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Emergency And Acute Medicine – Hepatic Encephalopathy
Basics And Description
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome characterized by alterations in behavior, level of consciousness, and motor function resulting from hepatic insufficiency and the accumulation of substances normally detoxified by the liver. The condition arises from a multifactorial process, most notably the accumulation of ammonia produced from protein degradation by colonic bacteria and deamination of glutamine in the small bowel, kidneys, and muscle. Ammonia crosses the blood–brain barrier and is metabolized by astrocytes into glutamine, leading to astrocytic swelling, cerebral edema, and mitochondrial dysfunction. Additional neurotoxins such as short-chain fatty acids, manganese, neurosteroids, phenols, mercaptans, and amino acids including tryptophan also contribute. Neurotransmitter imbalance plays a role, with increased inhibitory neurotransmitters such as benzodiazepines, γ-aminobutyric acid, and serotonin, and decreased excitatory neurotransmitters including glutamate, dopamine, aspartate, and catecholamines. Other contributing factors include reduced cerebral blood flow and oxygen delivery, increased cerebral glucose utilization with potential hypoglycemia, zinc deficiency affecting urea cycle enzymes, and rare inherited urea cycle disorders.
Etiology
Hepatic encephalopathy is classified according to the 11th World Congress of Gastroenterology. Type A is associated with acute liver injury and fulminant hepatic failure. Type B is related to portosystemic shunting without intrinsic liver disease. Type C is associated with cirrhosis and portal hypertension. Common precipitating factors include gastrointestinal bleeding, electrolyte abnormalities such as hypokalemia and hyponatremia, metabolic alkalosis reducing renal ammonium excretion, sepsis including spontaneous bacterial peritonitis, constipation, noncompliance with treatment in chronic liver disease, high-protein diet, hypoglycemia, hypovolemia following large-volume paracentesis, azotemia from diuretics or diarrhea, sedatives or narcotics including alcohol, zinc deficiency, hepatocellular injury from viral or drug-induced hepatitis, and post portosystemic shunt placement. Recurrent episodes may occur even without identifiable triggers.
Diagnosis – Signs And Symptoms
Type A HE progresses rapidly and may lead to seizures, decerebrate rigidity, coma, and death from cerebral edema. Type B and C HE are typically chronic and may present as minimal or overt encephalopathy. Minimal HE manifests as impaired psychomotor speed, attention, concentration, visual perception, memory deficits, and slowed mental processing, detectable only with psychometric testing. Overt HE includes slow and monotonous speech, impaired fine motor skills, hyperreflexia, clonus, hyperventilation, extrapyramidal movements, seizures, confusion, coma, and abnormal posturing. Episodic HE is characterized by transient changes in consciousness over hours to days with return to baseline after treatment, whereas persistent HE does not fully resolve.
Clinical Grading (West Haven Criteria)
Stage 0 shows no overt clinical changes but abnormal neuropsychological testing and no asterixis. Stage I includes personality changes, irritability, depression or euphoria, sleep–wake reversal, impaired writing or calculations, and possible asterixis. Stage II is marked by inappropriate behavior, lethargy, slowed responses, asterixis, slurred speech, and ataxia. Stage III presents with disorientation, amnesia, paranoia, nystagmus, hypoactive reflexes, positive Babinski sign, and stupor. Stage IV is characterized by coma and dilated pupils.
Essential Workup
Evaluation should include a detailed history of liver disease and prior HE episodes, identification of precipitating factors, and assessment for electrolyte disturbances, as even mild abnormalities may cause significant clinical deterioration.
Diagnostic Tests And Interpretation
Ammonia levels correlate poorly with disease severity but may assist in evaluating unexplained altered mental status. Samples must be handled correctly and processed promptly. A normal ammonia level should prompt investigation for alternative diagnoses. Additional studies include fecal occult blood testing and nasogastric lavage to assess for gastrointestinal bleeding, complete blood count for anemia or infection, electrolytes, renal function, glucose, coagulation studies, and liver enzymes. Urinalysis and cultures of urine and ascitic fluid help identify infection. Toxicology screening may be required to exclude other causes of altered consciousness. Additional testing may include thyroid function, arterial blood gases, magnesium, and viral serologies. Imaging includes chest radiography for pneumonia or heart failure and head CT for new-onset altered mental status, focal deficits, trauma, or suspected cerebral edema. Brain MRI may aid diagnosis in patients with portosystemic shunts without intrinsic liver disease. ECG assesses arrhythmias and electrolyte effects. Lumbar puncture is indicated for unexplained or worsening symptoms, and paracentesis is required when spontaneous bacterial peritonitis is suspected. EEG typically shows generalized slowing.
Differential Diagnosis
Consider alcohol withdrawal, cerebrovascular accident, congestive heart failure, carbon dioxide narcosis, head trauma, electrolyte disturbances, hypoglycemia, meningitis, encephalitis, metabolic encephalopathies, psychiatric illness, drug or alcohol intoxication, uremia, and in children, Reye syndrome or fatty acid oxidation disorders.
Initial Stabilization And Therapy
Management includes supplemental oxygen, cardiac monitoring, and airway protection, with intubation required for grade III or IV encephalopathy. Propofol is preferred for sedation if needed. Standard initial altered mental status treatment includes naloxone, glucose administration, and thiamine.
Emergency Department Treatment And Procedures
Identification and correction of precipitating factors is central to management. Frequent glucose monitoring is essential due to the risk of hypoglycemia. Complications such as gastrointestinal bleeding, sepsis, electrolyte abnormalities, coagulopathy, and renal dysfunction must be treated promptly. Sedatives and narcotics should be avoided when possible; if required, agents with minimal hepatic metabolism are preferred. Ammonia reduction is achieved with nonabsorbable disaccharides such as lactulose, administered orally, via nasogastric tube, or as retention enemas in severe cases. Intestinal flora reduction may include rifaximin, neomycin, metronidazole, or vancomycin, often in combination with lactulose. Rifaximin is preferred for lactulose-resistant HE due to its efficacy and favorable safety profile. Cerebral edema should be treated promptly if present. Zinc deficiency should be corrected, and short-term protein restriction may be considered. Flumazenil may provide transient improvement in select patients but should be avoided in chronic benzodiazepine or alcohol users. Liver transplantation is the definitive therapy for severe or recurrent HE. Additional therapies under investigation include L-carnitine, albumin dialysis, N-acetylcysteine, probiotics, branched-chain amino acids, and manganese chelation.
Medications
Therapy may include intravenous dextrose for hypoglycemia, lactulose titrated to achieve two to three soft stools daily, rifaximin 550 mg twice daily, neomycin or metronidazole when indicated, naloxone for suspected opioid effect, thiamine supplementation, zinc acetate or sulfate, and mannitol for cerebral edema.
Follow-Up And Disposition
Patients with grade II to IV HE, type A HE of any grade, type B or C HE grade II or higher, associated complications such as sepsis or gastrointestinal bleeding, or diagnostic uncertainty require admission, often to the intensive care unit with gastroenterology consultation. Discharge may be considered for patients with known chronic HE presenting with grade 0 or I symptoms, a reversible cause, and reliable supervision. Discharged patients should receive lactulose therapy and dietary guidance.
Follow-Up Recommendations
Patients should realize the importance of dietary counseling, medication adherence, and alcohol cessation when appropriate. Referral to gastroenterology is recommended for recurrent episodes, and patients with type A HE should be evaluated for liver transplantation.
Clinical Insights And Common Errors
Rifaximin is effective for lactulose-resistant hepatic encephalopathy. Hypoglycemia is common and easily overlooked. Sedatives and narcotics can worsen encephalopathy and should be avoided whenever possible or replaced with agents not metabolized by the liver.
Basics And Description
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome characterized by alterations in behavior, level of consciousness, and motor function resulting from hepatic insufficiency and the accumulation of substances normally detoxified by the liver. The condition arises from a multifactorial process, most notably the accumulation of ammonia produced from protein degradation by colonic bacteria and deamination of glutamine in the small bowel, kidneys, and muscle. Ammonia crosses the blood–brain barrier and is metabolized by astrocytes into glutamine, leading to astrocytic swelling, cerebral edema, and mitochondrial dysfunction. Additional neurotoxins such as short-chain fatty acids, manganese, neurosteroids, phenols, mercaptans, and amino acids including tryptophan also contribute. Neurotransmitter imbalance plays a role, with increased inhibitory neurotransmitters such as benzodiazepines, γ-aminobutyric acid, and serotonin, and decreased excitatory neurotransmitters including glutamate, dopamine, aspartate, and catecholamines. Other contributing factors include reduced cerebral blood flow and oxygen delivery, increased cerebral glucose utilization with potential hypoglycemia, zinc deficiency affecting urea cycle enzymes, and rare inherited urea cycle disorders.
Etiology
Hepatic encephalopathy is classified according to the 11th World Congress of Gastroenterology. Type A is associated with acute liver injury and fulminant hepatic failure. Type B is related to portosystemic shunting without intrinsic liver disease. Type C is associated with cirrhosis and portal hypertension. Common precipitating factors include gastrointestinal bleeding, electrolyte abnormalities such as hypokalemia and hyponatremia, metabolic alkalosis reducing renal ammonium excretion, sepsis including spontaneous bacterial peritonitis, constipation, noncompliance with treatment in chronic liver disease, high-protein diet, hypoglycemia, hypovolemia following large-volume paracentesis, azotemia from diuretics or diarrhea, sedatives or narcotics including alcohol, zinc deficiency, hepatocellular injury from viral or drug-induced hepatitis, and post portosystemic shunt placement. Recurrent episodes may occur even without identifiable triggers.
Diagnosis – Signs And Symptoms
Type A HE progresses rapidly and may lead to seizures, decerebrate rigidity, coma, and death from cerebral edema. Type B and C HE are typically chronic and may present as minimal or overt encephalopathy. Minimal HE manifests as impaired psychomotor speed, attention, concentration, visual perception, memory deficits, and slowed mental processing, detectable only with psychometric testing. Overt HE includes slow and monotonous speech, impaired fine motor skills, hyperreflexia, clonus, hyperventilation, extrapyramidal movements, seizures, confusion, coma, and abnormal posturing. Episodic HE is characterized by transient changes in consciousness over hours to days with return to baseline after treatment, whereas persistent HE does not fully resolve.
Clinical Grading (West Haven Criteria)
Stage 0 shows no overt clinical changes but abnormal neuropsychological testing and no asterixis. Stage I includes personality changes, irritability, depression or euphoria, sleep–wake reversal, impaired writing or calculations, and possible asterixis. Stage II is marked by inappropriate behavior, lethargy, slowed responses, asterixis, slurred speech, and ataxia. Stage III presents with disorientation, amnesia, paranoia, nystagmus, hypoactive reflexes, positive Babinski sign, and stupor. Stage IV is characterized by coma and dilated pupils.
Essential Workup
Evaluation should include a detailed history of liver disease and prior HE episodes, identification of precipitating factors, and assessment for electrolyte disturbances, as even mild abnormalities may cause significant clinical deterioration.
Diagnostic Tests And Interpretation
Ammonia levels correlate poorly with disease severity but may assist in evaluating unexplained altered mental status. Samples must be handled correctly and processed promptly. A normal ammonia level should prompt investigation for alternative diagnoses. Additional studies include fecal occult blood testing and nasogastric lavage to assess for gastrointestinal bleeding, complete blood count for anemia or infection, electrolytes, renal function, glucose, coagulation studies, and liver enzymes. Urinalysis and cultures of urine and ascitic fluid help identify infection. Toxicology screening may be required to exclude other causes of altered consciousness. Additional testing may include thyroid function, arterial blood gases, magnesium, and viral serologies. Imaging includes chest radiography for pneumonia or heart failure and head CT for new-onset altered mental status, focal deficits, trauma, or suspected cerebral edema. Brain MRI may aid diagnosis in patients with portosystemic shunts without intrinsic liver disease. ECG assesses arrhythmias and electrolyte effects. Lumbar puncture is indicated for unexplained or worsening symptoms, and paracentesis is required when spontaneous bacterial peritonitis is suspected. EEG typically shows generalized slowing.
Differential Diagnosis
Consider alcohol withdrawal, cerebrovascular accident, congestive heart failure, carbon dioxide narcosis, head trauma, electrolyte disturbances, hypoglycemia, meningitis, encephalitis, metabolic encephalopathies, psychiatric illness, drug or alcohol intoxication, uremia, and in children, Reye syndrome or fatty acid oxidation disorders.
Initial Stabilization And Therapy
Management includes supplemental oxygen, cardiac monitoring, and airway protection, with intubation required for grade III or IV encephalopathy. Propofol is preferred for sedation if needed. Standard initial altered mental status treatment includes naloxone, glucose administration, and thiamine.
Emergency Department Treatment And Procedures
Identification and correction of precipitating factors is central to management. Frequent glucose monitoring is essential due to the risk of hypoglycemia. Complications such as gastrointestinal bleeding, sepsis, electrolyte abnormalities, coagulopathy, and renal dysfunction must be treated promptly. Sedatives and narcotics should be avoided when possible; if required, agents with minimal hepatic metabolism are preferred. Ammonia reduction is achieved with nonabsorbable disaccharides such as lactulose, administered orally, via nasogastric tube, or as retention enemas in severe cases. Intestinal flora reduction may include rifaximin, neomycin, metronidazole, or vancomycin, often in combination with lactulose. Rifaximin is preferred for lactulose-resistant HE due to its efficacy and favorable safety profile. Cerebral edema should be treated promptly if present. Zinc deficiency should be corrected, and short-term protein restriction may be considered. Flumazenil may provide transient improvement in select patients but should be avoided in chronic benzodiazepine or alcohol users. Liver transplantation is the definitive therapy for severe or recurrent HE. Additional therapies under investigation include L-carnitine, albumin dialysis, N-acetylcysteine, probiotics, branched-chain amino acids, and manganese chelation.
Medications
Therapy may include intravenous dextrose for hypoglycemia, lactulose titrated to achieve two to three soft stools daily, rifaximin 550 mg twice daily, neomycin or metronidazole when indicated, naloxone for suspected opioid effect, thiamine supplementation, zinc acetate or sulfate, and mannitol for cerebral edema.
Follow-Up And Disposition
Patients with grade II to IV HE, type A HE of any grade, type B or C HE grade II or higher, associated complications such as sepsis or gastrointestinal bleeding, or diagnostic uncertainty require admission, often to the intensive care unit with gastroenterology consultation. Discharge may be considered for patients with known chronic HE presenting with grade 0 or I symptoms, a reversible cause, and reliable supervision. Discharged patients should receive lactulose therapy and dietary guidance.
Follow-Up Recommendations
Patients should realize the importance of dietary counseling, medication adherence, and alcohol cessation when appropriate. Referral to gastroenterology is recommended for recurrent episodes, and patients with type A HE should be evaluated for liver transplantation.
Clinical Insights And Common Errors
Rifaximin is effective for lactulose-resistant hepatic encephalopathy. Hypoglycemia is common and easily overlooked. Sedatives and narcotics can worsen encephalopathy and should be avoided whenever possible or replaced with agents not metabolized by the liver.
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Emergency And Acute Medicine – Hepatic Injury
Basics And Description
The liver’s size and anatomic location make it particularly vulnerable to injury. It is the most frequently injured solid organ in penetrating trauma and the second most commonly injured organ in blunt abdominal trauma, after the spleen. The liver is highly susceptible to blunt forces from direct impact or deceleration. Understanding the mechanism of injury is essential in evaluating for hepatic trauma. In blunt injury, the direction and magnitude of deceleration or compressive forces should be assessed. In penetrating trauma, the type, caliber, and distance of the weapon, as well as the length and characteristics of knives or impaling objects, are important. Hepatic injuries range from subcapsular hematomas and minor lacerations to severe fragmentation. Associated injuries commonly involve the ribs, spleen, diaphragm, kidneys, lungs, gallbladder, pancreas, and major blood vessels. Overall mortality is approximately 8–10%. Nonoperative management is increasingly common in isolated blunt hepatic trauma. In children, poorly developed abdominal musculature and a smaller anteroposterior diameter increase susceptibility to compressive forces.
Etiology
Hepatic injury most commonly results from trauma. Blunt mechanisms include deceleration, acceleration, and compression forces. Penetrating mechanisms include stab wounds, gunshot wounds, and impalement by foreign objects.
Diagnosis – Signs And Symptoms
Clinical presentation is variable, and neither history nor physical examination alone is sensitive or specific for hepatic injury. A history of trauma is usually available from the patient or prehospital providers. Systemic signs may reflect acute blood loss, including dizziness, weakness, tachycardia, and hypotension. Local findings may include right upper quadrant tenderness, guarding, abdominal distention, rigidity, rebound tenderness, contusions or abrasions, and penetrating wounds to the right chest, flank, or abdomen.
Essential Workup
Because physical examination is unreliable, objective evaluation is required. This includes imaging studies of the abdomen or surgical exploration when indicated.
Diagnostic Tests And Interpretation
No laboratory study is specific for liver injury. A baseline hemoglobin level should be obtained, and type and crossmatch considered if hemorrhage is suspected. Liver function tests are not useful in the acute setting. Plain abdominal radiographs have little diagnostic value. Bedside ultrasonography is an important screening tool in both blunt and penetrating trauma and is the procedure of choice in unstable patients. It may identify free intraperitoneal fluid in the hepatorenal (Morison) pouch or parenchymal injury, suggesting intra-abdominal hemorrhage. Contrast-enhanced CT scan is the best modality for defining the extent of hepatic injury and associated organ damage but requires hemodynamic stability. Active contrast extravasation during the arterial phase suggests vascular injury or high-grade liver trauma requiring intervention. Diagnostic peritoneal lavage is rarely used but is sensitive for hemoperitoneum, though nonspecific for bleeding source. Operative exploration is required if results are positive.
Differential Diagnosis
Consider other causes of intraperitoneal injury, retroperitoneal injury, thoracic or diaphragmatic injury, splenic injury, and vascular trauma.
Prehospital Management
Details of the injury mechanism should be obtained early. Large-bore intravenous access is essential due to the risk of rapid hemorrhage. Penetrating wounds or evisceration should be covered with moist saline dressings, and direct pressure applied to control bleeding. Full spinal immobilization is recommended except in isolated penetrating trauma.
Initial Stabilization And Therapy
Airway, breathing, and circulation take priority. Airway control may be required, particularly if associated head injury is present. Supplemental oxygen, cardiac monitoring, and pulse oximetry should be initiated. Adequate intravenous access is critical and may include peripheral large-bore lines, central venous access, intraosseous access, or venous cutdown. Fluid resuscitation typically begins with crystalloid solutions, followed by packed red blood cells and fresh frozen plasma as needed.
Emergency Department Treatment And Procedures
Immediate laparotomy is indicated in patients with hemodynamic instability, gunshot wounds to the anterior abdomen, clear signs of intraperitoneal hemorrhage, positive diagnostic studies such as DPL, or failure of nonoperative management. Stab wounds may be managed with local wound exploration and adjunct imaging when intraperitoneal penetration is uncertain. Nonoperative management may be appropriate in hemodynamically stable patients with normal mental status, no evidence of other intra-abdominal injury, isolated low-grade hepatic injuries confirmed by imaging, and minimal transfusion requirements. High-grade injuries have lower success rates with nonoperative strategies. Patients should remain NPO with strict bedrest. Selective angiography with embolization may control persistent bleeding and reduce the need for surgery. Adjunctive therapies such as recombinant factor VIIa or prothrombin complex concentrate have been used to aid hemostasis in select cases.
Medications
Management includes intravenous crystalloid fluids, packed red blood cells, fresh frozen plasma, and in select cases recombinant factor VIIa or prothrombin complex concentrate.
Follow-Up And Disposition
All patients with hepatic injury require hospital admission for operative management or close observation with serial examinations, hematocrit measurements, and repeat imaging as indicated. ICU admission is often required during the first 48 hours. Patients with suspected or confirmed hepatic injury should not be discharged from the emergency department.
Follow-Up Recommendations
Serial imaging, physical examinations, and hematocrit monitoring are essential to detect delayed deterioration. Penetrating injuries should be reported to appropriate authorities.
Clinical Insights And Common Errors
Early surgical consultation is critical in unstable patients. Failure to obtain appropriate imaging or relying on a negative ultrasound alone are common pitfalls. Inadequate resuscitation with fluids and blood products can worsen outcomes. Once hepatic injury is identified, associated injuries to surrounding organs must be actively excluded, and pregnancy testing should be performed in women of childbearing age.
Basics And Description
The liver’s size and anatomic location make it particularly vulnerable to injury. It is the most frequently injured solid organ in penetrating trauma and the second most commonly injured organ in blunt abdominal trauma, after the spleen. The liver is highly susceptible to blunt forces from direct impact or deceleration. Understanding the mechanism of injury is essential in evaluating for hepatic trauma. In blunt injury, the direction and magnitude of deceleration or compressive forces should be assessed. In penetrating trauma, the type, caliber, and distance of the weapon, as well as the length and characteristics of knives or impaling objects, are important. Hepatic injuries range from subcapsular hematomas and minor lacerations to severe fragmentation. Associated injuries commonly involve the ribs, spleen, diaphragm, kidneys, lungs, gallbladder, pancreas, and major blood vessels. Overall mortality is approximately 8–10%. Nonoperative management is increasingly common in isolated blunt hepatic trauma. In children, poorly developed abdominal musculature and a smaller anteroposterior diameter increase susceptibility to compressive forces.
Etiology
Hepatic injury most commonly results from trauma. Blunt mechanisms include deceleration, acceleration, and compression forces. Penetrating mechanisms include stab wounds, gunshot wounds, and impalement by foreign objects.
Diagnosis – Signs And Symptoms
Clinical presentation is variable, and neither history nor physical examination alone is sensitive or specific for hepatic injury. A history of trauma is usually available from the patient or prehospital providers. Systemic signs may reflect acute blood loss, including dizziness, weakness, tachycardia, and hypotension. Local findings may include right upper quadrant tenderness, guarding, abdominal distention, rigidity, rebound tenderness, contusions or abrasions, and penetrating wounds to the right chest, flank, or abdomen.
Essential Workup
Because physical examination is unreliable, objective evaluation is required. This includes imaging studies of the abdomen or surgical exploration when indicated.
Diagnostic Tests And Interpretation
No laboratory study is specific for liver injury. A baseline hemoglobin level should be obtained, and type and crossmatch considered if hemorrhage is suspected. Liver function tests are not useful in the acute setting. Plain abdominal radiographs have little diagnostic value. Bedside ultrasonography is an important screening tool in both blunt and penetrating trauma and is the procedure of choice in unstable patients. It may identify free intraperitoneal fluid in the hepatorenal (Morison) pouch or parenchymal injury, suggesting intra-abdominal hemorrhage. Contrast-enhanced CT scan is the best modality for defining the extent of hepatic injury and associated organ damage but requires hemodynamic stability. Active contrast extravasation during the arterial phase suggests vascular injury or high-grade liver trauma requiring intervention. Diagnostic peritoneal lavage is rarely used but is sensitive for hemoperitoneum, though nonspecific for bleeding source. Operative exploration is required if results are positive.
Differential Diagnosis
Consider other causes of intraperitoneal injury, retroperitoneal injury, thoracic or diaphragmatic injury, splenic injury, and vascular trauma.
Prehospital Management
Details of the injury mechanism should be obtained early. Large-bore intravenous access is essential due to the risk of rapid hemorrhage. Penetrating wounds or evisceration should be covered with moist saline dressings, and direct pressure applied to control bleeding. Full spinal immobilization is recommended except in isolated penetrating trauma.
Initial Stabilization And Therapy
Airway, breathing, and circulation take priority. Airway control may be required, particularly if associated head injury is present. Supplemental oxygen, cardiac monitoring, and pulse oximetry should be initiated. Adequate intravenous access is critical and may include peripheral large-bore lines, central venous access, intraosseous access, or venous cutdown. Fluid resuscitation typically begins with crystalloid solutions, followed by packed red blood cells and fresh frozen plasma as needed.
Emergency Department Treatment And Procedures
Immediate laparotomy is indicated in patients with hemodynamic instability, gunshot wounds to the anterior abdomen, clear signs of intraperitoneal hemorrhage, positive diagnostic studies such as DPL, or failure of nonoperative management. Stab wounds may be managed with local wound exploration and adjunct imaging when intraperitoneal penetration is uncertain. Nonoperative management may be appropriate in hemodynamically stable patients with normal mental status, no evidence of other intra-abdominal injury, isolated low-grade hepatic injuries confirmed by imaging, and minimal transfusion requirements. High-grade injuries have lower success rates with nonoperative strategies. Patients should remain NPO with strict bedrest. Selective angiography with embolization may control persistent bleeding and reduce the need for surgery. Adjunctive therapies such as recombinant factor VIIa or prothrombin complex concentrate have been used to aid hemostasis in select cases.
Medications
Management includes intravenous crystalloid fluids, packed red blood cells, fresh frozen plasma, and in select cases recombinant factor VIIa or prothrombin complex concentrate.
Follow-Up And Disposition
All patients with hepatic injury require hospital admission for operative management or close observation with serial examinations, hematocrit measurements, and repeat imaging as indicated. ICU admission is often required during the first 48 hours. Patients with suspected or confirmed hepatic injury should not be discharged from the emergency department.
Follow-Up Recommendations
Serial imaging, physical examinations, and hematocrit monitoring are essential to detect delayed deterioration. Penetrating injuries should be reported to appropriate authorities.
Clinical Insights And Common Errors
Early surgical consultation is critical in unstable patients. Failure to obtain appropriate imaging or relying on a negative ultrasound alone are common pitfalls. Inadequate resuscitation with fluids and blood products can worsen outcomes. Once hepatic injury is identified, associated injuries to surrounding organs must be actively excluded, and pregnancy testing should be performed in women of childbearing age.
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Emergency And Acute Medicine – Hepatitis
Basics And Description
Hepatitis refers to inflammation of the liver caused by infectious, toxic, metabolic, or autoimmune processes. Disease progression may range from transient hepatocellular injury to fibrosis, cirrhosis, and liver failure. Infectious causes, particularly viral hepatitis, account for the majority of cases encountered in emergency and acute care settings.
Etiology
No specific cause is identified in approximately 5–10% of acute and chronic hepatitis cases and up to 50% of fulminant hepatic failure.
Hepatitis A is transmitted via the fecal–oral route with an incubation period of 2–7 weeks. It does not cause chronic disease, though up to 10% of patients experience a relapsing course. Fulminant hepatic failure occurs in about 0.1%.
Hepatitis B is transmitted through percutaneous or mucosal exposure to body fluids and perinatally, with an incubation period of 8–22 weeks. Most infections are subclinical. Risk of chronic infection depends on age and immune status and carries long-term risks of cirrhosis and hepatocellular carcinoma.
Hepatitis C is primarily bloodborne, with sexual and perinatal transmission occurring less commonly. Incubation is 6–10 weeks. Fulminant hepatic failure is rare, but approximately 80% progress to chronic disease with risk of cirrhosis and hepatocellular carcinoma.
Hepatitis D occurs only in the presence of hepatitis B, either as coinfection or superinfection, and is associated with a higher risk of cirrhosis.
Hepatitis E is the most common cause of acute hepatitis worldwide, transmitted fecal–orally, often via contaminated water. Fulminant hepatic failure occurs in up to 10% and is particularly severe in pregnancy.
Alcoholic hepatitis results from chronic heavy alcohol use and may progress to cirrhosis. Severity can be estimated using the Maddrey discriminant function.
Other causes include abscess-related hepatitis, secondary viral infections such as CMV or EBV, medication- or toxin-induced injury, and autoimmune hepatitis.
In children, hepatitis A predominates, while perinatal hepatitis B commonly progresses to chronic disease. In pregnancy, hepatitis E carries high mortality, and pregnancy-specific liver diseases such as acute fatty liver of pregnancy and HELLP syndrome must be considered.
Diagnosis – Signs And Symptoms
Many patients are asymptomatic. The preicteric phase may mimic viral gastroenteritis with fever, malaise, nausea, vomiting, anorexia, and arthralgia. The icteric phase includes jaundice, dark urine, light stools, pruritus, rash, and right upper quadrant pain. Fulminant hepatic failure presents with coagulopathy, encephalopathy, cerebral edema, bleeding, and altered mental status.
Physical Examination
Findings vary by disease phase. Early disease may show fever, dehydration, or arthritis. Icteric findings include jaundice of skin and sclerae, tender hepatomegaly, rash, and dehydration. Severe disease may demonstrate bruising, asterixis, and disorientation.
Essential Workup
A detailed history focusing on travel, exposures, alcohol use, medications, and risk factors is critical. Viral serologies are central to diagnosis of infectious causes.
Diagnostic Tests And Interpretation
Laboratory evaluation includes CBC, metabolic panel, liver function tests, coagulation studies, albumin, and glucose. Transaminase elevation reflects hepatocellular injury but does not correlate reliably with severity. Markedly elevated alkaline phosphatase suggests cholestatic disease. Prolonged INR and low albumin indicate impaired synthetic function. Ammonia levels are useful in altered mental status.
Viral serologies define etiology, including HAV IgM, HBV surface and core antibodies, HCV antibody and RNA, HDV testing when indicated, and HEV IgM. Additional tests include α-fetoprotein in chronic viral hepatitis, Monospot testing for EBV, and urinalysis for bilirubin.
Imaging includes right upper quadrant ultrasound to assess for biliary obstruction and head CT when hepatic encephalopathy is suspected.
Differential Diagnosis
Consider nonalcoholic fatty liver disease, biliary disease, ischemic hepatitis, congestive heart failure, metabolic and genetic disorders, liver abscess, heat stroke, Wilson disease, Budd–Chiari syndrome, and pregnancy-related liver disease.
Initial Stabilization And Therapy
Airway, breathing, and circulation are priorities in fulminant hepatic failure or severe encephalopathy. Judicious intravenous fluid resuscitation is required.
Emergency Department Treatment And Procedures
Management is largely supportive. Correct hypovolemia and electrolyte disturbances, treat nausea and vomiting, and avoid hepatotoxic medications and alcohol. Use medications with minimal hepatic metabolism when sedation or analgesia is required. Correct coagulopathy only in the presence of active bleeding. Administer N-acetylcysteine for acetaminophen toxicity and consider its use in fulminant hepatic failure. Steroids may benefit severe alcoholic hepatitis. Manage pruritus with bile acid sequestrants. Perform paracentesis for tense ascites causing respiratory compromise. Provide postexposure prophylaxis for hepatitis A and B when indicated.
Medications
Commonly used agents include ondansetron or metoclopramide for nausea, cholestyramine or ursodeoxycholic acid for pruritus, N-acetylcysteine, prednisone for select alcoholic hepatitis cases, vitamin K for coagulopathy, and thiamine in malnourished patients.
Follow-Up And Disposition
Admit patients with intractable vomiting, dehydration, electrolyte abnormalities, pregnancy, immunocompromise, suspected toxic hepatitis, advanced age, or evidence of significant liver dysfunction. Fulminant hepatic failure requires ICU care and early transfer to a transplant center. Patients with mild disease and good oral tolerance may be discharged with close follow-up.
Follow-Up Recommendations
Arrange hepatology or gastroenterology follow-up for definitive diagnosis and management. Counsel on strict hygiene, avoidance of alcohol and acetaminophen, vaccination when appropriate, and limitation of strenuous activity.
Clinical Insights And Common Errors
Acute hepatitis is frequently misdiagnosed as a nonspecific viral illness. Emergency management is primarily supportive. Early recognition of fulminant hepatic failure and prompt transfer to a transplant-capable center are critical. Maintain high suspicion for pregnancy-related liver disease in pregnant patients with compatible symptoms.
Basics And Description
Hepatitis refers to inflammation of the liver caused by infectious, toxic, metabolic, or autoimmune processes. Disease progression may range from transient hepatocellular injury to fibrosis, cirrhosis, and liver failure. Infectious causes, particularly viral hepatitis, account for the majority of cases encountered in emergency and acute care settings.
Etiology
No specific cause is identified in approximately 5–10% of acute and chronic hepatitis cases and up to 50% of fulminant hepatic failure.
Hepatitis A is transmitted via the fecal–oral route with an incubation period of 2–7 weeks. It does not cause chronic disease, though up to 10% of patients experience a relapsing course. Fulminant hepatic failure occurs in about 0.1%.
Hepatitis B is transmitted through percutaneous or mucosal exposure to body fluids and perinatally, with an incubation period of 8–22 weeks. Most infections are subclinical. Risk of chronic infection depends on age and immune status and carries long-term risks of cirrhosis and hepatocellular carcinoma.
Hepatitis C is primarily bloodborne, with sexual and perinatal transmission occurring less commonly. Incubation is 6–10 weeks. Fulminant hepatic failure is rare, but approximately 80% progress to chronic disease with risk of cirrhosis and hepatocellular carcinoma.
Hepatitis D occurs only in the presence of hepatitis B, either as coinfection or superinfection, and is associated with a higher risk of cirrhosis.
Hepatitis E is the most common cause of acute hepatitis worldwide, transmitted fecal–orally, often via contaminated water. Fulminant hepatic failure occurs in up to 10% and is particularly severe in pregnancy.
Alcoholic hepatitis results from chronic heavy alcohol use and may progress to cirrhosis. Severity can be estimated using the Maddrey discriminant function.
Other causes include abscess-related hepatitis, secondary viral infections such as CMV or EBV, medication- or toxin-induced injury, and autoimmune hepatitis.
In children, hepatitis A predominates, while perinatal hepatitis B commonly progresses to chronic disease. In pregnancy, hepatitis E carries high mortality, and pregnancy-specific liver diseases such as acute fatty liver of pregnancy and HELLP syndrome must be considered.
Diagnosis – Signs And Symptoms
Many patients are asymptomatic. The preicteric phase may mimic viral gastroenteritis with fever, malaise, nausea, vomiting, anorexia, and arthralgia. The icteric phase includes jaundice, dark urine, light stools, pruritus, rash, and right upper quadrant pain. Fulminant hepatic failure presents with coagulopathy, encephalopathy, cerebral edema, bleeding, and altered mental status.
Physical Examination
Findings vary by disease phase. Early disease may show fever, dehydration, or arthritis. Icteric findings include jaundice of skin and sclerae, tender hepatomegaly, rash, and dehydration. Severe disease may demonstrate bruising, asterixis, and disorientation.
Essential Workup
A detailed history focusing on travel, exposures, alcohol use, medications, and risk factors is critical. Viral serologies are central to diagnosis of infectious causes.
Diagnostic Tests And Interpretation
Laboratory evaluation includes CBC, metabolic panel, liver function tests, coagulation studies, albumin, and glucose. Transaminase elevation reflects hepatocellular injury but does not correlate reliably with severity. Markedly elevated alkaline phosphatase suggests cholestatic disease. Prolonged INR and low albumin indicate impaired synthetic function. Ammonia levels are useful in altered mental status.
Viral serologies define etiology, including HAV IgM, HBV surface and core antibodies, HCV antibody and RNA, HDV testing when indicated, and HEV IgM. Additional tests include α-fetoprotein in chronic viral hepatitis, Monospot testing for EBV, and urinalysis for bilirubin.
Imaging includes right upper quadrant ultrasound to assess for biliary obstruction and head CT when hepatic encephalopathy is suspected.
Differential Diagnosis
Consider nonalcoholic fatty liver disease, biliary disease, ischemic hepatitis, congestive heart failure, metabolic and genetic disorders, liver abscess, heat stroke, Wilson disease, Budd–Chiari syndrome, and pregnancy-related liver disease.
Initial Stabilization And Therapy
Airway, breathing, and circulation are priorities in fulminant hepatic failure or severe encephalopathy. Judicious intravenous fluid resuscitation is required.
Emergency Department Treatment And Procedures
Management is largely supportive. Correct hypovolemia and electrolyte disturbances, treat nausea and vomiting, and avoid hepatotoxic medications and alcohol. Use medications with minimal hepatic metabolism when sedation or analgesia is required. Correct coagulopathy only in the presence of active bleeding. Administer N-acetylcysteine for acetaminophen toxicity and consider its use in fulminant hepatic failure. Steroids may benefit severe alcoholic hepatitis. Manage pruritus with bile acid sequestrants. Perform paracentesis for tense ascites causing respiratory compromise. Provide postexposure prophylaxis for hepatitis A and B when indicated.
Medications
Commonly used agents include ondansetron or metoclopramide for nausea, cholestyramine or ursodeoxycholic acid for pruritus, N-acetylcysteine, prednisone for select alcoholic hepatitis cases, vitamin K for coagulopathy, and thiamine in malnourished patients.
Follow-Up And Disposition
Admit patients with intractable vomiting, dehydration, electrolyte abnormalities, pregnancy, immunocompromise, suspected toxic hepatitis, advanced age, or evidence of significant liver dysfunction. Fulminant hepatic failure requires ICU care and early transfer to a transplant center. Patients with mild disease and good oral tolerance may be discharged with close follow-up.
Follow-Up Recommendations
Arrange hepatology or gastroenterology follow-up for definitive diagnosis and management. Counsel on strict hygiene, avoidance of alcohol and acetaminophen, vaccination when appropriate, and limitation of strenuous activity.
Clinical Insights And Common Errors
Acute hepatitis is frequently misdiagnosed as a nonspecific viral illness. Emergency management is primarily supportive. Early recognition of fulminant hepatic failure and prompt transfer to a transplant-capable center are critical. Maintain high suspicion for pregnancy-related liver disease in pregnant patients with compatible symptoms.
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Emergency And Acute Medicine – Hepatorenal Syndrome
Overview And Definition
Hepatorenal syndrome is a form of renal failure that occurs in patients with advanced acute or chronic liver disease in the absence of intrinsic renal pathology. It reflects a severe reduction in renal perfusion caused by advanced hepatic dysfunction. The kidneys are structurally normal, and renal failure does not improve despite adequate volume resuscitation.
Disease Classification And Mechanism
Type I hepatorenal syndrome is an acute and rapidly progressive condition characterized by a sudden decline in renal function, defined by a doubling of serum creatinine or a 50% reduction in creatinine clearance within two weeks. It is commonly associated with acute liver failure or severe alcoholic hepatitis, often presents with oliguria or anuria, and carries a mortality rate approaching 90% within three months.
Type II hepatorenal syndrome has a more indolent course and typically occurs in patients with cirrhosis and refractory ascites. Renal dysfunction progresses slowly, and overall survival is longer than in type I disease.
The underlying pathophysiology involves profound systemic vasodilation due to liver disease, resulting in reduced effective arterial blood volume. This triggers activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system, along with increased production of vasoactive substances. The net effect is dominant renal vasoconstriction, reduced renal blood flow, decreased glomerular filtration rate, and markedly low urinary sodium excretion.
Etiology And Precipitating Factors
Hepatorenal syndrome most commonly arises in chronic liver disease, particularly cirrhosis and severe alcoholic hepatitis, but may also occur in fulminant hepatic failure. Common precipitating factors include gastrointestinal bleeding, aggressive diuresis, large-volume paracentesis without albumin replacement, exposure to nephrotoxic medications such as NSAIDs or aminoglycosides, and systemic infections. Spontaneous bacterial peritonitis is a particularly important trigger and significantly increases the risk of renal failure.
Clinical Features
Patients typically exhibit signs of advanced liver disease, including ascites, portal hypertension, jaundice, hepatic encephalopathy, and coagulopathy. Progressive oliguria is common. Vital signs may reveal hypotension or tachycardia, particularly in the presence of bleeding or sepsis. Dyspnea and tachypnea may occur due to tense ascites or volume overload.
Diagnostic Evaluation
Laboratory findings usually demonstrate rising blood urea nitrogen and creatinine, though creatinine may underestimate renal dysfunction due to low muscle mass or interference from hyperbilirubinemia. Urinalysis typically shows no casts or protein, helping distinguish hepatorenal syndrome from acute tubular necrosis. Urine sodium is characteristically very low, with a fractional excretion of sodium below 1% and concentrated urine relative to plasma.
Additional studies include coagulation profiles, cultures to evaluate for infection, and renal ultrasound to exclude obstructive uropathy. Hepatorenal syndrome remains a diagnosis of exclusion, requiring elimination of other causes of renal failure such as hypovolemia, intrinsic renal disease, obstruction, and drug toxicity.
Differential Considerations
Important alternatives include prerenal azotemia due to volume depletion, acute tubular necrosis, glomerulonephritis related to viral hepatitis, obstructive uropathy, medication-induced nephrotoxicity, sepsis-related renal failure, and post–liver transplant renal dysfunction.
Initial Stabilization And Support
Management begins with standard airway, breathing, and circulation assessment. Hypotension and hypovolemia should be corrected promptly using isotonic fluids and albumin. Close monitoring of urine output and hemodynamic status is essential. Life-threatening complications of renal failure, including hyperkalemia, metabolic acidosis, hypoxemia, and uremic complications, must be addressed immediately.
Emergency Department Management
Treatment focuses on identifying and correcting reversible contributors while providing supportive care. All potentially nephrotoxic medications should be discontinued. Infections must be treated aggressively with early antibiotics. Electrolyte abnormalities, hypoglycemia, hepatic encephalopathy, and other complications of liver failure should be corrected. Large-volume paracentesis with albumin replacement may transiently improve renal perfusion in patients with tense ascites.
Advanced therapies such as transjugular intrahepatic portosystemic shunt placement may improve renal function in selected patients. Dialysis is reserved for management of complications and as a bridge to recovery or transplantation. Liver transplantation remains the only definitive treatment.
Pharmacologic Options
No medication is considered definitive therapy. Vasoconstrictor-based regimens may be used in select cases after excluding other causes of renal failure. Options include low-dose dopamine, combinations of midodrine and octreotide, or prostaglandin analogs. Vasopressin analogs such as terlipressin show benefit but are not widely available in all regions.
Disposition And Prognosis
All patients with suspected hepatorenal syndrome require hospital admission with gastroenterology and nephrology consultation. Intensive care admission is indicated for those with encephalopathy, severe electrolyte disturbances, or cardiopulmonary compromise. There are no circumstances in which discharge from the emergency department is appropriate.
Key Clinical Insights And Common Errors
Any degree of renal dysfunction in a patient with advanced liver disease must be treated as a medical emergency. Delayed recognition, failure to exclude reversible causes, or continued exposure to nephrotoxic agents significantly worsens outcomes. Early consultation and consideration of transplant eligibility are critical.
Overview And Definition
Hepatorenal syndrome is a form of renal failure that occurs in patients with advanced acute or chronic liver disease in the absence of intrinsic renal pathology. It reflects a severe reduction in renal perfusion caused by advanced hepatic dysfunction. The kidneys are structurally normal, and renal failure does not improve despite adequate volume resuscitation.
Disease Classification And Mechanism
Type I hepatorenal syndrome is an acute and rapidly progressive condition characterized by a sudden decline in renal function, defined by a doubling of serum creatinine or a 50% reduction in creatinine clearance within two weeks. It is commonly associated with acute liver failure or severe alcoholic hepatitis, often presents with oliguria or anuria, and carries a mortality rate approaching 90% within three months.
Type II hepatorenal syndrome has a more indolent course and typically occurs in patients with cirrhosis and refractory ascites. Renal dysfunction progresses slowly, and overall survival is longer than in type I disease.
The underlying pathophysiology involves profound systemic vasodilation due to liver disease, resulting in reduced effective arterial blood volume. This triggers activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system, along with increased production of vasoactive substances. The net effect is dominant renal vasoconstriction, reduced renal blood flow, decreased glomerular filtration rate, and markedly low urinary sodium excretion.
Etiology And Precipitating Factors
Hepatorenal syndrome most commonly arises in chronic liver disease, particularly cirrhosis and severe alcoholic hepatitis, but may also occur in fulminant hepatic failure. Common precipitating factors include gastrointestinal bleeding, aggressive diuresis, large-volume paracentesis without albumin replacement, exposure to nephrotoxic medications such as NSAIDs or aminoglycosides, and systemic infections. Spontaneous bacterial peritonitis is a particularly important trigger and significantly increases the risk of renal failure.
Clinical Features
Patients typically exhibit signs of advanced liver disease, including ascites, portal hypertension, jaundice, hepatic encephalopathy, and coagulopathy. Progressive oliguria is common. Vital signs may reveal hypotension or tachycardia, particularly in the presence of bleeding or sepsis. Dyspnea and tachypnea may occur due to tense ascites or volume overload.
Diagnostic Evaluation
Laboratory findings usually demonstrate rising blood urea nitrogen and creatinine, though creatinine may underestimate renal dysfunction due to low muscle mass or interference from hyperbilirubinemia. Urinalysis typically shows no casts or protein, helping distinguish hepatorenal syndrome from acute tubular necrosis. Urine sodium is characteristically very low, with a fractional excretion of sodium below 1% and concentrated urine relative to plasma.
Additional studies include coagulation profiles, cultures to evaluate for infection, and renal ultrasound to exclude obstructive uropathy. Hepatorenal syndrome remains a diagnosis of exclusion, requiring elimination of other causes of renal failure such as hypovolemia, intrinsic renal disease, obstruction, and drug toxicity.
Differential Considerations
Important alternatives include prerenal azotemia due to volume depletion, acute tubular necrosis, glomerulonephritis related to viral hepatitis, obstructive uropathy, medication-induced nephrotoxicity, sepsis-related renal failure, and post–liver transplant renal dysfunction.
Initial Stabilization And Support
Management begins with standard airway, breathing, and circulation assessment. Hypotension and hypovolemia should be corrected promptly using isotonic fluids and albumin. Close monitoring of urine output and hemodynamic status is essential. Life-threatening complications of renal failure, including hyperkalemia, metabolic acidosis, hypoxemia, and uremic complications, must be addressed immediately.
Emergency Department Management
Treatment focuses on identifying and correcting reversible contributors while providing supportive care. All potentially nephrotoxic medications should be discontinued. Infections must be treated aggressively with early antibiotics. Electrolyte abnormalities, hypoglycemia, hepatic encephalopathy, and other complications of liver failure should be corrected. Large-volume paracentesis with albumin replacement may transiently improve renal perfusion in patients with tense ascites.
Advanced therapies such as transjugular intrahepatic portosystemic shunt placement may improve renal function in selected patients. Dialysis is reserved for management of complications and as a bridge to recovery or transplantation. Liver transplantation remains the only definitive treatment.
Pharmacologic Options
No medication is considered definitive therapy. Vasoconstrictor-based regimens may be used in select cases after excluding other causes of renal failure. Options include low-dose dopamine, combinations of midodrine and octreotide, or prostaglandin analogs. Vasopressin analogs such as terlipressin show benefit but are not widely available in all regions.
Disposition And Prognosis
All patients with suspected hepatorenal syndrome require hospital admission with gastroenterology and nephrology consultation. Intensive care admission is indicated for those with encephalopathy, severe electrolyte disturbances, or cardiopulmonary compromise. There are no circumstances in which discharge from the emergency department is appropriate.
Key Clinical Insights And Common Errors
Any degree of renal dysfunction in a patient with advanced liver disease must be treated as a medical emergency. Delayed recognition, failure to exclude reversible causes, or continued exposure to nephrotoxic agents significantly worsens outcomes. Early consultation and consideration of transplant eligibility are critical.
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Emergency And Acute Medicine – Henoch–Schönlein Purpura
Basics And Description
Henoch–Schönlein purpura is a small-vessel vasculitis characterized by IgA-mediated inflammation affecting the skin, gastrointestinal tract, kidneys, joints, and, less commonly, the central nervous system. Multisystem involvement may lead to acute, life-threatening complications or long-term sequelae, particularly renal disease. Although often self-limited, careful evaluation and follow-up are essential.
Etiology
The underlying mechanism involves increased serum IgA with formation of circulating IgA immune complexes and mesangial IgA deposition in the glomeruli. The exact cause is unknown, but multiple associations have been identified. These include infections such as group A streptococcus, Mycoplasma, and viral illnesses including varicella and Epstein–Barr virus. Drug associations include penicillin, tetracycline, aspirin, sulfonamides, and erythromycin. Allergens such as insect bites and certain foods including chocolate, milk, and wheat have also been implicated. The condition most commonly affects school-aged children and young adults, occurs more frequently in males than females, is more common in white populations, and has a higher incidence in winter and spring.
Diagnosis – Signs And Symptoms
Patients are often well appearing despite extensive rash. Constitutional symptoms may include malaise, low-grade fever, and recent or current upper respiratory infection. Hypertension may be present when renal involvement develops. Infants younger than 3 months may present with skin findings alone, while children under 2 years may present with isolated facial edema.
Skin Manifestations
A purpuric rash is the hallmark and presenting feature in approximately half of patients, with eventual development in nearly all cases. Lesions begin as blanching pink papules and evolve within 24 hours into palpable purpura measuring 2–3 cm. The rash is typically symmetric, involves gravity-dependent areas such as the lower extremities and buttocks, and may extend to the trunk or upper extremities. Facial involvement is rare. Recurrence occurs in up to 40% of patients, usually within six weeks.
Abdominal Involvement
Abdominal pain occurs in 70–80% of cases and may range from colicky to severe. Gastrointestinal symptoms may precede the rash by up to four weeks. Gastrointestinal bleeding is common and ranges from occult blood loss to severe hemorrhage. Intussusception, usually ileoileal or ileocolic, is a serious complication.
Renal And Genitourinary Involvement
Asymptomatic hematuria is common and occurs in up to 80% of patients. Proteinuria suggests glomerulonephritis. Other manifestations include scrotal pain, testicular swelling, and, in severe cases, renal failure.
Musculoskeletal Involvement
Arthritis or arthralgia occurs in 70–80% of patients, is typically migratory, periarticular, and most commonly affects the knees and ankles. Angioedema may also occur.
Neurologic Involvement
Less common manifestations include headache, seizures, altered mental status, focal neurologic deficits, and visual or speech disturbances. Intracranial hemorrhage is rare but serious.
History
Key elements include recent infections, onset and progression of rash, presence of abdominal pain, vomiting, edema, joint symptoms, and timing and progression of multisystem complaints.
Physical Examination
Assessment should include vital signs with attention to blood pressure, cardiovascular perfusion, abdominal tenderness or distention, palpable masses, evidence of gastrointestinal bleeding, genitourinary examination for testicular involvement, careful skin inspection for nonblanching purpura, and a focused neurologic examination.
Essential Workup
The primary goal is to exclude life-threatening causes of purpura, abdominal pain, hematuria, and neurologic findings.
Diagnostic Tests And Interpretation
Laboratory studies typically show a normal platelet count and may reveal leukocytosis. Coagulation studies are indicated if bleeding is present or diagnosis is uncertain. Electrolytes, blood urea nitrogen, and creatinine should be obtained if hypertension or abnormal urinalysis is present. Urinalysis frequently shows hematuria, and proteinuria suggests renal involvement. Cultures may be obtained to exclude infectious triggers. Abdominal imaging with ultrasound, contrast enema, or CT is indicated for abdominal pain or gastrointestinal bleeding to evaluate for intussusception. Testicular ultrasound is indicated for scrotal symptoms. Head CT is required for neurologic findings. Lumbar puncture is performed only when clinically indicated.
Differential Diagnosis
Important considerations include gastroenteritis, appendicitis, inflammatory bowel disease, Meckel diverticulum, acute glomerulonephritis, systemic lupus erythematosus, polyarteritis nodosa, meningococcemia, bacterial sepsis, Rocky Mountain spotted fever, viral exanthems, thrombocytopenia, drug reactions, testicular torsion, and incarcerated hernia.
Treatment – Prehospital Care
Stabilization should be provided as clinically indicated.
Initial Stabilization And Therapy
Intravenous fluids are administered for shock. Packed red blood cells are indicated for massive gastrointestinal hemorrhage.
Emergency Department Treatment And Procedures
Life-threatening complications require immediate intervention. NSAIDs such as ibuprofen are used for arthralgia. Corticosteroids, typically prednisone, are indicated for severe abdominal pain after exclusion of surgical causes, painful subcutaneous edema, arthritis, significant renal involvement, or central nervous system disease. Severe nephritis may require high-dose pulse methylprednisolone. Immunosuppressive agents and intravenous immunoglobulin may be considered in severe, life-threatening disease, though evidence is limited.
Medications
First-line therapy includes ibuprofen 600 mg orally every 6 hours, or 5–10 mg/kg per dose in children. Second-line therapy includes prednisone 60 mg daily in adults or 1–2 mg/kg/day in children for 5–7 days.
Follow-Up And Disposition
Admission is required for severe abdominal pain, gastrointestinal bleeding, intussusception, central nervous system involvement, or evidence of renal failure. Patients may be discharged if platelet count and renal function are normal and abdominal pain is minimal or absent. Patients started on steroids should have follow-up within 24 hours.
Follow-Up Recommendations
Close follow-up with a primary care physician is required, with regular monitoring of blood pressure and repeat urinalysis and laboratory studies as indicated. In children, monitoring is recommended for at least six months.
Clinical Insights And Common Errors
Always exclude life-threatening causes of purpura and abdominal pain. NSAIDs are sufficient for most patients. Systemic corticosteroids do not alter the long-term prognosis of Henoch–Schönlein purpura nephritis and should be reserved for specific indications.
Basics And Description
Henoch–Schönlein purpura is a small-vessel vasculitis characterized by IgA-mediated inflammation affecting the skin, gastrointestinal tract, kidneys, joints, and, less commonly, the central nervous system. Multisystem involvement may lead to acute, life-threatening complications or long-term sequelae, particularly renal disease. Although often self-limited, careful evaluation and follow-up are essential.
Etiology
The underlying mechanism involves increased serum IgA with formation of circulating IgA immune complexes and mesangial IgA deposition in the glomeruli. The exact cause is unknown, but multiple associations have been identified. These include infections such as group A streptococcus, Mycoplasma, and viral illnesses including varicella and Epstein–Barr virus. Drug associations include penicillin, tetracycline, aspirin, sulfonamides, and erythromycin. Allergens such as insect bites and certain foods including chocolate, milk, and wheat have also been implicated. The condition most commonly affects school-aged children and young adults, occurs more frequently in males than females, is more common in white populations, and has a higher incidence in winter and spring.
Diagnosis – Signs And Symptoms
Patients are often well appearing despite extensive rash. Constitutional symptoms may include malaise, low-grade fever, and recent or current upper respiratory infection. Hypertension may be present when renal involvement develops. Infants younger than 3 months may present with skin findings alone, while children under 2 years may present with isolated facial edema.
Skin Manifestations
A purpuric rash is the hallmark and presenting feature in approximately half of patients, with eventual development in nearly all cases. Lesions begin as blanching pink papules and evolve within 24 hours into palpable purpura measuring 2–3 cm. The rash is typically symmetric, involves gravity-dependent areas such as the lower extremities and buttocks, and may extend to the trunk or upper extremities. Facial involvement is rare. Recurrence occurs in up to 40% of patients, usually within six weeks.
Abdominal Involvement
Abdominal pain occurs in 70–80% of cases and may range from colicky to severe. Gastrointestinal symptoms may precede the rash by up to four weeks. Gastrointestinal bleeding is common and ranges from occult blood loss to severe hemorrhage. Intussusception, usually ileoileal or ileocolic, is a serious complication.
Renal And Genitourinary Involvement
Asymptomatic hematuria is common and occurs in up to 80% of patients. Proteinuria suggests glomerulonephritis. Other manifestations include scrotal pain, testicular swelling, and, in severe cases, renal failure.
Musculoskeletal Involvement
Arthritis or arthralgia occurs in 70–80% of patients, is typically migratory, periarticular, and most commonly affects the knees and ankles. Angioedema may also occur.
Neurologic Involvement
Less common manifestations include headache, seizures, altered mental status, focal neurologic deficits, and visual or speech disturbances. Intracranial hemorrhage is rare but serious.
History
Key elements include recent infections, onset and progression of rash, presence of abdominal pain, vomiting, edema, joint symptoms, and timing and progression of multisystem complaints.
Physical Examination
Assessment should include vital signs with attention to blood pressure, cardiovascular perfusion, abdominal tenderness or distention, palpable masses, evidence of gastrointestinal bleeding, genitourinary examination for testicular involvement, careful skin inspection for nonblanching purpura, and a focused neurologic examination.
Essential Workup
The primary goal is to exclude life-threatening causes of purpura, abdominal pain, hematuria, and neurologic findings.
Diagnostic Tests And Interpretation
Laboratory studies typically show a normal platelet count and may reveal leukocytosis. Coagulation studies are indicated if bleeding is present or diagnosis is uncertain. Electrolytes, blood urea nitrogen, and creatinine should be obtained if hypertension or abnormal urinalysis is present. Urinalysis frequently shows hematuria, and proteinuria suggests renal involvement. Cultures may be obtained to exclude infectious triggers. Abdominal imaging with ultrasound, contrast enema, or CT is indicated for abdominal pain or gastrointestinal bleeding to evaluate for intussusception. Testicular ultrasound is indicated for scrotal symptoms. Head CT is required for neurologic findings. Lumbar puncture is performed only when clinically indicated.
Differential Diagnosis
Important considerations include gastroenteritis, appendicitis, inflammatory bowel disease, Meckel diverticulum, acute glomerulonephritis, systemic lupus erythematosus, polyarteritis nodosa, meningococcemia, bacterial sepsis, Rocky Mountain spotted fever, viral exanthems, thrombocytopenia, drug reactions, testicular torsion, and incarcerated hernia.
Treatment – Prehospital Care
Stabilization should be provided as clinically indicated.
Initial Stabilization And Therapy
Intravenous fluids are administered for shock. Packed red blood cells are indicated for massive gastrointestinal hemorrhage.
Emergency Department Treatment And Procedures
Life-threatening complications require immediate intervention. NSAIDs such as ibuprofen are used for arthralgia. Corticosteroids, typically prednisone, are indicated for severe abdominal pain after exclusion of surgical causes, painful subcutaneous edema, arthritis, significant renal involvement, or central nervous system disease. Severe nephritis may require high-dose pulse methylprednisolone. Immunosuppressive agents and intravenous immunoglobulin may be considered in severe, life-threatening disease, though evidence is limited.
Medications
First-line therapy includes ibuprofen 600 mg orally every 6 hours, or 5–10 mg/kg per dose in children. Second-line therapy includes prednisone 60 mg daily in adults or 1–2 mg/kg/day in children for 5–7 days.
Follow-Up And Disposition
Admission is required for severe abdominal pain, gastrointestinal bleeding, intussusception, central nervous system involvement, or evidence of renal failure. Patients may be discharged if platelet count and renal function are normal and abdominal pain is minimal or absent. Patients started on steroids should have follow-up within 24 hours.
Follow-Up Recommendations
Close follow-up with a primary care physician is required, with regular monitoring of blood pressure and repeat urinalysis and laboratory studies as indicated. In children, monitoring is recommended for at least six months.
Clinical Insights And Common Errors
Always exclude life-threatening causes of purpura and abdominal pain. NSAIDs are sufficient for most patients. Systemic corticosteroids do not alter the long-term prognosis of Henoch–Schönlein purpura nephritis and should be reserved for specific indications.
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Emergency And Acute Medicine – High-Altitude Illness
Basics
Description
High-altitude illness occurs due to hypobaric hypoxia following rapid ascent to higher elevations, typically above 8,000 ft (≈2,500 m), without adequate acclimatization. The incidence depends on the rate of ascent, final altitude reached, sleeping altitude, and duration of exposure.
Acute mountain sickness (AMS) occurs in up to 67% of individuals who ascend rapidly (1–2 days) to elevations above 14,000 ft. Among skiers sleeping at altitude, AMS occurs in approximately 22% at 7,000–9,000 ft and 40% at 10,000 ft.
High-altitude pulmonary edema (HAPE) occurs in fewer than 1–2% of exposed individuals, and high-altitude cerebral edema (HACE) occurs in less than 1%. HAPE and HACE are uncommon below 13,000 ft (≈4,000 m).
Risk Factors
Risk factors for AMS include a prior history of high-altitude illness, rapid ascent, physical exertion, younger age (<50 yr), obesity, and preexisting lung disease. physical fitness does not confer protection.< />pan>
Pregnancy Considerations
The relationship between pregnancy and high-altitude illness is not well defined. Pregnancy-induced hypertension, proteinuria, and peripheral edema are more common at altitude, likely related to maternal hypoxemia. There is no evidence of increased risk of spontaneous abortion or placental complications at moderate altitude. Travel above 13,000 ft should be approached cautiously, especially in complicated pregnancies.
Geriatric Considerations
Although older adults often have comorbidities such as hypertension, COPD, or coronary artery disease, individuals older than 55 years appear to have a lower risk of AMS than younger adults.
Etiology
The primary cause of high-altitude illness is rapid ascent without acclimatization. Susceptibility varies between individuals, and illness is influenced by ascent rate, altitude attained, sleeping altitude, and physiologic response to hypoxia.
Diagnosis
Signs and Symptoms
Acute Mountain Sickness (AMS)
AMS is defined by headache plus at least one of the following: nausea or vomiting, fatigue or lassitude, dizziness, or difficulty sleeping. Symptoms typically begin 4–12 hours after ascent and are usually self-limited but may become debilitating.
High-Altitude Pulmonary Edema (HAPE)
HAPE usually develops 2–4 days after ascent, often on the second night. It is potentially life-threatening and presents with dry cough progressing to productive cough, dyspnea at rest, and decreased exercise tolerance.
High-Altitude Cerebral Edema (HACE)
HACE is life-threatening and typically occurs in patients with AMS and/or HAPE. Onset usually requires 2–4 days but may occur as early as 12 hours after AMS symptoms. Findings include severe headache, nausea and vomiting, altered mental status, and ataxia.
Pediatric Considerations
In infants and young children, AMS may present as irritability, decreased playfulness, reduced appetite, vomiting, and sleep disturbances. HAPE occurs more frequently in individuals younger than 20 years, and cases have not been reported in children younger than 4 years.
Physical Examination
Essential Workup
Diagnosis is primarily clinical in the setting of recent altitude gain.
Diagnostic Tests and Interpretation
Differential Diagnosis
Treatment
Prehospital Care
Severe cases require immediate descent. Further ascent is contraindicated in symptomatic individuals. Supplemental oxygen or simulated descent using a portable hyperbaric chamber (e.g., Gamow bag) may be lifesaving when evacuation is delayed.
Initial Stabilization and Therapy
For HAPE and HACE, prioritize airway, breathing, and circulation. Provide supplemental oxygen, establish IV access, and monitor closely. Endotracheal intubation may be required for respiratory failure or airway protection. CPAP may be beneficial in HAPE.
Emergency Department Treatment and Procedures
AMS
Mild cases are usually self-limited. Management includes halting ascent, symptomatic treatment, acetazolamide for moderate to severe symptoms, analgesics for headache, antiemetics for nausea, and oxygen for severe cases. Descent is required if symptoms persist or worsen.
HAPE
Immediate descent is mandatory for moderate to severe disease. Mild cases may be managed at altitude only if oxygen and close monitoring are available. Bed rest, high-flow supplemental oxygen, and avoidance of exertion are critical. Nifedipine may be used when oxygen or descent is unavailable. Hyperbaric therapy may be used when descent is impossible.
HACE
Immediate evacuation to lower altitude is essential. Administer oxygen and dexamethasone. Maintain bed rest with head elevation and manage elevated intracranial pressure aggressively in severe cases.
Medications
First-Line Therapy
Acetazolamide for AMS, nifedipine for HAPE
Second-Line Therapy
Dexamethasone
Use of multiple medications concurrently is not supported by current evidence.
Follow-Up and Disposition
Admission Criteria
HAPE, HACE, or persistent symptoms after descent and observation require admission.
Discharge Criteria
Patients may be discharged after clinical improvement with oxygen saturation >95% on room air at sea level or appropriate baseline saturation at altitude.
Issues for Referral
Patients with recurrent AMS may benefit from acetazolamide prophylaxis for future ascents. Those with prior HAPE may benefit from nifedipine prophylaxis.
Clinical Pearls and Pitfalls
High-altitude illness often mimics viral syndromes, leading to missed diagnosis. Once symptoms develop, further ascent is contraindicated until complete resolution. Ataxia and dyspnea at rest are early warning signs of HACE and HAPE, respectively. When descent is not possible, hyperbaric therapy and adjunctive medications should be considered promptly.
Basics
Description
High-altitude illness occurs due to hypobaric hypoxia following rapid ascent to higher elevations, typically above 8,000 ft (≈2,500 m), without adequate acclimatization. The incidence depends on the rate of ascent, final altitude reached, sleeping altitude, and duration of exposure.
Acute mountain sickness (AMS) occurs in up to 67% of individuals who ascend rapidly (1–2 days) to elevations above 14,000 ft. Among skiers sleeping at altitude, AMS occurs in approximately 22% at 7,000–9,000 ft and 40% at 10,000 ft.
High-altitude pulmonary edema (HAPE) occurs in fewer than 1–2% of exposed individuals, and high-altitude cerebral edema (HACE) occurs in less than 1%. HAPE and HACE are uncommon below 13,000 ft (≈4,000 m).
Risk Factors
Risk factors for AMS include a prior history of high-altitude illness, rapid ascent, physical exertion, younger age (<50 yr), obesity, and preexisting lung disease. physical fitness does not confer protection.< />pan>
Pregnancy Considerations
The relationship between pregnancy and high-altitude illness is not well defined. Pregnancy-induced hypertension, proteinuria, and peripheral edema are more common at altitude, likely related to maternal hypoxemia. There is no evidence of increased risk of spontaneous abortion or placental complications at moderate altitude. Travel above 13,000 ft should be approached cautiously, especially in complicated pregnancies.
Geriatric Considerations
Although older adults often have comorbidities such as hypertension, COPD, or coronary artery disease, individuals older than 55 years appear to have a lower risk of AMS than younger adults.
Etiology
The primary cause of high-altitude illness is rapid ascent without acclimatization. Susceptibility varies between individuals, and illness is influenced by ascent rate, altitude attained, sleeping altitude, and physiologic response to hypoxia.
Diagnosis
Signs and Symptoms
Acute Mountain Sickness (AMS)
AMS is defined by headache plus at least one of the following: nausea or vomiting, fatigue or lassitude, dizziness, or difficulty sleeping. Symptoms typically begin 4–12 hours after ascent and are usually self-limited but may become debilitating.
High-Altitude Pulmonary Edema (HAPE)
HAPE usually develops 2–4 days after ascent, often on the second night. It is potentially life-threatening and presents with dry cough progressing to productive cough, dyspnea at rest, and decreased exercise tolerance.
High-Altitude Cerebral Edema (HACE)
HACE is life-threatening and typically occurs in patients with AMS and/or HAPE. Onset usually requires 2–4 days but may occur as early as 12 hours after AMS symptoms. Findings include severe headache, nausea and vomiting, altered mental status, and ataxia.
Pediatric Considerations
In infants and young children, AMS may present as irritability, decreased playfulness, reduced appetite, vomiting, and sleep disturbances. HAPE occurs more frequently in individuals younger than 20 years, and cases have not been reported in children younger than 4 years.
Physical Examination
- AMS: Often normal examination; mild cases may mimic viral illness or alcohol hangover.
- HAPE: Tachypnea, rales, cyanosis, possible fever, and signs of respiratory distress.
- HACE: Ataxia, altered mental status, papilledema, retinal hemorrhages, seizures (rare), and coma in severe cases.
Essential Workup
Diagnosis is primarily clinical in the setting of recent altitude gain.
Diagnostic Tests and Interpretation
- AMS: No laboratory or imaging studies required.
- HAPE:
- Arterial blood gas: Hypoxemia (PaO₂ 30–50 mm Hg) with respiratory alkalosis
- Chest radiograph: Patchy alveolar infiltrates with areas of sparing; cardiomegaly and classic signs of cardiogenic pulmonary edema are typically absent
- ECG: Tachycardia, possible right-heart strain
- HACE:
- CT or MRI: Vasogenic edema of the cerebral white matter
Differential Diagnosis
- AMS: Viral syndrome, alcohol hangover, carbon monoxide poisoning, meningitis, encephalitis, exhaustion
- HAPE: Pneumonia, pulmonary embolism (typically more acute with pleuritic chest pain), high-altitude bronchitis
- HACE: Stroke or transient ischemic attack (focal deficits suggest vascular etiology)
Treatment
Prehospital Care
Severe cases require immediate descent. Further ascent is contraindicated in symptomatic individuals. Supplemental oxygen or simulated descent using a portable hyperbaric chamber (e.g., Gamow bag) may be lifesaving when evacuation is delayed.
Initial Stabilization and Therapy
For HAPE and HACE, prioritize airway, breathing, and circulation. Provide supplemental oxygen, establish IV access, and monitor closely. Endotracheal intubation may be required for respiratory failure or airway protection. CPAP may be beneficial in HAPE.
Emergency Department Treatment and Procedures
AMS
Mild cases are usually self-limited. Management includes halting ascent, symptomatic treatment, acetazolamide for moderate to severe symptoms, analgesics for headache, antiemetics for nausea, and oxygen for severe cases. Descent is required if symptoms persist or worsen.
HAPE
Immediate descent is mandatory for moderate to severe disease. Mild cases may be managed at altitude only if oxygen and close monitoring are available. Bed rest, high-flow supplemental oxygen, and avoidance of exertion are critical. Nifedipine may be used when oxygen or descent is unavailable. Hyperbaric therapy may be used when descent is impossible.
HACE
Immediate evacuation to lower altitude is essential. Administer oxygen and dexamethasone. Maintain bed rest with head elevation and manage elevated intracranial pressure aggressively in severe cases.
Medications
- Acetazolamide:
- AMS treatment: 250–500 mg PO BID (peds: 5 mg/kg PO BID)
- AMS prophylaxis: 250 mg PO BID starting 24 hr before ascent
- Dexamethasone: 8 mg IV, then 4 mg PO/IV QID
- Ibuprofen: 800 mg PO TID (peds: 5–10 mg/kg)
- Nifedipine: 10 mg PO, then 30 mg sustained release PO daily
- Promethazine: 12.5–25 mg PO/IM/PR q4–6h
First-Line Therapy
Acetazolamide for AMS, nifedipine for HAPE
Second-Line Therapy
Dexamethasone
Use of multiple medications concurrently is not supported by current evidence.
Follow-Up and Disposition
Admission Criteria
HAPE, HACE, or persistent symptoms after descent and observation require admission.
Discharge Criteria
Patients may be discharged after clinical improvement with oxygen saturation >95% on room air at sea level or appropriate baseline saturation at altitude.
Issues for Referral
Patients with recurrent AMS may benefit from acetazolamide prophylaxis for future ascents. Those with prior HAPE may benefit from nifedipine prophylaxis.
Clinical Pearls and Pitfalls
High-altitude illness often mimics viral syndromes, leading to missed diagnosis. Once symptoms develop, further ascent is contraindicated until complete resolution. Ataxia and dyspnea at rest are early warning signs of HACE and HAPE, respectively. When descent is not possible, hyperbaric therapy and adjunctive medications should be considered promptly.
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Emergency And Acute Medicine – Hiccups
Basics
Description
Hiccups are sudden, involuntary contractions of the diaphragm (usually unilateral) and other inspiratory muscles, abruptly terminated by closure of the glottis. The medical term is singultus. Episodes typically occur at a frequency of 4–60 per minute and result from stimulation of the hiccup reflex arc involving irritation of the vagus and phrenic nerves. The hiccup center is believed to be located in the upper spinal cord or brainstem.
Classification includes hiccup bouts lasting less than 48 hours, persistent hiccups lasting 48 hours to 1 month, and intractable hiccups persisting longer than 1 month. Hiccups are more common in males than females (approximately 4:1).
Etiology
Gastrointestinal causes include gastric distention, overeating, rapid eating, gastroesophageal reflux disease, achalasia, candida esophagitis, esophageal or gastric cancer, ulcers, hepatitis, hepatoma, pancreatitis, pancreatic pseudocyst or cancer, bowel obstruction, inflammatory bowel disease, cholelithiasis, cholecystitis, appendicitis, abdominal aortic aneurysm, and postoperative or post–abdominal procedures.
Diaphragmatic irritation may result from hiatal hernia, intra-abdominal mass, pericarditis, diaphragmatic eventration, splenomegaly, hepatomegaly, or peritonitis.
Central nervous system causes include ischemic or hemorrhagic stroke, head trauma, arteriovenous malformations, encephalitis, meningitis, abscess, malignancy, Parkinson disease, multiple sclerosis, hydrocephalus, and ventriculoperitoneal shunts.
Thoracic causes include pneumonia, tuberculosis, myocardial infarction, pericarditis, aortic aneurysm, malignancy, and mediastinal lymphadenopathy.
Head and neck causes include otic foreign bodies irritating the tympanic membrane, pharyngitis, laryngitis, goiter, retropharyngeal or peritonsillar abscess, and neck masses.
Metabolic causes include uremia, hyponatremia, hypocalcemia, gout, and diabetes mellitus.
Toxic and drug-related causes include alcohol, tobacco, α-methyldopa, benzodiazepines, steroids, barbiturates, narcotics, chemotherapeutic agents, antibiotics, and general anesthesia.
Psychogenic causes include stress, excitement, grief, malingering, and conversion disorder. Many cases remain idiopathic.
Diagnosis
Signs And Symptoms
Hiccups produce a characteristic sound that abruptly ends an inspiratory effort. Attacks usually occur at brief intervals and last seconds to minutes. Episodes persisting longer than 48 hours or continuing during sleep strongly suggest an underlying organic cause.
History
A targeted history should assess the severity and duration of the current episode, prior episodes, previous treatment attempts, and associated symptoms that may suggest an underlying etiology.
Physical Examination
A focused examination should evaluate the head and neck, chest, abdomen, and neurologic system to identify potential causes.
Essential Workup
For persistent or intractable hiccups, further evaluation is guided by findings from the history and physical examination.
Diagnostic Tests And Interpretation
Laboratory evaluation may include a complete blood count with differential and measurement of electrolytes, blood urea nitrogen, and creatinine. A chest radiograph is commonly obtained. Additional imaging or testing should be based on clinical suspicion and is often appropriate for outpatient evaluation.
Differential Diagnosis
Eructation (belching).
Treatment
Emergency Department Treatment And Procedures
Specific causes should be treated when identified, such as removal of an ear foreign body or decompression of gastric distention with a nasogastric tube.
Nonpharmacologic maneuvers include posterior pharyngeal stimulation with a catheter or cotton swab, direct uvular stimulation, supraorbital pressure, carotid sinus massage, digital rectal massage, and suboccipital release with gentle traction and pressure to the posterior neck.
Pharmacologic therapy includes chlorpromazine, the only FDA-approved medication for hiccups. Other agents used include gabapentin, metoclopramide, baclofen, haloperidol, nebulized lidocaine, amitriptyline, and phenytoin.
Medications
Amitriptyline 10 mg PO TID
Baclofen 10 mg PO TID
Chlorpromazine 25–50 mg IV or IM, or 25–50 mg PO BID–TID
Gabapentin 100 mg PO TID–QID
Haloperidol 2–5 mg IM
Lidocaine 4% solution, 3 mL nebulized, may repeat
Metoclopramide 10 mg IV or IM, or 10–20 mg PO QID
Phenytoin 200 mg IV
Follow-Up And Disposition
Admission Criteria
Admission is indicated when hiccups interfere with daily activities or lead to complications such as poor oral intake, aspiration, insomnia, or wound dehiscence.
Discharge Criteria
Patients may be discharged if hiccups last less than 48 hours and evaluation does not suggest an underlying organic cause.
Issues For Referral
Referral is recommended for intractable hiccups requiring further investigation or advanced therapies such as phrenic nerve block or transection, hypnosis, behavioral modification, acupuncture, or psychiatric intervention.
Follow-Up Recommendations
Patients may try home remedies for recurrence, including swallowing a spoonful of sugar, sucking on hard candy, swallowing peanut butter, breath holding or Valsalva maneuver, biting a lemon, tongue traction, lifting the uvula with a cold spoon, drinking from the far side of a glass, applying noxious stimuli, or rebreathing into a paper bag.
Clinical Insights And Common Pitfalls
Prolonged or persistent hiccups are strongly suggestive of an underlying organic disease and should not be dismissed as benign without appropriate evaluation.
Basics
Description
Hiccups are sudden, involuntary contractions of the diaphragm (usually unilateral) and other inspiratory muscles, abruptly terminated by closure of the glottis. The medical term is singultus. Episodes typically occur at a frequency of 4–60 per minute and result from stimulation of the hiccup reflex arc involving irritation of the vagus and phrenic nerves. The hiccup center is believed to be located in the upper spinal cord or brainstem.
Classification includes hiccup bouts lasting less than 48 hours, persistent hiccups lasting 48 hours to 1 month, and intractable hiccups persisting longer than 1 month. Hiccups are more common in males than females (approximately 4:1).
Etiology
Gastrointestinal causes include gastric distention, overeating, rapid eating, gastroesophageal reflux disease, achalasia, candida esophagitis, esophageal or gastric cancer, ulcers, hepatitis, hepatoma, pancreatitis, pancreatic pseudocyst or cancer, bowel obstruction, inflammatory bowel disease, cholelithiasis, cholecystitis, appendicitis, abdominal aortic aneurysm, and postoperative or post–abdominal procedures.
Diaphragmatic irritation may result from hiatal hernia, intra-abdominal mass, pericarditis, diaphragmatic eventration, splenomegaly, hepatomegaly, or peritonitis.
Central nervous system causes include ischemic or hemorrhagic stroke, head trauma, arteriovenous malformations, encephalitis, meningitis, abscess, malignancy, Parkinson disease, multiple sclerosis, hydrocephalus, and ventriculoperitoneal shunts.
Thoracic causes include pneumonia, tuberculosis, myocardial infarction, pericarditis, aortic aneurysm, malignancy, and mediastinal lymphadenopathy.
Head and neck causes include otic foreign bodies irritating the tympanic membrane, pharyngitis, laryngitis, goiter, retropharyngeal or peritonsillar abscess, and neck masses.
Metabolic causes include uremia, hyponatremia, hypocalcemia, gout, and diabetes mellitus.
Toxic and drug-related causes include alcohol, tobacco, α-methyldopa, benzodiazepines, steroids, barbiturates, narcotics, chemotherapeutic agents, antibiotics, and general anesthesia.
Psychogenic causes include stress, excitement, grief, malingering, and conversion disorder. Many cases remain idiopathic.
Diagnosis
Signs And Symptoms
Hiccups produce a characteristic sound that abruptly ends an inspiratory effort. Attacks usually occur at brief intervals and last seconds to minutes. Episodes persisting longer than 48 hours or continuing during sleep strongly suggest an underlying organic cause.
History
A targeted history should assess the severity and duration of the current episode, prior episodes, previous treatment attempts, and associated symptoms that may suggest an underlying etiology.
Physical Examination
A focused examination should evaluate the head and neck, chest, abdomen, and neurologic system to identify potential causes.
Essential Workup
For persistent or intractable hiccups, further evaluation is guided by findings from the history and physical examination.
Diagnostic Tests And Interpretation
Laboratory evaluation may include a complete blood count with differential and measurement of electrolytes, blood urea nitrogen, and creatinine. A chest radiograph is commonly obtained. Additional imaging or testing should be based on clinical suspicion and is often appropriate for outpatient evaluation.
Differential Diagnosis
Eructation (belching).
Treatment
Emergency Department Treatment And Procedures
Specific causes should be treated when identified, such as removal of an ear foreign body or decompression of gastric distention with a nasogastric tube.
Nonpharmacologic maneuvers include posterior pharyngeal stimulation with a catheter or cotton swab, direct uvular stimulation, supraorbital pressure, carotid sinus massage, digital rectal massage, and suboccipital release with gentle traction and pressure to the posterior neck.
Pharmacologic therapy includes chlorpromazine, the only FDA-approved medication for hiccups. Other agents used include gabapentin, metoclopramide, baclofen, haloperidol, nebulized lidocaine, amitriptyline, and phenytoin.
Medications
Amitriptyline 10 mg PO TID
Baclofen 10 mg PO TID
Chlorpromazine 25–50 mg IV or IM, or 25–50 mg PO BID–TID
Gabapentin 100 mg PO TID–QID
Haloperidol 2–5 mg IM
Lidocaine 4% solution, 3 mL nebulized, may repeat
Metoclopramide 10 mg IV or IM, or 10–20 mg PO QID
Phenytoin 200 mg IV
Follow-Up And Disposition
Admission Criteria
Admission is indicated when hiccups interfere with daily activities or lead to complications such as poor oral intake, aspiration, insomnia, or wound dehiscence.
Discharge Criteria
Patients may be discharged if hiccups last less than 48 hours and evaluation does not suggest an underlying organic cause.
Issues For Referral
Referral is recommended for intractable hiccups requiring further investigation or advanced therapies such as phrenic nerve block or transection, hypnosis, behavioral modification, acupuncture, or psychiatric intervention.
Follow-Up Recommendations
Patients may try home remedies for recurrence, including swallowing a spoonful of sugar, sucking on hard candy, swallowing peanut butter, breath holding or Valsalva maneuver, biting a lemon, tongue traction, lifting the uvula with a cold spoon, drinking from the far side of a glass, applying noxious stimuli, or rebreathing into a paper bag.
Clinical Insights And Common Pitfalls
Prolonged or persistent hiccups are strongly suggestive of an underlying organic disease and should not be dismissed as benign without appropriate evaluation.
- Published on
Emergency And Acute Medicine – Genital Herpes
Overview And Definition
Genital herpes is a lifelong, recurrent viral infection caused by herpes simplex virus (HSV). Approximately one in four Americans older than 30 years are seropositive for HSV-2, though most are asymptomatic. The infection is characterized by periods of latency and reactivation, with viral shedding that can occur even in the absence of visible lesions, contributing to ongoing transmission.
Disease Course And Natural History
Primary infection has an incubation period of approximately 2–12 days, with symptoms typically peaking 8–10 days after onset and lesions healing within about three weeks. Primary disease may present with a more severe clinical syndrome and complications such as meningitis, encephalitis, or hepatitis. Importantly, more than half of first recognized episodes are not true primary infections, as earlier asymptomatic exposure is common.
Recurrent infection results from viral reactivation in the dorsal root ganglia. The average patient experiences about four recurrences per year. Recurrences are generally milder, involve fewer lesions, and resolve within 10 days. HSV-1 genital infections recur significantly less often than HSV-2.
Asymptomatic infection is common, with intermittent viral shedding that frequently leads to transmission by individuals without symptoms or lesions.
Etiology And Risk Factors
Most cases (70–90%) of genital herpes are caused by HSV-2, with the remainder caused by HSV-1. Genital HSV-1 infections are increasing in prevalence, likely due to higher rates of oral–genital contact and reduced childhood exposure to HSV-1, leaving more adolescents and adults susceptible. Acquisition of HSV-2 in individuals with prior HSV-1 infection tends to be less symptomatic, whereas acquisition of HSV-1 in those with HSV-2 is uncommon.
Genital herpes is strongly associated with HIV and other sexually transmitted infections. HSV infection increases both susceptibility to HIV and HIV viral shedding during HSV reactivation. Despite extensive research, no effective HSV vaccine is currently available.
Clinical Manifestations
Patients commonly report local pain, itching, or burning. A prodrome of tingling, itching, or pain may occur 1–2 days before lesion eruption and can sometimes mimic radicular pain such as sciatica. Lesions typically begin as macules and papules, progress to vesicles and pustules, and then ulcerate by approximately day five. Skin lesions crust over, whereas mucosal lesions heal without crusting.
Associated manifestations may include herpetic cervicitis, vaginitis, or urethritis, presenting with dysuria, urinary hesitancy or retention, vaginal discharge, or pelvic pain. Systemic symptoms such as fever, malaise, headache, myalgias, photophobia, anorexia, and lymphadenopathy are more common during primary infection.
Physical Examination Findings
Examination may reveal grouped vesicles on an erythematous base involving the vulva, vagina, cervix, perineum, buttocks, penile shaft, or glans. On moist mucosal surfaces, ulcers may predominate. Atypical findings include localized edema, erythema, fissures, or crusts.
Special Populations
Pediatric patients with genital herpes require careful evaluation, as neonatal infection is often disseminated or involves the central nervous system and carries high morbidity and mortality. Congenital HSV infection without vesicles may resemble other congenital infections. Sexual abuse must be considered in children with genital HSV, and evaluation for other sexually transmitted infections is recommended.
Pregnancy is a high-risk context, particularly with primary infection, which is associated with significant neonatal morbidity. Suppressive antiviral therapy after 36 weeks’ gestation reduces lesion recurrence at delivery and lowers cesarean section rates.
Diagnostic Approach
Diagnosis is usually clinical, based on history and examination. Laboratory testing is useful when confirmation is needed or in atypical or severe cases. Viral culture from vesicle fluid or ulcer base is positive in most early lesions but loses sensitivity as lesions heal. PCR testing is more sensitive and is the diagnostic test of choice, especially for central nervous system involvement. Serologic testing detects prior exposure but is not useful for diagnosing acute disease, as it cannot distinguish recent from chronic infection.
Differential Diagnosis
Important considerations include syphilis, chancroid, lymphogranuloma venereum, granuloma inguinale, candidiasis, and Behçet syndrome.
Emergency Management
Treatment reduces symptom severity and duration but does not eradicate latent virus or prevent future recurrences once therapy is stopped.
Episodic therapy for recurrences shortens lesion duration if started during the prodrome or within one day of lesion onset.
Suppressive therapy, recommended for patients with frequent recurrences (six or more per year), reduces recurrence frequency by approximately 75% and decreases viral shedding.
Severe disease, systemic involvement, or infection in immunocompromised patients requires intravenous antiviral therapy. Resistance to acyclovir occurs in a minority of immunocompromised patients, in which case foscarnet may be effective. Women with urinary retention may require bladder catheterization due to sacral nerve involvement.
Pharmacologic Treatment
First-episode, recurrent, suppressive, and HIV-associated genital herpes are treated with oral or intravenous acyclovir, valacyclovir, or famciclovir, with regimen selection based on severity, immune status, and recurrence pattern. Dosing adjustments may be necessary in renal impairment.
Disposition And Counseling
Hospital admission is indicated for patients with central nervous system involvement, disseminated disease, severe pain or urinary retention, or significant immunosuppression. Immunocompetent patients without systemic involvement can be managed as outpatients.
Discharge counseling is essential and should emphasize avoidance of sexual contact during prodrome and active lesions, consistent use of barrier protection even when asymptomatic, and the lifelong nature of infection. Patients should be informed about the likelihood of recurrence and the option of suppressive therapy.
Key Clinical Pearls
Primary genital herpes may be severe and should be treated promptly. Always consider sexual abuse in children presenting with genital HSV. Genital herpes is lifelong, with intermittent asymptomatic shedding that plays a major role in transmission.
Overview And Definition
Genital herpes is a lifelong, recurrent viral infection caused by herpes simplex virus (HSV). Approximately one in four Americans older than 30 years are seropositive for HSV-2, though most are asymptomatic. The infection is characterized by periods of latency and reactivation, with viral shedding that can occur even in the absence of visible lesions, contributing to ongoing transmission.
Disease Course And Natural History
Primary infection has an incubation period of approximately 2–12 days, with symptoms typically peaking 8–10 days after onset and lesions healing within about three weeks. Primary disease may present with a more severe clinical syndrome and complications such as meningitis, encephalitis, or hepatitis. Importantly, more than half of first recognized episodes are not true primary infections, as earlier asymptomatic exposure is common.
Recurrent infection results from viral reactivation in the dorsal root ganglia. The average patient experiences about four recurrences per year. Recurrences are generally milder, involve fewer lesions, and resolve within 10 days. HSV-1 genital infections recur significantly less often than HSV-2.
Asymptomatic infection is common, with intermittent viral shedding that frequently leads to transmission by individuals without symptoms or lesions.
Etiology And Risk Factors
Most cases (70–90%) of genital herpes are caused by HSV-2, with the remainder caused by HSV-1. Genital HSV-1 infections are increasing in prevalence, likely due to higher rates of oral–genital contact and reduced childhood exposure to HSV-1, leaving more adolescents and adults susceptible. Acquisition of HSV-2 in individuals with prior HSV-1 infection tends to be less symptomatic, whereas acquisition of HSV-1 in those with HSV-2 is uncommon.
Genital herpes is strongly associated with HIV and other sexually transmitted infections. HSV infection increases both susceptibility to HIV and HIV viral shedding during HSV reactivation. Despite extensive research, no effective HSV vaccine is currently available.
Clinical Manifestations
Patients commonly report local pain, itching, or burning. A prodrome of tingling, itching, or pain may occur 1–2 days before lesion eruption and can sometimes mimic radicular pain such as sciatica. Lesions typically begin as macules and papules, progress to vesicles and pustules, and then ulcerate by approximately day five. Skin lesions crust over, whereas mucosal lesions heal without crusting.
Associated manifestations may include herpetic cervicitis, vaginitis, or urethritis, presenting with dysuria, urinary hesitancy or retention, vaginal discharge, or pelvic pain. Systemic symptoms such as fever, malaise, headache, myalgias, photophobia, anorexia, and lymphadenopathy are more common during primary infection.
Physical Examination Findings
Examination may reveal grouped vesicles on an erythematous base involving the vulva, vagina, cervix, perineum, buttocks, penile shaft, or glans. On moist mucosal surfaces, ulcers may predominate. Atypical findings include localized edema, erythema, fissures, or crusts.
Special Populations
Pediatric patients with genital herpes require careful evaluation, as neonatal infection is often disseminated or involves the central nervous system and carries high morbidity and mortality. Congenital HSV infection without vesicles may resemble other congenital infections. Sexual abuse must be considered in children with genital HSV, and evaluation for other sexually transmitted infections is recommended.
Pregnancy is a high-risk context, particularly with primary infection, which is associated with significant neonatal morbidity. Suppressive antiviral therapy after 36 weeks’ gestation reduces lesion recurrence at delivery and lowers cesarean section rates.
Diagnostic Approach
Diagnosis is usually clinical, based on history and examination. Laboratory testing is useful when confirmation is needed or in atypical or severe cases. Viral culture from vesicle fluid or ulcer base is positive in most early lesions but loses sensitivity as lesions heal. PCR testing is more sensitive and is the diagnostic test of choice, especially for central nervous system involvement. Serologic testing detects prior exposure but is not useful for diagnosing acute disease, as it cannot distinguish recent from chronic infection.
Differential Diagnosis
Important considerations include syphilis, chancroid, lymphogranuloma venereum, granuloma inguinale, candidiasis, and Behçet syndrome.
Emergency Management
Treatment reduces symptom severity and duration but does not eradicate latent virus or prevent future recurrences once therapy is stopped.
Episodic therapy for recurrences shortens lesion duration if started during the prodrome or within one day of lesion onset.
Suppressive therapy, recommended for patients with frequent recurrences (six or more per year), reduces recurrence frequency by approximately 75% and decreases viral shedding.
Severe disease, systemic involvement, or infection in immunocompromised patients requires intravenous antiviral therapy. Resistance to acyclovir occurs in a minority of immunocompromised patients, in which case foscarnet may be effective. Women with urinary retention may require bladder catheterization due to sacral nerve involvement.
Pharmacologic Treatment
First-episode, recurrent, suppressive, and HIV-associated genital herpes are treated with oral or intravenous acyclovir, valacyclovir, or famciclovir, with regimen selection based on severity, immune status, and recurrence pattern. Dosing adjustments may be necessary in renal impairment.
Disposition And Counseling
Hospital admission is indicated for patients with central nervous system involvement, disseminated disease, severe pain or urinary retention, or significant immunosuppression. Immunocompetent patients without systemic involvement can be managed as outpatients.
Discharge counseling is essential and should emphasize avoidance of sexual contact during prodrome and active lesions, consistent use of barrier protection even when asymptomatic, and the lifelong nature of infection. Patients should be informed about the likelihood of recurrence and the option of suppressive therapy.
Key Clinical Pearls
Primary genital herpes may be severe and should be treated promptly. Always consider sexual abuse in children presenting with genital HSV. Genital herpes is lifelong, with intermittent asymptomatic shedding that plays a major role in transmission.
- Published on
Emergency And Acute Medicine – Herpes Simplex
Definition And Overview
Herpes simplex is a viral disease characterized by recurrent, painful vesicular lesions involving mucocutaneous surfaces. Commonly affected sites include the lips, oral cavity, genitalia, rectum, hands, and eyes. Infection occurs in two phases: a primary phase during which the virus establishes latency within sensory nerve ganglia, and a secondary phase marked by recurrent reactivation at the same anatomic site. The incubation period is approximately four days after exposure. Viral shedding lasts about 7–10 days in primary infection (up to 23 days) and 3–4 days during recurrences. Neonatal infection may occur in utero, intrapartum (most commonly), or postnatally, with an incidence of approximately 1 in 3,500 births annually in the United States. Transmission is human-to-human, and 60–90% of the population is infected with herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2). Infection is more common in Black populations than White populations under 40 years of age, and females are affected more frequently than males.
Etiology And Virology
HSV-1 and HSV-2 are DNA viruses belonging to the Herpesviridae family. Transmission occurs through contact with infected secretions via mucous membranes or abraded skin, as well as through respiratory droplets. Recurrent asymptomatic mucosal shedding can transmit infection. HSV-1 most commonly causes oral infections, while HSV-2 more frequently causes genital disease, though either virus may infect oral or genital mucosa. Recurrence rates vary depending on viral type and anatomic location; HSV-2 genital infections recur more frequently than HSV-1 genital infections, and HSV-1 oral infections recur more often than genital HSV-1 infections.
Clinical Manifestations
Many primary infections are subclinical and detected only by serologic evidence of antibodies. Symptomatic disease typically presents with grouped 1–2 mm vesicles on an erythematous base, containing clear or cloudy fluid or appearing pustular.
Orofacial Disease
Primary orofacial infection often manifests as gingivostomatitis or pharyngitis with ulcerative lesions of the gingiva and mucosa. Associated symptoms include fever, malaise, irritability, headache, myalgias, and cervical lymphadenopathy. Symptoms may last two to four weeks and usually heal without scarring. Pain may limit oral intake, increasing the risk of dehydration.
Recurrent disease typically involves the lips, especially the vermilion border, and is often preceded by a prodrome of tingling, itching, burning, or throbbing. Triggers include sunlight, stress, heat, trauma, and immunosuppression. Lesions progress from erythema to vesicle, ulcer, crusting, and healing. Transmission can occur even without visible lesions.
Cutaneous Disease
Herpetic whitlow involves infection of the fingers, most commonly caused by HSV-2, and presents with vesicles on the pulp or lateral finger. It may occur from autoinoculation or occupational exposure and can last three to four weeks.
Traumatic herpes may develop after cosmetic, surgical, dental procedures, sun exposure, or burns.
Herpes gladiatorum is a cutaneous infection seen in athletes, particularly wrestlers, affecting the face, chest, and hands.
Eczema herpeticum is a disseminated HSV infection occurring in patients with atopic dermatitis, often associated with fever, headache, fatigue, and risk of secondary bacterial infection.
Ocular Disease
HSV is the most common cause of corneal blindness in developed countries. Infection may result from direct inoculation or spread from facial lesions. Symptoms include eye pain, photophobia, blurry vision, conjunctivitis, chemosis, and periauricular lymphadenopathy. Dendritic corneal lesions are seen on fluorescein examination. Vesicles on the tip of the nose (Hutchinson sign) suggest involvement of the nasociliary nerve and increased risk of ocular disease.
Central Nervous System Involvement
HSV encephalitis is the most common cause of severe sporadic encephalitis in the Western world, usually due to HSV-1 reactivation. Patients may present with altered mental status, seizures, focal neurologic deficits, or coma, with or without a history of mucocutaneous herpes.
Special Populations
In neonates, up to 60–80% of infected infants are born to mothers without known genital herpes. Vesicular lesions may be absent initially. Primary maternal genital infection carries the highest risk of neonatal transmission.
In children, primary infection often occurs early in life, with gingivostomatitis being the most common presentation in those under five years of age.
In pregnancy, suppressive antiviral therapy near term may reduce recurrence and viral shedding.
Diagnostic Evaluation
Diagnosis is often clinical based on history and examination. Definitive testing is indicated in severe disease, immunocompromised patients, suspected abuse, ocular involvement, or CNS disease. PCR testing of vesicular fluid is the most sensitive and specific diagnostic method. Viral culture, fluorescent antibody detection, and Tzanck smear may also be used.
Ocular disease requires fluorescein examination, and CNS disease requires lumbar puncture with CSF PCR, along with neuroimaging.
Differential Diagnosis
Conditions to consider include bacterial pharyngitis, Stevens–Johnson syndrome, herpes zoster, varicella, impetigo, syphilis, contact dermatitis, conjunctivitis, corneal abrasion, glaucoma, and other causes of encephalitis.
Emergency Management
Supportive care with hydration and analgesia is sufficient for mild primary infections in immunocompetent patients. Antiviral therapy is indicated for severe primary disease, recurrent infections with significant symptoms, immunocompromised patients, ocular disease, neonatal infection, and encephalitis. Incision and drainage of herpetic lesions should be avoided. Ocular involvement requires urgent ophthalmology consultation, and corticosteroids should not be used.
Pharmacologic Therapy
First-line treatment includes acyclovir, valacyclovir, or famciclovir. Acyclovir is preferred in children and severe disease. Encephalitis requires high-dose IV acyclovir for 14–21 days. Long-term suppressive therapy may be used for frequent recurrences. Antiviral dosing should be adjusted in renal impairment.
Disposition And Follow-Up
Hospital admission is required for encephalitis, neonatal infection, disseminated disease, severe dehydration, immunocompromised patients, and significant ocular involvement. Uncomplicated localized disease may be managed on an outpatient basis. Patients should be counseled on transmission risk, avoidance of contact with lesions, and indications for suppressive therapy.
Clinical Pearls And Pitfalls
Failure to recognize HSV encephalitis or ocular herpes can result in significant morbidity. Transmission may occur without visible lesions. Patients should be warned about autoinoculation and spread to others, especially during outbreaks. Avoid topical or systemic steroids unless specifically indicated and supervised.
Definition And Overview
Herpes simplex is a viral disease characterized by recurrent, painful vesicular lesions involving mucocutaneous surfaces. Commonly affected sites include the lips, oral cavity, genitalia, rectum, hands, and eyes. Infection occurs in two phases: a primary phase during which the virus establishes latency within sensory nerve ganglia, and a secondary phase marked by recurrent reactivation at the same anatomic site. The incubation period is approximately four days after exposure. Viral shedding lasts about 7–10 days in primary infection (up to 23 days) and 3–4 days during recurrences. Neonatal infection may occur in utero, intrapartum (most commonly), or postnatally, with an incidence of approximately 1 in 3,500 births annually in the United States. Transmission is human-to-human, and 60–90% of the population is infected with herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2). Infection is more common in Black populations than White populations under 40 years of age, and females are affected more frequently than males.
Etiology And Virology
HSV-1 and HSV-2 are DNA viruses belonging to the Herpesviridae family. Transmission occurs through contact with infected secretions via mucous membranes or abraded skin, as well as through respiratory droplets. Recurrent asymptomatic mucosal shedding can transmit infection. HSV-1 most commonly causes oral infections, while HSV-2 more frequently causes genital disease, though either virus may infect oral or genital mucosa. Recurrence rates vary depending on viral type and anatomic location; HSV-2 genital infections recur more frequently than HSV-1 genital infections, and HSV-1 oral infections recur more often than genital HSV-1 infections.
Clinical Manifestations
Many primary infections are subclinical and detected only by serologic evidence of antibodies. Symptomatic disease typically presents with grouped 1–2 mm vesicles on an erythematous base, containing clear or cloudy fluid or appearing pustular.
Orofacial Disease
Primary orofacial infection often manifests as gingivostomatitis or pharyngitis with ulcerative lesions of the gingiva and mucosa. Associated symptoms include fever, malaise, irritability, headache, myalgias, and cervical lymphadenopathy. Symptoms may last two to four weeks and usually heal without scarring. Pain may limit oral intake, increasing the risk of dehydration.
Recurrent disease typically involves the lips, especially the vermilion border, and is often preceded by a prodrome of tingling, itching, burning, or throbbing. Triggers include sunlight, stress, heat, trauma, and immunosuppression. Lesions progress from erythema to vesicle, ulcer, crusting, and healing. Transmission can occur even without visible lesions.
Cutaneous Disease
Herpetic whitlow involves infection of the fingers, most commonly caused by HSV-2, and presents with vesicles on the pulp or lateral finger. It may occur from autoinoculation or occupational exposure and can last three to four weeks.
Traumatic herpes may develop after cosmetic, surgical, dental procedures, sun exposure, or burns.
Herpes gladiatorum is a cutaneous infection seen in athletes, particularly wrestlers, affecting the face, chest, and hands.
Eczema herpeticum is a disseminated HSV infection occurring in patients with atopic dermatitis, often associated with fever, headache, fatigue, and risk of secondary bacterial infection.
Ocular Disease
HSV is the most common cause of corneal blindness in developed countries. Infection may result from direct inoculation or spread from facial lesions. Symptoms include eye pain, photophobia, blurry vision, conjunctivitis, chemosis, and periauricular lymphadenopathy. Dendritic corneal lesions are seen on fluorescein examination. Vesicles on the tip of the nose (Hutchinson sign) suggest involvement of the nasociliary nerve and increased risk of ocular disease.
Central Nervous System Involvement
HSV encephalitis is the most common cause of severe sporadic encephalitis in the Western world, usually due to HSV-1 reactivation. Patients may present with altered mental status, seizures, focal neurologic deficits, or coma, with or without a history of mucocutaneous herpes.
Special Populations
In neonates, up to 60–80% of infected infants are born to mothers without known genital herpes. Vesicular lesions may be absent initially. Primary maternal genital infection carries the highest risk of neonatal transmission.
In children, primary infection often occurs early in life, with gingivostomatitis being the most common presentation in those under five years of age.
In pregnancy, suppressive antiviral therapy near term may reduce recurrence and viral shedding.
Diagnostic Evaluation
Diagnosis is often clinical based on history and examination. Definitive testing is indicated in severe disease, immunocompromised patients, suspected abuse, ocular involvement, or CNS disease. PCR testing of vesicular fluid is the most sensitive and specific diagnostic method. Viral culture, fluorescent antibody detection, and Tzanck smear may also be used.
Ocular disease requires fluorescein examination, and CNS disease requires lumbar puncture with CSF PCR, along with neuroimaging.
Differential Diagnosis
Conditions to consider include bacterial pharyngitis, Stevens–Johnson syndrome, herpes zoster, varicella, impetigo, syphilis, contact dermatitis, conjunctivitis, corneal abrasion, glaucoma, and other causes of encephalitis.
Emergency Management
Supportive care with hydration and analgesia is sufficient for mild primary infections in immunocompetent patients. Antiviral therapy is indicated for severe primary disease, recurrent infections with significant symptoms, immunocompromised patients, ocular disease, neonatal infection, and encephalitis. Incision and drainage of herpetic lesions should be avoided. Ocular involvement requires urgent ophthalmology consultation, and corticosteroids should not be used.
Pharmacologic Therapy
First-line treatment includes acyclovir, valacyclovir, or famciclovir. Acyclovir is preferred in children and severe disease. Encephalitis requires high-dose IV acyclovir for 14–21 days. Long-term suppressive therapy may be used for frequent recurrences. Antiviral dosing should be adjusted in renal impairment.
Disposition And Follow-Up
Hospital admission is required for encephalitis, neonatal infection, disseminated disease, severe dehydration, immunocompromised patients, and significant ocular involvement. Uncomplicated localized disease may be managed on an outpatient basis. Patients should be counseled on transmission risk, avoidance of contact with lesions, and indications for suppressive therapy.
Clinical Pearls And Pitfalls
Failure to recognize HSV encephalitis or ocular herpes can result in significant morbidity. Transmission may occur without visible lesions. Patients should be warned about autoinoculation and spread to others, especially during outbreaks. Avoid topical or systemic steroids unless specifically indicated and supervised.
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Emergency And Acute Medicine – Herpes Zoster
Definition And Overview
Herpes zoster, commonly known as shingles, is characterized by a unilateral eruption of painful vesicles distributed along a single dermatome. It results from reactivation of latent varicella zoster virus (VZV) in dorsal root ganglia. Dissemination is rare in immunocompetent hosts but occurs more frequently in immunocompromised patients. The disease is most common in individuals with impaired cell-mediated immunity, particularly adults older than 50 years, patients with malignancy, and those receiving immunosuppressive therapy.
Etiology And Risk Factors
Herpes zoster is caused by reactivation of VZV, a DNA virus in the Herpesviridae family. Most cases occur in individuals with a history of primary varicella (chickenpox), and only rarely in vaccinated individuals. Declining cell-mediated immunity with aging or immunosuppression is the primary risk factor.
Pregnancy is not associated with an increased risk of congenital varicella syndrome. In children, herpes zoster may occur following in utero exposure or primary varicella infection during the first six months of life.
Clinical Features
Dermatomal zoster typically begins with a prodrome of pain, paresthesias, or pruritus in the affected dermatome, occurring in approximately 75% of patients. Pain may be sharp, burning, tingling, or severe. The classic rash consists of grouped vesicles on an erythematous base, which progress to crusting over 7–10 days, with complete resolution in 2–3 weeks. Thoracic and lumbar dermatomes are most commonly involved, followed by trigeminal and cervical distributions.
Zoster sine herpete presents with dermatomal pain without rash and can be diagnostically challenging.
Herpes zoster ophthalmicus results from involvement of the ophthalmic division of the trigeminal nerve. Hutchinson sign, defined as vesicles on the tip of the nose, suggests nasociliary nerve involvement and increased risk of ocular complications. Ocular findings may include punctate keratitis or corneal pseudodendrites, which are less ulcerative and show less fluorescein uptake than HSV dendrites.
Ramsay Hunt syndrome is caused by involvement of cranial nerves VII and VIII and presents with vesicles in the external auditory canal, peripheral facial palsy, vertigo, and altered sensation of the anterior two-thirds of the tongue.
Disseminated disease may occur, particularly in immunocompromised patients, and can involve the central nervous system, liver, or lungs, leading to complications such as meningoencephalitis, myelitis, hepatitis, pneumonitis, and peripheral neuropathy.
Postherpetic neuralgia is defined as pain persisting at the site of zoster lesions for more than three months after cutaneous healing. It occurs in 10–70% of patients, with risk increasing in those older than 50 years and in patients with severe initial rash or pain.
Diagnostic Evaluation
Diagnosis is primarily clinical in typical presentations. Laboratory testing is reserved for atypical cases, disseminated disease, or immunocompromised patients. Tzanck smear may show multinucleated giant cells but cannot distinguish VZV from HSV and has low sensitivity. PCR testing from vesicle fluid, blood, cerebrospinal fluid, or bronchoalveolar lavage is the preferred diagnostic method due to high sensitivity and specificity. Serologic testing is less reliable in the acute setting, and viral culture is slow and insensitive.
Differential Diagnosis
Conditions to consider include primary varicella, herpes simplex infection, cellulitis, allergic contact dermatitis, bullous impetigo, molluscum contagiosum, insect bites, trigeminal neuralgia, radiculopathy, biliary or renal colic, Bell palsy, peripheral vertigo, conjunctivitis, and HSV keratitis.
Emergency Management
Herpes zoster is usually self-limited. Management focuses on reducing pain, shortening disease duration, and preventing postherpetic neuralgia. Lesions should be covered, and universal precautions maintained, as zoster can transmit varicella to nonimmune individuals.
In immunocompetent patients, oral antiviral therapy should be initiated within 72 hours of rash onset, though treatment may still be beneficial if new lesions are forming. Valacyclovir is preferred for ease of dosing, though acyclovir or famciclovir are acceptable alternatives. Analgesia should be tailored to pain severity, ranging from nonsteroidal anti-inflammatory drugs to opioids. Corticosteroids remain controversial and may modestly improve acute pain and rash healing but do not prevent postherpetic neuralgia.
Immunocompromised patients require intravenous acyclovir and close monitoring.
Herpes zoster ophthalmicus requires urgent ophthalmology consultation. Oral antivirals are indicated, with intravenous therapy for immunocompromised patients or those with cranial nerve involvement.
Postherpetic neuralgia is managed with analgesics, tricyclic antidepressants, gabapentin or pregabalin, and topical lidocaine; antivirals are not effective once PHN is established.
Postexposure Prophylaxis And Prevention
Varicella zoster immune globulin (VariZIG) is recommended within 72 hours of exposure for immunocompromised patients, pregnant individuals, and certain neonates. The live-attenuated zoster vaccine is recommended for adults over 60 years of age but is contraindicated in pregnancy and immunocompromised patients. Vaccination does not treat active disease or prevent postherpetic neuralgia in those with established zoster.
Disposition And Follow-Up
Most patients can be managed as outpatients. Admission is indicated for immunocompromised patients, disseminated disease, severe or intractable pain, neonatal infection, or herpes zoster ophthalmicus with cranial nerve involvement. Patients should be advised to avoid contact with pregnant or immunocompromised individuals until all lesions have crusted. Long-term follow-up may be required for management of postherpetic neuralgia.
Clinical Pearls And Pitfalls
Always assess for ocular involvement when lesions appear on the tip of the nose. Consider herpes zoster in patients with unexplained dermatomal pain, even in the absence of rash. Fully expose the skin in patients presenting with chest or abdominal pain. Counsel patients early about the risk and chronic nature of postherpetic neuralgia.
Definition And Overview
Herpes zoster, commonly known as shingles, is characterized by a unilateral eruption of painful vesicles distributed along a single dermatome. It results from reactivation of latent varicella zoster virus (VZV) in dorsal root ganglia. Dissemination is rare in immunocompetent hosts but occurs more frequently in immunocompromised patients. The disease is most common in individuals with impaired cell-mediated immunity, particularly adults older than 50 years, patients with malignancy, and those receiving immunosuppressive therapy.
Etiology And Risk Factors
Herpes zoster is caused by reactivation of VZV, a DNA virus in the Herpesviridae family. Most cases occur in individuals with a history of primary varicella (chickenpox), and only rarely in vaccinated individuals. Declining cell-mediated immunity with aging or immunosuppression is the primary risk factor.
Pregnancy is not associated with an increased risk of congenital varicella syndrome. In children, herpes zoster may occur following in utero exposure or primary varicella infection during the first six months of life.
Clinical Features
Dermatomal zoster typically begins with a prodrome of pain, paresthesias, or pruritus in the affected dermatome, occurring in approximately 75% of patients. Pain may be sharp, burning, tingling, or severe. The classic rash consists of grouped vesicles on an erythematous base, which progress to crusting over 7–10 days, with complete resolution in 2–3 weeks. Thoracic and lumbar dermatomes are most commonly involved, followed by trigeminal and cervical distributions.
Zoster sine herpete presents with dermatomal pain without rash and can be diagnostically challenging.
Herpes zoster ophthalmicus results from involvement of the ophthalmic division of the trigeminal nerve. Hutchinson sign, defined as vesicles on the tip of the nose, suggests nasociliary nerve involvement and increased risk of ocular complications. Ocular findings may include punctate keratitis or corneal pseudodendrites, which are less ulcerative and show less fluorescein uptake than HSV dendrites.
Ramsay Hunt syndrome is caused by involvement of cranial nerves VII and VIII and presents with vesicles in the external auditory canal, peripheral facial palsy, vertigo, and altered sensation of the anterior two-thirds of the tongue.
Disseminated disease may occur, particularly in immunocompromised patients, and can involve the central nervous system, liver, or lungs, leading to complications such as meningoencephalitis, myelitis, hepatitis, pneumonitis, and peripheral neuropathy.
Postherpetic neuralgia is defined as pain persisting at the site of zoster lesions for more than three months after cutaneous healing. It occurs in 10–70% of patients, with risk increasing in those older than 50 years and in patients with severe initial rash or pain.
Diagnostic Evaluation
Diagnosis is primarily clinical in typical presentations. Laboratory testing is reserved for atypical cases, disseminated disease, or immunocompromised patients. Tzanck smear may show multinucleated giant cells but cannot distinguish VZV from HSV and has low sensitivity. PCR testing from vesicle fluid, blood, cerebrospinal fluid, or bronchoalveolar lavage is the preferred diagnostic method due to high sensitivity and specificity. Serologic testing is less reliable in the acute setting, and viral culture is slow and insensitive.
Differential Diagnosis
Conditions to consider include primary varicella, herpes simplex infection, cellulitis, allergic contact dermatitis, bullous impetigo, molluscum contagiosum, insect bites, trigeminal neuralgia, radiculopathy, biliary or renal colic, Bell palsy, peripheral vertigo, conjunctivitis, and HSV keratitis.
Emergency Management
Herpes zoster is usually self-limited. Management focuses on reducing pain, shortening disease duration, and preventing postherpetic neuralgia. Lesions should be covered, and universal precautions maintained, as zoster can transmit varicella to nonimmune individuals.
In immunocompetent patients, oral antiviral therapy should be initiated within 72 hours of rash onset, though treatment may still be beneficial if new lesions are forming. Valacyclovir is preferred for ease of dosing, though acyclovir or famciclovir are acceptable alternatives. Analgesia should be tailored to pain severity, ranging from nonsteroidal anti-inflammatory drugs to opioids. Corticosteroids remain controversial and may modestly improve acute pain and rash healing but do not prevent postherpetic neuralgia.
Immunocompromised patients require intravenous acyclovir and close monitoring.
Herpes zoster ophthalmicus requires urgent ophthalmology consultation. Oral antivirals are indicated, with intravenous therapy for immunocompromised patients or those with cranial nerve involvement.
Postherpetic neuralgia is managed with analgesics, tricyclic antidepressants, gabapentin or pregabalin, and topical lidocaine; antivirals are not effective once PHN is established.
Postexposure Prophylaxis And Prevention
Varicella zoster immune globulin (VariZIG) is recommended within 72 hours of exposure for immunocompromised patients, pregnant individuals, and certain neonates. The live-attenuated zoster vaccine is recommended for adults over 60 years of age but is contraindicated in pregnancy and immunocompromised patients. Vaccination does not treat active disease or prevent postherpetic neuralgia in those with established zoster.
Disposition And Follow-Up
Most patients can be managed as outpatients. Admission is indicated for immunocompromised patients, disseminated disease, severe or intractable pain, neonatal infection, or herpes zoster ophthalmicus with cranial nerve involvement. Patients should be advised to avoid contact with pregnant or immunocompromised individuals until all lesions have crusted. Long-term follow-up may be required for management of postherpetic neuralgia.
Clinical Pearls And Pitfalls
Always assess for ocular involvement when lesions appear on the tip of the nose. Consider herpes zoster in patients with unexplained dermatomal pain, even in the absence of rash. Fully expose the skin in patients presenting with chest or abdominal pain. Counsel patients early about the risk and chronic nature of postherpetic neuralgia.
