured and correlated with gestational age, particularly when dates are uncertain. A sterile pelvic examination is required to assess cervical dilation and effacement, but digital examination is contraindicated in patients with vaginal bleeding until placental location is confirmed.
Essential workup
Patients with suspected labor require immediate sterile pelvic examination to evaluate cervical status and determine the likelihood of imminent delivery. Suspected rupture of membranes should be evaluated with sterile speculum examination for pooling, ferning, and nitrazine testing. Patients with preterm labor and cervical changes require urinalysis with culture and cervical cultures. Continuous fetal monitoring should be initiated when available. Digital or bimanual pelvic examination should be avoided in third-trimester bleeding until ultrasound excludes placenta previa or abruption.
Diagnostic tests and interpretation
If labor is confirmed, obtain a complete blood count and type and screen. Urinalysis should assess for proteinuria. Patients without prenatal care require Rh factor and antibody screening. Imaging is not routinely required, but emergent ultrasound is indicated in third-trimester patients with abdominal pain and vaginal bleeding to evaluate for placental pathology.
Differential diagnosis
False labor presents with irregular contractions without cervical change. Other considerations include round ligament pain, musculoskeletal back pain, appendicitis, ovarian cysts, diverticulitis, nephrolithiasis, and urinary tract infection.
Treatment and initial management
Prehospital management includes oxygen administration and left lateral positioning to optimize uteroplacental perfusion. Transport of high-risk obstetric patients prior to delivery improves outcomes compared with neonatal transfer after birth. If delivery is imminent, prepare for immediate vaginal delivery in the emergency department. Otherwise, patients should be transferred promptly to the labor and delivery unit.
If transfer is delayed or preterm labor is suspected, initiate maternal and fetal monitoring, provide intravenous hydration, and consider antibiotics for unknown group B Streptococcus status. Tocolysis with agents such as magnesium sulfate or terbutaline may be initiated for preterm labor when appropriate, with careful monitoring for toxicity.
Disposition
All patients in true labor should be admitted to labor and delivery. Preterm labor requires immediate obstetric consultation and admission. Patients with false labor may be discharged only after obstetric evaluation, confirmation of fetal well-being, and arrangement of close follow-up.
Pearls and pitfalls
Vaginal bleeding in labor requires urgent evaluation for placental abruption or previa, and digital pelvic examination must be avoided in these cases. Pelvic examinations in labor should always be sterile. False labor can progress to true labor and requires appropriate counseling and follow-up.
Basic description
Labor is the sequence of physiologic processes that results in transport of the fetus from the uterus through the birth canal. It is characterized by synchronous, coordinated uterine contractions that progressively increase in strength, duration, and frequency, leading to cervical effacement, dilation, and eventual delivery of the fetus and placenta.
Physiology and stages of labor
Labor produces cervical changes that allow passage of the fetus through the birth canal and is divided into three stages. Stage one extends from the onset of regular uterine contractions to complete cervical dilation and is subdivided into latent and active phases. During the latent phase, contractions are mild, irregular, and short, usually lasting less than 45 seconds, with minimal cervical change. The active phase typically begins at 3–4 cm dilation, with strong, regular contractions occurring every 2–3 minutes and lasting longer than 45 seconds. Stage two spans from complete cervical dilation to delivery of the infant. Stage three begins after delivery of the infant and ends with placental delivery.
The total duration of labor varies among patients. Nulliparous patients generally have longer labor, with an average first stage of 14.4 hours and a second stage of 1 hour. Parous patients have shorter labors, with an average first stage of 7.7 hours and a second stage of 0.2 hours. Progression of the second stage is influenced by the “three Ps”: passenger (fetal size and presentation), passageway (pelvic anatomy and soft tissues), and powers (uterine contractions). Abnormalities in any of these factors may lead to dysfunctional labor.
False labor, or Braxton Hicks contractions, consists of irregular, nonsynchronous uterine contractions occurring days to weeks before true labor and does not result in cervical dilation.
Etiology
Preterm labor occurs in approximately 8–10% of pregnancies. Uterine, cervical, or urinary tract infections account for 30–40% of cases. Premature rupture of membranes, defined as rupture of membranes at least two hours before labor onset in patients under 37 weeks’ gestation, occurs in about 3% of pregnancies but accounts for 30–40% of premature births.
Diagnosis: signs and symptoms
True labor presents with regular uterine contractions occurring at least every five minutes, lasting 30–60 seconds, and associated with progressive cervical dilation or effacement. Pain is typically intermittent, located in the lower abdomen, and may radiate to the lower back. Preterm labor produces these changes before 37 weeks’ gestation. Labor is not associated with vaginal bleeding, and bleeding in the third trimester should prompt concern for placental abruption or placenta previa. Sudden release of clear vaginal fluid or persistent perineal wetness suggests rupture of membranes, which may precede labor.
History and physical examination
Assessment should include gestational age, adequacy of prenatal care, prior obstetric history including cesarean delivery, and recent infections. Fundal height should be measured and correlated with gestational age, particularly when dates are uncertain. A sterile pelvic examination is required to assess cervical dilation and effacement, but digital examination is contraindicated in patients with vaginal bleeding until placental location is confirmed.
Essential workup
Patients with suspected labor require immediate sterile pelvic examination to evaluate cervical status and determine the likelihood of imminent delivery. Suspected rupture of membranes should be evaluated with sterile speculum examination for pooling, ferning, and nitrazine testing. Patients with preterm labor and cervical changes require urinalysis with culture and cervical cultures. Continuous fetal monitoring should be initiated when available. Digital or bimanual pelvic examination should be avoided in third-trimester bleeding until ultrasound excludes placenta previa or abruption.
Diagnostic tests and interpretation
If labor is confirmed, obtain a complete blood count and type and screen. Urinalysis should assess for proteinuria. Patients without prenatal care require Rh factor and antibody screening. Imaging is not routinely required, but emergent ultrasound is indicated in third-trimester patients with abdominal pain and vaginal bleeding to evaluate for placental pathology.
Differential diagnosis
False labor presents with irregular contractions without cervical change. Other considerations include round ligament pain, musculoskeletal back pain, appendicitis, ovarian cysts, diverticulitis, nephrolithiasis, and urinary tract infection.
Treatment and initial management
Prehospital management includes oxygen administration and left lateral positioning to optimize uteroplacental perfusion. Transport of high-risk obstetric patients prior to delivery improves outcomes compared with neonatal transfer after birth. If delivery is imminent, prepare for immediate vaginal delivery in the emergency department. Otherwise, patients should be transferred promptly to the labor and delivery unit.
If transfer is delayed or preterm labor is suspected, initiate maternal and fetal monitoring, provide intravenous hydration, and consider antibiotics for unknown group B Streptococcus status. Tocolysis with agents such as magnesium sulfate or terbutaline may be initiated for preterm labor when appropriate, with careful monitoring for toxicity.
Disposition
All patients in true labor should be admitted to labor and delivery. Preterm labor requires immediate obstetric consultation and admission. Patients with false labor may be discharged only after obstetric evaluation, confirmation of fetal well-being, and arrangement of close follow-up.
Pearls and pitfalls
Vaginal bleeding in labor requires urgent evaluation for placental abruption or previa, and digital pelvic examination must be avoided in these cases. Pelvic examinations in labor should always be sterile. False labor can progress to true labor and requires appropriate counseling and follow-up.
