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IEmergency And Acute Medicine – Duodenal Trauma
Basics Description
The duodenum is a 12-inch long, C-shaped structure extending from the pylorus to the ligament of Treitz and is divided into four sections. The distal portion of the first section and the remaining three sections are retroperitoneal. It lies mostly over the first three lumbar vertebrae, with the second portion being the most commonly injured. Types of injury include duodenal wall hematoma, wall perforation, hemorrhage including retroperitoneal bleeding, and crush injury. Duodenal trauma accounts for 3–5% of all traumatic abdominal injuries. Penetrating trauma causes approximately 75% of cases, with mortality ranging from 13–28%, often due to exsanguination. Blunt trauma carries higher mortality because of greater injury force and delayed diagnosis related to the retroperitoneal location. If diagnosed within 24 hours, mortality is approximately 11%; if delayed beyond 24 hours, mortality approaches 40%, with late deaths commonly due to sepsis.
Pediatric Considerations
Most pediatric duodenal injuries result from recreational trauma such as bicycle handlebar injuries. Intramural duodenal hematomas may be associated with nonaccidental trauma; suspected cases require immediate referral to child protective services. In children, hematomas most commonly involve the first portion of the duodenum.
Pregnancy Considerations
Retroperitoneal hemorrhage is more common due to increased abdominal and pelvic vascularity. The enlarged uterus may provide partial protection from bowel injury, and peritoneal irritation may be blunted, necessitating a higher index of suspicion.
Etiology
Blunt trauma mechanisms include shear strain from rapid acceleration–deceleration at points of fixation and tensile strain from direct compression or stretching. Penetrating trauma is the most common cause overall and may create cavitation with subsequent infection.
Diagnosis Signs And Symptoms
Symptoms may be minimal and nonspecific, including vague abdominal, flank, or back pain. High gastrointestinal obstruction may occur with duodenal hematomas.
History
Penetrating or blunt abdominal trauma.
Physical-Exam
Retroperitoneal injury may present subtly with right upper quadrant pain, nausea, vomiting, tachycardia, and fever. Intraperitoneal involvement presents with signs of peritonitis.
Essential Workup
Obtain basic laboratory studies including amylase. Perform an acute abdominal series or CT imaging. Diagnostic peritoneal lavage or exploratory laparotomy is indicated in unstable patients with high clinical suspicion.
Diagnosis Tests And Interpretation
Laboratory studies are generally nonspecific; approximately 50% of patients have elevated serum amylase, and rising leukocytosis may suggest missed injury. FAST examination is validated for hemoperitoneum but is unreliable for duodenal injury, with one-third of retroperitoneal injuries having a normal FAST. Upright chest and abdominal radiographs may show intraperitoneal or retroperitoneal air, air in the biliary tree, rightward scoliosis, loss of psoas shadow, or air around the right kidney. Air insufflation via nasogastric tube may enhance detection of retroperitoneal air. Intramural hematomas may show a coiled-spring appearance. CT with oral and IV contrast is the preferred diagnostic modality, identifying retroperitoneal gas, contrast extravasation, duodenal wall thickening, periduodenal fluid, sentinel clot, or sausage-shaped intramural masses. Exploratory laparotomy remains the definitive diagnostic test when suspicion persists despite negative studies. Diagnostic peritoneal lavage may reveal blood, bile, or bowel contents but has a false-negative rate of up to 65%.
Differential Diagnosis
Hollow viscus injuries involving stomach or intestines, liver and biliary injuries, vascular injuries including aortic or mesenteric vessels, and postoperative complications such as infection or suture dehiscence.
Treatment Pre Hospital
Follow standard trauma protocols. Clear documentation of mechanism of injury and transport to an appropriate trauma center are essential.
Initial Stabilization And Therapy
Secure the airway and initiate resuscitation as needed. Provide aggressive fluid resuscitation with warmed crystalloids and transfuse blood products when indicated. Place central venous access in unstable patients. Initiate nasogastric decompression and obtain early trauma surgery consultation.
Emergency Department Treatment And Procedures
Administer tetanus prophylaxis and broad-spectrum antibiotics for penetrating injuries. Definitive management typically requires laparotomy with duodenal exploration. Low-grade blunt injuries (grade I or II) are often managed nonoperatively, though up to 10% may fail conservative therapy. Antibiotics are essential in cases of perforation to prevent sepsis.
Medication
Cefoxitin 2 g IV every 6 hours (pediatric dose 40 mg/kg) or levofloxacin 750 mg IV or ciprofloxacin 400 mg IV daily combined with metronidazole 500 mg IV every 8 hours.
Follow-Up And Disposition
All patients with duodenal injury require admission to a trauma surgical service. Minor hematomas may require nasogastric decompression for obstruction for up to seven days with close observation for expansion or rupture. No patient with confirmed duodenal trauma should be discharged from the emergency department. Complications include intra-abdominal abscess, duodenal fistula, pancreatic fistula, and sepsis.
Issues For Referral
Duodenal injuries are graded using the American Association for the Surgery of Trauma Duodenal Injury Scale, with most injuries being grade II or III. Approximately 80% are managed with primary repair.
Follow-Up Recommendations
All confirmed injuries require inpatient management. If diagnostic studies are negative, arrange follow-up with a primary care physician within 24–48 hours. Begin with clear liquids and advance diet as tolerated.
Pearls And Pitfalls
Delayed or missed diagnosis significantly increases morbidity and mortality. Physical examination may be misleading due to the retroperitoneal location of the duodenum. Persistent clinical suspicion warrants immediate surgical consultation even with negative diagnostic tests.
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Emergency And Acute Medicine – Drowning
Basics Description
Drowning is a process resulting in primary respiratory impairment from submersion or immersion in a liquid medium. Fatal drowning refers to death at any time as a result of the drowning process, while nonfatal drowning occurs when the victim survives after interruption of submersion. Water rescue describes submersion or immersion without respiratory impairment. All drowning victims aspirate some amount of liquid; previously used terms such as “wet” and “dry” drowning are obsolete. The final common pathway is hypoxia, with no clinically significant difference between freshwater and saltwater drowning.
Pathophysiology
Aspiration of small volumes of water decreases lung compliance, causing ventilation–perfusion mismatch and intrapulmonary shunting, usually without major electrolyte disturbances. Grossly contaminated water increases the risk of pulmonary infection. Hypoxemia leads to lactic acidosis, multisystem organ dysfunction, noncardiogenic pulmonary edema, myocardial dysrhythmias, coagulation abnormalities including disseminated intravascular coagulation, acute renal failure, and cerebral hypoxia resulting in cerebral edema and increased intracranial pressure.
Pediatric Considerations
Hypothermia is more common in children due to a higher body surface area–to–mass ratio and may be neuroprotective by lowering metabolic rate. The diving reflex, particularly in young children exposed to cold water, causes bradycardia and preferential blood flow to the heart and brain, delaying hypoxic injury.
Alert
Risk factors include inadequate supervision, alcohol or drug use, limited swimming ability, trauma, seizure disorder, risky behavior, pre-existing medical conditions, suicide attempt, and poor water safety education.
Diagnosis Signs And Symptoms
Findings include cardiopulmonary arrest, cyanosis, dyspnea, copious pulmonary secretions, altered mental status or loss of consciousness, hypothermia, cerebral edema or neurologic injury, and evidence of trauma. Cervical spine injury is rare.
Essential Workup
Obtain witness and EMS information, initiate early airway management and cardiopulmonary resuscitation when indicated, and measure core temperature to assess hypothermia.
Diagnostic Tests And Interpretation
Laboratory studies include arterial blood gas, complete blood count, electrolytes, blood urea nitrogen, creatinine, glucose, and alcohol or toxicology screening. Imaging includes chest radiography, which may show infiltrates or acute respiratory distress syndrome but can be normal initially, electrocardiography showing bradyarrhythmias or tachyarrhythmias, and computed tomography of the brain or cervical spine when indicated.
Differential Diagnosis
Consider dysrhythmias such as long QT syndrome, myocardial infarction, seizure, syncope, trauma, or suicide attempt as causes of submersion. In pediatric patients, always consider abuse or neglect, particularly in bathtub incidents.
Treatment Prehospital
Address airway, breathing, and circulation, avoid further aspiration, secure the airway, initiate early cardiopulmonary resuscitation, apply cervical spine precautions when indicated, and begin rewarming. Abdominal thrusts are not recommended as they delay effective resuscitation and increase aspiration risk.
Initial Stabilization And Therapy
Manage airway and oxygenation, remove wet clothing, initiate rewarming, and support circulation.
Emergency Department Treatment
Correct hypoxemia, intubate with positive end-expiratory pressure if needed, treat acidosis, and evaluate for traumatic injuries. In cardiac arrest, follow advanced cardiac life support protocols and continue resuscitation until core temperature exceeds 32°C or return of spontaneous circulation occurs. Corticosteroids have no proven benefit. Poor prognostic indicators include prolonged submersion, severe acidosis, need for cardiopulmonary resuscitation, low oxygen saturation, and low Glasgow Coma Scale score.
Medication
Epinephrine, vasopressin, lidocaine, and sodium bicarbonate may be administered when clinically indicated.
Follow-Up And Disposition
Patients with respiratory symptoms, neurologic abnormalities, abnormal imaging or laboratory findings, or those requiring ventilatory support should be admitted, often to intensive care. Symptomatic patients or those with significant submersion history require observation. Patients may be discharged only after at least eight hours of observation with no respiratory distress, no neurologic impairment, and reliable caregivers.
Pearls And Pitfalls
All drowning patients require observation for delayed complications. Hypothermia may be protective. Prevention through supervision and water safety education is essential.
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Emergency and Acute Medicine – Domestic Violence
Basics
Description
Intimate partner violence (IPV) is physical, sexual, or psychological abuse by a current or former partner. It occurs in adult and adolescent intimate relationships across all socioeconomic groups.
Etiology
Most victims are women injured by male perpetrators, but men and individuals in same-sex relationships may also be victims. Risk factors include female sex, young age (20–24 years), and separation from a partner or spouse.
Diagnosis
Directly asking about IPV increases identification of victims.
Signs and symptoms
Traumatic injuries include a wide range of presentations. Unwitnessed head, neck, and facial injuries are common. Forearm bruises or fractures may suggest defensive posture. Injuries may be in various stages of healing.
Psychiatric and medical associations include chronic pain syndromes, depression, somatization, anxiety, suicidality, and substance abuse.
Alert
Clinical clues include discrepancies between history and physical findings, a partner refusing to leave the patient alone with the provider, delay in seeking care, any injury during pregnancy, concerning patient–partner interactions, and multiple symptoms without clear physical findings.
History
Screening questions can identify IPV. Evidence is mixed regarding improved outcomes, but IPV screening is required by the Joint Commission and supported by some professional organizations. Screening should be direct, nonjudgmental, supportive, and private. Computer-based ED screening may be effective. Consider IPV in patients with substance abuse or intoxication, who may be at higher risk and under-identified.
Physical examination
Perform a careful examination for traumatic injuries and a mental status assessment.
Essential workup
After IPV identification, perform a directed evaluation for traumatic injuries and acute medical or behavioral health conditions. Assess risk for future injury or victimization.
Differential diagnosis
Maintain a high index of suspicion for IPV in patients with traumatic injuries, behavioral health complaints, and medical presentations such as genitourinary or gynecologic complaints and multiple somatic symptoms.
Treatment
Prehospital
Provide standard trauma evaluation and treatment. Incorporate accurate EMS descriptions into the medical record.
Initial stabilization and therapy
Provide timely medical care and ongoing emotional support throughout evaluation and treatment.
Emergency department treatment and procedures
Interview the patient privately without family members present. Use a professional medical interpreter when needed. Document thoroughly using the patient’s exact words; careful documentation is admissible in court. Record extent and location of injuries; diagrams or photographs are helpful.
If stable for discharge, assess lethality risk, including escalating violence, threats of homicide or suicide, and access to lethal weapons. Collaborate with the patient to create a discharge plan aligned with their wishes. Arrange referrals for victim services, emergency shelter information, hotlines, restraining order information, and legal services.
Mandatory reporting varies by state and may increase risk or pose ethical challenges. Inform patients of reporting requirements and potential outcomes.
Medication
Acetaminophen 650–975 mg PO.
Morphine sulfate 0.1 mg/kg/dose IV or IM.
Follow-up and disposition
Admission criteria
Use standard admission guidelines based on injury severity. Medically stable patients with imminent safety risk may require hospitalization until a safe plan is established.
Discharge criteria
Patients whose safety is ensured and whose injuries are manageable as an outpatient may be discharged.
Issues for referral
Advocacy services availability varies by region.
Follow-up recommendations
Provide information on outpatient services and emergency shelter options.
Pearls and pitfalls
Failure to consider IPV in the differential diagnosis. Inadequate, nonobjective documentation of assault details and exam findings. Failure to assess discharge safety and arrange appropriate referrals. Mandatory reporting laws remain controversial and may have unintended consequences.
Basics
Description
Intimate partner violence (IPV) is physical, sexual, or psychological abuse by a current or former partner. It occurs in adult and adolescent intimate relationships across all socioeconomic groups.
Etiology
Most victims are women injured by male perpetrators, but men and individuals in same-sex relationships may also be victims. Risk factors include female sex, young age (20–24 years), and separation from a partner or spouse.
Diagnosis
Directly asking about IPV increases identification of victims.
Signs and symptoms
Traumatic injuries include a wide range of presentations. Unwitnessed head, neck, and facial injuries are common. Forearm bruises or fractures may suggest defensive posture. Injuries may be in various stages of healing.
Psychiatric and medical associations include chronic pain syndromes, depression, somatization, anxiety, suicidality, and substance abuse.
Alert
Clinical clues include discrepancies between history and physical findings, a partner refusing to leave the patient alone with the provider, delay in seeking care, any injury during pregnancy, concerning patient–partner interactions, and multiple symptoms without clear physical findings.
History
Screening questions can identify IPV. Evidence is mixed regarding improved outcomes, but IPV screening is required by the Joint Commission and supported by some professional organizations. Screening should be direct, nonjudgmental, supportive, and private. Computer-based ED screening may be effective. Consider IPV in patients with substance abuse or intoxication, who may be at higher risk and under-identified.
Physical examination
Perform a careful examination for traumatic injuries and a mental status assessment.
Essential workup
After IPV identification, perform a directed evaluation for traumatic injuries and acute medical or behavioral health conditions. Assess risk for future injury or victimization.
Differential diagnosis
Maintain a high index of suspicion for IPV in patients with traumatic injuries, behavioral health complaints, and medical presentations such as genitourinary or gynecologic complaints and multiple somatic symptoms.
Treatment
Prehospital
Provide standard trauma evaluation and treatment. Incorporate accurate EMS descriptions into the medical record.
Initial stabilization and therapy
Provide timely medical care and ongoing emotional support throughout evaluation and treatment.
Emergency department treatment and procedures
Interview the patient privately without family members present. Use a professional medical interpreter when needed. Document thoroughly using the patient’s exact words; careful documentation is admissible in court. Record extent and location of injuries; diagrams or photographs are helpful.
If stable for discharge, assess lethality risk, including escalating violence, threats of homicide or suicide, and access to lethal weapons. Collaborate with the patient to create a discharge plan aligned with their wishes. Arrange referrals for victim services, emergency shelter information, hotlines, restraining order information, and legal services.
Mandatory reporting varies by state and may increase risk or pose ethical challenges. Inform patients of reporting requirements and potential outcomes.
Medication
Acetaminophen 650–975 mg PO.
Morphine sulfate 0.1 mg/kg/dose IV or IM.
Follow-up and disposition
Admission criteria
Use standard admission guidelines based on injury severity. Medically stable patients with imminent safety risk may require hospitalization until a safe plan is established.
Discharge criteria
Patients whose safety is ensured and whose injuries are manageable as an outpatient may be discharged.
Issues for referral
Advocacy services availability varies by region.
Follow-up recommendations
Provide information on outpatient services and emergency shelter options.
Pearls and pitfalls
Failure to consider IPV in the differential diagnosis. Inadequate, nonobjective documentation of assault details and exam findings. Failure to assess discharge safety and arrange appropriate referrals. Mandatory reporting laws remain controversial and may have unintended consequences.
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Emergency and Acute Medicine – Disulfiram Reaction
Basics
Description
Disulfiram inhibits multiple enzymatic pathways, and its active metabolites contribute additional toxic effects. The classic disulfiram–ethanol reaction usually occurs 8–12 hours after drug ingestion and is not expected beyond 24 hours after dosing. Disulfiram competitively and irreversibly inhibits aldehyde dehydrogenase, blocking ethanol metabolism and causing accumulation of acetaldehyde. Acetaldehyde triggers histamine release, leading to vasodilation and hypotension. Severe reactions may occur at ethanol levels as low as 50–100 mg/dL, and severity correlates with the amount of ethanol consumed.
Disulfiram also inhibits dopamine β-hydroxylase, reducing conversion of dopamine to norepinephrine. Excess dopamine may contribute to behavioral changes, while norepinephrine depletion may worsen hypotension. Its metabolite, carbon disulfide, interferes with pyridoxal-5-phosphate, reducing pyridoxine availability for γ-aminobutyric acid synthesis and potentially lowering the seizure threshold. Carbon disulfide is additionally cardiotoxic, hepatotoxic, inhibits CYP2E1, chelates essential metals, and may cause dose- and duration-dependent peripheral neuropathy.
Etiology
Disulfiram is prescribed as a deterrent for chronic alcohol use disorder, and many patients wear medical alert identification. Disulfiram-like reactions may also occur with other agents, including metronidazole; certain cephalosporins with an N-methylthiotetrazole side chain such as cefoperazone, cefotetan, and cefmetazole; nitrofurantoin; sulfonylurea hypoglycemics; industrial exposures such as carbon disulfide and hydrogen sulfide; and mushrooms including Coprinus atramentarius and Clitocybe clavipes.
Diagnosis
Signs and symptoms
Disulfiram–ethanol reactions commonly present with hypotension, tachycardia, tachypnea, flushing of the face, neck, and torso, pruritus, diaphoresis, warmth, nausea, vomiting, abdominal pain, diarrhea, headache, ataxia, confusion, anxiety, and dizziness. Severe cases may involve dyspnea, pulmonary edema, chest pain, dysrhythmias, and myocardial infarction.
Disulfiram overdose is uncommon with ingestions under 3 g, while doses of 10–30 g may be fatal. Presentations may mimic shock or sepsis and include tachycardia, hypotension, tachypnea, abdominal pain, diarrhea, garlic- or rotten-egg breath, agitation, irritability, ataxia, dysarthria, hallucinations, lethargy, coma, seizures, flaccidity, or parkinsonian features.
History of disulfiram use, ingestion of causative agents, or ethanol exposure—including alcohol-containing foods, medications, or mouthwash—is key. Physical examination often reveals hemodynamic instability, flushing, diaphoresis, pulmonary edema, diffuse abdominal tenderness, altered mental status, cerebellar signs, or seizures.
Essential workup
Suspect a disulfiram–ethanol reaction when characteristic symptoms occur in a patient treated for alcohol use disorder with recent ethanol exposure.
Diagnosis tests and interpretation
Laboratory evaluation includes ethanol level, electrolytes, renal function, glucose, and liver function tests if hepatitis is suspected. Creatine phosphokinase should be checked if seizures or agitation raise concern for rhabdomyolysis. Urinalysis may detect myoglobin. Serum drug levels are not clinically useful.
Electrocardiography evaluates ischemia or dysrhythmias. Neuroimaging is indicated for altered mental status or seizures, as basal ganglia ischemia has been reported. EEG may show diffuse slowing in severe toxicity.
Differential diagnosis
Consider sepsis, meningitis or encephalitis, cardiogenic shock from acute coronary syndrome, anaphylactoid or anaphylactic reactions, gastroenteritis or pancreatitis with dehydration, and ethanol withdrawal.
Treatment
Prehospital care
Initial management includes airway assessment, intravenous access, fluid resuscitation if pulmonary edema is absent, and rapid glucose testing.
Initial stabilization and therapy
Provide airway protection as needed, supplemental oxygen, mechanical ventilation if required, aggressive isotonic fluid resuscitation for hypotension, and vasopressor support with norepinephrine for refractory shock.
Emergency department treatment and procedures
Management is primarily supportive, as no specific antidote exists. Activated charcoal may be considered after disulfiram overdose if the airway is protected and vomiting is controlled; gastric lavage and whole-bowel irrigation are not indicated. Flushing may be treated with antihistamines and prostaglandin inhibitors. Antiemetics are used for persistent vomiting. Seizures are treated with benzodiazepines, and pyridoxine supplementation is recommended.
Fomepizole is not indicated for routine reactions but may improve hemodynamics in severe overdoses. Hemodialysis may be considered after massive ingestion with refractory hypotension, though evidence of benefit is limited.
Medication
Commonly used agents include benzodiazepines for seizures, antihistamines for flushing and pruritus, antiemetics for nausea and vomiting, norepinephrine for refractory hypotension, and intravenous pyridoxine.
Follow-up and disposition
Admission criteria
Intensive care admission is required for coma, mechanical ventilation, refractory hypotension needing vasopressors, cardiac ischemia, uncontrolled seizures, severe agitation, persistent gastrointestinal symptoms, or in elderly patients and those with cardiac disease.
Discharge criteria
Patients with mild reactions that resolve after 8–12 hours of observation may be discharged. Ethanol abstinence is required for at least two weeks after the last dose of disulfiram or related agents, as reactions may recur for up to 7–10 days.
Follow-up recommendations
Psychiatric follow-up is indicated for intentional overdose, and detoxification or addiction follow-up is recommended after disulfiram–ethanol reactions to monitor for hepatic or neurologic sequelae.
Pearls and pitfalls
Patients prescribed disulfiram or drugs with disulfiram-like effects must avoid all alcohol sources, including mouthwash, hand sanitizers, aftershaves, cough syrups, and elixir-based medications. Abstinence should continue for several days beyond completion of therapy to minimize reaction risk.
Basics
Description
Disulfiram inhibits multiple enzymatic pathways, and its active metabolites contribute additional toxic effects. The classic disulfiram–ethanol reaction usually occurs 8–12 hours after drug ingestion and is not expected beyond 24 hours after dosing. Disulfiram competitively and irreversibly inhibits aldehyde dehydrogenase, blocking ethanol metabolism and causing accumulation of acetaldehyde. Acetaldehyde triggers histamine release, leading to vasodilation and hypotension. Severe reactions may occur at ethanol levels as low as 50–100 mg/dL, and severity correlates with the amount of ethanol consumed.
Disulfiram also inhibits dopamine β-hydroxylase, reducing conversion of dopamine to norepinephrine. Excess dopamine may contribute to behavioral changes, while norepinephrine depletion may worsen hypotension. Its metabolite, carbon disulfide, interferes with pyridoxal-5-phosphate, reducing pyridoxine availability for γ-aminobutyric acid synthesis and potentially lowering the seizure threshold. Carbon disulfide is additionally cardiotoxic, hepatotoxic, inhibits CYP2E1, chelates essential metals, and may cause dose- and duration-dependent peripheral neuropathy.
Etiology
Disulfiram is prescribed as a deterrent for chronic alcohol use disorder, and many patients wear medical alert identification. Disulfiram-like reactions may also occur with other agents, including metronidazole; certain cephalosporins with an N-methylthiotetrazole side chain such as cefoperazone, cefotetan, and cefmetazole; nitrofurantoin; sulfonylurea hypoglycemics; industrial exposures such as carbon disulfide and hydrogen sulfide; and mushrooms including Coprinus atramentarius and Clitocybe clavipes.
Diagnosis
Signs and symptoms
Disulfiram–ethanol reactions commonly present with hypotension, tachycardia, tachypnea, flushing of the face, neck, and torso, pruritus, diaphoresis, warmth, nausea, vomiting, abdominal pain, diarrhea, headache, ataxia, confusion, anxiety, and dizziness. Severe cases may involve dyspnea, pulmonary edema, chest pain, dysrhythmias, and myocardial infarction.
Disulfiram overdose is uncommon with ingestions under 3 g, while doses of 10–30 g may be fatal. Presentations may mimic shock or sepsis and include tachycardia, hypotension, tachypnea, abdominal pain, diarrhea, garlic- or rotten-egg breath, agitation, irritability, ataxia, dysarthria, hallucinations, lethargy, coma, seizures, flaccidity, or parkinsonian features.
History of disulfiram use, ingestion of causative agents, or ethanol exposure—including alcohol-containing foods, medications, or mouthwash—is key. Physical examination often reveals hemodynamic instability, flushing, diaphoresis, pulmonary edema, diffuse abdominal tenderness, altered mental status, cerebellar signs, or seizures.
Essential workup
Suspect a disulfiram–ethanol reaction when characteristic symptoms occur in a patient treated for alcohol use disorder with recent ethanol exposure.
Diagnosis tests and interpretation
Laboratory evaluation includes ethanol level, electrolytes, renal function, glucose, and liver function tests if hepatitis is suspected. Creatine phosphokinase should be checked if seizures or agitation raise concern for rhabdomyolysis. Urinalysis may detect myoglobin. Serum drug levels are not clinically useful.
Electrocardiography evaluates ischemia or dysrhythmias. Neuroimaging is indicated for altered mental status or seizures, as basal ganglia ischemia has been reported. EEG may show diffuse slowing in severe toxicity.
Differential diagnosis
Consider sepsis, meningitis or encephalitis, cardiogenic shock from acute coronary syndrome, anaphylactoid or anaphylactic reactions, gastroenteritis or pancreatitis with dehydration, and ethanol withdrawal.
Treatment
Prehospital care
Initial management includes airway assessment, intravenous access, fluid resuscitation if pulmonary edema is absent, and rapid glucose testing.
Initial stabilization and therapy
Provide airway protection as needed, supplemental oxygen, mechanical ventilation if required, aggressive isotonic fluid resuscitation for hypotension, and vasopressor support with norepinephrine for refractory shock.
Emergency department treatment and procedures
Management is primarily supportive, as no specific antidote exists. Activated charcoal may be considered after disulfiram overdose if the airway is protected and vomiting is controlled; gastric lavage and whole-bowel irrigation are not indicated. Flushing may be treated with antihistamines and prostaglandin inhibitors. Antiemetics are used for persistent vomiting. Seizures are treated with benzodiazepines, and pyridoxine supplementation is recommended.
Fomepizole is not indicated for routine reactions but may improve hemodynamics in severe overdoses. Hemodialysis may be considered after massive ingestion with refractory hypotension, though evidence of benefit is limited.
Medication
Commonly used agents include benzodiazepines for seizures, antihistamines for flushing and pruritus, antiemetics for nausea and vomiting, norepinephrine for refractory hypotension, and intravenous pyridoxine.
Follow-up and disposition
Admission criteria
Intensive care admission is required for coma, mechanical ventilation, refractory hypotension needing vasopressors, cardiac ischemia, uncontrolled seizures, severe agitation, persistent gastrointestinal symptoms, or in elderly patients and those with cardiac disease.
Discharge criteria
Patients with mild reactions that resolve after 8–12 hours of observation may be discharged. Ethanol abstinence is required for at least two weeks after the last dose of disulfiram or related agents, as reactions may recur for up to 7–10 days.
Follow-up recommendations
Psychiatric follow-up is indicated for intentional overdose, and detoxification or addiction follow-up is recommended after disulfiram–ethanol reactions to monitor for hepatic or neurologic sequelae.
Pearls and pitfalls
Patients prescribed disulfiram or drugs with disulfiram-like effects must avoid all alcohol sources, including mouthwash, hand sanitizers, aftershaves, cough syrups, and elixir-based medications. Abstinence should continue for several days beyond completion of therapy to minimize reaction risk.
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Emergency and Acute Medicine – Digoxin Poisoning
Basics
Description
Acute digitalis toxicity, typically seen with elevated levels in children or intentional overdose, occurs through inhibition of the sodium–potassium ATPase pump in cell membranes. This allows increased intracellular calcium, leading to stronger myocardial contraction, increased extracellular potassium, enhanced vagal tone, slowed atrioventricular (AV) node conduction (vagotonic effect), increased automaticity, prolonged refractory periods, and predominantly bradydysrhythmias.
Chronic digitalis toxicity, usually occurring in elderly patients at therapeutic to toxic levels, also involves sodium–potassium ATPase inhibition with increased intracellular calcium and vagal tone. These patients commonly develop bradydysrhythmias, increased automaticity, tachydysrhythmias, and are often hypokalemic due to concurrent diuretic use.
Etiology
Sources include digoxin and digitoxin pharmaceuticals as well as plants and animals containing cardiac glycosides such as foxglove, oleander (white and yellow), lily of the valley, dogbane, red squill, cane toad, and Colorado River toad.
Diagnosis
Signs and symptoms
Toxicity typically begins about 2 hours after oral ingestion and as early as 15 minutes after intravenous administration. Toxicity may occur at normal digoxin levels in chronic exposure and may be absent despite elevated levels in acute overdose.
Cardiovascular manifestations include a wide range of dysrhythmias: premature ventricular contractions (most common), paroxysmal atrial tachycardia with AV block, nonparoxysmal accelerated junctional tachycardia, atrial fibrillation or flutter, bigeminy, sinus arrhythmia, AV blocks, bradycardia, ventricular tachycardia, ventricular fibrillation, and the pathognomonic bidirectional ventricular tachycardia. Other findings include hypotension, syncope, shock, cardiovascular collapse, and exacerbation of congestive heart failure.
Central nervous system findings include agitation, lethargy, psychosis, and characteristic visual disturbances such as blurred vision, scotomas, photophobia, and green-to-yellow halos.
Gastrointestinal symptoms include anorexia, nausea, vomiting, and abdominal pain.
History may reveal accidental pediatric or adult overdose, intentional acute or chronic overdose, unintentional chronic toxicity due to declining renal clearance or dose escalation, or recent antibiotic use—especially macrolides—that alter gastrointestinal flora and increase digoxin absorption by reducing Eubacterium lentum.
Physical examination
Common findings include altered mental status, bradycardia or tachycardia, irregular rhythm, and hypotension.
Essential workup
Electrocardiography is required to evaluate for dysrhythmias. Serum digoxin level should be obtained, recognizing that steady-state levels are most accurate when measured more than 6 hours after oral ingestion. False elevations may occur with spironolactone use, pregnancy, hyperbilirubinemia, chronic renal failure, liver failure, or congestive heart failure. Levels may be falsely elevated after administration of digoxin-specific Fab fragments.
Diagnosis tests and interpretation
Laboratory studies
Electrolytes, blood urea nitrogen, creatinine, and glucose should be assessed. Hypokalemia predisposes to toxicity, whereas hyperkalemia in acute poisoning correlates more strongly with mortality than digoxin serum levels and should be followed serially. Calcium and magnesium levels should also be measured.
Serum digoxin concentration should not be obtained after digoxin-specific Fab fragments are administered, as results will be inaccurate.
Differential diagnosis
Consider overdoses involving calcium channel blockers, β-blockers, clonidine, organophosphates, quinidine, procainamide, other antidysrhythmics or antihypertensives, primary cardiac dysrhythmias, and acute gastroenteritis.
Treatment
Prehospital care
Establish intravenous access, initiate continuous cardiac monitoring, and apply defibrillation pads. If cardioversion is required for tachydysrhythmias, use low-energy shocks (around 50 J), as higher energy may precipitate refractory arrhythmias.
Initial stabilization
Follow airway, breathing, and circulation principles. Provide oxygen, intravenous fluids if hypovolemic, and administer naloxone, thiamine, and dextrose for altered mental status when indicated.
Emergency department treatment and procedures
Cardiac arrest should be managed according to standard advanced cardiac life support protocols, including defibrillation for ventricular fibrillation or pulseless ventricular tachycardia. Administer digoxin-specific antibody Fab fragments promptly, typically 5–20 vials intravenously as indicated. Magnesium sulfate 2 g IV may be given, and resuscitation should continue for at least 30 minutes after Fab administration.
Supportive care includes activated charcoal for acute ingestion, magnesium repletion, and treatment of hyperkalemia with insulin, dextrose, bicarbonate, or sodium polystyrene sulfonate. Calcium is generally avoided unless life-saving membrane stabilization is required in unstable patients. In hemodynamically stable patients with hyperkalemia from digoxin toxicity, digoxin-specific Fab fragments are the first-line therapy.
Dysrhythmia management
First-line therapy is digoxin-specific antibody Fab fragments (Digibind or DigiFab). Indications include serum digoxin concentration ≥15 ng/mL at any time or ≥10 ng/mL at steady state, ingestion of more than 10 mg in adults or 0.2 mg/kg (or 4 mg) in children, hyperkalemia >5–5.5 mEq/L, hemodynamic instability, or life-threatening dysrhythmias such as ventricular tachycardia, ventricular fibrillation, atrial tachycardia with variable AV block, atropine-resistant bradycardia, or hypotension.
If Fab fragments are unavailable, lidocaine may be used for ventricular dysrhythmias without AV block, atropine or pacing for symptomatic bradycardia, and magnesium sulfate for torsades de pointes. Quinidine and procainamide are contraindicated. Electrical cardioversion is a last resort and should begin at low energy (10–50 J).
Medication
Activated charcoal may be administered at 1 g/kg if within 1 hour of ingestion. Each 40-mg vial of digoxin-specific Fab fragments neutralizes approximately 0.5 mg of digoxin. Dosing may be calculated based on amount ingested, serum concentration, or given empirically (acute toxicity: 5–10 vials; chronic toxicity: 1–2 vials). Additional doses may be required for rebound toxicity. Standard therapies for hyperkalemia and bradycardia should be used, with calcium reserved only when absolutely necessary.
Special populations
In older adults, dosing of Fab fragments is based on weight and serum concentration and does not change with renal or hepatic dysfunction, though rebound toxicity may occur in renal failure. Pediatric dosing follows the same weight-based principles as adults. Digoxin-specific Fab fragments are pregnancy category C.
Follow-up and disposition
Admission criteria
Patients with unstable cardiovascular status from acute or chronic toxicity require intensive care admission. Telemetry admission is appropriate for asymptomatic or mildly symptomatic patients with dysrhythmias or high risk for progression.
Discharge criteria
Patients may be discharged if digoxin levels are below 2 ng/mL, they remain asymptomatic for at least 6 hours, and no ECG abnormalities are present.
Follow-up recommendations
Psychiatric referral is recommended for patients with intentional overdose.
Pearls and pitfalls
In patients known to be taking digoxin who present with cardiovascular instability or hyperkalemia, treatment should begin immediately with digoxin-specific Fab fragments rather than waiting for confirmatory testing.
Basics
Description
Acute digitalis toxicity, typically seen with elevated levels in children or intentional overdose, occurs through inhibition of the sodium–potassium ATPase pump in cell membranes. This allows increased intracellular calcium, leading to stronger myocardial contraction, increased extracellular potassium, enhanced vagal tone, slowed atrioventricular (AV) node conduction (vagotonic effect), increased automaticity, prolonged refractory periods, and predominantly bradydysrhythmias.
Chronic digitalis toxicity, usually occurring in elderly patients at therapeutic to toxic levels, also involves sodium–potassium ATPase inhibition with increased intracellular calcium and vagal tone. These patients commonly develop bradydysrhythmias, increased automaticity, tachydysrhythmias, and are often hypokalemic due to concurrent diuretic use.
Etiology
Sources include digoxin and digitoxin pharmaceuticals as well as plants and animals containing cardiac glycosides such as foxglove, oleander (white and yellow), lily of the valley, dogbane, red squill, cane toad, and Colorado River toad.
Diagnosis
Signs and symptoms
Toxicity typically begins about 2 hours after oral ingestion and as early as 15 minutes after intravenous administration. Toxicity may occur at normal digoxin levels in chronic exposure and may be absent despite elevated levels in acute overdose.
Cardiovascular manifestations include a wide range of dysrhythmias: premature ventricular contractions (most common), paroxysmal atrial tachycardia with AV block, nonparoxysmal accelerated junctional tachycardia, atrial fibrillation or flutter, bigeminy, sinus arrhythmia, AV blocks, bradycardia, ventricular tachycardia, ventricular fibrillation, and the pathognomonic bidirectional ventricular tachycardia. Other findings include hypotension, syncope, shock, cardiovascular collapse, and exacerbation of congestive heart failure.
Central nervous system findings include agitation, lethargy, psychosis, and characteristic visual disturbances such as blurred vision, scotomas, photophobia, and green-to-yellow halos.
Gastrointestinal symptoms include anorexia, nausea, vomiting, and abdominal pain.
History may reveal accidental pediatric or adult overdose, intentional acute or chronic overdose, unintentional chronic toxicity due to declining renal clearance or dose escalation, or recent antibiotic use—especially macrolides—that alter gastrointestinal flora and increase digoxin absorption by reducing Eubacterium lentum.
Physical examination
Common findings include altered mental status, bradycardia or tachycardia, irregular rhythm, and hypotension.
Essential workup
Electrocardiography is required to evaluate for dysrhythmias. Serum digoxin level should be obtained, recognizing that steady-state levels are most accurate when measured more than 6 hours after oral ingestion. False elevations may occur with spironolactone use, pregnancy, hyperbilirubinemia, chronic renal failure, liver failure, or congestive heart failure. Levels may be falsely elevated after administration of digoxin-specific Fab fragments.
Diagnosis tests and interpretation
Laboratory studies
Electrolytes, blood urea nitrogen, creatinine, and glucose should be assessed. Hypokalemia predisposes to toxicity, whereas hyperkalemia in acute poisoning correlates more strongly with mortality than digoxin serum levels and should be followed serially. Calcium and magnesium levels should also be measured.
Serum digoxin concentration should not be obtained after digoxin-specific Fab fragments are administered, as results will be inaccurate.
Differential diagnosis
Consider overdoses involving calcium channel blockers, β-blockers, clonidine, organophosphates, quinidine, procainamide, other antidysrhythmics or antihypertensives, primary cardiac dysrhythmias, and acute gastroenteritis.
Treatment
Prehospital care
Establish intravenous access, initiate continuous cardiac monitoring, and apply defibrillation pads. If cardioversion is required for tachydysrhythmias, use low-energy shocks (around 50 J), as higher energy may precipitate refractory arrhythmias.
Initial stabilization
Follow airway, breathing, and circulation principles. Provide oxygen, intravenous fluids if hypovolemic, and administer naloxone, thiamine, and dextrose for altered mental status when indicated.
Emergency department treatment and procedures
Cardiac arrest should be managed according to standard advanced cardiac life support protocols, including defibrillation for ventricular fibrillation or pulseless ventricular tachycardia. Administer digoxin-specific antibody Fab fragments promptly, typically 5–20 vials intravenously as indicated. Magnesium sulfate 2 g IV may be given, and resuscitation should continue for at least 30 minutes after Fab administration.
Supportive care includes activated charcoal for acute ingestion, magnesium repletion, and treatment of hyperkalemia with insulin, dextrose, bicarbonate, or sodium polystyrene sulfonate. Calcium is generally avoided unless life-saving membrane stabilization is required in unstable patients. In hemodynamically stable patients with hyperkalemia from digoxin toxicity, digoxin-specific Fab fragments are the first-line therapy.
Dysrhythmia management
First-line therapy is digoxin-specific antibody Fab fragments (Digibind or DigiFab). Indications include serum digoxin concentration ≥15 ng/mL at any time or ≥10 ng/mL at steady state, ingestion of more than 10 mg in adults or 0.2 mg/kg (or 4 mg) in children, hyperkalemia >5–5.5 mEq/L, hemodynamic instability, or life-threatening dysrhythmias such as ventricular tachycardia, ventricular fibrillation, atrial tachycardia with variable AV block, atropine-resistant bradycardia, or hypotension.
If Fab fragments are unavailable, lidocaine may be used for ventricular dysrhythmias without AV block, atropine or pacing for symptomatic bradycardia, and magnesium sulfate for torsades de pointes. Quinidine and procainamide are contraindicated. Electrical cardioversion is a last resort and should begin at low energy (10–50 J).
Medication
Activated charcoal may be administered at 1 g/kg if within 1 hour of ingestion. Each 40-mg vial of digoxin-specific Fab fragments neutralizes approximately 0.5 mg of digoxin. Dosing may be calculated based on amount ingested, serum concentration, or given empirically (acute toxicity: 5–10 vials; chronic toxicity: 1–2 vials). Additional doses may be required for rebound toxicity. Standard therapies for hyperkalemia and bradycardia should be used, with calcium reserved only when absolutely necessary.
Special populations
In older adults, dosing of Fab fragments is based on weight and serum concentration and does not change with renal or hepatic dysfunction, though rebound toxicity may occur in renal failure. Pediatric dosing follows the same weight-based principles as adults. Digoxin-specific Fab fragments are pregnancy category C.
Follow-up and disposition
Admission criteria
Patients with unstable cardiovascular status from acute or chronic toxicity require intensive care admission. Telemetry admission is appropriate for asymptomatic or mildly symptomatic patients with dysrhythmias or high risk for progression.
Discharge criteria
Patients may be discharged if digoxin levels are below 2 ng/mL, they remain asymptomatic for at least 6 hours, and no ECG abnormalities are present.
Follow-up recommendations
Psychiatric referral is recommended for patients with intentional overdose.
Pearls and pitfalls
In patients known to be taking digoxin who present with cardiovascular instability or hyperkalemia, treatment should begin immediately with digoxin-specific Fab fragments rather than waiting for confirmatory testing.
- Published on
Emergency and Acute Medicine – Diplopia
Basics
Description
Diplopia is double vision with simultaneous perception of two images. The images may be oriented horizontally, vertically, or diagonally. Diplopia most often results from abnormal movement of the extraocular muscles, which are innervated by three cranial nerves. Cranial nerve III innervates the superior, inferior, and medial rectus muscles and the inferior oblique. Cranial nerve IV innervates the superior oblique muscle, and cranial nerve VI innervates the lateral rectus muscle. Brainstem lesions may damage cranial nerve nuclei or their connections, particularly the medial longitudinal fasciculus, resulting in internuclear ophthalmoplegia. Cranial nerve dysfunction may occur due to compression along the subarachnoid space or venous sinuses, inflammation, or altered cerebrospinal fluid pressure, with elevated or reduced pressure commonly causing cranial nerve VI palsy. Disorders affecting the orbits or bony skull may mechanically restrict movement of one or both eyes or extraocular muscles.
Etiology
Traumatic diplopia may result from orbital fractures, contusions, or hematomas, and rarely from brainstem contusion or hematoma. Monocular diplopia is almost always due to intrinsic ocular pathology such as corneal surface disease including keratoconus, lens subluxation, structural defects within the eye, or functional disorders such as conversion disorder, factitious disorder, or somatization.
Nontraumatic binocular diplopia may arise from brain or brainstem dysfunction, including stroke and multiple sclerosis. Cortical causes such as migraine are rare. Cranial nerve dysfunction may be due to posterior communicating artery aneurysm causing cranial nerve III palsy, chronic lymphocytic meningitis with multiple cranial nerve involvement, pseudotumor cerebri causing cranial nerve VI palsy, or spontaneous intracranial hypotension also affecting cranial nerve VI. Disorders of the bony skull and orbits include tumors, thyroid eye disease, and inflammatory conditions such as Tolosa–Hunt syndrome. Neuromuscular junction disorders affecting extraocular muscles include myasthenia gravis.
Diagnosis
Signs and symptoms
History should establish whether diplopia followed head injury, whether it is constant or intermittent, and its duration. It is essential to determine whether diplopia is monocular or binocular and to ask about headache or other neurologic or visual symptoms. Clarify whether the images are separated horizontally, vertically, or diagonally.
On physical examination, monocular diplopia persists when one eye is covered and indicates pathology within the affected eye. Binocular diplopia resolves when either eye is covered and suggests misalignment. Traumatic and nontraumatic causes should be distinguished.
Monocular diplopia requires a careful ocular examination including visual acuity assessment. Binocular diplopia requires full eye examination for ptosis, anisocoria, extraocular movement limitation, proptosis, or exophthalmos, and assessment of visual acuity. Cranial nerve III palsy with pupil involvement typically causes diagonal diplopia with ptosis and a dilated pupil, whereas pupil-sparing cranial nerve III palsy causes diagonal diplopia with normal pupils and eyelids. Cranial nerve IV palsy produces vertical or diagonal diplopia and is the least common. Cranial nerve VI palsy produces horizontal diplopia that worsens with lateral gaze toward the affected side.
A complete neurologic examination is required. In traumatic diplopia, look for facial anesthesia, anisocoria, proptosis, or decreased visual acuity. Patients may appear well, so a systematic examination is critical to localize the lesion. Pupil-involving cranial nerve III palsy should prompt concern for aneurysm, whereas pupil-sparing palsy is usually microvascular. Facial numbness with diplopia suggests cavernous sinus or superior orbital fissure pathology. Decreased vision raises concern for orbital or superior orbital fissure syndrome.
Essential workup
A careful history and physical examination are the cornerstones of diagnosis, with particular attention to trauma history. In spontaneous cases, determine whether diplopia is isolated, which cranial nerve is involved, and whether additional neurologic deficits are present to aid localization. Cerebral angiography using CTA, MRA, or DSA is indicated for cranial nerve III palsy with a dilated pupil.
Diagnosis tests and interpretation
Laboratory testing is generally not useful in the emergency department, though thyroid function tests may occasionally be helpful. Serologic testing for myasthenia gravis is not required in the acute setting.
Diagnostic procedures may include an edrophonium or ice test if myasthenia gravis is suspected. Lumbar puncture is indicated when considering subarachnoid hemorrhage, chronic lymphocytic meningitis, or abnormal cerebrospinal fluid pressure states. Brain and cerebrovascular imaging should be obtained when evaluating for mass lesions, aneurysm, stroke, or multiple sclerosis, with specific tests guided by the suspected diagnosis.
Differential diagnosis
Post-traumatic diplopia includes orbital fracture or hematoma with direct cranial nerve injury or mechanical restriction, and rarely brainstem contusion affecting cranial nerve nuclei or the medial longitudinal fasciculus.
Monocular diplopia may be caused by nearly any ocular disorder involving the cornea, lens, iris, retina, or refractive system, and rarely bilateral monocular diplopia from cortical dysfunction.
Binocular diplopia may result from brainstem stroke or multiple sclerosis, Wernicke encephalopathy, rare cortical causes such as migraine, botulism, cranial nerve palsies due to stretch, ischemia, inflammation, or pressure abnormalities, cavernous sinus pathology, internuclear ophthalmoplegia, orbital infiltrative disorders, myasthenia gravis, or botulism.
Treatment
Initial stabilization and therapy
Most patients with diplopia do not require immediate stabilization. Management is guided by the underlying etiology.
Emergency department treatment and procedures
Lumbar puncture should be performed when lymphocytic meningitis, pseudotumor cerebri, or spontaneous intracranial hypotension is suspected, with mandatory measurement of opening pressure. An edrophonium test may be considered for suspected myasthenia gravis. Eye patching may be offered for symptomatic relief in patients discharged from the emergency department.
Special considerations
Pediatric patients share the same differential diagnosis. In pregnancy, hyperemesis gravidarum may lead to Wernicke encephalopathy or orbital hemorrhage presenting with diplopia. Postpartum diplopia may occur due to cavernous sinus thrombosis, post–dural puncture headache, or orbital hemorrhage.
Follow-up and disposition
Admission criteria
Admission depends on the underlying cause. Many patients require admission to expedite evaluation for serious etiologies, including advanced neuroimaging and specialty consultation.
Discharge criteria
Patients with monocular diplopia or traumatic diplopia with a clearly established, nonurgent cause may be safely discharged.
Follow-up recommendations
All discharged patients with diplopia require follow-up, typically with neurology or ophthalmology.
Pearls and pitfalls
Diplopia may be described as blurred vision if image separation is minimal. Never assume diplopia is an isolated cranial neuropathy without a thorough neurologic examination. Always assess pupils to avoid missing an aneurysmal cranial nerve III palsy, which may occur with normal CT and lumbar puncture. Myasthenia gravis often presents with intermittent diplopia and normal pupils. Facial sensory loss with diplopia localizes pathology to the cavernous sinus or superior orbital fissure. Decreased visual acuity with diplopia suggests orbital or superior orbital fissure disease and may represent a surgical emergency.
Basics
Description
Diplopia is double vision with simultaneous perception of two images. The images may be oriented horizontally, vertically, or diagonally. Diplopia most often results from abnormal movement of the extraocular muscles, which are innervated by three cranial nerves. Cranial nerve III innervates the superior, inferior, and medial rectus muscles and the inferior oblique. Cranial nerve IV innervates the superior oblique muscle, and cranial nerve VI innervates the lateral rectus muscle. Brainstem lesions may damage cranial nerve nuclei or their connections, particularly the medial longitudinal fasciculus, resulting in internuclear ophthalmoplegia. Cranial nerve dysfunction may occur due to compression along the subarachnoid space or venous sinuses, inflammation, or altered cerebrospinal fluid pressure, with elevated or reduced pressure commonly causing cranial nerve VI palsy. Disorders affecting the orbits or bony skull may mechanically restrict movement of one or both eyes or extraocular muscles.
Etiology
Traumatic diplopia may result from orbital fractures, contusions, or hematomas, and rarely from brainstem contusion or hematoma. Monocular diplopia is almost always due to intrinsic ocular pathology such as corneal surface disease including keratoconus, lens subluxation, structural defects within the eye, or functional disorders such as conversion disorder, factitious disorder, or somatization.
Nontraumatic binocular diplopia may arise from brain or brainstem dysfunction, including stroke and multiple sclerosis. Cortical causes such as migraine are rare. Cranial nerve dysfunction may be due to posterior communicating artery aneurysm causing cranial nerve III palsy, chronic lymphocytic meningitis with multiple cranial nerve involvement, pseudotumor cerebri causing cranial nerve VI palsy, or spontaneous intracranial hypotension also affecting cranial nerve VI. Disorders of the bony skull and orbits include tumors, thyroid eye disease, and inflammatory conditions such as Tolosa–Hunt syndrome. Neuromuscular junction disorders affecting extraocular muscles include myasthenia gravis.
Diagnosis
Signs and symptoms
History should establish whether diplopia followed head injury, whether it is constant or intermittent, and its duration. It is essential to determine whether diplopia is monocular or binocular and to ask about headache or other neurologic or visual symptoms. Clarify whether the images are separated horizontally, vertically, or diagonally.
On physical examination, monocular diplopia persists when one eye is covered and indicates pathology within the affected eye. Binocular diplopia resolves when either eye is covered and suggests misalignment. Traumatic and nontraumatic causes should be distinguished.
Monocular diplopia requires a careful ocular examination including visual acuity assessment. Binocular diplopia requires full eye examination for ptosis, anisocoria, extraocular movement limitation, proptosis, or exophthalmos, and assessment of visual acuity. Cranial nerve III palsy with pupil involvement typically causes diagonal diplopia with ptosis and a dilated pupil, whereas pupil-sparing cranial nerve III palsy causes diagonal diplopia with normal pupils and eyelids. Cranial nerve IV palsy produces vertical or diagonal diplopia and is the least common. Cranial nerve VI palsy produces horizontal diplopia that worsens with lateral gaze toward the affected side.
A complete neurologic examination is required. In traumatic diplopia, look for facial anesthesia, anisocoria, proptosis, or decreased visual acuity. Patients may appear well, so a systematic examination is critical to localize the lesion. Pupil-involving cranial nerve III palsy should prompt concern for aneurysm, whereas pupil-sparing palsy is usually microvascular. Facial numbness with diplopia suggests cavernous sinus or superior orbital fissure pathology. Decreased vision raises concern for orbital or superior orbital fissure syndrome.
Essential workup
A careful history and physical examination are the cornerstones of diagnosis, with particular attention to trauma history. In spontaneous cases, determine whether diplopia is isolated, which cranial nerve is involved, and whether additional neurologic deficits are present to aid localization. Cerebral angiography using CTA, MRA, or DSA is indicated for cranial nerve III palsy with a dilated pupil.
Diagnosis tests and interpretation
Laboratory testing is generally not useful in the emergency department, though thyroid function tests may occasionally be helpful. Serologic testing for myasthenia gravis is not required in the acute setting.
Diagnostic procedures may include an edrophonium or ice test if myasthenia gravis is suspected. Lumbar puncture is indicated when considering subarachnoid hemorrhage, chronic lymphocytic meningitis, or abnormal cerebrospinal fluid pressure states. Brain and cerebrovascular imaging should be obtained when evaluating for mass lesions, aneurysm, stroke, or multiple sclerosis, with specific tests guided by the suspected diagnosis.
Differential diagnosis
Post-traumatic diplopia includes orbital fracture or hematoma with direct cranial nerve injury or mechanical restriction, and rarely brainstem contusion affecting cranial nerve nuclei or the medial longitudinal fasciculus.
Monocular diplopia may be caused by nearly any ocular disorder involving the cornea, lens, iris, retina, or refractive system, and rarely bilateral monocular diplopia from cortical dysfunction.
Binocular diplopia may result from brainstem stroke or multiple sclerosis, Wernicke encephalopathy, rare cortical causes such as migraine, botulism, cranial nerve palsies due to stretch, ischemia, inflammation, or pressure abnormalities, cavernous sinus pathology, internuclear ophthalmoplegia, orbital infiltrative disorders, myasthenia gravis, or botulism.
Treatment
Initial stabilization and therapy
Most patients with diplopia do not require immediate stabilization. Management is guided by the underlying etiology.
Emergency department treatment and procedures
Lumbar puncture should be performed when lymphocytic meningitis, pseudotumor cerebri, or spontaneous intracranial hypotension is suspected, with mandatory measurement of opening pressure. An edrophonium test may be considered for suspected myasthenia gravis. Eye patching may be offered for symptomatic relief in patients discharged from the emergency department.
Special considerations
Pediatric patients share the same differential diagnosis. In pregnancy, hyperemesis gravidarum may lead to Wernicke encephalopathy or orbital hemorrhage presenting with diplopia. Postpartum diplopia may occur due to cavernous sinus thrombosis, post–dural puncture headache, or orbital hemorrhage.
Follow-up and disposition
Admission criteria
Admission depends on the underlying cause. Many patients require admission to expedite evaluation for serious etiologies, including advanced neuroimaging and specialty consultation.
Discharge criteria
Patients with monocular diplopia or traumatic diplopia with a clearly established, nonurgent cause may be safely discharged.
Follow-up recommendations
All discharged patients with diplopia require follow-up, typically with neurology or ophthalmology.
Pearls and pitfalls
Diplopia may be described as blurred vision if image separation is minimal. Never assume diplopia is an isolated cranial neuropathy without a thorough neurologic examination. Always assess pupils to avoid missing an aneurysmal cranial nerve III palsy, which may occur with normal CT and lumbar puncture. Myasthenia gravis often presents with intermittent diplopia and normal pupils. Facial sensory loss with diplopia localizes pathology to the cavernous sinus or superior orbital fissure. Decreased visual acuity with diplopia suggests orbital or superior orbital fissure disease and may represent a surgical emergency.
- Published on
Emergency and Acute Medicine – Disseminated Intravascular Coagulation
Basics
Description
Normal coagulation consists of a localized series of reactions involving blood vessels, platelets, and clotting factors. Disseminated intravascular coagulation is a systemic activation of coagulation and fibrinolysis triggered by an underlying disease process. Widespread activation leads to circulation of thrombin and plasmin.
Thrombin activation occurs through tissue factor and factor VIIIa via the extrinsic pathway, resulting in fibrinogen conversion to fibrin monomers that polymerize into fibrin clots within the circulation. These clots cause microvascular and macrovascular thrombosis, leading to peripheral ischemia and end-organ damage. Platelets are consumed within clots, producing thrombocytopenia.
Plasmin activity results in degradation of fibrinogen into fibrin degradation products, which interfere with fibrin polymerization and impair platelet function, worsening bleeding.
Failure of physiologic anticoagulation is necessary for DIC to occur, with impairment of antithrombin III, the protein C system, and tissue factor pathway inhibitor.
Acute DIC represents an uncompensated state where clotting factors are consumed faster than they are replaced, making hemorrhage the dominant feature. Chronic DIC is a compensated state in which factor production keeps pace with consumption, and thrombosis predominates.
Etiology
DIC may be precipitated by numerous conditions. Obstetric causes include retained fetus, amniotic fluid embolism, placental abruption, abortion, eclampsia, and HELLP syndrome. Sepsis is a major trigger and may be caused by gram-negative bacteria through endotoxin, gram-positive organisms through mucopolysaccharides, or other microorganisms including viruses and parasites. Trauma-related causes include crush injury, severe burns, severe head injury, and fat embolism. Malignancy-associated DIC may occur with solid tumors, metastatic disease, or hematologic malignancies such as leukemia. Intravascular hemolysis from transfusion reactions or massive transfusion, organ destruction from severe pancreatitis or hepatic failure, vascular abnormalities such as Kasabach–Merritt syndrome or large aneurysms, and hematologic disorders such as thrombotic thrombocytopenic purpura or immune thrombocytopenic purpura may also precipitate DIC. Miscellaneous causes include snake envenomation and recreational drug use.
Diagnosis
Signs and symptoms
Bleeding manifestations include petechiae, purpura, hemorrhagic bullae, wound bleeding, oozing from venipuncture or arterial lines, epistaxis, hemoptysis, and gastrointestinal bleeding. Thrombotic manifestations include large-vessel thrombosis, microvascular thrombosis with end-organ dysfunction involving the heart, lungs, kidneys, liver, and central nervous system, thrombophlebitis, pulmonary embolism, nonbacterial thrombotic endocarditis, gangrene, and ischemic infarcts of the kidney, liver, bowel, or brain.
Acute DIC is characterized predominantly by hemorrhagic complications, whereas chronic DIC is dominated by thrombotic events.
History should assess prior bleeding disorders, pregnancy status, recent obstetric events, malignancy, and immunocompromised states.
Physical examination may reveal altered mental status, hypotension, tachycardia, tachypnea, pulmonary crackles, gastrointestinal bleeding, abdominal distension, oliguria, hematuria, petechiae, purpura, jaundice, or skin necrosis.
Essential workup
Evaluation depends on the precipitating illness. The diagnosis is often not definitively established in the emergency department and evolves with serial assessment.
Diagnosis tests and interpretation
Laboratory findings typically include a falling platelet count, often below 100,000/mm³, though it may be normal in chronic DIC. Prothrombin time and partial thromboplastin time are usually prolonged but may be normal in chronic disease. Fibrinogen levels are decreased in most acute cases but may remain normal, limiting sensitivity. Fibrin degradation products and D-dimer levels are elevated. Peripheral smear may show schistocytes and thrombocytopenia, particularly in chronic DIC. Renal dysfunction may be reflected by elevated BUN and creatinine, and arterial blood gases assess oxygenation and acid–base status.
The ISTH scoring system incorporates the presence of an underlying disorder, platelet count, fibrin markers, PT prolongation, and fibrinogen level. A score greater than five indicates overt DIC and is associated with increased mortality.
Imaging may include chest radiography for suspected pneumonia, head CT for altered mental status, and obstetric ultrasound in pregnant patients.
Differential diagnosis
Consider inherited factor deficiencies, anticoagulant or drug-induced coagulopathy, hepatic disease, vitamin K deficiency, massive blood loss, platelet dysfunction, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, heparin-induced thrombocytopenia, and immune thrombocytopenic purpura.
Treatment
Initial stabilization and therapy
Management focuses on airway protection, hemodynamic resuscitation, control of bleeding, intravenous access, and restoration of circulating volume. Prompt treatment of the underlying cause is essential, including antibiotics for sepsis, evacuation of retained products of conception, chemotherapy for malignancy, or surgical debridement for trauma.
Emergency department treatment and procedures
Specific therapy for DIC is controversial and should be individualized based on age, hemodynamic status, severity of bleeding, and degree of thrombosis. Early consultation with the admitting service is recommended.
Replacement of depleted blood components may include fresh frozen plasma for prolonged coagulation times, platelet transfusion for severe thrombocytopenia or active bleeding, and cryoprecipitate for severe hypofibrinogenemia. Recombinant factor VIIa has been reported in selected cases, though benefit and safety remain uncertain.
Heparin use is controversial and may be considered when thrombosis predominates, such as in purpura fulminans, acute promyelocytic leukemia, or chronic DIC with large-vessel thrombosis. Activated protein C and antithrombin supplementation have not demonstrated mortality benefit. Antifibrinolytic agents such as aminocaproic acid or tranexamic acid should be reserved for extreme cases with documented excessive fibrinolysis and refractory bleeding.
Medication
Definitive DIC-directed pharmacologic therapy is rarely initiated in the emergency department. Management emphasizes treatment of the underlying cause. Low-dose heparin infusion may be considered when thrombosis predominates.
Follow-up and disposition
Admission criteria
Patients with severe precipitating illness and DIC require intensive care unit admission.
Discharge criteria
There are no discharge criteria for patients with active DIC.
Follow-up recommendations
Ongoing management includes close monitoring of platelet counts, coagulation parameters, and organ function.
Pearls and pitfalls
DIC should be suspected as a complication of severe, life-threatening illness. Early recognition is critical, as the consequences can be catastrophic. Always address and treat the underlying cause, even when bleeding or thrombotic manifestations dominate the clinical presentation.
Basics
Description
Normal coagulation consists of a localized series of reactions involving blood vessels, platelets, and clotting factors. Disseminated intravascular coagulation is a systemic activation of coagulation and fibrinolysis triggered by an underlying disease process. Widespread activation leads to circulation of thrombin and plasmin.
Thrombin activation occurs through tissue factor and factor VIIIa via the extrinsic pathway, resulting in fibrinogen conversion to fibrin monomers that polymerize into fibrin clots within the circulation. These clots cause microvascular and macrovascular thrombosis, leading to peripheral ischemia and end-organ damage. Platelets are consumed within clots, producing thrombocytopenia.
Plasmin activity results in degradation of fibrinogen into fibrin degradation products, which interfere with fibrin polymerization and impair platelet function, worsening bleeding.
Failure of physiologic anticoagulation is necessary for DIC to occur, with impairment of antithrombin III, the protein C system, and tissue factor pathway inhibitor.
Acute DIC represents an uncompensated state where clotting factors are consumed faster than they are replaced, making hemorrhage the dominant feature. Chronic DIC is a compensated state in which factor production keeps pace with consumption, and thrombosis predominates.
Etiology
DIC may be precipitated by numerous conditions. Obstetric causes include retained fetus, amniotic fluid embolism, placental abruption, abortion, eclampsia, and HELLP syndrome. Sepsis is a major trigger and may be caused by gram-negative bacteria through endotoxin, gram-positive organisms through mucopolysaccharides, or other microorganisms including viruses and parasites. Trauma-related causes include crush injury, severe burns, severe head injury, and fat embolism. Malignancy-associated DIC may occur with solid tumors, metastatic disease, or hematologic malignancies such as leukemia. Intravascular hemolysis from transfusion reactions or massive transfusion, organ destruction from severe pancreatitis or hepatic failure, vascular abnormalities such as Kasabach–Merritt syndrome or large aneurysms, and hematologic disorders such as thrombotic thrombocytopenic purpura or immune thrombocytopenic purpura may also precipitate DIC. Miscellaneous causes include snake envenomation and recreational drug use.
Diagnosis
Signs and symptoms
Bleeding manifestations include petechiae, purpura, hemorrhagic bullae, wound bleeding, oozing from venipuncture or arterial lines, epistaxis, hemoptysis, and gastrointestinal bleeding. Thrombotic manifestations include large-vessel thrombosis, microvascular thrombosis with end-organ dysfunction involving the heart, lungs, kidneys, liver, and central nervous system, thrombophlebitis, pulmonary embolism, nonbacterial thrombotic endocarditis, gangrene, and ischemic infarcts of the kidney, liver, bowel, or brain.
Acute DIC is characterized predominantly by hemorrhagic complications, whereas chronic DIC is dominated by thrombotic events.
History should assess prior bleeding disorders, pregnancy status, recent obstetric events, malignancy, and immunocompromised states.
Physical examination may reveal altered mental status, hypotension, tachycardia, tachypnea, pulmonary crackles, gastrointestinal bleeding, abdominal distension, oliguria, hematuria, petechiae, purpura, jaundice, or skin necrosis.
Essential workup
Evaluation depends on the precipitating illness. The diagnosis is often not definitively established in the emergency department and evolves with serial assessment.
Diagnosis tests and interpretation
Laboratory findings typically include a falling platelet count, often below 100,000/mm³, though it may be normal in chronic DIC. Prothrombin time and partial thromboplastin time are usually prolonged but may be normal in chronic disease. Fibrinogen levels are decreased in most acute cases but may remain normal, limiting sensitivity. Fibrin degradation products and D-dimer levels are elevated. Peripheral smear may show schistocytes and thrombocytopenia, particularly in chronic DIC. Renal dysfunction may be reflected by elevated BUN and creatinine, and arterial blood gases assess oxygenation and acid–base status.
The ISTH scoring system incorporates the presence of an underlying disorder, platelet count, fibrin markers, PT prolongation, and fibrinogen level. A score greater than five indicates overt DIC and is associated with increased mortality.
Imaging may include chest radiography for suspected pneumonia, head CT for altered mental status, and obstetric ultrasound in pregnant patients.
Differential diagnosis
Consider inherited factor deficiencies, anticoagulant or drug-induced coagulopathy, hepatic disease, vitamin K deficiency, massive blood loss, platelet dysfunction, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, heparin-induced thrombocytopenia, and immune thrombocytopenic purpura.
Treatment
Initial stabilization and therapy
Management focuses on airway protection, hemodynamic resuscitation, control of bleeding, intravenous access, and restoration of circulating volume. Prompt treatment of the underlying cause is essential, including antibiotics for sepsis, evacuation of retained products of conception, chemotherapy for malignancy, or surgical debridement for trauma.
Emergency department treatment and procedures
Specific therapy for DIC is controversial and should be individualized based on age, hemodynamic status, severity of bleeding, and degree of thrombosis. Early consultation with the admitting service is recommended.
Replacement of depleted blood components may include fresh frozen plasma for prolonged coagulation times, platelet transfusion for severe thrombocytopenia or active bleeding, and cryoprecipitate for severe hypofibrinogenemia. Recombinant factor VIIa has been reported in selected cases, though benefit and safety remain uncertain.
Heparin use is controversial and may be considered when thrombosis predominates, such as in purpura fulminans, acute promyelocytic leukemia, or chronic DIC with large-vessel thrombosis. Activated protein C and antithrombin supplementation have not demonstrated mortality benefit. Antifibrinolytic agents such as aminocaproic acid or tranexamic acid should be reserved for extreme cases with documented excessive fibrinolysis and refractory bleeding.
Medication
Definitive DIC-directed pharmacologic therapy is rarely initiated in the emergency department. Management emphasizes treatment of the underlying cause. Low-dose heparin infusion may be considered when thrombosis predominates.
Follow-up and disposition
Admission criteria
Patients with severe precipitating illness and DIC require intensive care unit admission.
Discharge criteria
There are no discharge criteria for patients with active DIC.
Follow-up recommendations
Ongoing management includes close monitoring of platelet counts, coagulation parameters, and organ function.
Pearls and pitfalls
DIC should be suspected as a complication of severe, life-threatening illness. Early recognition is critical, as the consequences can be catastrophic. Always address and treat the underlying cause, even when bleeding or thrombotic manifestations dominate the clinical presentation.
- Published on
Emergency And Acute Medicine - Ectopic Pregnancy
Core Overview
Ectopic pregnancy occurs when a fertilized ovum implants outside the uterine cavity, most commonly within the fallopian tube, accounting for approximately 93–97% of cases. Less common sites include abdominal and peritoneal locations, which are associated with higher morbidity due to diagnostic difficulty and increased bleeding risk. Ectopic pregnancy occurs in about 2–2.6% of all pregnancies and is responsible for roughly 6% of maternal deaths, making it the leading cause of pregnancy-related mortality in the first trimester. Despite this, approximately 60% of women with a prior ectopic pregnancy are able to achieve a subsequent normal intrauterine pregnancy.
Predisposing Factors And Causes
Risk factors include maternal age over 35 years, African American race, prior fallopian tube damage from pelvic inflammatory disease, previous tubal surgery or ectopic pregnancy, intrauterine device use (with 25–50% of pregnancies occurring with an IUD being ectopic), diethylstilbestrol exposure, in vitro fertilization, and current tobacco use. Importantly, more than half of affected women have no identifiable risk factors.
Clinical Manifestations
The classic triad of amenorrhea, vaginal bleeding, and abdominal pain is present in only a minority of patients. Amenorrhea occurs in most cases, abdominal pain—often unilateral—is very common, and abnormal vaginal bleeding is frequent. Some patients report symptoms of early pregnancy, while others may present with orthostatic hypotension, dizziness, or syncope. Physical findings may include abdominal tenderness, adnexal tenderness or mass, and cervical motion tenderness.
Focused History And Examination
History should address the last menstrual period, gestational and parity history, bleeding characteristics, pain location and severity, prior pelvic surgery or ectopic pregnancy, IUD use, and fertility treatments. Examination should assess for peritoneal signs and include a pelvic examination evaluating uterine size, adnexal masses or tenderness, cervical motion tenderness, and whether the cervical os is open or closed.
Essential Initial Evaluation
All women of reproductive age presenting with abdominal pain or vaginal bleeding must undergo pregnancy testing, regardless of contraception history or prior sterilization. A positive test requires quantitative serum β-hCG measurement. In unstable patients, establish two large-bore IV lines, obtain type and cross-match with hemoglobin and hematocrit, perform bedside ultrasound if available, and urgently consult obstetrics/gynecology. In stable patients, obtain hemoglobin and hematocrit, blood type and Rh status, and transvaginal ultrasound.
Diagnostic Studies And Interpretation
Urine pregnancy tests typically detect β-hCG levels of 25–50 mIU/L, while serum testing detects levels as low as 25 mIU/L. In normal early pregnancy, β-hCG levels double approximately every 48 hours; slower rises suggest ectopic pregnancy. Transvaginal ultrasound can identify a gestational sac at around 5 weeks and cardiac activity by approximately 6.5 weeks. The absence of an intrauterine pregnancy when β-hCG exceeds the discriminatory zone (generally 1,500–3,000 mIU/mL) strongly suggests ectopic pregnancy. Complex adnexal masses with pelvic free fluid are highly predictive when present. Culdocentesis may be considered if ultrasound is unavailable.
Alternative Diagnoses To Consider
Differential diagnoses include spontaneous or threatened abortion, cervicitis, trauma, ruptured ovarian or corpus luteum cyst, ovarian torsion, urinary tract infection, nephrolithiasis, appendicitis, pelvic inflammatory disease, and heterotopic pregnancy, particularly in patients undergoing fertility treatments.
Prehospital And Early Management Considerations
Any woman of childbearing age presenting in shock should be presumed to have a ruptured ectopic pregnancy until proven otherwise. Early recognition and rapid transport are critical.
Stabilization Priorities
Unstable patients require airway management, aggressive resuscitation with oxygen and IV fluids, blood transfusion as needed, immediate gynecology consultation, and urgent operative management. Stable patients with confirmed ectopic pregnancy require gynecologic evaluation to determine suitability for medical versus surgical treatment. Patients with pregnancy of unknown location require close follow-up and serial β-hCG testing.
Emergency Department Interventions
Methotrexate therapy may be considered in reliable, stable patients with unruptured ectopic pregnancies, small ectopic size, and lower β-hCG levels, under obstetric supervision. Contraindications include breastfeeding, immunodeficiency, hematologic disorders, significant anemia, hepatic or renal dysfunction, peptic ulcer disease, active pulmonary disease, and alcoholism. Serial β-hCG monitoring is mandatory, and patients must be counseled regarding expected side effects and warning signs of rupture.
Pharmacologic Therapy
Methotrexate is typically administered as a single dose of 50 mg/m² intramuscularly or intravenously, with repeat dosing guided by β-hCG response. Rh-negative women should receive Rho(D) immune globulin based on gestational age.
Disposition And Monitoring Decisions
Admission is required for hemodynamically unstable patients and those with confirmed ectopic pregnancy who cannot ensure close follow-up. Outpatient management may be appropriate for stable, reliable patients with coordinated obstetric follow-up. Clear return precautions must be provided, including instructions to seek immediate care for worsening abdominal pain, increased bleeding, dizziness, or syncope.
Follow-Up Planning
All patients with positive pregnancy tests and no confirmed intrauterine pregnancy must have close obstetric follow-up with serial β-hCG testing and repeat ultrasound as indicated.
Key Clinical Insights And Common Errors
Always obtain a pregnancy test in women of childbearing age. Combine quantitative β-hCG testing with transvaginal ultrasound in any pregnant patient with abdominal pain or vaginal bleeding. Maintain awareness of heterotopic pregnancy, especially after assisted reproduction. Ensure reliable follow-up and clear return precautions for any patient discharged during evaluation for ectopic pregnancy.
Core Overview
Ectopic pregnancy occurs when a fertilized ovum implants outside the uterine cavity, most commonly within the fallopian tube, accounting for approximately 93–97% of cases. Less common sites include abdominal and peritoneal locations, which are associated with higher morbidity due to diagnostic difficulty and increased bleeding risk. Ectopic pregnancy occurs in about 2–2.6% of all pregnancies and is responsible for roughly 6% of maternal deaths, making it the leading cause of pregnancy-related mortality in the first trimester. Despite this, approximately 60% of women with a prior ectopic pregnancy are able to achieve a subsequent normal intrauterine pregnancy.
Predisposing Factors And Causes
Risk factors include maternal age over 35 years, African American race, prior fallopian tube damage from pelvic inflammatory disease, previous tubal surgery or ectopic pregnancy, intrauterine device use (with 25–50% of pregnancies occurring with an IUD being ectopic), diethylstilbestrol exposure, in vitro fertilization, and current tobacco use. Importantly, more than half of affected women have no identifiable risk factors.
Clinical Manifestations
The classic triad of amenorrhea, vaginal bleeding, and abdominal pain is present in only a minority of patients. Amenorrhea occurs in most cases, abdominal pain—often unilateral—is very common, and abnormal vaginal bleeding is frequent. Some patients report symptoms of early pregnancy, while others may present with orthostatic hypotension, dizziness, or syncope. Physical findings may include abdominal tenderness, adnexal tenderness or mass, and cervical motion tenderness.
Focused History And Examination
History should address the last menstrual period, gestational and parity history, bleeding characteristics, pain location and severity, prior pelvic surgery or ectopic pregnancy, IUD use, and fertility treatments. Examination should assess for peritoneal signs and include a pelvic examination evaluating uterine size, adnexal masses or tenderness, cervical motion tenderness, and whether the cervical os is open or closed.
Essential Initial Evaluation
All women of reproductive age presenting with abdominal pain or vaginal bleeding must undergo pregnancy testing, regardless of contraception history or prior sterilization. A positive test requires quantitative serum β-hCG measurement. In unstable patients, establish two large-bore IV lines, obtain type and cross-match with hemoglobin and hematocrit, perform bedside ultrasound if available, and urgently consult obstetrics/gynecology. In stable patients, obtain hemoglobin and hematocrit, blood type and Rh status, and transvaginal ultrasound.
Diagnostic Studies And Interpretation
Urine pregnancy tests typically detect β-hCG levels of 25–50 mIU/L, while serum testing detects levels as low as 25 mIU/L. In normal early pregnancy, β-hCG levels double approximately every 48 hours; slower rises suggest ectopic pregnancy. Transvaginal ultrasound can identify a gestational sac at around 5 weeks and cardiac activity by approximately 6.5 weeks. The absence of an intrauterine pregnancy when β-hCG exceeds the discriminatory zone (generally 1,500–3,000 mIU/mL) strongly suggests ectopic pregnancy. Complex adnexal masses with pelvic free fluid are highly predictive when present. Culdocentesis may be considered if ultrasound is unavailable.
Alternative Diagnoses To Consider
Differential diagnoses include spontaneous or threatened abortion, cervicitis, trauma, ruptured ovarian or corpus luteum cyst, ovarian torsion, urinary tract infection, nephrolithiasis, appendicitis, pelvic inflammatory disease, and heterotopic pregnancy, particularly in patients undergoing fertility treatments.
Prehospital And Early Management Considerations
Any woman of childbearing age presenting in shock should be presumed to have a ruptured ectopic pregnancy until proven otherwise. Early recognition and rapid transport are critical.
Stabilization Priorities
Unstable patients require airway management, aggressive resuscitation with oxygen and IV fluids, blood transfusion as needed, immediate gynecology consultation, and urgent operative management. Stable patients with confirmed ectopic pregnancy require gynecologic evaluation to determine suitability for medical versus surgical treatment. Patients with pregnancy of unknown location require close follow-up and serial β-hCG testing.
Emergency Department Interventions
Methotrexate therapy may be considered in reliable, stable patients with unruptured ectopic pregnancies, small ectopic size, and lower β-hCG levels, under obstetric supervision. Contraindications include breastfeeding, immunodeficiency, hematologic disorders, significant anemia, hepatic or renal dysfunction, peptic ulcer disease, active pulmonary disease, and alcoholism. Serial β-hCG monitoring is mandatory, and patients must be counseled regarding expected side effects and warning signs of rupture.
Pharmacologic Therapy
Methotrexate is typically administered as a single dose of 50 mg/m² intramuscularly or intravenously, with repeat dosing guided by β-hCG response. Rh-negative women should receive Rho(D) immune globulin based on gestational age.
Disposition And Monitoring Decisions
Admission is required for hemodynamically unstable patients and those with confirmed ectopic pregnancy who cannot ensure close follow-up. Outpatient management may be appropriate for stable, reliable patients with coordinated obstetric follow-up. Clear return precautions must be provided, including instructions to seek immediate care for worsening abdominal pain, increased bleeding, dizziness, or syncope.
Follow-Up Planning
All patients with positive pregnancy tests and no confirmed intrauterine pregnancy must have close obstetric follow-up with serial β-hCG testing and repeat ultrasound as indicated.
Key Clinical Insights And Common Errors
Always obtain a pregnancy test in women of childbearing age. Combine quantitative β-hCG testing with transvaginal ultrasound in any pregnant patient with abdominal pain or vaginal bleeding. Maintain awareness of heterotopic pregnancy, especially after assisted reproduction. Ensure reliable follow-up and clear return precautions for any patient discharged during evaluation for ectopic pregnancy.
- Published on
Emergency and Acute Medicine – Diverticulitis
Basics
Description
Diverticulitis results from micro- or macroscopic perforation of a colonic diverticulum. The condition is classified as uncomplicated in approximately 75% of cases and complicated in the remainder. Its incidence is increasing worldwide, and obesity is a recognized risk factor.
Etiology
Fecal material may become trapped within a diverticulum and harden to form a fecalith, leading to increased intraluminal pressure. Progressive erosion of the diverticular wall causes inflammation, focal necrosis, and eventual perforation.
Microperforation leads to uncomplicated diverticulitis, characterized by colonic wall thickening and surrounding inflammatory changes, such as fat stranding on computed tomography.
Macroperforation results in complicated diverticulitis, which may include abscess formation, bowel obstruction, fistula formation after recurrent attacks, and peritonitis. Colovesical fistula is the most common fistula type and presents with dysuria, urinary frequency, urgency, pneumaturia, and fecaluria.
Diagnosis
Signs and symptoms
Symptoms typically evolve over several days, and nearly half of patients report prior similar episodes. Left lower quadrant abdominal pain occurs in about 70% of cases in Western populations, whereas right lower quadrant pain is more common in Asian patients. Pain is often initially vague before localizing. Associated symptoms include nausea, vomiting, constipation, diarrhea, and urinary complaints.
On examination, patients may have low-grade fever and left lower quadrant tenderness, with an occasional palpable mass representing a phlegmon. Abdominal distension and variable bowel sounds may be present. Rectal tenderness with heme-positive stool can occur, although massive rectal bleeding is rare. Peritoneal signs suggest perforation. Elderly, immunocompromised patients, or those on corticosteroids may have minimal findings.
Essential workup
Initial evaluation includes complete blood count and urinalysis. Blood cultures and lactate levels are obtained if sepsis is suspected. Computed tomography of the abdomen and pelvis is the preferred diagnostic modality, as it confirms diverticulitis, assesses severity, and identifies alternative diagnoses. Intravenous and oral or rectal contrast enhance diagnostic accuracy, while barium contrast should be avoided when perforation is suspected. Plain abdominal and chest radiographs may identify free air or obstruction.
Diagnosis tests and interpretation
Leukocytosis is common but not universal. Urinalysis may reveal sterile pyuria, and the presence of colonic bacteria suggests a colovesical fistula. Imaging findings on CT include colonic wall thickening greater than 5 mm, pericolic fat inflammation, and abscess formation. CT-guided percutaneous drainage of localized abscesses may avoid surgery. Endoscopy is not required during the acute phase, though rigid sigmoidoscopy may help exclude alternative diagnoses. Ultrasonography can identify wall thickening or abscesses but is operator dependent. Barium enema is reserved for post-resolution evaluation to exclude malignancy or fistula.
Differential diagnosis
Consider colon carcinoma with perforation, ischemic or infectious colitis, appendicitis, inflammatory bowel disease, irritable bowel syndrome, gynecologic pathology, pancreatic disease, pelvic inflammatory disease, peptic ulcer disease, and renal colic.
Treatment
Prehospital care
Initial management includes intravenous fluid administration.
Initial stabilization and therapy
Resuscitate with isotonic fluids, institute bowel rest with nothing by mouth or clear liquids, and place a nasogastric tube if persistent vomiting or bowel obstruction is suspected.
Emergency department treatment and procedures
Uncomplicated diverticulitis is usually managed medically, though up to 30% of patients may eventually require surgery. Complicated diverticulitis often requires percutaneous drainage or surgical intervention. Analgesia may include anticholinergics such as dicyclomine for colonic spasm or opioids for severe pain, avoiding opioids in unstable patients.
Antibiotics should cover gram-negative aerobic and anaerobic organisms. Mild uncomplicated cases may be treated as outpatients with oral regimens such as amoxicillin-clavulanate or trimethoprim-sulfamethoxazole plus metronidazole. Inpatient regimens include third-generation cephalosporins with metronidazole, beta-lactam/beta-lactamase inhibitor combinations, or carbapenems for severe disease.
Emergent surgery is indicated for generalized peritonitis due to perforation. Elective surgery may be considered after recurrent attacks, fistula formation, obstruction, or failure of medical therapy. Percutaneous drainage is appropriate for well-circumscribed abscesses.
Medication
Common agents include amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, ciprofloxacin, metronidazole, third-generation cephalosporins, beta-lactam/beta-lactamase inhibitors, and carbapenems, selected according to disease severity and patient factors.
Follow-up and disposition
Admission criteria
Hospitalization is indicated for intractable pain or vomiting, high fever, peritonitis, failure of outpatient therapy, severe disease on imaging, significant leukocytosis, immunocompromised status, recurrent episodes, major comorbidities, extremes of age, or diagnostic uncertainty.
Discharge criteria
Patients with mild disease, minimal comorbidities, and ability to tolerate oral intake may be discharged with close follow-up.
Follow-up recommendations
Patients should begin with clear liquids and advance diet as symptoms improve, usually within three days. They should seek care for worsening pain, fever, or inability to tolerate oral intake. Colonoscopy or contrast studies are recommended after recovery to exclude malignancy. Avoidance of seeds and nuts is not required.
Pearls and pitfalls
Computed tomography distinguishes uncomplicated from complicated diverticulitis and guides management. Most uncomplicated cases do not progress to complicated disease, and multiple attacks do not necessarily predict worsening severity. Severe findings on initial imaging are associated with higher risk of treatment failure and complications.
Basics
Description
Diverticulitis results from micro- or macroscopic perforation of a colonic diverticulum. The condition is classified as uncomplicated in approximately 75% of cases and complicated in the remainder. Its incidence is increasing worldwide, and obesity is a recognized risk factor.
Etiology
Fecal material may become trapped within a diverticulum and harden to form a fecalith, leading to increased intraluminal pressure. Progressive erosion of the diverticular wall causes inflammation, focal necrosis, and eventual perforation.
Microperforation leads to uncomplicated diverticulitis, characterized by colonic wall thickening and surrounding inflammatory changes, such as fat stranding on computed tomography.
Macroperforation results in complicated diverticulitis, which may include abscess formation, bowel obstruction, fistula formation after recurrent attacks, and peritonitis. Colovesical fistula is the most common fistula type and presents with dysuria, urinary frequency, urgency, pneumaturia, and fecaluria.
Diagnosis
Signs and symptoms
Symptoms typically evolve over several days, and nearly half of patients report prior similar episodes. Left lower quadrant abdominal pain occurs in about 70% of cases in Western populations, whereas right lower quadrant pain is more common in Asian patients. Pain is often initially vague before localizing. Associated symptoms include nausea, vomiting, constipation, diarrhea, and urinary complaints.
On examination, patients may have low-grade fever and left lower quadrant tenderness, with an occasional palpable mass representing a phlegmon. Abdominal distension and variable bowel sounds may be present. Rectal tenderness with heme-positive stool can occur, although massive rectal bleeding is rare. Peritoneal signs suggest perforation. Elderly, immunocompromised patients, or those on corticosteroids may have minimal findings.
Essential workup
Initial evaluation includes complete blood count and urinalysis. Blood cultures and lactate levels are obtained if sepsis is suspected. Computed tomography of the abdomen and pelvis is the preferred diagnostic modality, as it confirms diverticulitis, assesses severity, and identifies alternative diagnoses. Intravenous and oral or rectal contrast enhance diagnostic accuracy, while barium contrast should be avoided when perforation is suspected. Plain abdominal and chest radiographs may identify free air or obstruction.
Diagnosis tests and interpretation
Leukocytosis is common but not universal. Urinalysis may reveal sterile pyuria, and the presence of colonic bacteria suggests a colovesical fistula. Imaging findings on CT include colonic wall thickening greater than 5 mm, pericolic fat inflammation, and abscess formation. CT-guided percutaneous drainage of localized abscesses may avoid surgery. Endoscopy is not required during the acute phase, though rigid sigmoidoscopy may help exclude alternative diagnoses. Ultrasonography can identify wall thickening or abscesses but is operator dependent. Barium enema is reserved for post-resolution evaluation to exclude malignancy or fistula.
Differential diagnosis
Consider colon carcinoma with perforation, ischemic or infectious colitis, appendicitis, inflammatory bowel disease, irritable bowel syndrome, gynecologic pathology, pancreatic disease, pelvic inflammatory disease, peptic ulcer disease, and renal colic.
Treatment
Prehospital care
Initial management includes intravenous fluid administration.
Initial stabilization and therapy
Resuscitate with isotonic fluids, institute bowel rest with nothing by mouth or clear liquids, and place a nasogastric tube if persistent vomiting or bowel obstruction is suspected.
Emergency department treatment and procedures
Uncomplicated diverticulitis is usually managed medically, though up to 30% of patients may eventually require surgery. Complicated diverticulitis often requires percutaneous drainage or surgical intervention. Analgesia may include anticholinergics such as dicyclomine for colonic spasm or opioids for severe pain, avoiding opioids in unstable patients.
Antibiotics should cover gram-negative aerobic and anaerobic organisms. Mild uncomplicated cases may be treated as outpatients with oral regimens such as amoxicillin-clavulanate or trimethoprim-sulfamethoxazole plus metronidazole. Inpatient regimens include third-generation cephalosporins with metronidazole, beta-lactam/beta-lactamase inhibitor combinations, or carbapenems for severe disease.
Emergent surgery is indicated for generalized peritonitis due to perforation. Elective surgery may be considered after recurrent attacks, fistula formation, obstruction, or failure of medical therapy. Percutaneous drainage is appropriate for well-circumscribed abscesses.
Medication
Common agents include amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, ciprofloxacin, metronidazole, third-generation cephalosporins, beta-lactam/beta-lactamase inhibitors, and carbapenems, selected according to disease severity and patient factors.
Follow-up and disposition
Admission criteria
Hospitalization is indicated for intractable pain or vomiting, high fever, peritonitis, failure of outpatient therapy, severe disease on imaging, significant leukocytosis, immunocompromised status, recurrent episodes, major comorbidities, extremes of age, or diagnostic uncertainty.
Discharge criteria
Patients with mild disease, minimal comorbidities, and ability to tolerate oral intake may be discharged with close follow-up.
Follow-up recommendations
Patients should begin with clear liquids and advance diet as symptoms improve, usually within three days. They should seek care for worsening pain, fever, or inability to tolerate oral intake. Colonoscopy or contrast studies are recommended after recovery to exclude malignancy. Avoidance of seeds and nuts is not required.
Pearls and pitfalls
Computed tomography distinguishes uncomplicated from complicated diverticulitis and guides management. Most uncomplicated cases do not progress to complicated disease, and multiple attacks do not necessarily predict worsening severity. Severe findings on initial imaging are associated with higher risk of treatment failure and complications.
- Published on
Emergency and Acute Medicine – Diverticulosis
Basics
Description
Diverticulosis refers to the presence of single (diverticulum) or multiple (diverticula) outpouchings of the colonic wall that arise from colonic muscle dysfunction and are usually acquired. The typical sequence involves insufficient dietary fiber leading to reduced stool bulk, increased colonic contractions to propel stool, and a rise in intraluminal pressure. This pressure forces the mucosa and submucosa to herniate through the muscularis propria at points of weakness where the vasa recta penetrate.
Etiology
Diverticulosis can occur anywhere in the gastrointestinal tract but is predominantly a colonic disease. In Western countries, it is left-sided in approximately 95% of cases, whereas in Asian countries it is right-sided in about 70%. The sigmoid colon is the most commonly affected site.
Most colonic diverticula are pseudodiverticula, consisting only of mucosa and submucosa, and represent the most common form. True congenital diverticula, which contain all bowel wall layers, are uncommon.
The condition is common in Western societies due to refined diets and low fiber intake. Prevalence increases with age, affecting approximately 30% of individuals by age 50 and up to 65% by age 85.
Most patients are asymptomatic. About 15–25% develop diverticulitis, and 5–15% develop diverticular bleeding, with obesity as a recognized risk factor. Bleeding resolves spontaneously in roughly 75% of cases. Complications include inflammation, massive arterial bleeding (often from the right colon due to erosion of an arterial branch by a fecalith), perforation, abscess formation, and obstruction.
Diagnosis
Signs and symptoms
Patients may report chronic or intermittent abdominal pain, often triggered by eating and sometimes relieved by flatulence or bowel movements. Changes in bowel habits such as constipation or diarrhea may occur, along with dyspepsia.
Painless hematochezia is a classic presentation of diverticular bleeding and is self-limited in most cases. Bleeding from the left colon typically appears bright red, while right-sided bleeding is darker or maroon and mixed with stool. Diverticulitis and diverticular bleeding are distinct entities and rarely occur together.
On examination, patients are usually afebrile. The abdominal exam is often benign but may reveal left lower quadrant tenderness or a firm sigmoid colon. Rectal examination findings are variable, with stool either heme-negative or positive if bleeding is present.
Essential workup
A careful history and physical examination are essential and help prevent unnecessary diagnostic testing.
Diagnosis tests and interpretation
Asymptomatic diverticulosis requires no diagnostic workup. Recurrent uncomplicated painful disease also typically requires no testing. New-onset uncomplicated pain warrants evaluation to exclude carcinoma, particularly in the presence of weight loss, anorexia, or heme-positive stool.
Laboratory studies may include a complete blood count to assess leukocytosis or anemia and urinalysis to exclude urinary pathology. In hemorrhagic diverticulosis, additional studies include electrolytes, renal function tests, coagulation studies, type and crossmatch, and ECG.
Imaging options for uncomplicated painful diverticulosis include flexible sigmoidoscopy followed by barium enema, or colonoscopy, to identify diverticula and exclude malignancy.
For hemorrhagic diverticulosis, anoscopy may rule out hemorrhoids, while proctosigmoidoscopy helps localize rectal bleeding. Colonoscopy is the preferred diagnostic and therapeutic tool in stable patients, though visualization may be limited in active massive bleeding. Radionuclide imaging is sensitive for intermittent bleeding but lacks therapeutic capability. Angiography localizes active bleeding and allows intervention but carries a risk of intestinal infarction. Barium enema is rarely indicated and does not identify active bleeding.
Differential diagnosis
Painful diverticulosis should be differentiated from irritable bowel syndrome, diverticulitis, colon carcinoma, Crohn disease, renal colic, and gynecologic pathology.
Hemorrhagic diverticulosis should be distinguished from hemorrhoids, anal fissures, proctitis, colitis, carcinoma, polyps, ischemic enteritis, angiodysplasia, amyloidosis, vascular-enteric fistula, and upper gastrointestinal bleeding.
Treatment
Prehospital care
Opiates should be avoided when the cause of abdominal pain is uncertain. Establish intravenous access, and in cases of significant bleeding or hypotension administer isotonic fluid boluses and position the patient appropriately.
Initial stabilization and therapy
In massive hemorrhagic diverticulosis, priority is airway protection, supplemental oxygen, and aggressive intravenous fluid resuscitation. Large-bore intravenous access is required, with early blood transfusion if instability persists. Urinary catheterization aids in monitoring urine output, and surgical consultation is necessary for ongoing or severe bleeding.
Emergency department treatment and procedures
Uncomplicated symptomatic diverticulosis is managed conservatively with a high-fiber diet or bulk-forming agents such as psyllium, warm abdominal compresses, reassurance, and avoidance of cathartic laxatives. There is no evidence supporting routine use of antispasmodics.
Massive diverticular bleeding requires stabilization followed by colonoscopy for diagnosis and possible therapy. Radionuclide scanning or selective angiography may be used if bleeding persists, with embolization considered before surgical intervention. Segmental colectomy is reserved for refractory cases.
Medication
Medications may include bulk-forming agents and, in selected cases, anticholinergics such as dicyclomine or propantheline, although routine use is not strongly supported.
Follow-up and disposition
Admission criteria
Patients with massive hemorrhagic diverticulosis or hemodynamic instability require intensive care admission. Stable patients with ongoing or intermittent bleeding may require admission for localization and definitive management.
Discharge criteria
Patients with uncomplicated symptomatic diverticulosis or minimal bleeding who are stable, nonanemic, and without concerning features may be discharged.
Follow-up recommendations
Colonoscopy is recommended within 48 hours for stable patients. Aspirin and NSAIDs should be discontinued when possible, and dietary fiber intake increased. There is no evidence to support avoidance of nuts, corn, or popcorn.
Pearls and pitfalls
A significant proportion of patients with hematochezia have an upper gastrointestinal source. Most cases resolve spontaneously or with conservative management, though massive bleeding occurs in a minority, particularly in older patients or those with comorbidities. Colonoscopy is the preferred initial diagnostic procedure in stable patients.
Basics
Description
Diverticulosis refers to the presence of single (diverticulum) or multiple (diverticula) outpouchings of the colonic wall that arise from colonic muscle dysfunction and are usually acquired. The typical sequence involves insufficient dietary fiber leading to reduced stool bulk, increased colonic contractions to propel stool, and a rise in intraluminal pressure. This pressure forces the mucosa and submucosa to herniate through the muscularis propria at points of weakness where the vasa recta penetrate.
Etiology
Diverticulosis can occur anywhere in the gastrointestinal tract but is predominantly a colonic disease. In Western countries, it is left-sided in approximately 95% of cases, whereas in Asian countries it is right-sided in about 70%. The sigmoid colon is the most commonly affected site.
Most colonic diverticula are pseudodiverticula, consisting only of mucosa and submucosa, and represent the most common form. True congenital diverticula, which contain all bowel wall layers, are uncommon.
The condition is common in Western societies due to refined diets and low fiber intake. Prevalence increases with age, affecting approximately 30% of individuals by age 50 and up to 65% by age 85.
Most patients are asymptomatic. About 15–25% develop diverticulitis, and 5–15% develop diverticular bleeding, with obesity as a recognized risk factor. Bleeding resolves spontaneously in roughly 75% of cases. Complications include inflammation, massive arterial bleeding (often from the right colon due to erosion of an arterial branch by a fecalith), perforation, abscess formation, and obstruction.
Diagnosis
Signs and symptoms
Patients may report chronic or intermittent abdominal pain, often triggered by eating and sometimes relieved by flatulence or bowel movements. Changes in bowel habits such as constipation or diarrhea may occur, along with dyspepsia.
Painless hematochezia is a classic presentation of diverticular bleeding and is self-limited in most cases. Bleeding from the left colon typically appears bright red, while right-sided bleeding is darker or maroon and mixed with stool. Diverticulitis and diverticular bleeding are distinct entities and rarely occur together.
On examination, patients are usually afebrile. The abdominal exam is often benign but may reveal left lower quadrant tenderness or a firm sigmoid colon. Rectal examination findings are variable, with stool either heme-negative or positive if bleeding is present.
Essential workup
A careful history and physical examination are essential and help prevent unnecessary diagnostic testing.
Diagnosis tests and interpretation
Asymptomatic diverticulosis requires no diagnostic workup. Recurrent uncomplicated painful disease also typically requires no testing. New-onset uncomplicated pain warrants evaluation to exclude carcinoma, particularly in the presence of weight loss, anorexia, or heme-positive stool.
Laboratory studies may include a complete blood count to assess leukocytosis or anemia and urinalysis to exclude urinary pathology. In hemorrhagic diverticulosis, additional studies include electrolytes, renal function tests, coagulation studies, type and crossmatch, and ECG.
Imaging options for uncomplicated painful diverticulosis include flexible sigmoidoscopy followed by barium enema, or colonoscopy, to identify diverticula and exclude malignancy.
For hemorrhagic diverticulosis, anoscopy may rule out hemorrhoids, while proctosigmoidoscopy helps localize rectal bleeding. Colonoscopy is the preferred diagnostic and therapeutic tool in stable patients, though visualization may be limited in active massive bleeding. Radionuclide imaging is sensitive for intermittent bleeding but lacks therapeutic capability. Angiography localizes active bleeding and allows intervention but carries a risk of intestinal infarction. Barium enema is rarely indicated and does not identify active bleeding.
Differential diagnosis
Painful diverticulosis should be differentiated from irritable bowel syndrome, diverticulitis, colon carcinoma, Crohn disease, renal colic, and gynecologic pathology.
Hemorrhagic diverticulosis should be distinguished from hemorrhoids, anal fissures, proctitis, colitis, carcinoma, polyps, ischemic enteritis, angiodysplasia, amyloidosis, vascular-enteric fistula, and upper gastrointestinal bleeding.
Treatment
Prehospital care
Opiates should be avoided when the cause of abdominal pain is uncertain. Establish intravenous access, and in cases of significant bleeding or hypotension administer isotonic fluid boluses and position the patient appropriately.
Initial stabilization and therapy
In massive hemorrhagic diverticulosis, priority is airway protection, supplemental oxygen, and aggressive intravenous fluid resuscitation. Large-bore intravenous access is required, with early blood transfusion if instability persists. Urinary catheterization aids in monitoring urine output, and surgical consultation is necessary for ongoing or severe bleeding.
Emergency department treatment and procedures
Uncomplicated symptomatic diverticulosis is managed conservatively with a high-fiber diet or bulk-forming agents such as psyllium, warm abdominal compresses, reassurance, and avoidance of cathartic laxatives. There is no evidence supporting routine use of antispasmodics.
Massive diverticular bleeding requires stabilization followed by colonoscopy for diagnosis and possible therapy. Radionuclide scanning or selective angiography may be used if bleeding persists, with embolization considered before surgical intervention. Segmental colectomy is reserved for refractory cases.
Medication
Medications may include bulk-forming agents and, in selected cases, anticholinergics such as dicyclomine or propantheline, although routine use is not strongly supported.
Follow-up and disposition
Admission criteria
Patients with massive hemorrhagic diverticulosis or hemodynamic instability require intensive care admission. Stable patients with ongoing or intermittent bleeding may require admission for localization and definitive management.
Discharge criteria
Patients with uncomplicated symptomatic diverticulosis or minimal bleeding who are stable, nonanemic, and without concerning features may be discharged.
Follow-up recommendations
Colonoscopy is recommended within 48 hours for stable patients. Aspirin and NSAIDs should be discontinued when possible, and dietary fiber intake increased. There is no evidence to support avoidance of nuts, corn, or popcorn.
Pearls and pitfalls
A significant proportion of patients with hematochezia have an upper gastrointestinal source. Most cases resolve spontaneously or with conservative management, though massive bleeding occurs in a minority, particularly in older patients or those with comorbidities. Colonoscopy is the preferred initial diagnostic procedure in stable patients.
