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Emergency And Acute Medicine - Gastric Outlet Obstruction
Core Overview
Gastric outlet obstruction refers to any condition that impedes the passage of gastric contents into the duodenum. The underlying cause may originate from the stomach, duodenum, or extraluminal structures. Both benign and malignant etiologies are implicated, with malignancy being the most common cause in adults. Neoplasms may be intrinsic or extrinsic, including pancreatic tumors, gastric lymphoma, duodenal tumors, and gallbladder cancer, which can compress the pylorus or proximal duodenum. Peptic ulcer disease is no longer the leading adult cause due to effective Helicobacter pylori treatment and acid suppression therapy. In children, hypertrophic pyloric stenosis is the most common cause. Additional mechanisms include postoperative complications, gastric volvulus, polyps, bezoars, duplication cysts, and pyloric or duodenal edema, scarring, strictures, webs, or hyperplasia related to caustic injury or chronic pancreatitis.
Pathophysiologic Basis
Regardless of etiology, gastric outlet obstruction leads to impaired gastric emptying, resulting in nausea and predominantly nonbilious vomiting. Persistent emesis causes dehydration and electrolyte abnormalities, particularly hypokalemic, hypochloremic metabolic alkalosis. Chronic obstruction may result in weight loss, malnutrition, and failure to thrive.
Clinical Presentation
Patients often report intermittent symptoms that worsen as obstruction progresses. Common complaints include nausea, nonbilious vomiting, vague or epigastric abdominal pain, early satiety, epigastric fullness, and relief of discomfort after emesis. Chronic cases are associated with weight loss and nutritional decline.
Physical Examination Findings
Vital signs may initially be normal but can reveal tachycardia or hypotension in significant volume depletion. Abdominal examination may show epigastric or generalized distention with tympany. A succussion splash more than four hours after eating is suggestive. Digital rectal examination should assess for occult blood. Signs of dehydration include dry mucous membranes and decreased skin turgor, while chronic cases may show evidence of malnutrition.
Special Population Considerations
In elderly patients, symptoms such as abdominal pain and vomiting may be subtle or atypical, and alternative diagnoses including cardiac or neurologic causes should be considered. In pediatrics, idiopathic hypertrophic pyloric stenosis is the classic presentation, typically affecting male infants between two and eight weeks of age. Vomiting progresses from intermittent and nonprojectile to forceful projectile emesis. A visible midepigastric peristaltic wave may precede vomiting, and an epigastric “olive” mass is palpable in most cases.
Initial Diagnostic Approach
Evaluation begins with a thorough history and physical examination to assess symptom progression, hydration status, and risk factors for malignancy or peptic ulcer disease.
Laboratory And Imaging Assessment
Laboratory studies may show anemia from malignancy or gastrointestinal bleeding, hemoconcentration from dehydration, hypokalemia, hypochloremic metabolic alkalosis, hypoglycemia, and prerenal azotemia. Additional tests include urinalysis, amylase, lipase, liver function studies, and Helicobacter pylori testing when indicated. Plain abdominal radiographs are often nondiagnostic but may reveal gastric dilation or absence of distal bowel gas. In pediatric patients, abdominal ultrasound is preferred and may demonstrate an elongated hypertrophic pyloric sphincter. In adults, abdominal CT is highly useful for identifying intraluminal, extraluminal, and neoplastic causes. Upper gastrointestinal contrast studies may show characteristic signs of pyloric stenosis, and upper endoscopy allows direct visualization of the gastric outlet and proximal duodenum.
Alternative Diagnoses To Consider
Differential diagnoses include proximal bowel obstruction, peptic ulcer disease exacerbation, gastroenteritis, cholelithiasis, cholecystitis, acute pancreatitis, diabetic gastroparesis, and psychogenic vomiting.
Early Management Principles
Prehospital care focuses on airway assessment, oxygen administration, intravenous access, and fluid resuscitation in patients with dehydration or active vomiting.
Resuscitation And Stabilization
Initial therapy includes isotonic fluid resuscitation with 0.9% normal saline. Adults typically receive one-liter boluses, while children receive 20 mL/kg. Electrolyte abnormalities, especially hypokalemia, must be corrected promptly.
Emergency Department Interventions
Placement of a nasogastric tube for decompression is recommended. A Foley catheter may be used to monitor urine output. Definitive management often requires surgical or gastroenterologic intervention, including endoscopic balloon dilation for benign strictures, enteral stent placement or gastrojejunostomy for malignant causes, and surgical procedures such as pyloroplasty, antrectomy, vagotomy, or gastrojejunostomy for benign disease.
Pharmacologic Therapy
Acid suppression may be initiated with intravenous H2 blockers such as famotidine or ranitidine, or proton pump inhibitors such as pantoprazole. Helicobacter pylori eradication therapy should be considered when appropriate.
Disposition And Follow-Up
Most patients with gastric outlet obstruction require hospital admission for fluid resuscitation, electrolyte correction, and specialist evaluation. Discharge is uncommon and should only be considered if symptoms have resolved, volume status and laboratory values are normal, and the patient has been evaluated and cleared by surgery or gastroenterology.
Key Clinical Insights And Pitfalls
Common errors include misdiagnosing gastric outlet obstruction as gastroenteritis, overreliance on plain radiographs, failure to consider malignancy in patients with epigastric pain and vomiting, and inadequate fluid resuscitation, particularly in elderly and pediatric populations.
Core Overview
Gastric outlet obstruction refers to any condition that impedes the passage of gastric contents into the duodenum. The underlying cause may originate from the stomach, duodenum, or extraluminal structures. Both benign and malignant etiologies are implicated, with malignancy being the most common cause in adults. Neoplasms may be intrinsic or extrinsic, including pancreatic tumors, gastric lymphoma, duodenal tumors, and gallbladder cancer, which can compress the pylorus or proximal duodenum. Peptic ulcer disease is no longer the leading adult cause due to effective Helicobacter pylori treatment and acid suppression therapy. In children, hypertrophic pyloric stenosis is the most common cause. Additional mechanisms include postoperative complications, gastric volvulus, polyps, bezoars, duplication cysts, and pyloric or duodenal edema, scarring, strictures, webs, or hyperplasia related to caustic injury or chronic pancreatitis.
Pathophysiologic Basis
Regardless of etiology, gastric outlet obstruction leads to impaired gastric emptying, resulting in nausea and predominantly nonbilious vomiting. Persistent emesis causes dehydration and electrolyte abnormalities, particularly hypokalemic, hypochloremic metabolic alkalosis. Chronic obstruction may result in weight loss, malnutrition, and failure to thrive.
Clinical Presentation
Patients often report intermittent symptoms that worsen as obstruction progresses. Common complaints include nausea, nonbilious vomiting, vague or epigastric abdominal pain, early satiety, epigastric fullness, and relief of discomfort after emesis. Chronic cases are associated with weight loss and nutritional decline.
Physical Examination Findings
Vital signs may initially be normal but can reveal tachycardia or hypotension in significant volume depletion. Abdominal examination may show epigastric or generalized distention with tympany. A succussion splash more than four hours after eating is suggestive. Digital rectal examination should assess for occult blood. Signs of dehydration include dry mucous membranes and decreased skin turgor, while chronic cases may show evidence of malnutrition.
Special Population Considerations
In elderly patients, symptoms such as abdominal pain and vomiting may be subtle or atypical, and alternative diagnoses including cardiac or neurologic causes should be considered. In pediatrics, idiopathic hypertrophic pyloric stenosis is the classic presentation, typically affecting male infants between two and eight weeks of age. Vomiting progresses from intermittent and nonprojectile to forceful projectile emesis. A visible midepigastric peristaltic wave may precede vomiting, and an epigastric “olive” mass is palpable in most cases.
Initial Diagnostic Approach
Evaluation begins with a thorough history and physical examination to assess symptom progression, hydration status, and risk factors for malignancy or peptic ulcer disease.
Laboratory And Imaging Assessment
Laboratory studies may show anemia from malignancy or gastrointestinal bleeding, hemoconcentration from dehydration, hypokalemia, hypochloremic metabolic alkalosis, hypoglycemia, and prerenal azotemia. Additional tests include urinalysis, amylase, lipase, liver function studies, and Helicobacter pylori testing when indicated. Plain abdominal radiographs are often nondiagnostic but may reveal gastric dilation or absence of distal bowel gas. In pediatric patients, abdominal ultrasound is preferred and may demonstrate an elongated hypertrophic pyloric sphincter. In adults, abdominal CT is highly useful for identifying intraluminal, extraluminal, and neoplastic causes. Upper gastrointestinal contrast studies may show characteristic signs of pyloric stenosis, and upper endoscopy allows direct visualization of the gastric outlet and proximal duodenum.
Alternative Diagnoses To Consider
Differential diagnoses include proximal bowel obstruction, peptic ulcer disease exacerbation, gastroenteritis, cholelithiasis, cholecystitis, acute pancreatitis, diabetic gastroparesis, and psychogenic vomiting.
Early Management Principles
Prehospital care focuses on airway assessment, oxygen administration, intravenous access, and fluid resuscitation in patients with dehydration or active vomiting.
Resuscitation And Stabilization
Initial therapy includes isotonic fluid resuscitation with 0.9% normal saline. Adults typically receive one-liter boluses, while children receive 20 mL/kg. Electrolyte abnormalities, especially hypokalemia, must be corrected promptly.
Emergency Department Interventions
Placement of a nasogastric tube for decompression is recommended. A Foley catheter may be used to monitor urine output. Definitive management often requires surgical or gastroenterologic intervention, including endoscopic balloon dilation for benign strictures, enteral stent placement or gastrojejunostomy for malignant causes, and surgical procedures such as pyloroplasty, antrectomy, vagotomy, or gastrojejunostomy for benign disease.
Pharmacologic Therapy
Acid suppression may be initiated with intravenous H2 blockers such as famotidine or ranitidine, or proton pump inhibitors such as pantoprazole. Helicobacter pylori eradication therapy should be considered when appropriate.
Disposition And Follow-Up
Most patients with gastric outlet obstruction require hospital admission for fluid resuscitation, electrolyte correction, and specialist evaluation. Discharge is uncommon and should only be considered if symptoms have resolved, volume status and laboratory values are normal, and the patient has been evaluated and cleared by surgery or gastroenterology.
Key Clinical Insights And Pitfalls
Common errors include misdiagnosing gastric outlet obstruction as gastroenteritis, overreliance on plain radiographs, failure to consider malignancy in patients with epigastric pain and vomiting, and inadequate fluid resuscitation, particularly in elderly and pediatric populations.
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Emergency And Acute Medicine - Gangrene
Core Overview
Gas gangrene, also called clostridial myonecrosis, is an acute, rapidly progressive, gas-forming necrotizing infection involving muscle and subcutaneous tissue. It most commonly occurs in post-traumatic or postoperative settings and is characterized by aggressive invasion and destruction of healthy muscle with severe systemic toxicity.
Underlying Causes
The condition is caused by clostridial organisms, which are facultative anaerobic, spore-forming, gram-positive bacilli that produce multiple toxins, the most lethal being alpha-toxin. Clostridium perfringens is responsible for approximately 80–90% of cases. Other causative species include Clostridium novyi, Clostridium septicum, Clostridium histolyticum, Clostridium bifermentans, and Clostridium fallax. Organisms are introduced either through traumatic or postoperative contamination or via nontraumatic mechanisms associated with diabetes mellitus, peripheral vascular disease, alcoholism, intravenous drug use, or malignancy.
Diagnostic Evaluation
Patients typically present with sudden, severe pain in the affected extremity or region. Early findings include low-grade fever and marked tachycardia out of proportion to fever. Skin changes progress from bronze discoloration to purple or red hues. Crepitus, bleb and bullae formation, thin serosanguinous discharge with a sweet odor, rapid tissue spread, altered mental status, and systemic toxicity are common.
Initial Assessment Requirements
Diagnosis is primarily clinical and requires careful history and physical examination, with particular attention to crepitus and rapidly progressive soft-tissue changes. Plain soft-tissue radiographs may demonstrate gas dissecting along fascial planes, although absence of gas does not exclude disease. A stat Gram stain of wound exudate often shows gram-positive bacilli with few leukocytes.
Investigations And Interpretation
Laboratory evaluation includes complete blood count with differential, electrolytes, blood urea nitrogen, creatinine, and coagulation studies. Assessment for hemolysis is essential. Gram stain and anaerobic cultures from wound exudate or tissue biopsy should be obtained. Imaging with plain radiographs may reveal soft-tissue gas, while computed tomography is useful when abdominal or flank involvement is suspected.
Procedural And Surgical Evaluation
All patients with suspected gas gangrene require immediate surgical intervention. Aggressive surgical débridement is mandatory and may include fasciotomy or amputation depending on disease extent.
Conditions To Consider
Differential diagnoses include cellulitis, necrotizing fasciitis, nonclostridial myositis or myonecrosis, and other causes of gas within soft tissues such as dissection from respiratory or gastrointestinal sources.
Management Approach
Early management focuses on rapid resuscitation and definitive therapy. Prehospital care includes establishing intravenous access and initiating isotonic fluid resuscitation.
Early Stabilization Measures
Airway protection and hemodynamic stabilization are priorities. Rapid sequence intubation may be required. Supplemental oxygen, continuous cardiac and pulse oximetry monitoring, aggressive fluid resuscitation, central venous access, and sepsis protocol initiation are recommended, especially in patients with septic shock.
Emergency Department Management
Immediate broad-spectrum intravenous antibiotics should be administered, targeting Clostridium species, group A Streptococcus, and mixed aerobic and anaerobic organisms. Definitive antimicrobial therapy consists of penicillin G combined with clindamycin. Alternatives include ceftriaxone or erythromycin. For polymicrobial infections, combination therapy with penicillin, clindamycin, metronidazole or vancomycin, and gram-negative coverage such as gentamicin is indicated. Emergent surgical consultation is essential. Hyperbaric oxygen therapy may be used as an adjunct in stable patients. Tetanus prophylaxis should be provided. Patients must be closely monitored for complications such as acute respiratory distress syndrome, renal failure, myocardial instability, and disseminated intravascular coagulation.
Pharmacologic Therapy
Recommended medications include penicillin G 24 million units per day IV divided every 4–6 hours, clindamycin 900 mg IV every 8 hours, ceftriaxone 2 g IV every 12 hours, erythromycin 1 g IV every 6 hours, gentamicin 2 mg/kg IV every 8 hours, metronidazole 500 mg IV every 8 hours, tetanus immune globulin 500 IU IM, and tetanus toxoid 0.5 mg IM.
Disposition And Follow-Up
All patients with gas gangrene and evidence of myonecrosis require admission for urgent surgical débridement and intravenous antibiotics. No patient with acute gangrene should be discharged. Referral for hyperbaric oxygen therapy may be considered after stabilization.
Clinical Insights And Common Pitfalls
Bacteremia occurs in approximately 15% of cases and can rapidly progress to intravascular hemolysis. Early recognition, prompt surgical intervention, and immediate antibiotic therapy are critical. Hyperbaric oxygen therapy should only be used as an adjunct and never as a substitute for surgery.
Core Overview
Gas gangrene, also called clostridial myonecrosis, is an acute, rapidly progressive, gas-forming necrotizing infection involving muscle and subcutaneous tissue. It most commonly occurs in post-traumatic or postoperative settings and is characterized by aggressive invasion and destruction of healthy muscle with severe systemic toxicity.
Underlying Causes
The condition is caused by clostridial organisms, which are facultative anaerobic, spore-forming, gram-positive bacilli that produce multiple toxins, the most lethal being alpha-toxin. Clostridium perfringens is responsible for approximately 80–90% of cases. Other causative species include Clostridium novyi, Clostridium septicum, Clostridium histolyticum, Clostridium bifermentans, and Clostridium fallax. Organisms are introduced either through traumatic or postoperative contamination or via nontraumatic mechanisms associated with diabetes mellitus, peripheral vascular disease, alcoholism, intravenous drug use, or malignancy.
Diagnostic Evaluation
Patients typically present with sudden, severe pain in the affected extremity or region. Early findings include low-grade fever and marked tachycardia out of proportion to fever. Skin changes progress from bronze discoloration to purple or red hues. Crepitus, bleb and bullae formation, thin serosanguinous discharge with a sweet odor, rapid tissue spread, altered mental status, and systemic toxicity are common.
Initial Assessment Requirements
Diagnosis is primarily clinical and requires careful history and physical examination, with particular attention to crepitus and rapidly progressive soft-tissue changes. Plain soft-tissue radiographs may demonstrate gas dissecting along fascial planes, although absence of gas does not exclude disease. A stat Gram stain of wound exudate often shows gram-positive bacilli with few leukocytes.
Investigations And Interpretation
Laboratory evaluation includes complete blood count with differential, electrolytes, blood urea nitrogen, creatinine, and coagulation studies. Assessment for hemolysis is essential. Gram stain and anaerobic cultures from wound exudate or tissue biopsy should be obtained. Imaging with plain radiographs may reveal soft-tissue gas, while computed tomography is useful when abdominal or flank involvement is suspected.
Procedural And Surgical Evaluation
All patients with suspected gas gangrene require immediate surgical intervention. Aggressive surgical débridement is mandatory and may include fasciotomy or amputation depending on disease extent.
Conditions To Consider
Differential diagnoses include cellulitis, necrotizing fasciitis, nonclostridial myositis or myonecrosis, and other causes of gas within soft tissues such as dissection from respiratory or gastrointestinal sources.
Management Approach
Early management focuses on rapid resuscitation and definitive therapy. Prehospital care includes establishing intravenous access and initiating isotonic fluid resuscitation.
Early Stabilization Measures
Airway protection and hemodynamic stabilization are priorities. Rapid sequence intubation may be required. Supplemental oxygen, continuous cardiac and pulse oximetry monitoring, aggressive fluid resuscitation, central venous access, and sepsis protocol initiation are recommended, especially in patients with septic shock.
Emergency Department Management
Immediate broad-spectrum intravenous antibiotics should be administered, targeting Clostridium species, group A Streptococcus, and mixed aerobic and anaerobic organisms. Definitive antimicrobial therapy consists of penicillin G combined with clindamycin. Alternatives include ceftriaxone or erythromycin. For polymicrobial infections, combination therapy with penicillin, clindamycin, metronidazole or vancomycin, and gram-negative coverage such as gentamicin is indicated. Emergent surgical consultation is essential. Hyperbaric oxygen therapy may be used as an adjunct in stable patients. Tetanus prophylaxis should be provided. Patients must be closely monitored for complications such as acute respiratory distress syndrome, renal failure, myocardial instability, and disseminated intravascular coagulation.
Pharmacologic Therapy
Recommended medications include penicillin G 24 million units per day IV divided every 4–6 hours, clindamycin 900 mg IV every 8 hours, ceftriaxone 2 g IV every 12 hours, erythromycin 1 g IV every 6 hours, gentamicin 2 mg/kg IV every 8 hours, metronidazole 500 mg IV every 8 hours, tetanus immune globulin 500 IU IM, and tetanus toxoid 0.5 mg IM.
Disposition And Follow-Up
All patients with gas gangrene and evidence of myonecrosis require admission for urgent surgical débridement and intravenous antibiotics. No patient with acute gangrene should be discharged. Referral for hyperbaric oxygen therapy may be considered after stabilization.
Clinical Insights And Common Pitfalls
Bacteremia occurs in approximately 15% of cases and can rapidly progress to intravascular hemolysis. Early recognition, prompt surgical intervention, and immediate antibiotic therapy are critical. Hyperbaric oxygen therapy should only be used as an adjunct and never as a substitute for surgery.
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Emergency And Acute Medicine - Gallstone Ileus
Fundamental Overview
Clinical Description Mechanical intestinal obstruction caused by impaction of a gallstone within the bowel lumen. Stones are typically larger than 2.5 cm. Gallstone ileus accounts for 1–3% of all intestinal obstructions and occurs most commonly in patients older than 65 years. Females are affected more frequently than males with a ratio of approximately 5:1. Mortality remains high at 15–18%.
Underlying Causes
Chronic inflammation of the gallbladder leads to adhesion formation between the gallbladder and adjacent bowel. Over time, a cholecystoenteric fistula develops, allowing gallstones to migrate into the intestinal tract. The duodenum is the most common site of fistula formation, followed by the colon, while gastric fistulas are rare. Stone impaction most frequently occurs in the terminal ileum (54–65%), the narrowest segment of the small intestine at the ileocecal valve. Other sites include the jejunum (27%) and duodenum (1–3%). Duodenal impaction causing gastric outlet obstruction is referred to as Bouveret syndrome. Large bowel obstruction is uncommon.
Diagnostic Evaluation
Presenting Features And Symptoms Patients often experience “tumbling” abdominal pain characterized by intermittent discomfort as the stone moves through the bowel before becoming lodged. Complete obstruction results in severe and often acute abdominal pain. Common associated symptoms include nausea, bilious or feculent vomiting, obstipation, abdominal distention with tympany, abdominal tenderness with late peritoneal signs, and abnormal bowel sounds. Only 50–60% of patients report a prior history of biliary colic or known gallstone disease. Gallstone ileus is frequently associated with cardiovascular disease, diabetes, and obesity. Physical examination typically reveals abdominal distention and tenderness, and jaundice may be present.
Initial Assessment Requirements Evaluation should focus on confirming the presence of mechanical intestinal obstruction and identifying complications
.
Investigations And Interpretation
Laboratory Studies Electrolytes, blood urea nitrogen, creatinine, and glucose should be assessed due to dehydration and vomiting. Liver function tests and bilirubin may be elevated. Amylase may increase in late obstruction. Complete blood count and hematocrit may demonstrate hemoconcentration from dehydration, with nonspecific leukocytosis.
Imaging Studies
Upright and supine abdominal radiographs may show multiple air–fluid levels and bowel distention. The Rigler triad is diagnostic when two of three findings are present: pneumobilia, partial or complete bowel obstruction, and an ectopic gallstone. Chest radiography is used to assess for pneumoperitoneum. Abdominal CT scanning is the diagnostic modality of choice and allows direct visualization and localization of the obstructing stone. Abdominal ultrasound may identify pneumobilia and gallstones but is less sensitive for detecting the site of obstruction.
Conditions To Consider
Paralytic ileus, adhesive bowel obstruction, volvulus, hernia, intussusception, gastrointestinal malignancy, diverticulitis, bezoar, inflammatory bowel disease, pseudo-obstruction, cholecystitis, ascending cholangitis, and pancreatitis.
Management Approach
Prehospital Considerations Establish intravenous access as early as possible.
Early Stabilization Measures Initiate intravenous fluid resuscitation to correct dehydration and maintain hemodynamic stability.
Emergency Department
Management Insert a nasogastric tube for gastric and intestinal decompression. Maintain nil per os status. Correct electrolyte abnormalities and monitor urine output. Provide adequate analgesia. Begin broad-spectrum antibiotics covering bowel flora, such as piperacillin/tazobactam, ampicillin/sulbactam, or ticarcillin/clavulanate. Acceptable alternatives include carbapenems or a third-generation cephalosporin combined with metronidazole. Prompt surgical consultation is mandatory.
Pharmacologic Therapy
Ampicillin/sulbactam 3 g IV every 6 hours. Piperacillin/tazobactam 3.375 g IV every 6 hours. Ticarcillin/clavulanate 3.1 g IV every 4–6 hours.
Disposition And Follow Up
Indications For Admission All patients with gallstone ileus require hospital admission and urgent surgical evaluation for operative intervention.
Criteria For Discharge None.
Ongoing Care
Recommendations Immediate surgical consultation in the emergency department for definitive operative management.
Clinical Pearls And Common Errors
Gallstone ileus represents a true mechanical intestinal obstruction rather than a functional ileus. Definitive management requires urgent surgical intervention. Mortality is high due to delayed diagnosis and significant comorbidities in affected patients. Maintain a high index of suspicion in elderly patients, particularly women, presenting with bowel obstruction and no prior abdominal surgery. Plain radiographs detect only about 10% of ectopic gallstones, whereas CT imaging is significantly more sensitive. Only half of patients have a known history of biliary colic or gallstone disease.
Fundamental Overview
Clinical Description Mechanical intestinal obstruction caused by impaction of a gallstone within the bowel lumen. Stones are typically larger than 2.5 cm. Gallstone ileus accounts for 1–3% of all intestinal obstructions and occurs most commonly in patients older than 65 years. Females are affected more frequently than males with a ratio of approximately 5:1. Mortality remains high at 15–18%.
Underlying Causes
Chronic inflammation of the gallbladder leads to adhesion formation between the gallbladder and adjacent bowel. Over time, a cholecystoenteric fistula develops, allowing gallstones to migrate into the intestinal tract. The duodenum is the most common site of fistula formation, followed by the colon, while gastric fistulas are rare. Stone impaction most frequently occurs in the terminal ileum (54–65%), the narrowest segment of the small intestine at the ileocecal valve. Other sites include the jejunum (27%) and duodenum (1–3%). Duodenal impaction causing gastric outlet obstruction is referred to as Bouveret syndrome. Large bowel obstruction is uncommon.
Diagnostic Evaluation
Presenting Features And Symptoms Patients often experience “tumbling” abdominal pain characterized by intermittent discomfort as the stone moves through the bowel before becoming lodged. Complete obstruction results in severe and often acute abdominal pain. Common associated symptoms include nausea, bilious or feculent vomiting, obstipation, abdominal distention with tympany, abdominal tenderness with late peritoneal signs, and abnormal bowel sounds. Only 50–60% of patients report a prior history of biliary colic or known gallstone disease. Gallstone ileus is frequently associated with cardiovascular disease, diabetes, and obesity. Physical examination typically reveals abdominal distention and tenderness, and jaundice may be present.
Initial Assessment Requirements Evaluation should focus on confirming the presence of mechanical intestinal obstruction and identifying complications
.
Investigations And Interpretation
Laboratory Studies Electrolytes, blood urea nitrogen, creatinine, and glucose should be assessed due to dehydration and vomiting. Liver function tests and bilirubin may be elevated. Amylase may increase in late obstruction. Complete blood count and hematocrit may demonstrate hemoconcentration from dehydration, with nonspecific leukocytosis.
Imaging Studies
Upright and supine abdominal radiographs may show multiple air–fluid levels and bowel distention. The Rigler triad is diagnostic when two of three findings are present: pneumobilia, partial or complete bowel obstruction, and an ectopic gallstone. Chest radiography is used to assess for pneumoperitoneum. Abdominal CT scanning is the diagnostic modality of choice and allows direct visualization and localization of the obstructing stone. Abdominal ultrasound may identify pneumobilia and gallstones but is less sensitive for detecting the site of obstruction.
Conditions To Consider
Paralytic ileus, adhesive bowel obstruction, volvulus, hernia, intussusception, gastrointestinal malignancy, diverticulitis, bezoar, inflammatory bowel disease, pseudo-obstruction, cholecystitis, ascending cholangitis, and pancreatitis.
Management Approach
Prehospital Considerations Establish intravenous access as early as possible.
Early Stabilization Measures Initiate intravenous fluid resuscitation to correct dehydration and maintain hemodynamic stability.
Emergency Department
Management Insert a nasogastric tube for gastric and intestinal decompression. Maintain nil per os status. Correct electrolyte abnormalities and monitor urine output. Provide adequate analgesia. Begin broad-spectrum antibiotics covering bowel flora, such as piperacillin/tazobactam, ampicillin/sulbactam, or ticarcillin/clavulanate. Acceptable alternatives include carbapenems or a third-generation cephalosporin combined with metronidazole. Prompt surgical consultation is mandatory.
Pharmacologic Therapy
Ampicillin/sulbactam 3 g IV every 6 hours. Piperacillin/tazobactam 3.375 g IV every 6 hours. Ticarcillin/clavulanate 3.1 g IV every 4–6 hours.
Disposition And Follow Up
Indications For Admission All patients with gallstone ileus require hospital admission and urgent surgical evaluation for operative intervention.
Criteria For Discharge None.
Ongoing Care
Recommendations Immediate surgical consultation in the emergency department for definitive operative management.
Clinical Pearls And Common Errors
Gallstone ileus represents a true mechanical intestinal obstruction rather than a functional ileus. Definitive management requires urgent surgical intervention. Mortality is high due to delayed diagnosis and significant comorbidities in affected patients. Maintain a high index of suspicion in elderly patients, particularly women, presenting with bowel obstruction and no prior abdominal surgery. Plain radiographs detect only about 10% of ectopic gallstones, whereas CT imaging is significantly more sensitive. Only half of patients have a known history of biliary colic or gallstone disease.
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Emergency And Acute Medicine – Frostbite
Basics Description
Frostbite is tissue injury caused by exposure to cold temperatures. Tissue damage occurs through direct cellular injury from intracellular ice crystal formation, indirect injury from extracellular ice crystals causing cellular dehydration and enzymatic disruption, and reperfusion injury during rewarming. Reperfusion leads to release of inflammatory mediators such as prostaglandins and thromboxane, resulting in vasoconstriction, platelet aggregation, endothelial injury, and thrombosis. Clear blisters result from extracellular fluid exudation, while hemorrhagic blisters indicate deeper vascular injury. Progressive arterial thrombosis leads to ischemia and necrosis. Tissue demarcation evolves over weeks to months, leading to delayed definitive surgical decisions.
Etiology
Cold exposure severity depends on duration, wind chill, humidity, and wet skin or clothing. Predisposing factors include extremes of age, altered mental status from intoxication or psychiatric illness, and impaired circulation.
Diagnosis Signs And Symptoms
Fingers, toes, ears, and nose are most commonly affected. Classification after rewarming helps describe injury severity but does not change initial management.
Superficial frostbite involves skin only and usually heals without tissue loss. First-degree injuries present with erythema, edema, burning, and throbbing without blisters. Second-degree injuries cause marked edema, clear blisters, and numbness.
Deep frostbite results in inevitable tissue loss. Third-degree injuries involve subcutaneous tissue with hemorrhagic blisters and severe pain after rewarming. Fourth-degree injuries extend to muscle, tendon, and bone with deep cyanosis, mottling, or anesthesia. Poor prognostic signs include hemorrhagic blisters, persistent cyanosis, mottling, anesthesia, and impaired mobility after rewarming.
Essential Workup
Diagnosis is clinical. Document skin color, temperature, blister type, and tissue consistency. Perform vascular and neurologic exams including pulses, Doppler assessment, capillary refill, and two-point discrimination. Evaluate for associated conditions such as hypothermia, trauma, hypoglycemia, intoxication, cardiac or neurologic illness, and compartment syndrome.
Diagnosis Tests And Interpretation
Lab
Not required for mild cases. Severe frostbite may require CBC, electrolytes, renal function, glucose, creatine kinase, urinalysis for myoglobinuria, and cultures if infection is suspected.
Imaging
Technetium-99 scintigraphy or MR angiography may help identify viable tissue early and guide surgical planning.
Diagnostic Procedures
Rapid rewarming is performed using a water bath maintained at 40–42°C. Temperatures outside this range increase risk of thermal injury or worsen tissue loss.
Differential Diagnosis
Frostnip causes reversible numbness without tissue injury. Trench foot results from prolonged wet cold exposure without ice crystal formation and presents with neurovascular compromise. Chilblains occur with chronic cold exposure and present as erythematous or cyanotic plaques.
Treatment Prehospital
Protect and immobilize affected areas. Remove wet or constrictive clothing. Avoid rubbing, massage, snow application, or dry rewarming if refreezing is possible. Treat hypothermia cautiously to prevent arrhythmias.
Initial Stabilization Therapy
Address airway, breathing, and circulation. Correct hypothermia. Provide IV fluids for severe cases. Minimize handling of frozen tissue.
ED Treatment Procedures
If injury is recent and not rewarmed, initiate rapid rewarming in a 40–42°C water bath for 15–30 minutes until tissue is pliable and erythematous. Provide aggressive analgesia with opioids and NSAIDs. Apply topical aloe vera to intact skin. Debride or aspirate clear blisters but avoid hemorrhagic blister intervention. Provide tetanus prophylaxis. Consider short-term antibiotics during hyperemic recovery for severe injuries. Elevate and splint affected areas and change dressings frequently. Avoid vasoconstrictive agents including nicotine. Thrombolytic therapy within 24 hours may improve tissue salvage and requires specialist consultation.
Medication
Aloe vera topical cream applied every 6 hours.
Ibuprofen 800 mg PO TID (pediatric dosing weight-based).
Morphine sulfate titrated IV or IM for pain control.
Antibiotics such as cephalexin, dicloxacillin, or ciprofloxacin when indicated.
Follow Up Disposition
Admission Criteria
All but minimal superficial injuries should be admitted, especially when refreezing risk exists.
Discharge Criteria
Only very mild superficial frostbite with reliable follow-up.
Issues For Referral
Consult burn, plastic, hand, or general surgery for all but the mildest cases.
Key Practice Insights And Common Pitfalls
Avoid freeze–thaw–refreeze cycles. Maintain correct rewarming temperature. Always address hypothermia and systemic illness. Consider compartment syndrome in pulseless or tense extremities.
Basics Description
Frostbite is tissue injury caused by exposure to cold temperatures. Tissue damage occurs through direct cellular injury from intracellular ice crystal formation, indirect injury from extracellular ice crystals causing cellular dehydration and enzymatic disruption, and reperfusion injury during rewarming. Reperfusion leads to release of inflammatory mediators such as prostaglandins and thromboxane, resulting in vasoconstriction, platelet aggregation, endothelial injury, and thrombosis. Clear blisters result from extracellular fluid exudation, while hemorrhagic blisters indicate deeper vascular injury. Progressive arterial thrombosis leads to ischemia and necrosis. Tissue demarcation evolves over weeks to months, leading to delayed definitive surgical decisions.
Etiology
Cold exposure severity depends on duration, wind chill, humidity, and wet skin or clothing. Predisposing factors include extremes of age, altered mental status from intoxication or psychiatric illness, and impaired circulation.
Diagnosis Signs And Symptoms
Fingers, toes, ears, and nose are most commonly affected. Classification after rewarming helps describe injury severity but does not change initial management.
Superficial frostbite involves skin only and usually heals without tissue loss. First-degree injuries present with erythema, edema, burning, and throbbing without blisters. Second-degree injuries cause marked edema, clear blisters, and numbness.
Deep frostbite results in inevitable tissue loss. Third-degree injuries involve subcutaneous tissue with hemorrhagic blisters and severe pain after rewarming. Fourth-degree injuries extend to muscle, tendon, and bone with deep cyanosis, mottling, or anesthesia. Poor prognostic signs include hemorrhagic blisters, persistent cyanosis, mottling, anesthesia, and impaired mobility after rewarming.
Essential Workup
Diagnosis is clinical. Document skin color, temperature, blister type, and tissue consistency. Perform vascular and neurologic exams including pulses, Doppler assessment, capillary refill, and two-point discrimination. Evaluate for associated conditions such as hypothermia, trauma, hypoglycemia, intoxication, cardiac or neurologic illness, and compartment syndrome.
Diagnosis Tests And Interpretation
Lab
Not required for mild cases. Severe frostbite may require CBC, electrolytes, renal function, glucose, creatine kinase, urinalysis for myoglobinuria, and cultures if infection is suspected.
Imaging
Technetium-99 scintigraphy or MR angiography may help identify viable tissue early and guide surgical planning.
Diagnostic Procedures
Rapid rewarming is performed using a water bath maintained at 40–42°C. Temperatures outside this range increase risk of thermal injury or worsen tissue loss.
Differential Diagnosis
Frostnip causes reversible numbness without tissue injury. Trench foot results from prolonged wet cold exposure without ice crystal formation and presents with neurovascular compromise. Chilblains occur with chronic cold exposure and present as erythematous or cyanotic plaques.
Treatment Prehospital
Protect and immobilize affected areas. Remove wet or constrictive clothing. Avoid rubbing, massage, snow application, or dry rewarming if refreezing is possible. Treat hypothermia cautiously to prevent arrhythmias.
Initial Stabilization Therapy
Address airway, breathing, and circulation. Correct hypothermia. Provide IV fluids for severe cases. Minimize handling of frozen tissue.
ED Treatment Procedures
If injury is recent and not rewarmed, initiate rapid rewarming in a 40–42°C water bath for 15–30 minutes until tissue is pliable and erythematous. Provide aggressive analgesia with opioids and NSAIDs. Apply topical aloe vera to intact skin. Debride or aspirate clear blisters but avoid hemorrhagic blister intervention. Provide tetanus prophylaxis. Consider short-term antibiotics during hyperemic recovery for severe injuries. Elevate and splint affected areas and change dressings frequently. Avoid vasoconstrictive agents including nicotine. Thrombolytic therapy within 24 hours may improve tissue salvage and requires specialist consultation.
Medication
Aloe vera topical cream applied every 6 hours.
Ibuprofen 800 mg PO TID (pediatric dosing weight-based).
Morphine sulfate titrated IV or IM for pain control.
Antibiotics such as cephalexin, dicloxacillin, or ciprofloxacin when indicated.
Follow Up Disposition
Admission Criteria
All but minimal superficial injuries should be admitted, especially when refreezing risk exists.
Discharge Criteria
Only very mild superficial frostbite with reliable follow-up.
Issues For Referral
Consult burn, plastic, hand, or general surgery for all but the mildest cases.
Key Practice Insights And Common Pitfalls
Avoid freeze–thaw–refreeze cycles. Maintain correct rewarming temperature. Always address hypothermia and systemic illness. Consider compartment syndrome in pulseless or tense extremities.
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Emergency And Acute Medicine – Fracture, Open
Basics Description
An open fracture is defined by continuity between a skin violation and the fracture site, ranging from a small puncture wound to grossly exposed bone. These injuries represent a surgical urgency because delays in care significantly increase infection risk and complication rates. Certain factors increase morbidity, including massive soft tissue damage, severe wound contamination, compromised vascular supply, fracture instability, and host factors such as diabetes or peripheral vascular disease.
Etiology
Open fractures usually result from significant blunt trauma or penetrating injury.
Diagnosis Signs And Symptoms
Patients typically present with deformity and a nearby break in skin integrity. Neurovascular compromise may be present, and associated traumatic injuries are common.
History
A history of significant trauma is typical.
Physical Exam
Perform a complete neurologic and vascular examination of the affected limb. A thorough trauma evaluation is essential to identify associated injuries.
Essential Workup
Obtain plain radiographs including the joints above and below the injury. Additional diagnostic evaluation should be guided by the mechanism of injury and evidence of multisystem trauma.
Diagnosis Tests And Interpretation
Lab
CBC, basic chemistry panel, and coagulation studies are indicated for large-bone fractures (e.g., femur, pelvis) or in polytrauma. Type and screen or type and cross-match should be obtained if significant blood loss is anticipated. Pre- and post-débridement wound cultures have limited value and are not recommended.
Imaging
Doppler ultrasonography or angiography is indicated when vascular injury is suspected, such as with posterior knee dislocation, ischemic extremity, or extensive soft tissue damage in high-risk areas.
Diagnostic Procedures/Surgery
Measure compartment pressures if compartment syndrome is suspected. Consider saline or methylene blue arthrogram if joint violation is a concern. Angiography is warranted if noninvasive testing cannot adequately exclude vascular compromise.
Differential Diagnosis
Noncontiguous laceration or abrasion unrelated to the fracture site.
Treatment
Prehospital
Cover open wounds with moist, sterile dressings. Immobilize joints above and below the fracture. Control bleeding with direct pressure; use a tourniquet for traumatic amputations or uncontrolled hemorrhage. Apply gentle longitudinal traction if distal pulses are absent.
Initial Stabilization/Therapy
Prioritize airway, breathing, and circulation. Perform gentle reduction and immobilization when indicated.
ED Treatment/Procedures
Establish intravenous access and keep the patient NPO. Administer tetanus prophylaxis as indicated. Initiate intravenous antibiotics as early as possible to reduce infection risk. Minimize repeated wound exposure to prevent secondary contamination. Reassess frequently for compartment syndrome and neurovascular compromise. Certain large joint open fracture–dislocations (ankle, elbow, knee) require emergent reduction in the ED. Obtain urgent orthopedic consultation for formal irrigation, débridement, and possible operative fixation. Consult vascular surgery when vascular injury is suspected.
Medication
Cefazolin 1–2 g IM/IV (pediatric: 20 mg/kg).
Add gentamicin 1.5–2 mg/kg IV for severe or highly contaminated wounds (pediatric: 2–2.5 mg/kg).
Add penicillin G 4–5 million units IV for farm-related injuries, vascular injuries, or wounds at risk for Clostridium contamination (pediatric: 50,000 U/kg).
Tetanus booster 0.5 mL IM; tetanus immunoglobulin 250 IU IM if not previously immunized.
Morphine sulfate 2–10 mg IV (pediatric: 0.05–0.1 mg/kg per dose) or equivalent analgesia.
Pediatric Considerations
Administer DTaP booster in children younger than 7 years when indicated.
Follow Up Disposition
Admission Criteria
Most patients require admission for operative irrigation, débridement, intravenous antibiotics, and possible fixation.
Discharge Criteria
Selected simple open fractures may be irrigated and immobilized in the ED after orthopedic consultation, with discharge on oral antibiotics and close follow-up.
Issues For Referral
Nearly all open fractures require emergent orthopedic consultation and may necessitate trauma team involvement due to associated injuries.
Follow Up Recommendations
Patients discharged from the ED should be evaluated by an orthopedic surgeon within 1–2 days.
Key Practice Insights And Common Pitfalls
Open fractures are surgical urgencies requiring prompt antibiotics and orthopedic consultation. A high proportion of patients have associated traumatic injuries, which must not be overlooked. Early, thorough emergency department management significantly reduces morbidity and infection risk.
Basics Description
An open fracture is defined by continuity between a skin violation and the fracture site, ranging from a small puncture wound to grossly exposed bone. These injuries represent a surgical urgency because delays in care significantly increase infection risk and complication rates. Certain factors increase morbidity, including massive soft tissue damage, severe wound contamination, compromised vascular supply, fracture instability, and host factors such as diabetes or peripheral vascular disease.
Etiology
Open fractures usually result from significant blunt trauma or penetrating injury.
Diagnosis Signs And Symptoms
Patients typically present with deformity and a nearby break in skin integrity. Neurovascular compromise may be present, and associated traumatic injuries are common.
History
A history of significant trauma is typical.
Physical Exam
Perform a complete neurologic and vascular examination of the affected limb. A thorough trauma evaluation is essential to identify associated injuries.
Essential Workup
Obtain plain radiographs including the joints above and below the injury. Additional diagnostic evaluation should be guided by the mechanism of injury and evidence of multisystem trauma.
Diagnosis Tests And Interpretation
Lab
CBC, basic chemistry panel, and coagulation studies are indicated for large-bone fractures (e.g., femur, pelvis) or in polytrauma. Type and screen or type and cross-match should be obtained if significant blood loss is anticipated. Pre- and post-débridement wound cultures have limited value and are not recommended.
Imaging
Doppler ultrasonography or angiography is indicated when vascular injury is suspected, such as with posterior knee dislocation, ischemic extremity, or extensive soft tissue damage in high-risk areas.
Diagnostic Procedures/Surgery
Measure compartment pressures if compartment syndrome is suspected. Consider saline or methylene blue arthrogram if joint violation is a concern. Angiography is warranted if noninvasive testing cannot adequately exclude vascular compromise.
Differential Diagnosis
Noncontiguous laceration or abrasion unrelated to the fracture site.
Treatment
Prehospital
Cover open wounds with moist, sterile dressings. Immobilize joints above and below the fracture. Control bleeding with direct pressure; use a tourniquet for traumatic amputations or uncontrolled hemorrhage. Apply gentle longitudinal traction if distal pulses are absent.
Initial Stabilization/Therapy
Prioritize airway, breathing, and circulation. Perform gentle reduction and immobilization when indicated.
ED Treatment/Procedures
Establish intravenous access and keep the patient NPO. Administer tetanus prophylaxis as indicated. Initiate intravenous antibiotics as early as possible to reduce infection risk. Minimize repeated wound exposure to prevent secondary contamination. Reassess frequently for compartment syndrome and neurovascular compromise. Certain large joint open fracture–dislocations (ankle, elbow, knee) require emergent reduction in the ED. Obtain urgent orthopedic consultation for formal irrigation, débridement, and possible operative fixation. Consult vascular surgery when vascular injury is suspected.
Medication
Cefazolin 1–2 g IM/IV (pediatric: 20 mg/kg).
Add gentamicin 1.5–2 mg/kg IV for severe or highly contaminated wounds (pediatric: 2–2.5 mg/kg).
Add penicillin G 4–5 million units IV for farm-related injuries, vascular injuries, or wounds at risk for Clostridium contamination (pediatric: 50,000 U/kg).
Tetanus booster 0.5 mL IM; tetanus immunoglobulin 250 IU IM if not previously immunized.
Morphine sulfate 2–10 mg IV (pediatric: 0.05–0.1 mg/kg per dose) or equivalent analgesia.
Pediatric Considerations
Administer DTaP booster in children younger than 7 years when indicated.
Follow Up Disposition
Admission Criteria
Most patients require admission for operative irrigation, débridement, intravenous antibiotics, and possible fixation.
Discharge Criteria
Selected simple open fractures may be irrigated and immobilized in the ED after orthopedic consultation, with discharge on oral antibiotics and close follow-up.
Issues For Referral
Nearly all open fractures require emergent orthopedic consultation and may necessitate trauma team involvement due to associated injuries.
Follow Up Recommendations
Patients discharged from the ED should be evaluated by an orthopedic surgeon within 1–2 days.
Key Practice Insights And Common Pitfalls
Open fractures are surgical urgencies requiring prompt antibiotics and orthopedic consultation. A high proportion of patients have associated traumatic injuries, which must not be overlooked. Early, thorough emergency department management significantly reduces morbidity and infection risk.
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Emergency And Acute Medicine – Fournier Gangrene
Basics Description
Inadequate hygiene can lead to maceration and excoriation of scrotal skin, creating a portal of entry for bacteria. Once the skin barrier is disrupted, polymicrobial organisms spread rapidly along fascial planes of the perineum. Colles fascia fuses with the urogenital diaphragm, limiting posterior and lateral spread, while continuity of Buck and Scarpa fascia allows rapid anterior extension to the abdominal wall and lateral spread along the fascia lata. The testes and urethra are typically spared.
Most cases originate from three anatomic sources: lower urinary tract infections such as urethral strictures or indwelling catheters, penile or scrotal sources including condom catheters, hidradenitis, or balanitis, and anorectal sources such as fistulas, perirectal infections, or hemorrhoids. Rarely, intra-abdominal pathology including perforated appendicitis, diverticulitis, or pancreatitis may spread contiguously.
Etiology
Fournier gangrene is caused by polymicrobial infection involving mixed aerobic and anaerobic organisms that act synergistically to destroy tissue. End-arterial thrombosis in subcutaneous tissues creates an anaerobic environment that promotes rapid progression. Bacterial toxins and tissue necrosis factors contribute to systemic toxicity. Predisposing risk factors include trauma, diabetes mellitus, alcoholism, immunocompromised states, morbid obesity, and recent abdominal surgery.
Diagnosis Signs And Symptoms
This condition is a rapidly progressive necrotizing infection of the perineum involving subcutaneous tissue, fascia, and often muscle. It most commonly affects diabetic or immunocompromised patients. Early pain is often severe and out of proportion to physical findings; as necrosis progresses, affected tissue may become insensate. Associated symptoms include fever, chills, nausea, vomiting, urinary symptoms, lethargy, and inappropriate indifference to illness.
On examination, patients are often toxic appearing. Findings may include bronze or violaceous skin discoloration, thin brown malodorous discharge, ulceration, bullae, crepitus from subcutaneous air, frank necrosis, and eschar formation.
Essential Workup
Fournier gangrene is primarily a clinical diagnosis. A thorough history and focused examination of the perineum are critical. Evaluation for sepsis is mandatory, and early surgical consultation for emergent débridement is essential. Additional assessment should address underlying comorbidities such as diabetes or immunosuppression.
Diagnosis Tests And Interpretation
No laboratory test is diagnostic, but supportive findings include leukocytosis, anemia, electrolyte abnormalities, metabolic acidosis, renal failure, and possible disseminated intravascular coagulation. Urinalysis should be obtained. If diabetes is suspected or known, serum glucose, electrolytes, and ketones should be checked to evaluate for diabetic ketoacidosis. Blood, urine, and tissue cultures should be obtained when possible.
Imaging may show subcutaneous emphysema or ileus on plain pelvic radiographs. CT imaging is helpful when an intra-abdominal or ischiorectal source is suspected. Ultrasound may assist in differentiating Fournier gangrene from other causes of acute scrotum.
Differential Diagnosis
Epididymitis or orchitis, insect or human bites, perirectal infections, scrotal or inguinal abscess, scrotal cellulitis, testicular torsion, and tinea cruris.
Treatment
Prehospital care focuses on early recognition of septic shock with aggressive fluid resuscitation and vasopressor support if needed. Initial stabilization includes airway management, hemodynamic resuscitation, and avoidance of femoral venous access when possible.
Emergency department management requires immediate broad-spectrum intravenous antibiotics and emergent aggressive surgical débridement. Adjunctive hyperbaric oxygen therapy may be considered in coordination with surgical teams. Metabolic derangements, dehydration, anemia, and coagulopathy should be corrected, and tetanus prophylaxis administered as indicated.
Medication
Empiric antibiotic therapy should provide broad aerobic and anaerobic coverage and include agents such as ampicillin with clindamycin and gentamicin, or single-agent regimens like piperacillin–tazobactam, ampicillin–sulbactam, or carbapenems. Coverage for methicillin-resistant Staphylococcus aureus with vancomycin should be added when indicated. Insulin therapy is required for glycemic control, and vasopressors may be necessary for persistent hypotension.
Follow Up Disposition
All patients with Fournier gangrene require admission to a surgical intensive care unit. Mortality remains high despite treatment, emphasizing the importance of early recognition and aggressive management. Transfer to a facility capable of providing hyperbaric oxygen therapy should be considered when appropriate.
Key Practice Insights And Common Pitfalls
Failure to perform a careful genital and perineal examination can delay diagnosis. Delayed initiation of broad-spectrum antibiotics and surgical consultation significantly worsens outcomes. Early suspicion, prompt antibiotics, and immediate surgical intervention are critical to survival.
Basics Description
Inadequate hygiene can lead to maceration and excoriation of scrotal skin, creating a portal of entry for bacteria. Once the skin barrier is disrupted, polymicrobial organisms spread rapidly along fascial planes of the perineum. Colles fascia fuses with the urogenital diaphragm, limiting posterior and lateral spread, while continuity of Buck and Scarpa fascia allows rapid anterior extension to the abdominal wall and lateral spread along the fascia lata. The testes and urethra are typically spared.
Most cases originate from three anatomic sources: lower urinary tract infections such as urethral strictures or indwelling catheters, penile or scrotal sources including condom catheters, hidradenitis, or balanitis, and anorectal sources such as fistulas, perirectal infections, or hemorrhoids. Rarely, intra-abdominal pathology including perforated appendicitis, diverticulitis, or pancreatitis may spread contiguously.
Etiology
Fournier gangrene is caused by polymicrobial infection involving mixed aerobic and anaerobic organisms that act synergistically to destroy tissue. End-arterial thrombosis in subcutaneous tissues creates an anaerobic environment that promotes rapid progression. Bacterial toxins and tissue necrosis factors contribute to systemic toxicity. Predisposing risk factors include trauma, diabetes mellitus, alcoholism, immunocompromised states, morbid obesity, and recent abdominal surgery.
Diagnosis Signs And Symptoms
This condition is a rapidly progressive necrotizing infection of the perineum involving subcutaneous tissue, fascia, and often muscle. It most commonly affects diabetic or immunocompromised patients. Early pain is often severe and out of proportion to physical findings; as necrosis progresses, affected tissue may become insensate. Associated symptoms include fever, chills, nausea, vomiting, urinary symptoms, lethargy, and inappropriate indifference to illness.
On examination, patients are often toxic appearing. Findings may include bronze or violaceous skin discoloration, thin brown malodorous discharge, ulceration, bullae, crepitus from subcutaneous air, frank necrosis, and eschar formation.
Essential Workup
Fournier gangrene is primarily a clinical diagnosis. A thorough history and focused examination of the perineum are critical. Evaluation for sepsis is mandatory, and early surgical consultation for emergent débridement is essential. Additional assessment should address underlying comorbidities such as diabetes or immunosuppression.
Diagnosis Tests And Interpretation
No laboratory test is diagnostic, but supportive findings include leukocytosis, anemia, electrolyte abnormalities, metabolic acidosis, renal failure, and possible disseminated intravascular coagulation. Urinalysis should be obtained. If diabetes is suspected or known, serum glucose, electrolytes, and ketones should be checked to evaluate for diabetic ketoacidosis. Blood, urine, and tissue cultures should be obtained when possible.
Imaging may show subcutaneous emphysema or ileus on plain pelvic radiographs. CT imaging is helpful when an intra-abdominal or ischiorectal source is suspected. Ultrasound may assist in differentiating Fournier gangrene from other causes of acute scrotum.
Differential Diagnosis
Epididymitis or orchitis, insect or human bites, perirectal infections, scrotal or inguinal abscess, scrotal cellulitis, testicular torsion, and tinea cruris.
Treatment
Prehospital care focuses on early recognition of septic shock with aggressive fluid resuscitation and vasopressor support if needed. Initial stabilization includes airway management, hemodynamic resuscitation, and avoidance of femoral venous access when possible.
Emergency department management requires immediate broad-spectrum intravenous antibiotics and emergent aggressive surgical débridement. Adjunctive hyperbaric oxygen therapy may be considered in coordination with surgical teams. Metabolic derangements, dehydration, anemia, and coagulopathy should be corrected, and tetanus prophylaxis administered as indicated.
Medication
Empiric antibiotic therapy should provide broad aerobic and anaerobic coverage and include agents such as ampicillin with clindamycin and gentamicin, or single-agent regimens like piperacillin–tazobactam, ampicillin–sulbactam, or carbapenems. Coverage for methicillin-resistant Staphylococcus aureus with vancomycin should be added when indicated. Insulin therapy is required for glycemic control, and vasopressors may be necessary for persistent hypotension.
Follow Up Disposition
All patients with Fournier gangrene require admission to a surgical intensive care unit. Mortality remains high despite treatment, emphasizing the importance of early recognition and aggressive management. Transfer to a facility capable of providing hyperbaric oxygen therapy should be considered when appropriate.
Key Practice Insights And Common Pitfalls
Failure to perform a careful genital and perineal examination can delay diagnosis. Delayed initiation of broad-spectrum antibiotics and surgical consultation significantly worsens outcomes. Early suspicion, prompt antibiotics, and immediate surgical intervention are critical to survival.
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Emergency And Acute Medicine – Rectal Foreign Body
Basics Description
Rectal foreign bodies most commonly result from self-insertion, often related to autoerotic activity, typically involving phallic-shaped objects inserted by the patient or partner. This presentation occurs predominantly in men aged 20–40 years, with a marked male predominance. Other causes include ingested objects such as chicken or fish bones and toothpicks that become lodged in the rectum, iatrogenic accidents involving thermometers or enema tips, and objects used to aid fecal removal. Assault-related cases involve forcible insertion of objects such as knives or pipes and carry a high risk of perforation. Concealment for illicit drug transport, known as body packing, is another important etiology.
Diagnosis Signs And Symptoms
Patients may present with a clear complaint of a rectal foreign body, rectal fullness, or rectal pain. Complications include perirectal abscesses, particularly with sharp objects like bones or toothpicks. On rectal examination, low-lying foreign bodies located in the rectal ampulla are usually palpable, whereas high-lying foreign bodies proximal to the rectosigmoid junction are not. Some patients may provide vague or misleading histories and present with nonspecific abdominal pain, bowel obstruction, or signs of perforation with generalized peritonitis. Presentation is often delayed, sometimes hours or days after insertion, following repeated failed removal attempts. Rectal injuries are commonly classified using the Rectal Organ Injury Scale, with most foreign body–related injuries being low-grade contusions or hematomas.
Essential Workup
Evaluation begins with identifying the number, type, duration, and mechanism of insertion of the foreign body. A thorough physical examination with focused abdominal and rectal assessment is required, including classification as high-riding or low-riding based on the rectosigmoid junction. Biplane radiographs are recommended to confirm the number, size, and location of foreign bodies, especially as serious injury is more common in assault-related cases.
Diagnosis Tests And Interpretation
Laboratory studies may include a complete blood count to assess for bleeding or infection and urinalysis if genitourinary injury is suspected. Plain abdominal radiographs, often including a KUB view, should be obtained before rectal examination to protect the examiner and define the object’s location. Serial imaging may be used to monitor descent. CT imaging of the abdomen and pelvis is indicated when perforation, abscess, or other complications are suspected.
Differential Diagnosis
Consider pseudo–foreign body presentations in which patients insist on the presence of an object despite normal imaging and examinations. Other considerations include perirectal abscesses and hemorrhoids.
Treatment
Prehospital care emphasizes avoidance of repeated extraction attempts, as these increase the risk of perforation. Initial stabilization focuses on managing perforation, peritonitis, or sepsis with intravenous fluids, broad-spectrum antibiotics targeting anaerobic and gram-negative organisms, and urgent surgical consultation. In the emergency department, adequate analgesia and sedation are essential to overcome sphincter spasm and edema. Enemas and suppositories should be avoided.
Low-lying, small, nonfragile, and nonsharp foreign bodies may be removed transanally in the emergency department using gentle, continuous traction, often aided by patient Valsalva. A Foley catheter passed beyond the object with balloon insufflation can relieve the vacuum effect and facilitate removal. Various instruments may assist extraction, and a majority of low-lying foreign bodies can be successfully removed transanally under proper sedation. After removal, thorough anorectal evaluation is mandatory.
High-lying foreign bodies usually require surgical or gastroenterology consultation. Attempts may be made to reposition the object with gentle abdominal pressure, but blind extraction should be avoided. Admission for observation or operative intervention may be required, particularly for sharp objects, prolonged retention, or signs of perforation. Body packers require special caution due to the risk of packet rupture and systemic toxicity.
Medication
Broad-spectrum antibiotics such as ampicillin–sulbactam, piperacillin–tazobactam, ceftriaxone with metronidazole, or appropriate alternatives should be administered when infection or perforation is suspected. Pediatric dosing adjustments are required. Analgesia and procedural sedation should be provided as indicated.
Follow Up Disposition
Admission is required for failed emergency department extraction, evidence of perforation, mucosal injury requiring observation, or suspected abscess formation. Discharge may be appropriate for reliable patients with atraumatic insertion and uncomplicated removal, with strict return precautions for pain, fever, abdominal symptoms, or significant rectal bleeding.
Follow Up Recommendations
Flexible sigmoidoscopy or rigid proctoscopy is recommended after retrieval of any rectal foreign body to assess for mucosal injury, regardless of the method of removal.
Key Practice Insights And Common Pitfalls
Passing a Foley catheter beyond the object and insufflating air can effectively break the rectal vacuum and aid retrieval. Adequate sedation and analgesia are crucial for safe and successful removal. Avoid repeated blind attempts, which significantly increase the risk of rectal perforation.
Basics Description
Rectal foreign bodies most commonly result from self-insertion, often related to autoerotic activity, typically involving phallic-shaped objects inserted by the patient or partner. This presentation occurs predominantly in men aged 20–40 years, with a marked male predominance. Other causes include ingested objects such as chicken or fish bones and toothpicks that become lodged in the rectum, iatrogenic accidents involving thermometers or enema tips, and objects used to aid fecal removal. Assault-related cases involve forcible insertion of objects such as knives or pipes and carry a high risk of perforation. Concealment for illicit drug transport, known as body packing, is another important etiology.
Diagnosis Signs And Symptoms
Patients may present with a clear complaint of a rectal foreign body, rectal fullness, or rectal pain. Complications include perirectal abscesses, particularly with sharp objects like bones or toothpicks. On rectal examination, low-lying foreign bodies located in the rectal ampulla are usually palpable, whereas high-lying foreign bodies proximal to the rectosigmoid junction are not. Some patients may provide vague or misleading histories and present with nonspecific abdominal pain, bowel obstruction, or signs of perforation with generalized peritonitis. Presentation is often delayed, sometimes hours or days after insertion, following repeated failed removal attempts. Rectal injuries are commonly classified using the Rectal Organ Injury Scale, with most foreign body–related injuries being low-grade contusions or hematomas.
Essential Workup
Evaluation begins with identifying the number, type, duration, and mechanism of insertion of the foreign body. A thorough physical examination with focused abdominal and rectal assessment is required, including classification as high-riding or low-riding based on the rectosigmoid junction. Biplane radiographs are recommended to confirm the number, size, and location of foreign bodies, especially as serious injury is more common in assault-related cases.
Diagnosis Tests And Interpretation
Laboratory studies may include a complete blood count to assess for bleeding or infection and urinalysis if genitourinary injury is suspected. Plain abdominal radiographs, often including a KUB view, should be obtained before rectal examination to protect the examiner and define the object’s location. Serial imaging may be used to monitor descent. CT imaging of the abdomen and pelvis is indicated when perforation, abscess, or other complications are suspected.
Differential Diagnosis
Consider pseudo–foreign body presentations in which patients insist on the presence of an object despite normal imaging and examinations. Other considerations include perirectal abscesses and hemorrhoids.
Treatment
Prehospital care emphasizes avoidance of repeated extraction attempts, as these increase the risk of perforation. Initial stabilization focuses on managing perforation, peritonitis, or sepsis with intravenous fluids, broad-spectrum antibiotics targeting anaerobic and gram-negative organisms, and urgent surgical consultation. In the emergency department, adequate analgesia and sedation are essential to overcome sphincter spasm and edema. Enemas and suppositories should be avoided.
Low-lying, small, nonfragile, and nonsharp foreign bodies may be removed transanally in the emergency department using gentle, continuous traction, often aided by patient Valsalva. A Foley catheter passed beyond the object with balloon insufflation can relieve the vacuum effect and facilitate removal. Various instruments may assist extraction, and a majority of low-lying foreign bodies can be successfully removed transanally under proper sedation. After removal, thorough anorectal evaluation is mandatory.
High-lying foreign bodies usually require surgical or gastroenterology consultation. Attempts may be made to reposition the object with gentle abdominal pressure, but blind extraction should be avoided. Admission for observation or operative intervention may be required, particularly for sharp objects, prolonged retention, or signs of perforation. Body packers require special caution due to the risk of packet rupture and systemic toxicity.
Medication
Broad-spectrum antibiotics such as ampicillin–sulbactam, piperacillin–tazobactam, ceftriaxone with metronidazole, or appropriate alternatives should be administered when infection or perforation is suspected. Pediatric dosing adjustments are required. Analgesia and procedural sedation should be provided as indicated.
Follow Up Disposition
Admission is required for failed emergency department extraction, evidence of perforation, mucosal injury requiring observation, or suspected abscess formation. Discharge may be appropriate for reliable patients with atraumatic insertion and uncomplicated removal, with strict return precautions for pain, fever, abdominal symptoms, or significant rectal bleeding.
Follow Up Recommendations
Flexible sigmoidoscopy or rigid proctoscopy is recommended after retrieval of any rectal foreign body to assess for mucosal injury, regardless of the method of removal.
Key Practice Insights And Common Pitfalls
Passing a Foley catheter beyond the object and insufflating air can effectively break the rectal vacuum and aid retrieval. Adequate sedation and analgesia are crucial for safe and successful removal. Avoid repeated blind attempts, which significantly increase the risk of rectal perforation.
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Emergency And Acute Medicine – Nasal Foreign Body
Basics Description
A nasal foreign body is an object lodged within the nasal cavity and represents the most common site of foreign body insertion in children. The type of object is limited primarily by the size of the nostril. Children between 2–6 years are most commonly affected, with increased risk in those with intellectual disability or psychiatric illness. Impaction and removal difficulty worsen over time due to mucosal swelling or expansion of organic material when moistened. Sinusitis is the most frequent complication, though foreign bodies may migrate into the sinuses. Serious complications include septal perforation, bronchial aspiration, and, with button batteries, ischemic mucosal injury, turbinate or septal damage, and saddle-nose deformity.
Etiology
Common objects include food items such as beans and seeds, beads, rocks, paper, toy parts, sponge fragments, vegetable matter, insects, and live worms. Button batteries pose a particularly high risk and require rapid removal due to tissue necrosis and structural damage. Magnets, often used to mimic nasal piercings, may become embedded in tissue and are difficult to remove; ingestion carries a risk of intestinal perforation. Glass fragments are less common but possible.
Diagnosis Signs And Symptoms
Many nasal foreign bodies are asymptomatic. When present, symptoms include unilateral nasal obstruction, nasal pain, difficulty breathing through the nose, and unilateral nasal discharge that may be foul-smelling or chronic. Other findings include halitosis, sinus discomfort, persistent epistaxis, local inflammation, and septal perforation. Delayed presentations are common when insertion is unwitnessed and may be misdiagnosed as sinusitis.
Essential Workup
Direct visualization of the foreign body within the nostril is essential. Both nostrils must always be examined.
Diagnosis Tests And Interpretation
Fiberoptic visualization may be required if the object is not seen on routine examination. Sinus imaging may be considered for prolonged retention or persistent symptoms despite removal and antibiotics. Chest or abdominal imaging may be needed if aspiration or ingestion is suspected.
Differential Diagnosis
Conditions to consider include sinusitis, swollen inferior turbinate, rhinitis, nasal polyps, benign tumors such as hemangioma, malignant tumors including lymphoma or rhabdomyosarcoma, congenital nasal masses, retropharyngeal abscess, traumatic nasal injury, structural nasal deformities, and rhinitis medicamentosa.
Treatment
Prehospital care emphasizes transport in the sitting position and avoidance of distressing interventions that may provoke aspiration. In the emergency department, topical vasoconstrictors may be used to reduce mucosal edema or bleeding. Positive-pressure techniques are particularly effective in children and involve occluding the unaffected nostril while applying a brisk puff of air to the mouth, often performed by a caregiver.
Mechanical removal options include hooked probes or alligator forceps for anterior, graspable objects; suction catheters for smooth, round objects; cyanoacrylate tissue glue applied to a swab handle; balloon catheters such as Foley or Fogarty passed beyond the object and withdrawn after inflation; magnets for metallic objects; and snare techniques using fine wire. Procedural sedation may be required if the child is uncooperative or removal attempts fail.
Medication
Topical agents may include cocaine 4%, lidocaine 4%, oxymetazoline 0.05%, or phenylephrine 0.125–0.5%. Procedural sedation is used selectively.
Follow Up Disposition
Admission or referral for operative removal is required if the foreign body cannot be removed in the emergency department or if general anesthesia is necessary. Discharge is appropriate once removal is successful and airway compromise is excluded. Patients with button battery exposure require monitoring for delayed complications.
Follow Up Recommendations
Parents should seek immediate care if the child develops coughing, wheezing, noisy or difficult breathing, vomiting, choking, drooling, neck or throat pain, or inability to swallow. Medical review is also advised for fever, headache or facial pain, persistent epistaxis, or ongoing nasal discharge.
Key Practice Insights And Common Pitfalls
Always consider a nasal foreign body in children aged 2–6 years presenting with unilateral, foul-smelling nasal discharge. Caregiver-assisted positive-pressure techniques are often effective and minimally traumatic. Combining topical lidocaine with oxymetazoline can improve comfort and visualization during removal.
Basics Description
A nasal foreign body is an object lodged within the nasal cavity and represents the most common site of foreign body insertion in children. The type of object is limited primarily by the size of the nostril. Children between 2–6 years are most commonly affected, with increased risk in those with intellectual disability or psychiatric illness. Impaction and removal difficulty worsen over time due to mucosal swelling or expansion of organic material when moistened. Sinusitis is the most frequent complication, though foreign bodies may migrate into the sinuses. Serious complications include septal perforation, bronchial aspiration, and, with button batteries, ischemic mucosal injury, turbinate or septal damage, and saddle-nose deformity.
Etiology
Common objects include food items such as beans and seeds, beads, rocks, paper, toy parts, sponge fragments, vegetable matter, insects, and live worms. Button batteries pose a particularly high risk and require rapid removal due to tissue necrosis and structural damage. Magnets, often used to mimic nasal piercings, may become embedded in tissue and are difficult to remove; ingestion carries a risk of intestinal perforation. Glass fragments are less common but possible.
Diagnosis Signs And Symptoms
Many nasal foreign bodies are asymptomatic. When present, symptoms include unilateral nasal obstruction, nasal pain, difficulty breathing through the nose, and unilateral nasal discharge that may be foul-smelling or chronic. Other findings include halitosis, sinus discomfort, persistent epistaxis, local inflammation, and septal perforation. Delayed presentations are common when insertion is unwitnessed and may be misdiagnosed as sinusitis.
Essential Workup
Direct visualization of the foreign body within the nostril is essential. Both nostrils must always be examined.
Diagnosis Tests And Interpretation
Fiberoptic visualization may be required if the object is not seen on routine examination. Sinus imaging may be considered for prolonged retention or persistent symptoms despite removal and antibiotics. Chest or abdominal imaging may be needed if aspiration or ingestion is suspected.
Differential Diagnosis
Conditions to consider include sinusitis, swollen inferior turbinate, rhinitis, nasal polyps, benign tumors such as hemangioma, malignant tumors including lymphoma or rhabdomyosarcoma, congenital nasal masses, retropharyngeal abscess, traumatic nasal injury, structural nasal deformities, and rhinitis medicamentosa.
Treatment
Prehospital care emphasizes transport in the sitting position and avoidance of distressing interventions that may provoke aspiration. In the emergency department, topical vasoconstrictors may be used to reduce mucosal edema or bleeding. Positive-pressure techniques are particularly effective in children and involve occluding the unaffected nostril while applying a brisk puff of air to the mouth, often performed by a caregiver.
Mechanical removal options include hooked probes or alligator forceps for anterior, graspable objects; suction catheters for smooth, round objects; cyanoacrylate tissue glue applied to a swab handle; balloon catheters such as Foley or Fogarty passed beyond the object and withdrawn after inflation; magnets for metallic objects; and snare techniques using fine wire. Procedural sedation may be required if the child is uncooperative or removal attempts fail.
Medication
Topical agents may include cocaine 4%, lidocaine 4%, oxymetazoline 0.05%, or phenylephrine 0.125–0.5%. Procedural sedation is used selectively.
Follow Up Disposition
Admission or referral for operative removal is required if the foreign body cannot be removed in the emergency department or if general anesthesia is necessary. Discharge is appropriate once removal is successful and airway compromise is excluded. Patients with button battery exposure require monitoring for delayed complications.
Follow Up Recommendations
Parents should seek immediate care if the child develops coughing, wheezing, noisy or difficult breathing, vomiting, choking, drooling, neck or throat pain, or inability to swallow. Medical review is also advised for fever, headache or facial pain, persistent epistaxis, or ongoing nasal discharge.
Key Practice Insights And Common Pitfalls
Always consider a nasal foreign body in children aged 2–6 years presenting with unilateral, foul-smelling nasal discharge. Caregiver-assisted positive-pressure techniques are often effective and minimally traumatic. Combining topical lidocaine with oxymetazoline can improve comfort and visualization during removal.
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Emergency And Acute Medicine – Foreign Body, Esophageal
Basics Description
Esophageal foreign bodies typically lodge at physiologic narrowing points: the cricopharyngeal muscle at C6 (≈63%, most common), the level of the aortic arch at T4 (≈10%), and the gastroesophageal junction at T11 (≈20%). Approximately 90% of ingested foreign bodies pass spontaneously, 10–20% require endoscopic removal, and fewer than 1% require surgical intervention.
Etiology
In adults and adolescents, food boluses and bones are most common. Risk is increased in edentulous patients, intoxicated individuals, and those with underlying esophageal pathology such as Schatzki B-rings or peptic strictures.
Pediatric ingestions account for about 80% of cases, most commonly between 6 months and 6 years of age, especially under 2 years. Coins are the most frequent pediatric esophageal foreign body. Additional pediatric constriction sites include the thoracic inlet (T1) and the tracheal bifurcation (T6).
Diagnosis Signs And Symptoms
Acute ingestion may cause dysphagia, odynophagia, drooling, gagging, choking, retching, blood-stained saliva, or chest discomfort. Chronically retained foreign bodies often present with respiratory symptoms such as cough, stridor, or hoarseness due to paraesophageal swelling compressing the airway.
Sharp object ingestion carries a 15–35% risk of esophageal perforation, with findings including neck swelling, erythema, crepitus, chest pain, pleurisy, or peritonitis.
Adults usually provide a clear history and often present within 24 hours. Children may be asymptomatic or present with drooling, refusal to eat, unexplained gagging, cough, wheeze, or choking; history may be unclear if ingestion was unwitnessed.
Essential Workup
Obtain a detailed history regarding the type, size, and timing of ingestion. Physical examination should assess for obstruction, perforation, aspiration, hemorrhage, and airway compromise, including evaluation of the neck, chest, lungs, abdomen, and oropharynx.
Diagnosis Tests And Interpretation
Biplane chest and neck radiographs are used to localize radiopaque foreign bodies; esophageal objects often align in the coronal plane. Signs of perforation include retropharyngeal air, cervical soft tissue air, or pneumomediastinum. Many bones and food boluses are radiolucent.
CT scanning is increasingly used for radiolucent objects and to detect perforation or infection.
Endoscopy is the diagnostic and therapeutic modality of choice, allowing direct visualization, removal, and evaluation of underlying mucosal pathology.
Differential Diagnosis
Globus sensation, esophagitis, esophageal mucosal irritation, croup, epiglottitis, upper respiratory tract infection, and retropharyngeal abscess.
Treatment
Prehospital care prioritizes airway protection and aspiration prevention; emetics and cathartics are contraindicated.
In the emergency department, airway, breathing, and circulation take priority. Direct laryngoscopy may remove very proximal objects.
Urgent endoscopy is indicated for sharp or elongated objects (>6 cm long or >2.5 cm wide), irregular edges, multiple objects (especially magnets), suspected perforation, airway compromise, food bolus with complete obstruction, foreign bodies present for more than 24 hours, or coins lodged at the cricopharyngeus in children.
Asymptomatic patients with smooth objects in the distal esophagus (excluding button batteries) may be observed for up to 24 hours.
Glucagon may be considered for recent distal food bolus impaction but is less effective with strictures and is falling out of favor.
Fluoroscopically guided Foley catheter extraction or bougienage may be used in selected cases by experienced providers.
Button batteries require emergent removal due to rapid liquefaction necrosis. Magnets require early GI or surgical consultation. Surgical intervention is reserved for failed endoscopic removal or complications.
Medication
Glucagon 1–2 mg IV may be used selectively for distal food bolus impaction after assessing for contraindications.
Follow Up Disposition
Admission is required for airway compromise, perforation, significant bleeding, migration of the foreign body, or failed removal.
Discharge is appropriate for asymptomatic patients after removal or confirmed passage into the stomach, with re-evaluation within 12–24 hours if distal esophageal objects are observed.
Follow Up Recommendations
GI referral is recommended when underlying esophageal pathology is suspected or for follow-up after complicated ingestions.
Key Practice Insights And Common Pitfalls
Always localize radiopaque foreign bodies with imaging and maintain a high index of suspicion for esophageal perforation, particularly with sharp objects or delayed presentation.
Basics Description
Esophageal foreign bodies typically lodge at physiologic narrowing points: the cricopharyngeal muscle at C6 (≈63%, most common), the level of the aortic arch at T4 (≈10%), and the gastroesophageal junction at T11 (≈20%). Approximately 90% of ingested foreign bodies pass spontaneously, 10–20% require endoscopic removal, and fewer than 1% require surgical intervention.
Etiology
In adults and adolescents, food boluses and bones are most common. Risk is increased in edentulous patients, intoxicated individuals, and those with underlying esophageal pathology such as Schatzki B-rings or peptic strictures.
Pediatric ingestions account for about 80% of cases, most commonly between 6 months and 6 years of age, especially under 2 years. Coins are the most frequent pediatric esophageal foreign body. Additional pediatric constriction sites include the thoracic inlet (T1) and the tracheal bifurcation (T6).
Diagnosis Signs And Symptoms
Acute ingestion may cause dysphagia, odynophagia, drooling, gagging, choking, retching, blood-stained saliva, or chest discomfort. Chronically retained foreign bodies often present with respiratory symptoms such as cough, stridor, or hoarseness due to paraesophageal swelling compressing the airway.
Sharp object ingestion carries a 15–35% risk of esophageal perforation, with findings including neck swelling, erythema, crepitus, chest pain, pleurisy, or peritonitis.
Adults usually provide a clear history and often present within 24 hours. Children may be asymptomatic or present with drooling, refusal to eat, unexplained gagging, cough, wheeze, or choking; history may be unclear if ingestion was unwitnessed.
Essential Workup
Obtain a detailed history regarding the type, size, and timing of ingestion. Physical examination should assess for obstruction, perforation, aspiration, hemorrhage, and airway compromise, including evaluation of the neck, chest, lungs, abdomen, and oropharynx.
Diagnosis Tests And Interpretation
Biplane chest and neck radiographs are used to localize radiopaque foreign bodies; esophageal objects often align in the coronal plane. Signs of perforation include retropharyngeal air, cervical soft tissue air, or pneumomediastinum. Many bones and food boluses are radiolucent.
CT scanning is increasingly used for radiolucent objects and to detect perforation or infection.
Endoscopy is the diagnostic and therapeutic modality of choice, allowing direct visualization, removal, and evaluation of underlying mucosal pathology.
Differential Diagnosis
Globus sensation, esophagitis, esophageal mucosal irritation, croup, epiglottitis, upper respiratory tract infection, and retropharyngeal abscess.
Treatment
Prehospital care prioritizes airway protection and aspiration prevention; emetics and cathartics are contraindicated.
In the emergency department, airway, breathing, and circulation take priority. Direct laryngoscopy may remove very proximal objects.
Urgent endoscopy is indicated for sharp or elongated objects (>6 cm long or >2.5 cm wide), irregular edges, multiple objects (especially magnets), suspected perforation, airway compromise, food bolus with complete obstruction, foreign bodies present for more than 24 hours, or coins lodged at the cricopharyngeus in children.
Asymptomatic patients with smooth objects in the distal esophagus (excluding button batteries) may be observed for up to 24 hours.
Glucagon may be considered for recent distal food bolus impaction but is less effective with strictures and is falling out of favor.
Fluoroscopically guided Foley catheter extraction or bougienage may be used in selected cases by experienced providers.
Button batteries require emergent removal due to rapid liquefaction necrosis. Magnets require early GI or surgical consultation. Surgical intervention is reserved for failed endoscopic removal or complications.
Medication
Glucagon 1–2 mg IV may be used selectively for distal food bolus impaction after assessing for contraindications.
Follow Up Disposition
Admission is required for airway compromise, perforation, significant bleeding, migration of the foreign body, or failed removal.
Discharge is appropriate for asymptomatic patients after removal or confirmed passage into the stomach, with re-evaluation within 12–24 hours if distal esophageal objects are observed.
Follow Up Recommendations
GI referral is recommended when underlying esophageal pathology is suspected or for follow-up after complicated ingestions.
Key Practice Insights And Common Pitfalls
Always localize radiopaque foreign bodies with imaging and maintain a high index of suspicion for esophageal perforation, particularly with sharp objects or delayed presentation.
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Emergency And Acute Medicine - Erythema Infectiosum
Basic description
Erythema infectiosum is a characteristic viral exanthem, also known as fifth disease, historically the fifth most commonly described childhood rash. It typically presents with a mild viral prodrome followed by a “slapped-cheek” facial rash and a subsequent diffuse, lacy, reticular eruption, with or without arthropathy. It most commonly affects school-aged children younger than 14 years and is usually self-limited with lifelong immunity. Chronic or severe disease is rare but may occur in patients with congenital anemias or immunosuppression. Infection during pregnancy carries a risk of serious fetal complications.
Etiology
The condition is caused by human parvovirus B19, a small single-stranded DNA virus that infects human erythroid progenitor cells and transiently suppresses erythropoiesis. Transmission occurs via respiratory droplets, blood products, and vertical maternal–fetal spread. It is most common in late winter and spring. The incubation period ranges from 4 to 21 days, and patients are most contagious during the week before rash onset. Most adults have serologic evidence of prior infection.
Diagnosis – signs and symptoms
Young children typically develop a bright erythematous “slapped-cheek” rash accompanied by low-grade fever and malaise. Four to fourteen days later, a diffuse, pruritic, lacy rash may appear, most prominent on the extremities and usually sparing the palms and soles. Adolescents and adults may develop symmetric polyarthropathy, particularly involving small joints, while children more commonly experience knee involvement. Many patients remain asymptomatic or experience only mild viral symptoms.
History
Symptoms often begin with mild constitutional complaints such as fever, headache, nasal congestion, nausea, or sore throat. Patients are contagious only before the facial rash appears.
Physical examination
Stage one consists of coalescent, warm, erythematous, edematous facial papules with circumoral pallor. Stage two features a diffuse, maculopapular, reticular rash that may persist for weeks. Stage three is marked by fading of the rash with recurrence triggered by heat, sunlight, stress, or exercise, eventually resolving without scarring.
Essential workup
Diagnosis is clinical and based on classic presentation.
Diagnosis tests and interpretation
Laboratory testing is usually unnecessary. A CBC and reticulocyte count are indicated if aplastic crisis is suspected. In immunocompromised or pregnant patients, confirmation may be obtained with parvovirus B19 PCR or serology. IgM antibodies indicate acute infection, while IgG antibodies confirm immunity. Pregnant patients may require ultrasound monitoring for hydrops fetalis.
Differential diagnosis
Allergic reaction, drug eruption, nonspecific viral exanthem, measles, rubella, roseola, scarlet fever, erysipelas, infectious mononucleosis, collagen vascular disease, rheumatoid arthritis, sunburn, and enteroviral infections.
Treatment
The disease is typically self-limited and requires no specific therapy.
Prehospital care
Supportive care and standard ABCs for severe presentations.
Initial stabilization and therapy
Airway, breathing, and circulation management as needed. Supplemental oxygen and intravenous fluids may be required for severe dehydration. Severe anemia should be treated with packed red blood cell transfusion. Analgesia may be provided for arthropathy.
Emergency department treatment and procedures
No antiviral therapy or vaccine is available. Management is supportive, including antipyretics for fever, NSAIDs for joint pain if renal function permits, antihistamines for pruritus, and IV fluids when indicated. Immunocompromised patients with chronic infection or red cell aplasia may benefit from IVIG in consultation with infectious disease specialists. Hospitalization is indicated for aplastic crisis or severe complications.
Medication
Acetaminophen or ibuprofen for fever and pain. Diphenhydramine may be used for pruritus with caution regarding sedation. IVIG is reserved for select cases under specialist guidance.
Follow-up and disposition
Admission criteria
Aplastic crisis, severe anemia, hydrops fetalis, severe immunosuppression, toxic appearance, or debilitating arthritis.
Discharge criteria
Most patients can be safely discharged. Once the facial rash appears, patients are no longer contagious and may return to school or work if clinically stable.
Issues for referral
Hematology referral for patients with hereditary anemias or aplastic crisis. Infectious disease consultation for immunocompromised patients. Obstetric referral for pregnant patients with confirmed or suspected acute infection.
Follow-up recommendations
Pregnant patients with new infection require serial ultrasounds for 10–12 weeks. Patients at risk for aplastic crisis should have repeat CBC testing within 1–2 days.
Patient education
There is no vaccine. Hand hygiene reduces transmission. Children are usually no longer contagious by the time the rash appears, so exclusion from school is generally unnecessary.
Complications
Transient aplastic crisis in patients with underlying anemias, chronic anemia in immunocompromised individuals, arthropathy in adults, rare neurologic or cardiac involvement, and pregnancy-related complications including hydrops fetalis and fetal loss.
Clinical pearls and common missteps
Parvovirus B19 infection is usually mild and self-limited. Patients are not contagious once the rash appears. Always evaluate patients with anemia or immunosuppression for complications. Confirm infection in pregnancy and ensure appropriate fetal monitoring.
Basic description
Erythema infectiosum is a characteristic viral exanthem, also known as fifth disease, historically the fifth most commonly described childhood rash. It typically presents with a mild viral prodrome followed by a “slapped-cheek” facial rash and a subsequent diffuse, lacy, reticular eruption, with or without arthropathy. It most commonly affects school-aged children younger than 14 years and is usually self-limited with lifelong immunity. Chronic or severe disease is rare but may occur in patients with congenital anemias or immunosuppression. Infection during pregnancy carries a risk of serious fetal complications.
Etiology
The condition is caused by human parvovirus B19, a small single-stranded DNA virus that infects human erythroid progenitor cells and transiently suppresses erythropoiesis. Transmission occurs via respiratory droplets, blood products, and vertical maternal–fetal spread. It is most common in late winter and spring. The incubation period ranges from 4 to 21 days, and patients are most contagious during the week before rash onset. Most adults have serologic evidence of prior infection.
Diagnosis – signs and symptoms
Young children typically develop a bright erythematous “slapped-cheek” rash accompanied by low-grade fever and malaise. Four to fourteen days later, a diffuse, pruritic, lacy rash may appear, most prominent on the extremities and usually sparing the palms and soles. Adolescents and adults may develop symmetric polyarthropathy, particularly involving small joints, while children more commonly experience knee involvement. Many patients remain asymptomatic or experience only mild viral symptoms.
History
Symptoms often begin with mild constitutional complaints such as fever, headache, nasal congestion, nausea, or sore throat. Patients are contagious only before the facial rash appears.
Physical examination
Stage one consists of coalescent, warm, erythematous, edematous facial papules with circumoral pallor. Stage two features a diffuse, maculopapular, reticular rash that may persist for weeks. Stage three is marked by fading of the rash with recurrence triggered by heat, sunlight, stress, or exercise, eventually resolving without scarring.
Essential workup
Diagnosis is clinical and based on classic presentation.
Diagnosis tests and interpretation
Laboratory testing is usually unnecessary. A CBC and reticulocyte count are indicated if aplastic crisis is suspected. In immunocompromised or pregnant patients, confirmation may be obtained with parvovirus B19 PCR or serology. IgM antibodies indicate acute infection, while IgG antibodies confirm immunity. Pregnant patients may require ultrasound monitoring for hydrops fetalis.
Differential diagnosis
Allergic reaction, drug eruption, nonspecific viral exanthem, measles, rubella, roseola, scarlet fever, erysipelas, infectious mononucleosis, collagen vascular disease, rheumatoid arthritis, sunburn, and enteroviral infections.
Treatment
The disease is typically self-limited and requires no specific therapy.
Prehospital care
Supportive care and standard ABCs for severe presentations.
Initial stabilization and therapy
Airway, breathing, and circulation management as needed. Supplemental oxygen and intravenous fluids may be required for severe dehydration. Severe anemia should be treated with packed red blood cell transfusion. Analgesia may be provided for arthropathy.
Emergency department treatment and procedures
No antiviral therapy or vaccine is available. Management is supportive, including antipyretics for fever, NSAIDs for joint pain if renal function permits, antihistamines for pruritus, and IV fluids when indicated. Immunocompromised patients with chronic infection or red cell aplasia may benefit from IVIG in consultation with infectious disease specialists. Hospitalization is indicated for aplastic crisis or severe complications.
Medication
Acetaminophen or ibuprofen for fever and pain. Diphenhydramine may be used for pruritus with caution regarding sedation. IVIG is reserved for select cases under specialist guidance.
Follow-up and disposition
Admission criteria
Aplastic crisis, severe anemia, hydrops fetalis, severe immunosuppression, toxic appearance, or debilitating arthritis.
Discharge criteria
Most patients can be safely discharged. Once the facial rash appears, patients are no longer contagious and may return to school or work if clinically stable.
Issues for referral
Hematology referral for patients with hereditary anemias or aplastic crisis. Infectious disease consultation for immunocompromised patients. Obstetric referral for pregnant patients with confirmed or suspected acute infection.
Follow-up recommendations
Pregnant patients with new infection require serial ultrasounds for 10–12 weeks. Patients at risk for aplastic crisis should have repeat CBC testing within 1–2 days.
Patient education
There is no vaccine. Hand hygiene reduces transmission. Children are usually no longer contagious by the time the rash appears, so exclusion from school is generally unnecessary.
Complications
Transient aplastic crisis in patients with underlying anemias, chronic anemia in immunocompromised individuals, arthropathy in adults, rare neurologic or cardiac involvement, and pregnancy-related complications including hydrops fetalis and fetal loss.
Clinical pearls and common missteps
Parvovirus B19 infection is usually mild and self-limited. Patients are not contagious once the rash appears. Always evaluate patients with anemia or immunosuppression for complications. Confirm infection in pregnancy and ensure appropriate fetal monitoring.
