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Emergency And Acute Medicine - Esophageal trauma
Basic description
The adult esophagus is approximately 25–30 cm in length and lies in close proximity to the mediastinum, with potential access to the pleural space. It begins at the hypopharynx posterior to the larynx at the level of the cricoid cartilage. On either side are the piriform recesses, which are common sites for foreign body lodgment.
Physiologic narrowing occurs at the cricopharyngeal muscle (upper esophageal sphincter), at the crossover of the left mainstem bronchus and aortic arch, and at the gastroesophageal junction (lower esophageal sphincter). Additional narrowing may occur in areas of disease such as malignancy, webs, or Schatzki rings.
The upper third of the esophagus consists of striated muscle and initiates swallowing. The middle third contains both striated and smooth muscle, and the distal third is composed entirely of smooth muscle. Although relatively fixed, the esophagus may be displaced by adjacent structures such as goiter, enlarged atria, or mediastinal masses.
Etiology
Esophageal trauma may result from external or internal forces.
External mechanisms include penetrating injuries such as stab or missile wounds, direct perforation from foreign bodies, pressure necrosis, chemical or radiation injury, and iatrogenic trauma from instrumentation. Blunt trauma, most commonly from motor vehicle collisions, may also cause injury.
Internal mechanisms include caustic ingestions, infections, medication-induced injury, swallowed foreign bodies, iatrogenic causes, and barotrauma.
Caustic ingestions include alkali substances, which cause liquefaction necrosis and deep tissue penetration, and acids, which cause coagulation necrosis and thermal injury. Chlorine bleach typically causes mucosal edema and superficial erythema.
Infectious causes include viral infections such as CMV, HPV, and HSV, and fungal infections in immunocompromised patients.
Medication-related injury has been reported with agents such as alendronate, doxycycline, NSAIDs, and mycophenolate mofetil.
Swallowed foreign bodies include food bolus impaction, coins, bones, pins, and button batteries. Meat impaction is the most common type in adults, particularly among prisoners, psychiatric patients, intoxicated individuals, and edentulous patients.
Iatrogenic injury accounts for more than half of cases, most commonly due to endoscopy, nasogastric tube placement, or nasotracheal intubation.
Increased intraluminal pressure from vomiting or retching may result in Mallory–Weiss tears, which are mucosal lacerations with bleeding, or Boerhaave syndrome, which is a spontaneous full-thickness rupture of the distal esophagus.
Pediatric considerations
Foreign body ingestion accounts for most cases of esophageal trauma in children, particularly in those aged 18–48 months. Perforations are most often iatrogenic. Caustic ingestions are more common in children younger than five years. Button batteries lodged in the esophagus require urgent removal due to their highly alkaline nature. Single-use laundry detergent packets are an increasingly common hazard.
Diagnosis – signs and symptoms
Common symptoms include dysphagia, odynophagia, chest pain that may be pleuritic and severe, hoarseness, and dyspnea.
Tears or perforations may present with bleeding or hematemesis.
Foreign body ingestion may cause drooling, choking, gagging, vomiting, stridor, wheezing, or inability to tolerate oral intake.
Caustic ingestion may produce oral pain, abdominal pain, vomiting, and drooling.
History
Key historical elements include the type, amount, and timing of ingestions; history of prolonged vomiting; sudden inability to swallow after eating; foreign body sensation; penetrating trauma; or prior cancer therapy.
Physical examination
Findings suggestive of perforation include subcutaneous emphysema at the base of the neck, a Hamman crunch due to mediastinal air, signs of shock, septicemia, or peritonitis.
Penetrating trauma may be associated with injuries to the trachea, neck, chest, or abdomen.
Caustic ingestions may cause airway edema with stridor and visible oral burns.
Essential workup
A high index of suspicion and early diagnosis are critical. Mortality for esophageal perforation is less than 5% if repaired within 24 hours but increases dramatically with delayed diagnosis. Early endoscopy is indicated for caustic ingestions. Chest and lateral neck radiographs are part of the initial evaluation.
Diagnosis tests and interpretation
Laboratory studies may include complete blood count, type and crossmatch for significant bleeding, coagulation studies, electrolytes for prolonged vomiting or retained foreign body, and arterial blood gas analysis in acid ingestions.
Imaging includes chest radiography to assess for pneumomediastinum, pneumothorax, widened mediastinum, or pleural effusion. Lateral cervical spine radiographs may reveal retropharyngeal air or fluid.
Esophagram is useful for suspected perforation, with water-soluble contrast preferred initially. Endoscopy is indicated for suspected perforation, caustic injury, or foreign body removal. CT with dilute oral contrast may aid in identifying perforation and associated complications.
Differential diagnosis
Pulmonary causes include tracheal injury and pneumothorax. Cardiovascular causes include myocardial infarction and aortic dissection. Other esophageal conditions include strictures, neoplasm, Schatzki ring, diverticula, achalasia, esophageal spasm, gastroesophageal reflux, and medication-induced esophagitis.
Treatment
Prehospital care
Chest pain should be presumed cardiac until proven otherwise. Airway protection, suctioning of secretions, intravenous fluids for hypotension or bleeding, and analgesia are indicated. Neutralizing agents and large volumes of oral fluids should be avoided in caustic ingestions.
Initial stabilization and therapy
Airway management and resuscitation are priorities. Establish intravenous access, initiate monitoring, and consider early intubation for penetrating neck or chest injuries.
Emergency department treatment and procedures
Most foreign bodies pass spontaneously, but endoscopic removal is required in a significant minority. Pharmacologic measures such as glucagon, nitroglycerin, or benzodiazepines may be attempted for food impaction. Gastroenterology consultation is indicated if these measures fail.
Caustic ingestions require avoidance of emesis and lavage, cautious dilution with milk, and early endoscopy for prognostication. Corticosteroids are not recommended.
Partial-thickness tears generally heal spontaneously. Full-thickness perforations require surgical consultation, broad-spectrum intravenous antibiotics, and possible operative repair.
Medication
For food impaction, glucagon, nitroglycerin, or diazepam may be used selectively.
For perforation, broad-spectrum intravenous antibiotics such as cefoxitin with gentamicin are indicated. Steroids are not indicated in caustic injury.
Follow-up and disposition
Admission criteria
Indications for admission include caustic ingestion, sharp foreign bodies, airway compromise, penetrating neck or chest trauma, evidence of sepsis or mediastinitis, esophageal perforation, significant bleeding, and inability to tolerate oral intake.
Discharge criteria
Patients may be discharged if bleeding from a partial-thickness tear is self-limited or if a foreign body or food bolus has passed beyond the lower esophageal sphincter without complications.
Clinical pearls and common pitfalls
Time to diagnosis and definitive therapy is the most important predictor of outcome, with intervention within 24 hours significantly reducing mortality. Cervical injuries have better outcomes than thoracic or abdominal injuries. Spontaneous perforation carries the highest mortality, followed by iatrogenic and then traumatic causes.
Basic description
The adult esophagus is approximately 25–30 cm in length and lies in close proximity to the mediastinum, with potential access to the pleural space. It begins at the hypopharynx posterior to the larynx at the level of the cricoid cartilage. On either side are the piriform recesses, which are common sites for foreign body lodgment.
Physiologic narrowing occurs at the cricopharyngeal muscle (upper esophageal sphincter), at the crossover of the left mainstem bronchus and aortic arch, and at the gastroesophageal junction (lower esophageal sphincter). Additional narrowing may occur in areas of disease such as malignancy, webs, or Schatzki rings.
The upper third of the esophagus consists of striated muscle and initiates swallowing. The middle third contains both striated and smooth muscle, and the distal third is composed entirely of smooth muscle. Although relatively fixed, the esophagus may be displaced by adjacent structures such as goiter, enlarged atria, or mediastinal masses.
Etiology
Esophageal trauma may result from external or internal forces.
External mechanisms include penetrating injuries such as stab or missile wounds, direct perforation from foreign bodies, pressure necrosis, chemical or radiation injury, and iatrogenic trauma from instrumentation. Blunt trauma, most commonly from motor vehicle collisions, may also cause injury.
Internal mechanisms include caustic ingestions, infections, medication-induced injury, swallowed foreign bodies, iatrogenic causes, and barotrauma.
Caustic ingestions include alkali substances, which cause liquefaction necrosis and deep tissue penetration, and acids, which cause coagulation necrosis and thermal injury. Chlorine bleach typically causes mucosal edema and superficial erythema.
Infectious causes include viral infections such as CMV, HPV, and HSV, and fungal infections in immunocompromised patients.
Medication-related injury has been reported with agents such as alendronate, doxycycline, NSAIDs, and mycophenolate mofetil.
Swallowed foreign bodies include food bolus impaction, coins, bones, pins, and button batteries. Meat impaction is the most common type in adults, particularly among prisoners, psychiatric patients, intoxicated individuals, and edentulous patients.
Iatrogenic injury accounts for more than half of cases, most commonly due to endoscopy, nasogastric tube placement, or nasotracheal intubation.
Increased intraluminal pressure from vomiting or retching may result in Mallory–Weiss tears, which are mucosal lacerations with bleeding, or Boerhaave syndrome, which is a spontaneous full-thickness rupture of the distal esophagus.
Pediatric considerations
Foreign body ingestion accounts for most cases of esophageal trauma in children, particularly in those aged 18–48 months. Perforations are most often iatrogenic. Caustic ingestions are more common in children younger than five years. Button batteries lodged in the esophagus require urgent removal due to their highly alkaline nature. Single-use laundry detergent packets are an increasingly common hazard.
Diagnosis – signs and symptoms
Common symptoms include dysphagia, odynophagia, chest pain that may be pleuritic and severe, hoarseness, and dyspnea.
Tears or perforations may present with bleeding or hematemesis.
Foreign body ingestion may cause drooling, choking, gagging, vomiting, stridor, wheezing, or inability to tolerate oral intake.
Caustic ingestion may produce oral pain, abdominal pain, vomiting, and drooling.
History
Key historical elements include the type, amount, and timing of ingestions; history of prolonged vomiting; sudden inability to swallow after eating; foreign body sensation; penetrating trauma; or prior cancer therapy.
Physical examination
Findings suggestive of perforation include subcutaneous emphysema at the base of the neck, a Hamman crunch due to mediastinal air, signs of shock, septicemia, or peritonitis.
Penetrating trauma may be associated with injuries to the trachea, neck, chest, or abdomen.
Caustic ingestions may cause airway edema with stridor and visible oral burns.
Essential workup
A high index of suspicion and early diagnosis are critical. Mortality for esophageal perforation is less than 5% if repaired within 24 hours but increases dramatically with delayed diagnosis. Early endoscopy is indicated for caustic ingestions. Chest and lateral neck radiographs are part of the initial evaluation.
Diagnosis tests and interpretation
Laboratory studies may include complete blood count, type and crossmatch for significant bleeding, coagulation studies, electrolytes for prolonged vomiting or retained foreign body, and arterial blood gas analysis in acid ingestions.
Imaging includes chest radiography to assess for pneumomediastinum, pneumothorax, widened mediastinum, or pleural effusion. Lateral cervical spine radiographs may reveal retropharyngeal air or fluid.
Esophagram is useful for suspected perforation, with water-soluble contrast preferred initially. Endoscopy is indicated for suspected perforation, caustic injury, or foreign body removal. CT with dilute oral contrast may aid in identifying perforation and associated complications.
Differential diagnosis
Pulmonary causes include tracheal injury and pneumothorax. Cardiovascular causes include myocardial infarction and aortic dissection. Other esophageal conditions include strictures, neoplasm, Schatzki ring, diverticula, achalasia, esophageal spasm, gastroesophageal reflux, and medication-induced esophagitis.
Treatment
Prehospital care
Chest pain should be presumed cardiac until proven otherwise. Airway protection, suctioning of secretions, intravenous fluids for hypotension or bleeding, and analgesia are indicated. Neutralizing agents and large volumes of oral fluids should be avoided in caustic ingestions.
Initial stabilization and therapy
Airway management and resuscitation are priorities. Establish intravenous access, initiate monitoring, and consider early intubation for penetrating neck or chest injuries.
Emergency department treatment and procedures
Most foreign bodies pass spontaneously, but endoscopic removal is required in a significant minority. Pharmacologic measures such as glucagon, nitroglycerin, or benzodiazepines may be attempted for food impaction. Gastroenterology consultation is indicated if these measures fail.
Caustic ingestions require avoidance of emesis and lavage, cautious dilution with milk, and early endoscopy for prognostication. Corticosteroids are not recommended.
Partial-thickness tears generally heal spontaneously. Full-thickness perforations require surgical consultation, broad-spectrum intravenous antibiotics, and possible operative repair.
Medication
For food impaction, glucagon, nitroglycerin, or diazepam may be used selectively.
For perforation, broad-spectrum intravenous antibiotics such as cefoxitin with gentamicin are indicated. Steroids are not indicated in caustic injury.
Follow-up and disposition
Admission criteria
Indications for admission include caustic ingestion, sharp foreign bodies, airway compromise, penetrating neck or chest trauma, evidence of sepsis or mediastinitis, esophageal perforation, significant bleeding, and inability to tolerate oral intake.
Discharge criteria
Patients may be discharged if bleeding from a partial-thickness tear is self-limited or if a foreign body or food bolus has passed beyond the lower esophageal sphincter without complications.
Clinical pearls and common pitfalls
Time to diagnosis and definitive therapy is the most important predictor of outcome, with intervention within 24 hours significantly reducing mortality. Cervical injuries have better outcomes than thoracic or abdominal injuries. Spontaneous perforation carries the highest mortality, followed by iatrogenic and then traumatic causes.
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Emergency And Acute Medicine - Ethylene glycol poisoning
Basic description
Peak serum concentration occurs in 1–4 hr. The half-life is 2.5–4.5 hr, and less than 20% is excreted unchanged by the kidneys.
Ethylene glycol is metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase to acidic metabolites that ultimately form oxalic acid. Aldehyde and acid metabolites are directly toxic to the CNS, heart, and kidneys.
Etiology
Exposure is typically from ethylene-glycol–containing products such as antifreeze and certain solvents. The minimum reported lethal dose is approximately 30 mL of 100% ethylene glycol.
Diagnosis – signs and symptoms
Cardiovascular: tachycardia, bradycardia, dysrhythmias, hypertension, hypotension.
Cns: inebriation, irritability, ataxia, obtundation, coma, cerebral edema, seizures; may also have peripheral nervous system findings including cranial nerve abnormalities.
Gi: nausea, vomiting, abdominal pain.
Pulmonary: tachypnea, hyperventilation, Kussmaul respirations, pulmonary edema.
Renal: crystalluria and acute renal failure.
Three overlapping stages may be seen:
History
Intentional or unintentional ingestion may be reported. Consider this diagnosis even without a clear history when there is an unexplained high anion gap metabolic acidosis and/or an elevated, unexplained osmol gap.
Physical examination
Tachypnea and altered mental status are common.
Essential workup
Obtain a complete ingestion history. Draw the following simultaneously:
Diagnosis tests and interpretation
Calculate the anion gap: (Na⁺) − (Cl⁻ + HCO₃⁻); normal is approximately 8–12.
Calculate the osmol gap: measured osmolality − calculated osmolarity; an increased gap is generally >10.
Calculated osmolarity: 2(Na⁺) + glucose/18 + BUN/2.8 + ethanol (mg/dL)/4.6.
The osmol gap is most useful early after ingestion (and may be larger with concurrent ethanol ingestion, with less severe acidosis). A normal osmol gap does not exclude ethylene glycol poisoning, especially with late presentation when metabolites drive an anion gap acidosis.
Urinalysis may show envelope-shaped calcium oxalate crystals (specific but insensitive). Absence of crystals does not rule out exposure.
Wood lamp inspection of urine or gastric contents may show fluorescein from antifreeze, but this is insensitive and nonspecific.
Differential diagnosis
Elevated osmol gap: methanol, ethanol, isopropyl alcohol, mannitol/glycerin/propylene glycol/sorbitol, acetone/ammonia, propylene glycol.
Elevated anion gap metabolic acidosis: alcoholic ketoacidosis, toxic asphyxiants (e.g., cyanide/CO/H₂S), acetaminophen-related causes, antiretrovirals (NRTIs), toluene, metformin, uremia, DKA, iron/INH, lactic acidosis, salicylates, starvation ketosis, methanol, ethylene glycol.
Treatment
Prehospital care
Bring containers of suspected substances. Monitor airway and mental status. For dermal exposure, remove contaminated clothing/jewelry and irrigate with soap and water.
Initial stabilization and therapy
ABCs. Provide supplemental oxygen, cardiac monitoring, and IV access with 0.9% saline. For altered mental status, check glucose and consider dextrose, naloxone, and thiamine as appropriate.
Emergency department treatment and procedures
Pregnancy considerations
Fomepizole is class C in pregnancy. Ethanol is not recommended.
Pediatric considerations
Ethanol can cause significant CNS depression and hypoglycemia in children.
Medication
Activated charcoal: 1 g/kg PO.
Dextrose: D50W 25 g IV (peds: D25W 2–4 mL/kg).
Ethanol: oral (via NG) or IV 10% ethanol in D5W per dosing protocols; adjust during hemodialysis.
Fomepizole: 15 mg/kg IV load over 30 min, then 10 mg/kg q12h ×4 doses, then 15 mg/kg q12h until level <25 mg />L; dose adjustments required during hemodialysis.
Magnesium: 25–50 mg/kg IV once (max 2 g).
Naloxone: 2 mg IV/IM (peds: 0.1 mg/kg).
Pyridoxine: 100 mg daily for 2 days.
Sodium bicarbonate: 1–2 mEq/kg IV in D5W.
Thiamine: 100 mg daily for 2 days (peds: 50 mg).
Follow-up and disposition
Admission criteria
Admit all patients with significant suspected or confirmed ethylene glycol ingestion, even if initially asymptomatic. ICU admission is indicated for serious illness, metabolic acidosis, or renal failure. Transfer if fomepizole or hemodialysis is indicated but not available.
Discharge criteria
An asymptomatic patient with isolated exposure may be discharged only if ethylene glycol concentration is undetectable and there is no metabolic acidosis.
Follow-up recommendations
Psychiatric evaluation is indicated after intentional ingestion.
Clinical pearls and common pitfalls
An osmol gap <10 does not exclude ethylene glycol poisoning. treat early with fomepizole when the diagnosis is on table and confirm serum levels available. presentations may show only an osmol gap, while late anion gap. do use absence of urinary crystals or lack fluorescence under a wood lamp to rule out exposure. if confirmation, antidote availability, 24 /> hemodialysis capability is uncertain, transfer to a facility that has all of these resources.
Basic description
Peak serum concentration occurs in 1–4 hr. The half-life is 2.5–4.5 hr, and less than 20% is excreted unchanged by the kidneys.
Ethylene glycol is metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase to acidic metabolites that ultimately form oxalic acid. Aldehyde and acid metabolites are directly toxic to the CNS, heart, and kidneys.
Etiology
Exposure is typically from ethylene-glycol–containing products such as antifreeze and certain solvents. The minimum reported lethal dose is approximately 30 mL of 100% ethylene glycol.
Diagnosis – signs and symptoms
Cardiovascular: tachycardia, bradycardia, dysrhythmias, hypertension, hypotension.
Cns: inebriation, irritability, ataxia, obtundation, coma, cerebral edema, seizures; may also have peripheral nervous system findings including cranial nerve abnormalities.
Gi: nausea, vomiting, abdominal pain.
Pulmonary: tachypnea, hyperventilation, Kussmaul respirations, pulmonary edema.
Renal: crystalluria and acute renal failure.
Three overlapping stages may be seen:
- First stage (1–12 hr): CNS depression, GI symptoms, worsening acidosis, coma, seizures, cerebral edema, tetany or myoclonus from hypocalcemia.
- Second stage (12–36 hr): cardiopulmonary manifestations; many deaths occur in this period.
- Third stage (36–72 hr): oliguria, flank pain, acute renal failure.
History
Intentional or unintentional ingestion may be reported. Consider this diagnosis even without a clear history when there is an unexplained high anion gap metabolic acidosis and/or an elevated, unexplained osmol gap.
Physical examination
Tachypnea and altered mental status are common.
Essential workup
Obtain a complete ingestion history. Draw the following simultaneously:
- Arterial blood gas
- Serum ethylene glycol, methanol, isopropyl alcohol, and ethanol concentrations
- Electrolytes, BUN/creatinine, glucose
- Measured serum osmolality (freezing point depression)
- Serum calcium, phosphorus, magnesium
Diagnosis tests and interpretation
Calculate the anion gap: (Na⁺) − (Cl⁻ + HCO₃⁻); normal is approximately 8–12.
Calculate the osmol gap: measured osmolality − calculated osmolarity; an increased gap is generally >10.
Calculated osmolarity: 2(Na⁺) + glucose/18 + BUN/2.8 + ethanol (mg/dL)/4.6.
The osmol gap is most useful early after ingestion (and may be larger with concurrent ethanol ingestion, with less severe acidosis). A normal osmol gap does not exclude ethylene glycol poisoning, especially with late presentation when metabolites drive an anion gap acidosis.
Urinalysis may show envelope-shaped calcium oxalate crystals (specific but insensitive). Absence of crystals does not rule out exposure.
Wood lamp inspection of urine or gastric contents may show fluorescein from antifreeze, but this is insensitive and nonspecific.
Differential diagnosis
Elevated osmol gap: methanol, ethanol, isopropyl alcohol, mannitol/glycerin/propylene glycol/sorbitol, acetone/ammonia, propylene glycol.
Elevated anion gap metabolic acidosis: alcoholic ketoacidosis, toxic asphyxiants (e.g., cyanide/CO/H₂S), acetaminophen-related causes, antiretrovirals (NRTIs), toluene, metformin, uremia, DKA, iron/INH, lactic acidosis, salicylates, starvation ketosis, methanol, ethylene glycol.
Treatment
Prehospital care
Bring containers of suspected substances. Monitor airway and mental status. For dermal exposure, remove contaminated clothing/jewelry and irrigate with soap and water.
Initial stabilization and therapy
ABCs. Provide supplemental oxygen, cardiac monitoring, and IV access with 0.9% saline. For altered mental status, check glucose and consider dextrose, naloxone, and thiamine as appropriate.
Emergency department treatment and procedures
- Limit absorption: gastric lavage may be considered only in select cases (<1 hr since ingestion, coma, or reported large ingestion). activated charcoal may be given for coingestants but adsorbs ethylene glycol poorly.< />pan>
- Block toxic metabolism: initiate fomepizole promptly when a potentially toxic ingestion is suspected (intentional ingestion, more than a “sip,” or unexplained osmol gap and/or anion gap acidosis with concerning presentation). Do not wait for confirmatory levels if suspicion is high.
- Alternative antidote: ethanol is second-line if fomepizole is unavailable, targeting a serum ethanol level of 100–150 mg/dL, and continuing until ethylene glycol level is ~25 mg/dL.
- Adjunct cofactors: thiamine, pyridoxine, and magnesium may be given to support metabolism toward less toxic pathways (human outcome data are limited).
- Hemodialysis: use to accelerate clearance of ethylene glycol and metabolites. Consider for severe acidosis, persistent metabolic derangements, renal insufficiency, pulmonary edema, cerebral edema, or ethylene glycol concentration >25 mg/dL; continue until level approaches 25 mg/dL and acidosis resolves.
- Correct complications: ensure urine output with IV fluids. Use sodium bicarbonate for severe acidemia (commonly when pH <7.1) to maintain ph in the normal range. monitor and replace calcium as needed because oxalate formation can lower serum calcium.< />pan>
Pregnancy considerations
Fomepizole is class C in pregnancy. Ethanol is not recommended.
Pediatric considerations
Ethanol can cause significant CNS depression and hypoglycemia in children.
Medication
Activated charcoal: 1 g/kg PO.
Dextrose: D50W 25 g IV (peds: D25W 2–4 mL/kg).
Ethanol: oral (via NG) or IV 10% ethanol in D5W per dosing protocols; adjust during hemodialysis.
Fomepizole: 15 mg/kg IV load over 30 min, then 10 mg/kg q12h ×4 doses, then 15 mg/kg q12h until level <25 mg />L; dose adjustments required during hemodialysis.
Magnesium: 25–50 mg/kg IV once (max 2 g).
Naloxone: 2 mg IV/IM (peds: 0.1 mg/kg).
Pyridoxine: 100 mg daily for 2 days.
Sodium bicarbonate: 1–2 mEq/kg IV in D5W.
Thiamine: 100 mg daily for 2 days (peds: 50 mg).
Follow-up and disposition
Admission criteria
Admit all patients with significant suspected or confirmed ethylene glycol ingestion, even if initially asymptomatic. ICU admission is indicated for serious illness, metabolic acidosis, or renal failure. Transfer if fomepizole or hemodialysis is indicated but not available.
Discharge criteria
An asymptomatic patient with isolated exposure may be discharged only if ethylene glycol concentration is undetectable and there is no metabolic acidosis.
Follow-up recommendations
Psychiatric evaluation is indicated after intentional ingestion.
Clinical pearls and common pitfalls
An osmol gap <10 does not exclude ethylene glycol poisoning. treat early with fomepizole when the diagnosis is on table and confirm serum levels available. presentations may show only an osmol gap, while late anion gap. do use absence of urinary crystals or lack fluorescence under a wood lamp to rule out exposure. if confirmation, antidote availability, 24 /> hemodialysis capability is uncertain, transfer to a facility that has all of these resources.
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Emergency And Acute Medicine - External Ear Chondritis And Abscess
Condition overview
This condition involves inflammation and/or infection of the auricular cartilage of the pinna. Because the cartilage of the external ear has minimal subcutaneous tissue, limited blood supply, and is exposed, it is particularly vulnerable to injury and infection. Chondritis often develops as a delayed complication after trauma or burns, sometimes appearing after the ear seems to have healed. Inadequate or delayed treatment can lead to cartilage avascular necrosis and permanent deformity of the pinna, ranging from a cauliflower-like ear to near-total loss of the external ear with possible narrowing of the auditory canal.
Underlying causes
Damage to the auricular cartilage may result from chemical or thermal burns, frostbite, auricular hematomas, blunt or penetrating trauma, human or insect bites, deep abrasions, otitis externa, and high ear piercings—especially when performed with poor technique, hygiene, or aftercare. Common causative organisms include Pseudomonas aeruginosa, Staphylococcus species, and Proteus species.
Clinical presentation
Symptoms often begin with a dull ache that progressively worsens. Fever and chills may occur in more advanced cases. Patients frequently report a history of ear trauma or recent ear piercing. On examination, the pinna is painful with marked tenderness, erythema, and warmth. Swelling leads to loss of normal auricular contours, typically sparing the lobule. The auriculocephalic angle may increase. As infection progresses, fluctuance can develop, followed by skin breakdown and purulent drainage.
Diagnostic approach
The diagnosis is primarily clinical, based on characteristic physical findings and a compatible history. Laboratory testing is reserved for patients with systemic signs of infection and may include a complete blood count and blood cultures. When drainage is performed for abscess or advanced chondritis, local cultures should be obtained to guide antibiotic therapy.
Conditions to consider
Important alternatives include allergic reactions, mastoiditis, dermatitis, and auricular hematoma.
Management principles
Early prevention and treatment are critical to avoid permanent deformity. Pressure to the injured ear should be avoided. Eschars and crusts should not be aggressively debrided. The ear should be gently cleansed twice daily with antibacterial soap and water, thoroughly dried, and treated with topical antibiotics if the skin barrier is disrupted. Hair should be kept away from the affected ear. Mild, early infections limited to the lobule may be treated with oral antibiotics. Established chondritis or abscess formation requires parenteral antibiotics and prompt surgical drainage.
Pharmacologic therapy
Antibiotic regimens must include coverage for Pseudomonas. Oral options for mild cases include ciprofloxacin, cephalexin, or dicloxacillin, adjusted for age and weight in pediatric patients. Severe infections require intravenous antibiotics. Topical antibiotics are indicated when there is a break in the skin.
Disposition and follow-up
Admission is indicated for patients with significant edema, erythema, marked tenderness, systemic toxicity, fever, chills, or immunocompromise. Stable patients without systemic signs may be discharged with close otolaryngology follow-up. ENT consultation is recommended for all cases of chondritis, abscess, or cartilage necrosis, and early surgical drainage is essential when abscess is present.
Key clinical lessons
Prompt and aggressive early management is essential to prevent severe and permanent ear deformity. Antibiotic therapy should always include reliable antipseudomonal coverage.
Condition overview
This condition involves inflammation and/or infection of the auricular cartilage of the pinna. Because the cartilage of the external ear has minimal subcutaneous tissue, limited blood supply, and is exposed, it is particularly vulnerable to injury and infection. Chondritis often develops as a delayed complication after trauma or burns, sometimes appearing after the ear seems to have healed. Inadequate or delayed treatment can lead to cartilage avascular necrosis and permanent deformity of the pinna, ranging from a cauliflower-like ear to near-total loss of the external ear with possible narrowing of the auditory canal.
Underlying causes
Damage to the auricular cartilage may result from chemical or thermal burns, frostbite, auricular hematomas, blunt or penetrating trauma, human or insect bites, deep abrasions, otitis externa, and high ear piercings—especially when performed with poor technique, hygiene, or aftercare. Common causative organisms include Pseudomonas aeruginosa, Staphylococcus species, and Proteus species.
Clinical presentation
Symptoms often begin with a dull ache that progressively worsens. Fever and chills may occur in more advanced cases. Patients frequently report a history of ear trauma or recent ear piercing. On examination, the pinna is painful with marked tenderness, erythema, and warmth. Swelling leads to loss of normal auricular contours, typically sparing the lobule. The auriculocephalic angle may increase. As infection progresses, fluctuance can develop, followed by skin breakdown and purulent drainage.
Diagnostic approach
The diagnosis is primarily clinical, based on characteristic physical findings and a compatible history. Laboratory testing is reserved for patients with systemic signs of infection and may include a complete blood count and blood cultures. When drainage is performed for abscess or advanced chondritis, local cultures should be obtained to guide antibiotic therapy.
Conditions to consider
Important alternatives include allergic reactions, mastoiditis, dermatitis, and auricular hematoma.
Management principles
Early prevention and treatment are critical to avoid permanent deformity. Pressure to the injured ear should be avoided. Eschars and crusts should not be aggressively debrided. The ear should be gently cleansed twice daily with antibacterial soap and water, thoroughly dried, and treated with topical antibiotics if the skin barrier is disrupted. Hair should be kept away from the affected ear. Mild, early infections limited to the lobule may be treated with oral antibiotics. Established chondritis or abscess formation requires parenteral antibiotics and prompt surgical drainage.
Pharmacologic therapy
Antibiotic regimens must include coverage for Pseudomonas. Oral options for mild cases include ciprofloxacin, cephalexin, or dicloxacillin, adjusted for age and weight in pediatric patients. Severe infections require intravenous antibiotics. Topical antibiotics are indicated when there is a break in the skin.
Disposition and follow-up
Admission is indicated for patients with significant edema, erythema, marked tenderness, systemic toxicity, fever, chills, or immunocompromise. Stable patients without systemic signs may be discharged with close otolaryngology follow-up. ENT consultation is recommended for all cases of chondritis, abscess, or cartilage necrosis, and early surgical drainage is essential when abscess is present.
Key clinical lessons
Prompt and aggressive early management is essential to prevent severe and permanent ear deformity. Antibiotic therapy should always include reliable antipseudomonal coverage.
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Emergency And Acute Medicine – Adult Fever
Basics Description
Fever is an elevation of core body temperature caused by an increase in the hypothalamic thermoregulatory set point. Prostaglandin E2 synthesis within the anterior hypothalamus mediates this process and is the primary target of antipyretic therapy. Normal core temperature is regulated around 37°C with circadian variation, typically lowest in the early morning and highest in the late afternoon. Fever must be distinguished from hyperthermia, in which temperature elevation occurs despite a normal hypothalamic set point, and from hyperpyrexia, defined as extreme temperatures above 41.5°C, often associated with central nervous system injury. Endogenous pyrogens such as interleukins and tumor necrosis factor, as well as exogenous pyrogens including bacterial endotoxins, raise the thermoregulatory set point. Patients receiving anticytokine agents or glucocorticoids may exhibit a blunted febrile response. Fever of unknown origin is defined as a temperature above 38.3°C for more than three weeks without an established diagnosis after appropriate evaluation.
Etiology
Fever may result from infectious processes involving the central nervous system, respiratory tract, gastrointestinal tract, genitourinary system, skin, soft tissue, bone, vascular structures, or cardiac endocardium. Noninfectious causes include neoplastic disease, drug reactions, toxidromes, hypersensitivity reactions, systemic inflammatory and rheumatologic disorders, endocrine abnormalities such as hyperthyroidism or pheochromocytoma, withdrawal syndromes, and miscellaneous conditions including pulmonary embolism and hemolytic anemia. Common causes of fever of unknown origin include occult infections such as tuberculosis or abscesses, malignancies such as lymphoma or renal cell carcinoma, and inflammatory disorders.
Diagnosis Signs And Symptoms
Patients may report chills, rigors, weight loss, or night sweats, which can suggest bacteremia, malignancy, or chronic infection. Certain fever patterns provide diagnostic clues, including relapsing, remittent, intermittent, or double quotidian fevers. High-risk features include immunosuppression, anticytokine therapy, incomplete vaccination status, intravenous drug use, pregnancy, recent chemotherapy, recent travel, and splenectomy. Physical examination should focus on accurate core temperature measurement, assessment for diaphoresis, heart rate response relative to temperature, mental status changes, muscle rigidity or clonus, and skin findings such as rash or petechiae. Signs of endocrine disease, including goiter or exophthalmos, should also be assessed.
Essential Workup
Rectal temperature measurement provides the most accurate assessment of core temperature. A thorough history and physical examination guide the need for further diagnostic testing, including evaluation of recent infections, travel, medication use, occupational exposures, animal or tick contact, and immunization history.
Diagnosis Tests And Interpretation
Laboratory evaluation may include a complete blood count to assess for neutropenia, leukocytosis, or atypical lymphocytosis. Serum lactate is useful for identifying sepsis and guiding resuscitation. Urinalysis, urine culture, and blood cultures should be obtained in systemically ill patients or those at risk for bacteremia. Additional testing such as malaria smears, stool studies, heterophile antibody testing, or inflammatory markers may be indicated based on clinical context. Imaging studies such as chest radiography are useful in patients with respiratory findings or unclear fever sources, while advanced imaging is reserved for suspected deep or focal infections.
Treatment
Prehospital care focuses on monitoring and stabilization in unstable patients. Initial emergency department management prioritizes airway, breathing, and circulation in critically ill individuals. Early administration of broad-spectrum antibiotics is indicated in patients with suspected sepsis, neutropenia, or other high-risk features. Antipyretics such as acetaminophen or nonsteroidal anti-inflammatory drugs may be administered for comfort. Empiric antimicrobial therapy should be tailored to patient risk factors, including coverage for neutropenic, asplenic, or immunocompromised patients. External cooling measures are rarely required.
Follow Up Disposition
Patients with unstable vital signs or severe illness require hospital or intensive care admission. High-risk populations, including neutropenic, immunocompromised, asplenic, elderly, or intravenous drug–using patients, warrant a lower threshold for admission even in the absence of a clear source. Stable, immunocompetent patients with an identified benign source or suspected viral illness may be discharged with appropriate follow-up. Referral is guided by the suspected underlying etiology.
Key Clinical Insights And Common Errors
Early identification of sepsis using lactate screening and prompt initiation of broad-spectrum antibiotics are critical. Clinicians should maintain a broad differential diagnosis and carefully evaluate immunosuppressed, elderly, and high-risk patients, as fever may be the only manifestation of serious disease. Failure to recognize atypical presentations or delayed treatment in vulnerable populations can lead to significant morbidity and mortality.
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Emergency And Acute Medicine - Extremity Trauma, Penetrating
Condition overview
Penetrating extremity trauma refers to injuries in which an object breaches the skin and underlying tissues of an arm or leg. These injuries range from minor puncture wounds to severe limb-threatening trauma involving vascular, neurologic, musculoskeletal, or compartment compromise.
Mechanisms of injury
Common mechanisms include stab or puncture wounds, gunshot wounds, lacerations, animal or human bites, and high-pressure injection injuries. High-muzzle-velocity gunshot wounds are particularly destructive, as the shock wave may cause extensive tissue damage beyond the visible wound tract, often with more damage at the exit wound than the entry site.
Clinical presentation
Findings may include entry and exit wounds, lacerations, or punctures. Vascular injury should be suspected with decreased or absent distal pulses, ischemic changes, expanding hematoma, or a bruit or thrill over the injury; the presence of a distal pulse does not exclude proximal vascular damage. Neurologic injury may present with paresthesias, weakness, or loss of sensation distal to the wound. Musculoskeletal injury may manifest as deformity, joint effusion, ligamentous laxity, or limited range of motion. Compartment syndrome is suggested by severe, constant pain, pain with passive stretch, compartment tenderness, weakness, and sensory deficits, with pallor and pulselessness being late findings.
History and examination priorities
Key historical elements include the mechanism and timing of injury, circumstances such as assault or self-harm, and comorbid conditions including diabetes, immunosuppression, peripheral vascular disease, valvular heart disease, or asplenia. Examination should document wound location, size, depth, and shape, and assess for exit wounds. Distal pulses should be compared bilaterally by palpation and Doppler. Capillary refill, motor and sensory function, joint stability, and signs of compartment syndrome must be evaluated. The wound should be carefully inspected for foreign bodies.
Diagnostic evaluation
The physical examination guides further testing. Acute wound cultures are not routinely indicated. Plain radiographs with at least anteroposterior and lateral views are used to detect fractures or radiopaque foreign bodies. Ultrasound, fluoroscopy, or CT may help identify radiolucent foreign bodies. When vascular injury is suspected and immediate surgery is not required, arteriography may be indicated.
Management principles
Prehospital care focuses on hemorrhage control with direct pressure, limb elevation, pain control, neurovascular assessment, and stabilization of impaled objects in place. In the emergency department, airway and hemodynamic stabilization take priority. The wound should be fully exposed, constricting items removed, and bleeding controlled with direct pressure; blind clamping and prolonged tourniquet use are discouraged. After a full neurologic exam, pain control is provided. Visible debris and devitalized tissue are removed, with copious high-pressure saline irrigation as the cornerstone of wound care. Tetanus prophylaxis is essential.
Stab and gunshot wounds should receive a single dose of cefazolin in the emergency department. Extremities should be immobilized when vascular injury, fracture, tendon injury, or joint violation is suspected. Loss of distal pulse or signs of ischemia mandate emergent surgical consultation without delay for imaging. Clean lacerations seen within 6–8 hours may be closed primarily; puncture wounds and gunshot wounds should not be closed primarily, with delayed primary closure considered for contaminated or older wounds.
Special considerations
Plantar puncture wounds require careful inspection and removal of foreign material; aggressive probing or irrigation may worsen contamination. Prophylactic antibiotics are generally not recommended unless the patient is diabetic, immunocompromised, or the wound is highly contaminated or delayed in presentation. High-pressure injection injuries of the hand require immediate orthopedic evaluation, as surface wounds may underestimate deep tissue involvement. Small inert foreign bodies, including bullets, may be left in place if not near vital structures, whereas organic material should always be removed.
Disposition and follow-up
Admission and emergent surgical consultation are required for suspected vascular injury, compartment syndrome, joint penetration, high-velocity gunshot wounds, or contaminated wounds in high-risk patients. Stable patients without indications for surgery may be discharged after appropriate wound care with instructions for elevation, wound hygiene, and close follow-up within 24–48 hours.
Key clinical lessons
A normal distal pulse does not exclude significant vascular injury. High-pressure hand injuries and plantar puncture wounds are commonly underestimated. Failure of a puncture wound infection to improve with antibiotics should prompt concern for a retained foreign body.
Condition overview
Penetrating extremity trauma refers to injuries in which an object breaches the skin and underlying tissues of an arm or leg. These injuries range from minor puncture wounds to severe limb-threatening trauma involving vascular, neurologic, musculoskeletal, or compartment compromise.
Mechanisms of injury
Common mechanisms include stab or puncture wounds, gunshot wounds, lacerations, animal or human bites, and high-pressure injection injuries. High-muzzle-velocity gunshot wounds are particularly destructive, as the shock wave may cause extensive tissue damage beyond the visible wound tract, often with more damage at the exit wound than the entry site.
Clinical presentation
Findings may include entry and exit wounds, lacerations, or punctures. Vascular injury should be suspected with decreased or absent distal pulses, ischemic changes, expanding hematoma, or a bruit or thrill over the injury; the presence of a distal pulse does not exclude proximal vascular damage. Neurologic injury may present with paresthesias, weakness, or loss of sensation distal to the wound. Musculoskeletal injury may manifest as deformity, joint effusion, ligamentous laxity, or limited range of motion. Compartment syndrome is suggested by severe, constant pain, pain with passive stretch, compartment tenderness, weakness, and sensory deficits, with pallor and pulselessness being late findings.
History and examination priorities
Key historical elements include the mechanism and timing of injury, circumstances such as assault or self-harm, and comorbid conditions including diabetes, immunosuppression, peripheral vascular disease, valvular heart disease, or asplenia. Examination should document wound location, size, depth, and shape, and assess for exit wounds. Distal pulses should be compared bilaterally by palpation and Doppler. Capillary refill, motor and sensory function, joint stability, and signs of compartment syndrome must be evaluated. The wound should be carefully inspected for foreign bodies.
Diagnostic evaluation
The physical examination guides further testing. Acute wound cultures are not routinely indicated. Plain radiographs with at least anteroposterior and lateral views are used to detect fractures or radiopaque foreign bodies. Ultrasound, fluoroscopy, or CT may help identify radiolucent foreign bodies. When vascular injury is suspected and immediate surgery is not required, arteriography may be indicated.
Management principles
Prehospital care focuses on hemorrhage control with direct pressure, limb elevation, pain control, neurovascular assessment, and stabilization of impaled objects in place. In the emergency department, airway and hemodynamic stabilization take priority. The wound should be fully exposed, constricting items removed, and bleeding controlled with direct pressure; blind clamping and prolonged tourniquet use are discouraged. After a full neurologic exam, pain control is provided. Visible debris and devitalized tissue are removed, with copious high-pressure saline irrigation as the cornerstone of wound care. Tetanus prophylaxis is essential.
Stab and gunshot wounds should receive a single dose of cefazolin in the emergency department. Extremities should be immobilized when vascular injury, fracture, tendon injury, or joint violation is suspected. Loss of distal pulse or signs of ischemia mandate emergent surgical consultation without delay for imaging. Clean lacerations seen within 6–8 hours may be closed primarily; puncture wounds and gunshot wounds should not be closed primarily, with delayed primary closure considered for contaminated or older wounds.
Special considerations
Plantar puncture wounds require careful inspection and removal of foreign material; aggressive probing or irrigation may worsen contamination. Prophylactic antibiotics are generally not recommended unless the patient is diabetic, immunocompromised, or the wound is highly contaminated or delayed in presentation. High-pressure injection injuries of the hand require immediate orthopedic evaluation, as surface wounds may underestimate deep tissue involvement. Small inert foreign bodies, including bullets, may be left in place if not near vital structures, whereas organic material should always be removed.
Disposition and follow-up
Admission and emergent surgical consultation are required for suspected vascular injury, compartment syndrome, joint penetration, high-velocity gunshot wounds, or contaminated wounds in high-risk patients. Stable patients without indications for surgery may be discharged after appropriate wound care with instructions for elevation, wound hygiene, and close follow-up within 24–48 hours.
Key clinical lessons
A normal distal pulse does not exclude significant vascular injury. High-pressure hand injuries and plantar puncture wounds are commonly underestimated. Failure of a puncture wound infection to improve with antibiotics should prompt concern for a retained foreign body.
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Emergency And Acute Medicine – Foot Fracture
Basics Description
Foot fractures involve injury to the tarsal bones or metatarsals, including the calcaneus, talus, navicular, cuboid, cuneiforms, and metatarsals.
Etiology
The most common foot fractures involve the metatarsals and phalanges. The calcaneus is the most frequently fractured tarsal bone.
Calcaneus fractures usually result from high-velocity axial compression to the heel; approximately 75% are intra-articular and 50% are associated with other injuries, including spinal fractures, lower extremity trauma, bilateral involvement, or open wounds.
Metatarsal fractures may result from stress, twisting injuries, or direct trauma. The first metatarsal is often injured by direct force. The second and third metatarsals are most commonly affected by stress or twisting injuries. The fifth metatarsal commonly sustains avulsion fractures at the proximal apophysis (dancer’s fracture) or a Jones fracture at the metaphyseal–diaphyseal junction from inversion injury.
Talus fractures are typically caused by dorsiflexion with axial loading. Navicular fractures result from axial compression or stress. Cuboid and cuneiform fractures are rare and usually occur with associated injuries, particularly tarsometatarsal (Lisfranc) injuries. Lisfranc injuries are high-energy injuries caused by axial load on a plantar-flexed foot or forced eversion and are frequently missed on initial evaluation.
Pediatric considerations include a predominance of metatarsal fractures, often from direct trauma, with physeal injury possible. Calcaneal fractures in children are less commonly intra-articular and less often associated with spinal injury.
Diagnosis Signs And Symptoms
History usually reveals trauma; stress fractures may present with progressive pain related to repetitive activity.
Physical examination may show ecchymosis, swelling, deformity, localized tenderness, pain with weight bearing, or joint instability.
Essential Workup
A focused extremity examination is required to assess neurovascular status, skin integrity, swelling, deformity, and function. In suspected calcaneal fractures, evaluation of the spine is essential due to the risk of associated injury. Standard anteroposterior, lateral, and oblique foot radiographs are required.
Diagnosis Tests And Interpretation
Imaging may require special views depending on the suspected injury. Lisfranc injuries may require weight-bearing stress views, MRI for ligamentous assessment, or CT. Talar fractures may require oblique views or CT. Calcaneal fractures require axial views, with a Böhler angle less than 20° suggesting compression fracture, and often CT for further definition. Lumbar spine imaging is recommended in calcaneal fractures. Stress fractures may not be visible on initial radiographs and may require delayed imaging, bone scan, or CT.
Complications to assess include compartment syndrome, nonunion, avascular necrosis (especially with talar neck fractures), and sural nerve injury with calcaneal fractures.
Differential Diagnosis
Ankle sprain, foot contusion, talar dome injury, and Freiberg disease may mimic foot fractures.
Treatment
Prehospital care includes ice application, immobilization, and spinal precautions when calcaneal fracture is suspected.
Initial stabilization prioritizes management of associated injuries.
Emergency department management includes airway, breathing, and circulation assessment, neurovascular evaluation, prompt reduction of dislocations with reassessment, immobilization in a bulky splint, elevation, ice, and crutches. Circumferential casting should be delayed until swelling subsides. Pain control is essential. Compartment syndrome should be suspected with severe pain, swelling, or pain on passive toe movement. Early orthopedic consultation is required for displaced, open, or midfoot fractures.
Medication
Analgesics and sedatives may be used as indicated for pain control and procedural sedation. Antibiotics are indicated for open fractures.
Follow Up Disposition
Admission criteria include open fractures, compartment syndrome, neurovascular compromise, or need for immediate operative fixation.
Discharge criteria include stable patients with isolated, nondisplaced metatarsal fractures who can be managed with immobilization and close orthopedic follow-up.
Clinical Insights And Frequent Errors
Calcaneal fractures should prompt evaluation for spinal injury. Lisfranc injuries are commonly missed and require a high index of suspicion. Persistent pain or swelling despite normal initial imaging warrants reevaluation for occult or stress fractures.
Basics Description
Foot fractures involve injury to the tarsal bones or metatarsals, including the calcaneus, talus, navicular, cuboid, cuneiforms, and metatarsals.
Etiology
The most common foot fractures involve the metatarsals and phalanges. The calcaneus is the most frequently fractured tarsal bone.
Calcaneus fractures usually result from high-velocity axial compression to the heel; approximately 75% are intra-articular and 50% are associated with other injuries, including spinal fractures, lower extremity trauma, bilateral involvement, or open wounds.
Metatarsal fractures may result from stress, twisting injuries, or direct trauma. The first metatarsal is often injured by direct force. The second and third metatarsals are most commonly affected by stress or twisting injuries. The fifth metatarsal commonly sustains avulsion fractures at the proximal apophysis (dancer’s fracture) or a Jones fracture at the metaphyseal–diaphyseal junction from inversion injury.
Talus fractures are typically caused by dorsiflexion with axial loading. Navicular fractures result from axial compression or stress. Cuboid and cuneiform fractures are rare and usually occur with associated injuries, particularly tarsometatarsal (Lisfranc) injuries. Lisfranc injuries are high-energy injuries caused by axial load on a plantar-flexed foot or forced eversion and are frequently missed on initial evaluation.
Pediatric considerations include a predominance of metatarsal fractures, often from direct trauma, with physeal injury possible. Calcaneal fractures in children are less commonly intra-articular and less often associated with spinal injury.
Diagnosis Signs And Symptoms
History usually reveals trauma; stress fractures may present with progressive pain related to repetitive activity.
Physical examination may show ecchymosis, swelling, deformity, localized tenderness, pain with weight bearing, or joint instability.
Essential Workup
A focused extremity examination is required to assess neurovascular status, skin integrity, swelling, deformity, and function. In suspected calcaneal fractures, evaluation of the spine is essential due to the risk of associated injury. Standard anteroposterior, lateral, and oblique foot radiographs are required.
Diagnosis Tests And Interpretation
Imaging may require special views depending on the suspected injury. Lisfranc injuries may require weight-bearing stress views, MRI for ligamentous assessment, or CT. Talar fractures may require oblique views or CT. Calcaneal fractures require axial views, with a Böhler angle less than 20° suggesting compression fracture, and often CT for further definition. Lumbar spine imaging is recommended in calcaneal fractures. Stress fractures may not be visible on initial radiographs and may require delayed imaging, bone scan, or CT.
Complications to assess include compartment syndrome, nonunion, avascular necrosis (especially with talar neck fractures), and sural nerve injury with calcaneal fractures.
Differential Diagnosis
Ankle sprain, foot contusion, talar dome injury, and Freiberg disease may mimic foot fractures.
Treatment
Prehospital care includes ice application, immobilization, and spinal precautions when calcaneal fracture is suspected.
Initial stabilization prioritizes management of associated injuries.
Emergency department management includes airway, breathing, and circulation assessment, neurovascular evaluation, prompt reduction of dislocations with reassessment, immobilization in a bulky splint, elevation, ice, and crutches. Circumferential casting should be delayed until swelling subsides. Pain control is essential. Compartment syndrome should be suspected with severe pain, swelling, or pain on passive toe movement. Early orthopedic consultation is required for displaced, open, or midfoot fractures.
Medication
Analgesics and sedatives may be used as indicated for pain control and procedural sedation. Antibiotics are indicated for open fractures.
Follow Up Disposition
Admission criteria include open fractures, compartment syndrome, neurovascular compromise, or need for immediate operative fixation.
Discharge criteria include stable patients with isolated, nondisplaced metatarsal fractures who can be managed with immobilization and close orthopedic follow-up.
Clinical Insights And Frequent Errors
Calcaneal fractures should prompt evaluation for spinal injury. Lisfranc injuries are commonly missed and require a high index of suspicion. Persistent pain or swelling despite normal initial imaging warrants reevaluation for occult or stress fractures.
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Emergency And Acute Medicine – Flail Chest
Basics Description
Flail chest is defined by a free-floating segment of the chest wall created when three or more adjacent ribs are fractured in two or more locations. It may also occur with rib fractures combined with sternal fractures or costochondral separations. The unstable segment characteristically moves inward during inspiration and outward during expiration (paradoxical motion). The primary clinical problem in flail chest is not the chest wall instability itself but the associated pulmonary contusion, which leads to impaired gas exchange rather than altered ventilatory mechanics.
Etiology
Flail chest results from high-energy blunt thoracic trauma, most commonly motor vehicle collisions, falls from height, assaults, or missile injuries. Rib fractures usually occur at the point of impact or at the posterior rib angle, with ribs 4–9 most frequently involved. Energy transfer to adjacent lung tissue disrupts the alveolocapillary membrane, producing pulmonary contusion, ventilation–perfusion mismatch, arteriovenous shunting, hypoxemia, and potential respiratory failure.
Pediatric considerations: Children have more elastic chest walls, making rib fractures less common; when present, they imply severe energy transfer.
Geriatric considerations: Older adults are more susceptible to rib fractures, often from low-energy mechanisms, and outcomes are worsened by osteoporosis.
Diagnosis Signs And Symptoms
History typically includes significant blunt chest trauma with localized chest wall pain that worsens with inspiration, coughing, or movement. Patients may report pleuritic chest pain, dyspnea, or hemoptysis.
Physical examination may reveal paradoxical chest wall motion, which can be subtle or absent early due to muscle spasm and splinting. Additional findings include multiple rib fractures with tenderness, crepitus, ecchymosis, edema, and bony step-offs. Respiratory findings range from tachypnea and splinting respirations to cyanosis, hypoxia, tachycardia, hypotension, and progressive crackles or diminished breath sounds as pulmonary contusion evolves.
Essential Workup
Diagnosis is primarily clinical and supported by imaging. Continuous monitoring of oxygenation and respiratory status is essential.
Diagnosis Tests And Interpretation
Laboratory studies may include arterial blood gas analysis demonstrating hypoxemia and an elevated alveolar–arterial gradient.
Chest radiography may show rib fractures and associated intrathoracic injuries such as pneumothorax, hemothorax, pneumomediastinum, or pulmonary contusion, which often becomes radiographically apparent within 6–12 hours.
Thoracic CT is more sensitive than plain radiographs and frequently identifies additional rib fractures and associated injuries not seen on initial chest X-ray.
Differential Diagnosis
Chest wall contusion, intercostal muscle strain, costochondral separation, sternal fracture or dislocation, and pulmonary conditions such as ARDS, pulmonary laceration, embolism, heart failure, pneumonia, or noncardiogenic pulmonary edema.
Treatment
Prehospital care includes positioning the patient with the injured side down to stabilize the chest wall and improve ventilation of the unaffected lung. Patients with significant thoracic trauma should be transported to a trauma center.
Initial stabilization follows airway, breathing, and circulation priorities with supplemental oxygen, IV access, cardiac monitoring, and pulse oximetry. Endotracheal intubation is indicated for severe hypoxemia, significant underlying lung disease, or impending respiratory failure.
Emergency department management focuses on maintaining adequate oxygenation and ventilation. High-flow oxygen is first-line in alert patients; noninvasive positive pressure ventilation may be used if oxygenation remains inadequate. Early invasive mechanical ventilation is indicated when noninvasive measures fail, providing physiologic internal stabilization of the flail segment. External fixation of the chest wall is not recommended.
Aggressive pain control is critical to prevent hypoventilation, atelectasis, and pneumonia. Intercostal nerve blocks with bupivacaine can provide effective temporary analgesia. Careful fluid management is essential to avoid worsening pulmonary edema in the presence of contusion. Prophylactic antibiotics are not indicated.
Medication
Analgesia may include acetaminophen–opioid combinations, IV or oral opioids such as morphine or hydromorphone, patient-controlled analgesia, and regional techniques. Bupivacaine 0.5% may be used for intercostal nerve blocks. Thoracic epidural analgesia should be considered in patients with severe pain or opioid-related hypoventilation. NSAIDs are generally discouraged due to bleeding risk. Acetaminophen dosing should not exceed recommended daily limits.
Follow Up Disposition
All patients with flail chest require admission to a critical care or closely monitored setting for respiratory observation and pain management. Discharge from the emergency department is not appropriate.
Clinical Takeaways And Common Pitfalls
Early and adequate pain control is essential to prevent respiratory complications. Always assess for associated injuries, particularly pulmonary contusion and pneumothorax. Elderly patients have markedly worse outcomes and require vigilant monitoring and aggressive supportive care.
Basics Description
Flail chest is defined by a free-floating segment of the chest wall created when three or more adjacent ribs are fractured in two or more locations. It may also occur with rib fractures combined with sternal fractures or costochondral separations. The unstable segment characteristically moves inward during inspiration and outward during expiration (paradoxical motion). The primary clinical problem in flail chest is not the chest wall instability itself but the associated pulmonary contusion, which leads to impaired gas exchange rather than altered ventilatory mechanics.
Etiology
Flail chest results from high-energy blunt thoracic trauma, most commonly motor vehicle collisions, falls from height, assaults, or missile injuries. Rib fractures usually occur at the point of impact or at the posterior rib angle, with ribs 4–9 most frequently involved. Energy transfer to adjacent lung tissue disrupts the alveolocapillary membrane, producing pulmonary contusion, ventilation–perfusion mismatch, arteriovenous shunting, hypoxemia, and potential respiratory failure.
Pediatric considerations: Children have more elastic chest walls, making rib fractures less common; when present, they imply severe energy transfer.
Geriatric considerations: Older adults are more susceptible to rib fractures, often from low-energy mechanisms, and outcomes are worsened by osteoporosis.
Diagnosis Signs And Symptoms
History typically includes significant blunt chest trauma with localized chest wall pain that worsens with inspiration, coughing, or movement. Patients may report pleuritic chest pain, dyspnea, or hemoptysis.
Physical examination may reveal paradoxical chest wall motion, which can be subtle or absent early due to muscle spasm and splinting. Additional findings include multiple rib fractures with tenderness, crepitus, ecchymosis, edema, and bony step-offs. Respiratory findings range from tachypnea and splinting respirations to cyanosis, hypoxia, tachycardia, hypotension, and progressive crackles or diminished breath sounds as pulmonary contusion evolves.
Essential Workup
Diagnosis is primarily clinical and supported by imaging. Continuous monitoring of oxygenation and respiratory status is essential.
Diagnosis Tests And Interpretation
Laboratory studies may include arterial blood gas analysis demonstrating hypoxemia and an elevated alveolar–arterial gradient.
Chest radiography may show rib fractures and associated intrathoracic injuries such as pneumothorax, hemothorax, pneumomediastinum, or pulmonary contusion, which often becomes radiographically apparent within 6–12 hours.
Thoracic CT is more sensitive than plain radiographs and frequently identifies additional rib fractures and associated injuries not seen on initial chest X-ray.
Differential Diagnosis
Chest wall contusion, intercostal muscle strain, costochondral separation, sternal fracture or dislocation, and pulmonary conditions such as ARDS, pulmonary laceration, embolism, heart failure, pneumonia, or noncardiogenic pulmonary edema.
Treatment
Prehospital care includes positioning the patient with the injured side down to stabilize the chest wall and improve ventilation of the unaffected lung. Patients with significant thoracic trauma should be transported to a trauma center.
Initial stabilization follows airway, breathing, and circulation priorities with supplemental oxygen, IV access, cardiac monitoring, and pulse oximetry. Endotracheal intubation is indicated for severe hypoxemia, significant underlying lung disease, or impending respiratory failure.
Emergency department management focuses on maintaining adequate oxygenation and ventilation. High-flow oxygen is first-line in alert patients; noninvasive positive pressure ventilation may be used if oxygenation remains inadequate. Early invasive mechanical ventilation is indicated when noninvasive measures fail, providing physiologic internal stabilization of the flail segment. External fixation of the chest wall is not recommended.
Aggressive pain control is critical to prevent hypoventilation, atelectasis, and pneumonia. Intercostal nerve blocks with bupivacaine can provide effective temporary analgesia. Careful fluid management is essential to avoid worsening pulmonary edema in the presence of contusion. Prophylactic antibiotics are not indicated.
Medication
Analgesia may include acetaminophen–opioid combinations, IV or oral opioids such as morphine or hydromorphone, patient-controlled analgesia, and regional techniques. Bupivacaine 0.5% may be used for intercostal nerve blocks. Thoracic epidural analgesia should be considered in patients with severe pain or opioid-related hypoventilation. NSAIDs are generally discouraged due to bleeding risk. Acetaminophen dosing should not exceed recommended daily limits.
Follow Up Disposition
All patients with flail chest require admission to a critical care or closely monitored setting for respiratory observation and pain management. Discharge from the emergency department is not appropriate.
Clinical Takeaways And Common Pitfalls
Early and adequate pain control is essential to prevent respiratory complications. Always assess for associated injuries, particularly pulmonary contusion and pneumothorax. Elderly patients have markedly worse outcomes and require vigilant monitoring and aggressive supportive care.
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Emergency And Acute Medicine – Fibromyalgia
Basics Description
Fibromyalgia is a nonarticular, noninflammatory syndrome characterized by chronic, widespread musculoskeletal pain and heightened pain sensitivity to normally nonpainful stimuli (allodynia). It is more common in females and is associated with diffuse tenderness at multiple sites, fatigue, sleep disturbance, muscle stiffness, and cognitive difficulties involving attention and memory. Physical examination findings are often limited. Fibromyalgia is not a diagnosis of exclusion and may coexist with other rheumatologic or medical conditions.
Etiology
The underlying mechanism is believed to involve central pain processing abnormalities, with increased activity of pronociceptive pathways and reduced activity of antinociceptive pathways in the brain and spinal cord. Identified contributors include elevated substance P levels and decreased biogenic amines such as norepinephrine, serotonin, and dopamine. Reduced gray matter volume in certain brain regions has also been described. A genetic predisposition is suggested, with approximately one third of patients having an affected first-degree relative; candidate genes include those related to serotonin and dopamine pathways. Psychological factors are common, and many patients have comorbid psychiatric conditions. In susceptible individuals, fibromyalgia may be triggered by physical trauma, illness, inflammation, or chronic stress, with hypothalamic–pituitary–adrenal axis dysfunction often preceding symptom onset.
Diagnosis Signs And Symptoms
Patients report widespread pain involving both sides of the body, above and below the waist, and the axial skeleton, persisting for more than three months. Common associated symptoms include morning stiffness, generalized weakness, persistent fatigue not relieved by rest, sleep disturbance, muscle spasms, paresthesias, impaired concentration or memory, headaches, gastrointestinal discomfort relieved by bowel movements, pelvic or bladder discomfort, jaw or facial pain, and mood disturbances. Physical examination is typically unremarkable aside from tenderness at characteristic sites.
Essential Workup
History is the most important diagnostic tool. In the emergency department, evaluation is primarily focused on distinguishing chronic fibromyalgia pain from acute pain due to trauma, injury, or new medical conditions. If diagnostic confirmation is required, American College of Rheumatology criteria may be applied, including widespread pain for at least three months with either tender point assessment or use of the Widespread Pain Index (WPI) and Symptom Severity (SS) scale. Tender points are classically located at bilateral sites including the occiput, low cervical region, trapezius, supraspinatus, second rib, lateral epicondyle, gluteal region, greater trochanter, and medial knee fat pad.
Diagnosis Tests And Interpretation
Laboratory testing is not diagnostic and should be reserved for exclusion of alternative or acute conditions. Studies may include CBC, basic chemistries, ESR, muscle enzymes, thyroid function tests, and urinalysis when clinically indicated. Imaging and invasive procedures are not routinely useful and should only be performed to evaluate suspected alternative diagnoses.
Differential Diagnosis
Conditions to consider include myofascial pain syndrome, chronic fatigue syndrome, major depression, polymyalgia rheumatica, Lyme disease, hypothyroidism, collagen vascular diseases, electrolyte abnormalities, metabolic or drug-induced myopathies, osteomalacia, spondyloarthropathies, interstitial cystitis, and urinary tract infection.
Treatment
Emergency department management focuses on patient education, reassurance, and exclusion of acute pathology. Patients should be informed that fibromyalgia is chronic but not life-threatening, deforming, or associated with reduced life expectancy. Long-term management aims to reduce pain and improve function and requires outpatient follow-up. Pharmacologic therapy with central nervous system–acting agents is most effective, including gabapentin, pregabalin, tricyclic antidepressants, and serotonin–norepinephrine reuptake inhibitors. Opioids are not recommended and may worsen long-term pain. NSAIDs and corticosteroids have not demonstrated benefit. Local injections into tender points remain controversial due to lack of strong evidence.
Medication
Acetaminophen 650 mg PO q4h. Amitriptyline 25–50 mg PO at bedtime. Cyclobenzaprine 5–10 mg PO TID. Duloxetine 60 mg PO daily or BID. Gabapentin starting at 300 mg PO TID with gradual titration. Milnacipran starting at 12.5 mg daily and titrated to 50–100 mg PO BID. Pregabalin starting at 50 mg PO TID, titrated to a maximum of 450 mg/day. Tramadol may be used as an adjunct in selected patients.
Follow Up Disposition
Patients with uncomplicated fibromyalgia can be discharged with outpatient follow-up. Admission is reserved for those with serious underlying disease, intractable pain, immunocompromised status, or suicidal ideation.
Follow Up Recommendations
Patients should be referred to a primary care provider, rheumatologist, or pain specialist for ongoing management. Gradual aerobic exercise programs are encouraged, along with sleep hygiene measures such as regular sleep schedules and avoidance of caffeine in the evening. Stress management strategies and cognitive-behavioral therapy can provide sustained benefit.
Practical Takeaways And Frequent Missteps
Careful distinction between chronic fibromyalgia symptoms and new or acute pain is essential, as patients may still develop unrelated emergent conditions. Avoid unnecessary diagnostic testing once acute pathology has been excluded, and avoid opioid prescribing, which may worsen long-term outcomes.
Basics Description
Fibromyalgia is a nonarticular, noninflammatory syndrome characterized by chronic, widespread musculoskeletal pain and heightened pain sensitivity to normally nonpainful stimuli (allodynia). It is more common in females and is associated with diffuse tenderness at multiple sites, fatigue, sleep disturbance, muscle stiffness, and cognitive difficulties involving attention and memory. Physical examination findings are often limited. Fibromyalgia is not a diagnosis of exclusion and may coexist with other rheumatologic or medical conditions.
Etiology
The underlying mechanism is believed to involve central pain processing abnormalities, with increased activity of pronociceptive pathways and reduced activity of antinociceptive pathways in the brain and spinal cord. Identified contributors include elevated substance P levels and decreased biogenic amines such as norepinephrine, serotonin, and dopamine. Reduced gray matter volume in certain brain regions has also been described. A genetic predisposition is suggested, with approximately one third of patients having an affected first-degree relative; candidate genes include those related to serotonin and dopamine pathways. Psychological factors are common, and many patients have comorbid psychiatric conditions. In susceptible individuals, fibromyalgia may be triggered by physical trauma, illness, inflammation, or chronic stress, with hypothalamic–pituitary–adrenal axis dysfunction often preceding symptom onset.
Diagnosis Signs And Symptoms
Patients report widespread pain involving both sides of the body, above and below the waist, and the axial skeleton, persisting for more than three months. Common associated symptoms include morning stiffness, generalized weakness, persistent fatigue not relieved by rest, sleep disturbance, muscle spasms, paresthesias, impaired concentration or memory, headaches, gastrointestinal discomfort relieved by bowel movements, pelvic or bladder discomfort, jaw or facial pain, and mood disturbances. Physical examination is typically unremarkable aside from tenderness at characteristic sites.
Essential Workup
History is the most important diagnostic tool. In the emergency department, evaluation is primarily focused on distinguishing chronic fibromyalgia pain from acute pain due to trauma, injury, or new medical conditions. If diagnostic confirmation is required, American College of Rheumatology criteria may be applied, including widespread pain for at least three months with either tender point assessment or use of the Widespread Pain Index (WPI) and Symptom Severity (SS) scale. Tender points are classically located at bilateral sites including the occiput, low cervical region, trapezius, supraspinatus, second rib, lateral epicondyle, gluteal region, greater trochanter, and medial knee fat pad.
Diagnosis Tests And Interpretation
Laboratory testing is not diagnostic and should be reserved for exclusion of alternative or acute conditions. Studies may include CBC, basic chemistries, ESR, muscle enzymes, thyroid function tests, and urinalysis when clinically indicated. Imaging and invasive procedures are not routinely useful and should only be performed to evaluate suspected alternative diagnoses.
Differential Diagnosis
Conditions to consider include myofascial pain syndrome, chronic fatigue syndrome, major depression, polymyalgia rheumatica, Lyme disease, hypothyroidism, collagen vascular diseases, electrolyte abnormalities, metabolic or drug-induced myopathies, osteomalacia, spondyloarthropathies, interstitial cystitis, and urinary tract infection.
Treatment
Emergency department management focuses on patient education, reassurance, and exclusion of acute pathology. Patients should be informed that fibromyalgia is chronic but not life-threatening, deforming, or associated with reduced life expectancy. Long-term management aims to reduce pain and improve function and requires outpatient follow-up. Pharmacologic therapy with central nervous system–acting agents is most effective, including gabapentin, pregabalin, tricyclic antidepressants, and serotonin–norepinephrine reuptake inhibitors. Opioids are not recommended and may worsen long-term pain. NSAIDs and corticosteroids have not demonstrated benefit. Local injections into tender points remain controversial due to lack of strong evidence.
Medication
Acetaminophen 650 mg PO q4h. Amitriptyline 25–50 mg PO at bedtime. Cyclobenzaprine 5–10 mg PO TID. Duloxetine 60 mg PO daily or BID. Gabapentin starting at 300 mg PO TID with gradual titration. Milnacipran starting at 12.5 mg daily and titrated to 50–100 mg PO BID. Pregabalin starting at 50 mg PO TID, titrated to a maximum of 450 mg/day. Tramadol may be used as an adjunct in selected patients.
Follow Up Disposition
Patients with uncomplicated fibromyalgia can be discharged with outpatient follow-up. Admission is reserved for those with serious underlying disease, intractable pain, immunocompromised status, or suicidal ideation.
Follow Up Recommendations
Patients should be referred to a primary care provider, rheumatologist, or pain specialist for ongoing management. Gradual aerobic exercise programs are encouraged, along with sleep hygiene measures such as regular sleep schedules and avoidance of caffeine in the evening. Stress management strategies and cognitive-behavioral therapy can provide sustained benefit.
Practical Takeaways And Frequent Missteps
Careful distinction between chronic fibromyalgia symptoms and new or acute pain is essential, as patients may still develop unrelated emergent conditions. Avoid unnecessary diagnostic testing once acute pathology has been excluded, and avoid opioid prescribing, which may worsen long-term outcomes.
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Emergency And Acute Medicine – Pediatric Fever
Basics Description
Fever in children is defined as a rectal temperature of 38°C (100.4°F) or higher. Oral and tympanic temperatures are typically 0.6°C to 1°C lower than rectal measurements, and tympanic readings are unreliable in infants younger than six months. Axillary temperatures are generally inaccurate. Children who present afebrile but have a reliable history of documented fever should be considered febrile to the reported degree.
Etiology
Common causes of pediatric fever include bacteremia, viral illnesses often associated with exanthems, and localized infections. Vaccination against Haemophilus influenzae type B and Streptococcus pneumoniae has significantly reduced invasive disease caused by these organisms. Central nervous system causes include meningitis and encephalitis. Head and neck sources include otitis media, pharyngitis, cervical adenitis, sinusitis, mastoiditis, periorbital cellulitis, and deep neck space abscesses. Respiratory causes include croup, bronchiolitis, pneumonia, empyema, influenza, and epiglottitis. Additional etiologies include cardiac infections, urinary tract infections, gastrointestinal disease, osteomyelitis, septic arthritis, cellulitis, Kawasaki disease, neonatal herpes simplex virus infection, malignancy, drug reactions, heat-related illness, endocrine disorders, and inflammatory or autoimmune disease.
Diagnosis Signs And Symptoms
Clinical appearance is the most important factor in assessment. Airway, breathing, and circulation must be evaluated carefully, with special attention to hydration and perfusion. Toxic features include lethargy, poor feeding, delayed capillary refill, abnormal respirations, weak cry, hypotonia, and petechial or purpuric rash. Tachycardia and tachypnea may be the only early signs of serious illness. Fever increases heart rate by approximately ten beats per minute per degree Fahrenheit. Temperatures above 40°C are associated with increased bacteremia risk in children younger than twenty-four months, while temperatures above 42°C are more often noninfectious. Altered mental status may present as lethargy, irritability, or impaired interaction. Pneumonia should be suspected with tachypnea or hypoxia, and urinary tract infection should be considered in young females, uncircumcised males, and children with fever without a source. Febrile seizures may occur, and serious infection can be present even without fever. Antipyretics may improve clinical appearance without affecting underlying pathology, which can aid assessment. Approximately twenty percent of children will have fever without an identifiable source after initial evaluation.
Essential Workup
Oxygen saturation should be considered a mandatory vital sign. Resuscitation is initiated as needed. A focused history should include duration and pattern of fever, antipyretic use, immunization status, medical history, medications, birth history for infants younger than six months, exposures, feeding and elimination patterns, travel history, and review of systems. A thorough physical examination is performed to identify a source, and antipyretic therapy is initiated.
Diagnosis Tests And Interpretation
Laboratory evaluation may include a complete blood count with differential and urinalysis with culture in all male infants younger than six months, uncircumcised males younger than twelve months, and females younger than two years, using catheterized or suprapubic specimens. Blood cultures are obtained when bacteremia is suspected. Cerebrospinal fluid analysis is required for toxic children and neonates and considered selectively in older infants. Stool studies are indicated when bacterial diarrhea is suspected. Inflammatory markers such as C-reactive protein, erythrocyte sedimentation rate, and procalcitonin may provide supportive information. Chest radiography is indicated for tachypnea, hypoxia, or respiratory findings, with additional imaging guided by suspected source.
Treatment
Prehospital care focuses on stabilization and early antipyretic administration. Initial emergency department management prioritizes treatment of life-threatening conditions. Antipyretics are administered, while evaporative cooling has a limited role. Toxic-appearing children require immediate sepsis evaluation and empiric antibiotics. Neonates younger than twenty-eight days require full sepsis workup and admission with empiric antimicrobial therapy. Infants aged twenty-nine to ninety days are managed based on risk stratification, with selective laboratory evaluation, antibiotic use, and close follow-up. Children three months to three years of age are evaluated selectively, with focused testing based on clinical findings. Immunocompromised children, those with petechiae or purpura, sickle cell disease, malignancy, indwelling devices, or incomplete immunizations require aggressive evaluation and management.
Follow Up Disposition
Admission is required for toxic patients, neonates with fever, higher-risk infants who do not meet low-risk criteria, immunocompromised children, and those with unreliable follow-up. Discharge may be considered for well-appearing infants meeting low-risk criteria and older children who are nontoxic with reliable caregivers and follow-up. Clear return precautions and re-evaluation within twenty-four to forty-eight hours are essential.
Follow Up Recommendations
Children discharged with fever require close follow-up with a primary care provider and explicit instructions for return if symptoms worsen or new signs develop.
Key Clinical Insights And Common Errors
Fever is the most frequent presenting complaint in pediatric patients and may indicate life-threatening disease. Neonates require empiric treatment until serious infection is excluded. Older children may appear well despite significant illness, making subtle findings such as tachycardia, tachypnea, or altered mental status critically important. Inadequate follow-up and failure to recognize early signs of serious infection are common sources of error.
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Emergency And Acute Medicine – Feeding Problems, Pediatric
Overview And Definitions
Feeding problems may involve one or more components of feeding, including oral intake initiation, swallowing, or gastrointestinal ingestion and absorption. Acute feeding difficulties may reflect systemic illness such as infection or bowel obstruction, whereas chronic feeding problems often result from neuromuscular, cardiovascular, behavioral, or social factors. Minor feeding difficulties occur in up to half of otherwise healthy children, while more severe feeding disorders are common in premature infants and children with chronic medical conditions.
Etiology And Pathophysiology
Feeding problems often arise from overlapping etiologies. Structural abnormalities may involve the naso-oropharynx, larynx, trachea, or esophagus, including cleft lip or palate, choanal atresia, micrognathia, macroglossia, tonsillar hypertrophy, laryngeal clefts, tracheomalacia, esophageal strictures, webs, vascular rings, masses, or foreign bodies. Neurologic conditions include cerebral palsy, neuromuscular disorders, mitochondrial disease, Arnold–Chiari malformation, myasthenia gravis, brainstem injury, autism spectrum disorder, infant botulism, and prematurity. Immune-mediated disorders include food allergy, eosinophilic esophagitis, and celiac disease. Cardiac disease may cause feeding intolerance due to fatigue or increased metabolic demand, both before and after corrective surgery. Metabolic disorders such as hypothyroidism and inborn errors of metabolism may impair feeding. Acute illnesses including sepsis, pharyngitis, intussusception, malrotation, or abusive head trauma may present with feeding refusal. Behavioral and environmental factors include dysfunctional caregiver–child interaction, selective eating, rumination, feeding-related anxiety, neglect, depression, and poverty.
Clinical Presentation
Common presentations include caregiver concern regarding feeding behavior, poor weight gain or failure to thrive, and recurrent or chronic respiratory illness. Aspiration is frequently silent in infants and may present as recurrent pneumonia or wheezing.
History And Physical Examination
History should address onset and duration of feeding problems, meal length, food refusal or oral aversion, independent feeding ability, vomiting or gagging, diarrhea or rectal bleeding, respiratory symptoms, irritability or lethargy during feeds, and feeding frequency and volume appropriate for age. Feeding times consistently longer than 30 minutes are concerning. Physical examination includes vital signs and pulse oximetry, growth measurements plotted on standardized growth curves, and assessment of nutritional status. Severe cases may show emaciation, weakness, or apathy. Examination should focus on affect and social responsiveness, dysmorphic features, ENT abnormalities, cardiovascular and pulmonary status, abdominal findings, neurologic tone and coordination, and skin signs of malnutrition or allergy. Direct observation of feeding is essential, assessing oral motor function, pacing, airway sounds, gagging, coughing, emesis, respiratory distress, fatigue, irritability, and feeding duration.
Essential Evaluation
A well-appearing, hydrated child with normal examination findings and adequate recent weight gain may not require emergency department testing beyond ensuring appropriate follow-up. Children with distress, dehydration, respiratory compromise, or poor growth require further evaluation.
Diagnostic Studies And Interpretation
Initial laboratory evaluation in children with failure to thrive or malnutrition may include complete blood count, urinalysis, electrolytes, BUN, glucose, ESR or CRP, thyroid function tests, liver function tests, total protein, and albumin. Blood, urine, and cerebrospinal fluid cultures are indicated if infection is suspected. Metabolic testing may include serum ammonia and urine organic acids. Imaging may include chest radiograph for cardiopulmonary disease, ECG for suspected cardiac pathology, and ultrasound or advanced imaging as indicated. Videofluoroscopic or fiberoptic swallowing studies may be required. MRI is indicated when brainstem or spinal pathology is suspected. Multidisciplinary evaluation involving speech therapy, pediatrics, and otolaryngology is often necessary.
Differential Diagnosis
Feeding disorders represent a final common pathway for numerous conditions. Prolonged feeding with fatigue suggests cardiac disease. Recurrent pneumonias suggest chronic aspiration. Stridor during feeds raises concern for airway anomalies. Poor suck–swallow–breathing coordination suggests nasal obstruction or choanal atresia. Vomiting, diarrhea, abdominal pain, or colic may indicate allergy or gastroesophageal reflux.
Management And Initial Therapy
Initial management includes assessment of airway, breathing, circulation, hydration status, and glucose. Cardiopulmonary and fluid resuscitation are provided as needed. Hypoglycemia should be promptly identified and treated. Certain inborn errors of metabolism may cause severe hypoglycemia with feeding interruption and require immediate intravenous dextrose. Bilious vomiting in infants raises concern for malrotation with volvulus and mandates emergent surgical consultation.
Emergency Department Treatment
Dehydration should be treated with oral rehydration when feasible or intravenous fluids when oral intake is not tolerated. Ondansetron may be used for acute vomiting in appropriate patients. Respiratory distress should be addressed, including nasal suctioning prior to feeding in young infants with upper respiratory symptoms. Oxygen and additional respiratory support should be provided as needed. Infection should be treated promptly, recognizing that severely malnourished children may have blunted physiologic responses to sepsis.
Disposition And Follow Up
Admission is indicated for suspected systemic infection, inability to maintain hydration, sustained hypoxia during feeding, significant failure to thrive—particularly in infants younger than three months—decompensated cardiopulmonary disease, symptomatic anemia or endocrine dysfunction, or concerns regarding caregiver capacity. Discharge may be considered when the child demonstrates adequate oral intake, weight stability or gain, reliable caregiving, and assured follow-up. Referral should be tailored to the underlying etiology, with multidisciplinary care often required for complex or chronic feeding disorders. Nonoral nutritional support may be necessary when oral feeding is insufficient.
Key Clinical Insights And Common Errors
Effective feeding requires coordinated interaction among physiologic, developmental, and environmental factors, and disruption of one component often affects others. Acute-onset feeding problems are more likely to have a single identifiable cause such as infection or obstruction, whereas chronic feeding difficulties are often multifactorial. Simple interventions such as aggressive nasal suctioning before feeding may resolve symptoms in infants with upper respiratory congestion. Swallowing disorders and aspiration are frequently occult. Feeding difficulties may persist behaviorally even after correction of the underlying medical condition, particularly when early negative feeding experiences have occurred.
