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Emergency And Acute Medicine - Eating Disorder
Foundational Overview
Eating disorders are complex psychiatric illnesses with significant medical morbidity and mortality.
Anorexia nervosa is defined by restriction of energy intake resulting in markedly low body weight for age, sex, or developmental trajectory, accompanied by an intense fear of weight gain and a disturbed perception of body image or denial of illness severity. Lifetime prevalence in U.S. females is approximately 0.5%, with bimodal onset peaks at ages 13–14 and 17–18 years.
Bulimia nervosa is characterized by recurrent binge-eating episodes involving consumption of unusually large amounts of food with loss of control, followed by compensatory behaviors such as self-induced vomiting, misuse of laxatives, diuretics, diet pills, fasting, or excessive exercise. These behaviors occur at least weekly for three months, with self-evaluation overly influenced by weight or shape. Lifetime prevalence is about 2% of U.S. females, typically beginning in late adolescence or early adulthood.
Binge eating disorder involves recurrent binge-eating episodes with loss of control, associated with marked distress and at least three characteristic behaviors such as rapid eating, eating until uncomfortably full, eating when not hungry, eating alone due to embarrassment, or feelings of guilt and disgust afterward. Episodes occur at least weekly for three months without compensatory behaviors. Lifetime prevalence is approximately 3.5% in females and 2% in males, with onset in late adolescence or early adulthood.
Underlying Causes And Contributing Factors
Twin studies support a strong genetic contribution. Sociocultural emphasis on thinness, personality traits such as perfectionism and rigidity, family stress, and dieting as a precipitating factor are common. Neurochemical and neuroendocrine abnormalities involving serotonin, leptin, and the hypothalamic–pituitary–adrenal axis have been described.
Clinical Presentation
Patients may report rapid or sustained weight loss, restrictive eating, bingeing, purging behaviors, excessive exercise, dizziness, syncope, bloating, constipation, abdominal pain, fatigue, palpitations, cold intolerance, amenorrhea, or loss of libido. A family history of eating disorders or obesity and comorbid psychiatric illness are common.
Physical Examination Findings
Findings may include weight less than 85% of ideal body weight or BMI below 17.5 in anorexia nervosa, hypothermia, hypotension with orthostasis, bradycardia or arrhythmias, dry skin, lanugo, carotenoderma, breast atrophy, parotid or submandibular swelling, abnormal dentition, abrasions on the dorsum of the hand, poor wound healing, peripheral edema, and proximal muscle weakness.
Core Evaluation Strategy
Assessment includes a detailed history, focused physical examination, nutritional assessment, and psychiatric evaluation with suicide risk assessment. Psychosocial context and family dynamics should be explored, particularly in adolescents.
Diagnostic Studies And Interpretation
Laboratory testing may reveal cytopenias, electrolyte disturbances such as hypokalemia, hyponatremia, hypoglycemia, metabolic alkalosis, renal dysfunction, hypocalcemia, hypomagnesemia, hypophosphatemia, hypoalbuminemia, and hepatic enzyme abnormalities. Urinalysis with specific gravity, toxicology screening, pregnancy testing, amylase and lipase levels, and thyroid-stimulating hormone may be useful. ECG may show QTc prolongation or arrhythmias. Consider echocardiography for suspected cardiomyopathy, bone density testing for osteoporosis, and targeted imaging to exclude alternative diagnoses when indicated.
Conditions To Distinguish From Eating Disorders
Medical causes include gastrointestinal disease, endocrine disorders, malignancy, and chronic infection. Psychiatric differentials include mood disorders, obsessive–compulsive disorder, borderline personality disorder, and substance use disorders.
Immediate Stabilization Principles
Initial management prioritizes airway, breathing, and circulation. Fluids should be administered cautiously to avoid precipitating edema. Correct hypoglycemia, electrolyte abnormalities, and vitamin deficiencies, particularly phosphate and thiamine, to prevent refeeding syndrome. Active warming may be required for hypothermia.
Emergency Department Management
Care focuses on medical stabilization and early psychiatric consultation, including evaluation for suicidality and comorbid psychiatric conditions.
Pharmacologic Considerations
No medication has proven efficacy for anorexia nervosa itself, though small studies suggest potential benefit of atypical antipsychotics such as olanzapine. Fluoxetine is FDA approved for bulimia nervosa and reduces binge–purge behavior; other SSRIs and selected antidepressants may be used. Evidence supports antidepressants and topiramate for binge eating disorder. Pharmacotherapy should be used alongside psychotherapy.
Disposition And Level Of Care Decisions
Admission is indicated for severe medical instability, including extremely low body weight, rapid weight loss, significant electrolyte abnormalities, bradycardia, hypotension, orthostasis, hypothermia, arrhythmias, or organ dysfunction. Psychiatric admission is required for suicidality, severe depression or psychosis, lack of treatment cooperation, or failure of outpatient care. Discharge is appropriate only when the patient is medically and psychologically stable with a multidisciplinary outpatient plan in place.
Follow-Up And Ongoing Care
Effective outpatient management requires a coordinated team including a physician, mental health professional, nutritionist, and often family or group therapy support. Monitoring includes vital signs, weight trends, electrolytes, ECGs, dietary intake, and exercise behaviors. Psychotherapy—particularly cognitive behavioral therapy and family-based treatment—is central. Pharmacologic therapy is adjunctive and targeted to comorbid conditions.
Key Clinical Insights And Common Errors
Eating disorders carry high medical and suicide risk, making safety assessment paramount. Rapid nutritional repletion without electrolyte and vitamin replacement can cause fatal refeeding syndrome. Avoid confrontational approaches that reinforce obsessive thinking. Optimal outcomes depend on early recognition and coordinated multidisciplinary care.
Foundational Overview
Eating disorders are complex psychiatric illnesses with significant medical morbidity and mortality.
Anorexia nervosa is defined by restriction of energy intake resulting in markedly low body weight for age, sex, or developmental trajectory, accompanied by an intense fear of weight gain and a disturbed perception of body image or denial of illness severity. Lifetime prevalence in U.S. females is approximately 0.5%, with bimodal onset peaks at ages 13–14 and 17–18 years.
Bulimia nervosa is characterized by recurrent binge-eating episodes involving consumption of unusually large amounts of food with loss of control, followed by compensatory behaviors such as self-induced vomiting, misuse of laxatives, diuretics, diet pills, fasting, or excessive exercise. These behaviors occur at least weekly for three months, with self-evaluation overly influenced by weight or shape. Lifetime prevalence is about 2% of U.S. females, typically beginning in late adolescence or early adulthood.
Binge eating disorder involves recurrent binge-eating episodes with loss of control, associated with marked distress and at least three characteristic behaviors such as rapid eating, eating until uncomfortably full, eating when not hungry, eating alone due to embarrassment, or feelings of guilt and disgust afterward. Episodes occur at least weekly for three months without compensatory behaviors. Lifetime prevalence is approximately 3.5% in females and 2% in males, with onset in late adolescence or early adulthood.
Underlying Causes And Contributing Factors
Twin studies support a strong genetic contribution. Sociocultural emphasis on thinness, personality traits such as perfectionism and rigidity, family stress, and dieting as a precipitating factor are common. Neurochemical and neuroendocrine abnormalities involving serotonin, leptin, and the hypothalamic–pituitary–adrenal axis have been described.
Clinical Presentation
Patients may report rapid or sustained weight loss, restrictive eating, bingeing, purging behaviors, excessive exercise, dizziness, syncope, bloating, constipation, abdominal pain, fatigue, palpitations, cold intolerance, amenorrhea, or loss of libido. A family history of eating disorders or obesity and comorbid psychiatric illness are common.
Physical Examination Findings
Findings may include weight less than 85% of ideal body weight or BMI below 17.5 in anorexia nervosa, hypothermia, hypotension with orthostasis, bradycardia or arrhythmias, dry skin, lanugo, carotenoderma, breast atrophy, parotid or submandibular swelling, abnormal dentition, abrasions on the dorsum of the hand, poor wound healing, peripheral edema, and proximal muscle weakness.
Core Evaluation Strategy
Assessment includes a detailed history, focused physical examination, nutritional assessment, and psychiatric evaluation with suicide risk assessment. Psychosocial context and family dynamics should be explored, particularly in adolescents.
Diagnostic Studies And Interpretation
Laboratory testing may reveal cytopenias, electrolyte disturbances such as hypokalemia, hyponatremia, hypoglycemia, metabolic alkalosis, renal dysfunction, hypocalcemia, hypomagnesemia, hypophosphatemia, hypoalbuminemia, and hepatic enzyme abnormalities. Urinalysis with specific gravity, toxicology screening, pregnancy testing, amylase and lipase levels, and thyroid-stimulating hormone may be useful. ECG may show QTc prolongation or arrhythmias. Consider echocardiography for suspected cardiomyopathy, bone density testing for osteoporosis, and targeted imaging to exclude alternative diagnoses when indicated.
Conditions To Distinguish From Eating Disorders
Medical causes include gastrointestinal disease, endocrine disorders, malignancy, and chronic infection. Psychiatric differentials include mood disorders, obsessive–compulsive disorder, borderline personality disorder, and substance use disorders.
Immediate Stabilization Principles
Initial management prioritizes airway, breathing, and circulation. Fluids should be administered cautiously to avoid precipitating edema. Correct hypoglycemia, electrolyte abnormalities, and vitamin deficiencies, particularly phosphate and thiamine, to prevent refeeding syndrome. Active warming may be required for hypothermia.
Emergency Department Management
Care focuses on medical stabilization and early psychiatric consultation, including evaluation for suicidality and comorbid psychiatric conditions.
Pharmacologic Considerations
No medication has proven efficacy for anorexia nervosa itself, though small studies suggest potential benefit of atypical antipsychotics such as olanzapine. Fluoxetine is FDA approved for bulimia nervosa and reduces binge–purge behavior; other SSRIs and selected antidepressants may be used. Evidence supports antidepressants and topiramate for binge eating disorder. Pharmacotherapy should be used alongside psychotherapy.
Disposition And Level Of Care Decisions
Admission is indicated for severe medical instability, including extremely low body weight, rapid weight loss, significant electrolyte abnormalities, bradycardia, hypotension, orthostasis, hypothermia, arrhythmias, or organ dysfunction. Psychiatric admission is required for suicidality, severe depression or psychosis, lack of treatment cooperation, or failure of outpatient care. Discharge is appropriate only when the patient is medically and psychologically stable with a multidisciplinary outpatient plan in place.
Follow-Up And Ongoing Care
Effective outpatient management requires a coordinated team including a physician, mental health professional, nutritionist, and often family or group therapy support. Monitoring includes vital signs, weight trends, electrolytes, ECGs, dietary intake, and exercise behaviors. Psychotherapy—particularly cognitive behavioral therapy and family-based treatment—is central. Pharmacologic therapy is adjunctive and targeted to comorbid conditions.
Key Clinical Insights And Common Errors
Eating disorders carry high medical and suicide risk, making safety assessment paramount. Rapid nutritional repletion without electrolyte and vitamin replacement can cause fatal refeeding syndrome. Avoid confrontational approaches that reinforce obsessive thinking. Optimal outcomes depend on early recognition and coordinated multidisciplinary care.
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Emergency And Acute Medicine - Dystonic Reaction
Foundational Overview
Normal CNS motor control depends on a balance between dopaminergic and cholinergic activity. Certain medications block dopamine receptors in the basal ganglia, creating relative cholinergic excess. This imbalance produces acute, involuntary muscle contractions, most often affecting the face and neck, though the trunk, pelvis, and extremities may also be involved. Symptoms are typically alarming but rarely life threatening, except in uncommon cases involving the laryngeal muscles. Onset usually occurs within hours of exposure and almost always within the first week. Children and young adults are at highest risk; males are affected more often. Prior dystonic reactions and recent cocaine use increase susceptibility, while occurrence after age 45 is rare.
Causes And Risk Factors
Most reactions follow exposure to dopamine antagonists, particularly antipsychotics, antiemetics, and some antidepressants. Incidence varies widely and correlates with drug potency—higher with agents such as haloperidol or fluphenazine, lower with chlorpromazine or thioridazine, and lowest with atypical antipsychotics. Common antiemetic triggers include metoclopramide, prochlorperazine, promethazine, and droperidol. Other implicated agents include cyclic antidepressants, H2 blockers, selected antimalarials, antihistamines, anticonvulsants, lithium, doxepin, and phencyclidine. Children are particularly vulnerable when febrile or dehydrated.
Clinical Recognition
History typically reveals recent ingestion or dose escalation of a neuroleptic or antiemetic, or reduction of prophylactic anticholinergic therapy. Patients remain alert and oriented, though speech may be impaired by facial or tongue involvement. Involuntary sustained muscle contractions are characteristic. Examination may reveal oculogyric crisis with painful eye deviation, blepharospasm, buccolingual involvement with facial grimacing, trismus, tongue protrusion, dysphagia, spasmodic torticollis, truncal arching (opisthotonos), abdominal wall spasm, or, rarely, laryngeal dystonia presenting with stridor or dysphonia.
Essential Evaluation
Diagnosis is clinical, supported by a compatible medication history and rapid resolution after treatment. Failure to improve should prompt reconsideration of the diagnosis.
Diagnostic Studies
Routine laboratory or imaging studies are unnecessary. If symptoms persist despite therapy, evaluate for alternative causes such as hypocalcemia.
Differential Considerations
Distinguish acute dystonia from tardive dyskinesia, akathisia, seizures, psychogenic events, tetanus, strychnine poisoning, chronic neurologic dystonias, scorpion envenomation, meningitis, encephalitis, mandibular dislocation, and metabolic disturbances such as hypocalcemia.
Prehospital Care
These reactions are rarely fatal. Attention should focus on airway protection, especially with tongue or laryngeal involvement. Obtain information on recent medication or substance exposure and transport medication containers when possible.
Initial Stabilization
Ensure airway patency and monitor for respiratory compromise related to oropharyngeal or laryngeal spasm.
Emergency Department Management
First-line therapy is intravenous anticholinergic medication, which rapidly restores neurotransmitter balance. Diphenhydramine or benztropine typically produces improvement within minutes, with complete resolution within 30 minutes. Intramuscular administration is an alternative when IV access is unavailable. Oral therapy should continue for several days to prevent recurrence. Benzodiazepines are reserved for refractory cases. Lack of response should prompt reevaluation for alternate diagnoses.
Pharmacologic Therapy
Diphenhydramine 1–2 mg/kg IV or IM (maximum 100 mg), followed by oral dosing for three days, is first line. Benztropine 1–2 mg IV or IM followed by oral dosing is an alternative, avoiding use in children under three years. Diazepam may be used for persistent symptoms.
Disposition And Follow-Up
Admission is rarely required unless symptoms fail to resolve, airway protection is a concern, or the diagnosis is uncertain. Patients with laryngeal involvement should be observed after symptom resolution. Discharge is appropriate once symptoms resolve; the offending agent should be discontinued, and patients cautioned about sedating medications. Follow-up with the prescribing clinician is recommended.
Key Clinical Insights And Common Errors
Acute dystonia is diagnosed by characteristic presentation and rapid response to anticholinergic therapy. Diphenhydramine is the preferred first-line treatment. Failure to improve should prompt reassessment for alternative or more serious conditions.
Foundational Overview
Normal CNS motor control depends on a balance between dopaminergic and cholinergic activity. Certain medications block dopamine receptors in the basal ganglia, creating relative cholinergic excess. This imbalance produces acute, involuntary muscle contractions, most often affecting the face and neck, though the trunk, pelvis, and extremities may also be involved. Symptoms are typically alarming but rarely life threatening, except in uncommon cases involving the laryngeal muscles. Onset usually occurs within hours of exposure and almost always within the first week. Children and young adults are at highest risk; males are affected more often. Prior dystonic reactions and recent cocaine use increase susceptibility, while occurrence after age 45 is rare.
Causes And Risk Factors
Most reactions follow exposure to dopamine antagonists, particularly antipsychotics, antiemetics, and some antidepressants. Incidence varies widely and correlates with drug potency—higher with agents such as haloperidol or fluphenazine, lower with chlorpromazine or thioridazine, and lowest with atypical antipsychotics. Common antiemetic triggers include metoclopramide, prochlorperazine, promethazine, and droperidol. Other implicated agents include cyclic antidepressants, H2 blockers, selected antimalarials, antihistamines, anticonvulsants, lithium, doxepin, and phencyclidine. Children are particularly vulnerable when febrile or dehydrated.
Clinical Recognition
History typically reveals recent ingestion or dose escalation of a neuroleptic or antiemetic, or reduction of prophylactic anticholinergic therapy. Patients remain alert and oriented, though speech may be impaired by facial or tongue involvement. Involuntary sustained muscle contractions are characteristic. Examination may reveal oculogyric crisis with painful eye deviation, blepharospasm, buccolingual involvement with facial grimacing, trismus, tongue protrusion, dysphagia, spasmodic torticollis, truncal arching (opisthotonos), abdominal wall spasm, or, rarely, laryngeal dystonia presenting with stridor or dysphonia.
Essential Evaluation
Diagnosis is clinical, supported by a compatible medication history and rapid resolution after treatment. Failure to improve should prompt reconsideration of the diagnosis.
Diagnostic Studies
Routine laboratory or imaging studies are unnecessary. If symptoms persist despite therapy, evaluate for alternative causes such as hypocalcemia.
Differential Considerations
Distinguish acute dystonia from tardive dyskinesia, akathisia, seizures, psychogenic events, tetanus, strychnine poisoning, chronic neurologic dystonias, scorpion envenomation, meningitis, encephalitis, mandibular dislocation, and metabolic disturbances such as hypocalcemia.
Prehospital Care
These reactions are rarely fatal. Attention should focus on airway protection, especially with tongue or laryngeal involvement. Obtain information on recent medication or substance exposure and transport medication containers when possible.
Initial Stabilization
Ensure airway patency and monitor for respiratory compromise related to oropharyngeal or laryngeal spasm.
Emergency Department Management
First-line therapy is intravenous anticholinergic medication, which rapidly restores neurotransmitter balance. Diphenhydramine or benztropine typically produces improvement within minutes, with complete resolution within 30 minutes. Intramuscular administration is an alternative when IV access is unavailable. Oral therapy should continue for several days to prevent recurrence. Benzodiazepines are reserved for refractory cases. Lack of response should prompt reevaluation for alternate diagnoses.
Pharmacologic Therapy
Diphenhydramine 1–2 mg/kg IV or IM (maximum 100 mg), followed by oral dosing for three days, is first line. Benztropine 1–2 mg IV or IM followed by oral dosing is an alternative, avoiding use in children under three years. Diazepam may be used for persistent symptoms.
Disposition And Follow-Up
Admission is rarely required unless symptoms fail to resolve, airway protection is a concern, or the diagnosis is uncertain. Patients with laryngeal involvement should be observed after symptom resolution. Discharge is appropriate once symptoms resolve; the offending agent should be discontinued, and patients cautioned about sedating medications. Follow-up with the prescribing clinician is recommended.
Key Clinical Insights And Common Errors
Acute dystonia is diagnosed by characteristic presentation and rapid response to anticholinergic therapy. Diphenhydramine is the preferred first-line treatment. Failure to improve should prompt reassessment for alternative or more serious conditions.
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Emergency And Acute Medicine – Dyspnea
Core Concept Overview
Dyspnea is the subjective sensation of uncomfortable or difficult breathing and represents a symptom rather than a diagnosis. It differs from objective signs of increased work of breathing and ranges from mild air hunger to a sensation of suffocation. Although breathing is usually an unconscious activity, dyspnea reflects a conscious perception arising from disruption of normal gas exchange, acid–base balance, metabolic demands, or central nervous system drive. It is a common emergency department complaint, accounting for approximately 3.5% of visits. The sensation results from impaired ventilation, perfusion, metabolic function, or neural control. Respiratory control depends on brainstem and cortical centers, chemoreceptors responsive to carbon dioxide and oxygen levels, mechanoreceptors within respiratory muscles and lung tissue, and intact neuromuscular pathways to the diaphragm and chest wall. Dysfunction at any point in this complex system can produce dyspnea.
Causes And Pathophysiologic Categories
Upper airway causes include epiglottitis, laryngeal obstruction, tracheitis or tracheobronchitis, and angioedema. Pulmonary etiologies encompass asthma, bronchitis, pneumonia, pneumothorax, pulmonary embolism, pulmonary hypertension, emphysema, restrictive lung disease, effusions, malignancy, chest wall trauma, and drug-induced lung injury. Cardiovascular causes include arrhythmias, coronary artery disease, intracardiac shunts, left ventricular failure, valvular disease, pericardial pathology, and cardiac tumors. Neuromuscular causes involve central nervous system disorders, peripheral neuropathies, myopathies, spinal cord disease, and diaphragmatic or phrenic nerve dysfunction. Metabolic acidosis from sepsis, diabetic or alcoholic ketoacidosis, renal failure, or severe thiamine deficiency may drive dyspnea. Toxic causes include methemoglobinemia, salicylate poisoning, and cellular asphyxiants such as carbon monoxide, cyanide, hydrogen sulfide, sodium azide, and toxic alcohols. Abdominal compression from ascites, pregnancy, or morbid obesity may impair ventilation. Psychogenic causes include anxiety and hyperventilation. Other contributors include anemia, altitude exposure, and anaphylaxis.
Special Population Considerations
In older adults, the most common causes of dyspnea are decompensated heart failure, pneumonia, chronic obstructive pulmonary disease, pulmonary embolism, and asthma. In children under two years of age, common causes include asthma, croup, congenital airway or cardiac anomalies, foreign-body aspiration, nasopharyngeal obstruction, and shock.
Clinical Manifestations
Patients may report difficult, labored, or uncomfortable breathing. Upper airway involvement may present with stridor. Pulmonary findings include tachypnea, accessory muscle use, wheezing, rales, asymmetric breath sounds, poor air movement, or prolonged expiration. Cardiovascular findings may include jugular venous distention, murmurs, or an S3 gallop. Neurologic involvement may cause altered mental status. General signs include diaphoresis, pallor, cyanosis, edema, clubbing, upright posture, or ketotic breath odor.
Focused History Assessment
Key elements include prior episodes of dyspnea, onset and time course, precipitating factors, severity, and progression. Elicit history of stridor or wheezing, exercise tolerance, medication use and compliance, allergen exposure, and past medical conditions. Associated symptoms such as chest pain, fever, cough, and hemoptysis should be explored.
Physical Examination Priorities
Assess for signs of acute distress including altered mental status, cyanosis, severe tachypnea, and retractions. Auscultate carefully for stridor, rales, wheezing, or diminished breath sounds and evaluate cardiovascular and neurologic status.
Essential Diagnostic Evaluation
Continuous pulse oximetry should be applied, recognizing that values may be misleading in hyperventilation or carbon monoxide exposure. End-tidal carbon dioxide monitoring provides rapid estimation of ventilation and waveform clues to etiology. Chest radiography evaluates pulmonary pathology and cardiac size. Arterial blood gas analysis assesses oxygenation and acid–base status and allows calculation of the alveolar–arterial gradient to identify gas exchange abnormalities.
Diagnostic Studies And Interpretation
Laboratory testing may include complete blood count for anemia or infection, metabolic panel for renal or metabolic derangements, B-type natriuretic peptide for heart failure, toxicology screening, methemoglobin or carboxyhemoglobin levels, thyroid studies, and D-dimer when pulmonary embolism is suspected. Imaging includes chest radiography, CT pulmonary angiography or ventilation–perfusion scanning for embolism, and soft tissue neck imaging or fiberoptic evaluation for upper airway obstruction. Electrocardiography assesses for ischemia, arrhythmias, or pericardial disease. Pulmonary function testing or peak flow may help evaluate reactive airway disease, and specialized testing may be considered for neuromuscular disorders.
Alternative Diagnoses To Consider
Less common considerations include anticholinergic or adrenergic toxidromes, thyroid storm, and factitious disorders.
Prehospital Management Principles
All patients should receive supplemental oxygen, continuous monitoring, and early intervention directed at the suspected cause, such as bronchodilators for asthma, diuretics for heart failure, or ventilatory support when indicated. Advanced airway management should be used for impending respiratory failure.
Initial Resuscitation Strategy
Follow airway, breathing, and circulation priorities. Immediate intubation is required for respiratory arrest, severe altered mental status, or unstable vital signs. Noninvasive ventilation may be used in alert patients but is contraindicated in hemodynamic instability, suspected upper airway obstruction, inability to protect the airway, active gastrointestinal bleeding, or ongoing seizures.
Emergency Department Management
Treatment is directed at the underlying etiology, including antibiotics and fluids for pneumonia, positive pressure ventilation and diuretics for heart failure, bronchodilators and corticosteroids for asthma, and antiplatelet or anticoagulant therapy for myocardial infarction when appropriate. Symptom-directed and palliative measures, including opioids, may be appropriate for refractory dyspnea in terminal illness.
Disposition Planning
Hospital admission is indicated for patients requiring assisted ventilation, persistent hypoxia, significantly elevated alveolar–arterial gradients, or conditions requiring inpatient therapy. Discharge may be considered for patients with stable disease, adequate oxygenation, and safe ambulatory pulse oximetry.
Referral And Follow-Up Needs
Specialty referral should be based on the identified or suspected etiology.
Discharge Instructions And Return Precautions
Patients should avoid smoking and be counseled on cessation. They should return for worsening symptoms, lack of improvement within 24 hours, new chest pain, high fever, worsening cough or wheeze, gastrointestinal symptoms, neurologic changes, or any significant new concern.
Clinical Pearls And Common Errors
Altered mental status in a dyspneic patient mandates immediate airway consideration. Dyspnea severity should be quantified and reassessed. Not all dyspnea is respiratory in origin; metabolic disturbances and catastrophic neurologic events must remain in the differential.
Core Concept Overview
Dyspnea is the subjective sensation of uncomfortable or difficult breathing and represents a symptom rather than a diagnosis. It differs from objective signs of increased work of breathing and ranges from mild air hunger to a sensation of suffocation. Although breathing is usually an unconscious activity, dyspnea reflects a conscious perception arising from disruption of normal gas exchange, acid–base balance, metabolic demands, or central nervous system drive. It is a common emergency department complaint, accounting for approximately 3.5% of visits. The sensation results from impaired ventilation, perfusion, metabolic function, or neural control. Respiratory control depends on brainstem and cortical centers, chemoreceptors responsive to carbon dioxide and oxygen levels, mechanoreceptors within respiratory muscles and lung tissue, and intact neuromuscular pathways to the diaphragm and chest wall. Dysfunction at any point in this complex system can produce dyspnea.
Causes And Pathophysiologic Categories
Upper airway causes include epiglottitis, laryngeal obstruction, tracheitis or tracheobronchitis, and angioedema. Pulmonary etiologies encompass asthma, bronchitis, pneumonia, pneumothorax, pulmonary embolism, pulmonary hypertension, emphysema, restrictive lung disease, effusions, malignancy, chest wall trauma, and drug-induced lung injury. Cardiovascular causes include arrhythmias, coronary artery disease, intracardiac shunts, left ventricular failure, valvular disease, pericardial pathology, and cardiac tumors. Neuromuscular causes involve central nervous system disorders, peripheral neuropathies, myopathies, spinal cord disease, and diaphragmatic or phrenic nerve dysfunction. Metabolic acidosis from sepsis, diabetic or alcoholic ketoacidosis, renal failure, or severe thiamine deficiency may drive dyspnea. Toxic causes include methemoglobinemia, salicylate poisoning, and cellular asphyxiants such as carbon monoxide, cyanide, hydrogen sulfide, sodium azide, and toxic alcohols. Abdominal compression from ascites, pregnancy, or morbid obesity may impair ventilation. Psychogenic causes include anxiety and hyperventilation. Other contributors include anemia, altitude exposure, and anaphylaxis.
Special Population Considerations
In older adults, the most common causes of dyspnea are decompensated heart failure, pneumonia, chronic obstructive pulmonary disease, pulmonary embolism, and asthma. In children under two years of age, common causes include asthma, croup, congenital airway or cardiac anomalies, foreign-body aspiration, nasopharyngeal obstruction, and shock.
Clinical Manifestations
Patients may report difficult, labored, or uncomfortable breathing. Upper airway involvement may present with stridor. Pulmonary findings include tachypnea, accessory muscle use, wheezing, rales, asymmetric breath sounds, poor air movement, or prolonged expiration. Cardiovascular findings may include jugular venous distention, murmurs, or an S3 gallop. Neurologic involvement may cause altered mental status. General signs include diaphoresis, pallor, cyanosis, edema, clubbing, upright posture, or ketotic breath odor.
Focused History Assessment
Key elements include prior episodes of dyspnea, onset and time course, precipitating factors, severity, and progression. Elicit history of stridor or wheezing, exercise tolerance, medication use and compliance, allergen exposure, and past medical conditions. Associated symptoms such as chest pain, fever, cough, and hemoptysis should be explored.
Physical Examination Priorities
Assess for signs of acute distress including altered mental status, cyanosis, severe tachypnea, and retractions. Auscultate carefully for stridor, rales, wheezing, or diminished breath sounds and evaluate cardiovascular and neurologic status.
Essential Diagnostic Evaluation
Continuous pulse oximetry should be applied, recognizing that values may be misleading in hyperventilation or carbon monoxide exposure. End-tidal carbon dioxide monitoring provides rapid estimation of ventilation and waveform clues to etiology. Chest radiography evaluates pulmonary pathology and cardiac size. Arterial blood gas analysis assesses oxygenation and acid–base status and allows calculation of the alveolar–arterial gradient to identify gas exchange abnormalities.
Diagnostic Studies And Interpretation
Laboratory testing may include complete blood count for anemia or infection, metabolic panel for renal or metabolic derangements, B-type natriuretic peptide for heart failure, toxicology screening, methemoglobin or carboxyhemoglobin levels, thyroid studies, and D-dimer when pulmonary embolism is suspected. Imaging includes chest radiography, CT pulmonary angiography or ventilation–perfusion scanning for embolism, and soft tissue neck imaging or fiberoptic evaluation for upper airway obstruction. Electrocardiography assesses for ischemia, arrhythmias, or pericardial disease. Pulmonary function testing or peak flow may help evaluate reactive airway disease, and specialized testing may be considered for neuromuscular disorders.
Alternative Diagnoses To Consider
Less common considerations include anticholinergic or adrenergic toxidromes, thyroid storm, and factitious disorders.
Prehospital Management Principles
All patients should receive supplemental oxygen, continuous monitoring, and early intervention directed at the suspected cause, such as bronchodilators for asthma, diuretics for heart failure, or ventilatory support when indicated. Advanced airway management should be used for impending respiratory failure.
Initial Resuscitation Strategy
Follow airway, breathing, and circulation priorities. Immediate intubation is required for respiratory arrest, severe altered mental status, or unstable vital signs. Noninvasive ventilation may be used in alert patients but is contraindicated in hemodynamic instability, suspected upper airway obstruction, inability to protect the airway, active gastrointestinal bleeding, or ongoing seizures.
Emergency Department Management
Treatment is directed at the underlying etiology, including antibiotics and fluids for pneumonia, positive pressure ventilation and diuretics for heart failure, bronchodilators and corticosteroids for asthma, and antiplatelet or anticoagulant therapy for myocardial infarction when appropriate. Symptom-directed and palliative measures, including opioids, may be appropriate for refractory dyspnea in terminal illness.
Disposition Planning
Hospital admission is indicated for patients requiring assisted ventilation, persistent hypoxia, significantly elevated alveolar–arterial gradients, or conditions requiring inpatient therapy. Discharge may be considered for patients with stable disease, adequate oxygenation, and safe ambulatory pulse oximetry.
Referral And Follow-Up Needs
Specialty referral should be based on the identified or suspected etiology.
Discharge Instructions And Return Precautions
Patients should avoid smoking and be counseled on cessation. They should return for worsening symptoms, lack of improvement within 24 hours, new chest pain, high fever, worsening cough or wheeze, gastrointestinal symptoms, neurologic changes, or any significant new concern.
Clinical Pearls And Common Errors
Altered mental status in a dyspneic patient mandates immediate airway consideration. Dyspnea severity should be quantified and reassessed. Not all dyspnea is respiratory in origin; metabolic disturbances and catastrophic neurologic events must remain in the differential.
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Emergency And Acute Medicine – Dysphagia
Basics Description
Dysphagia is defined as difficulty swallowing and may result from neuromuscular or mechanical causes. It can involve impairment at the oropharyngeal or esophageal level, and careful clinical distinction is essential because etiologies, workup, and urgency differ significantly.
Etiology
Oropharyngeal (transfer) dysphagia is characterized by difficulty initiating a swallow and impaired transfer of food from the mouth to the proximal esophagus. Patients often swallow solids more easily than liquids and develop symptoms immediately upon swallowing. Associated features include nasal or oral regurgitation, coughing, choking, drooling, and aspiration. This form is usually due to neuromuscular disorders causing bulbar muscle weakness or impaired coordination.
Esophageal (transport) dysphagia results from failure of normal transit through the esophagus and is associated with a retrosternal sticking sensation occurring seconds after swallowing. Patients may experience nocturnal regurgitation, aspiration, or regurgitation of undigested food, which is characteristic of esophageal obstruction. Causes include motility disorders and mechanical obstruction.
Functional dysphagia is a diagnosis of exclusion after a full evaluation shows no mechanical or neuromuscular pathology, with symptoms lasting longer than 12 weeks.
Odynophagia refers to pain with swallowing and is a separate but often related condition. Pain localization is generally poor; upper esophageal pain is better localized due to somatic innervation, while lower esophageal visceral pain is poorly localized and may mimic acute coronary syndrome.
Pediatric Considerations
In infants and newborns, common causes include prematurity, congenital malformations, neuromuscular disease, infection such as candidiasis, and inflammation. Foreign body aspiration must always be considered. Other pediatric causes include caustic ingestions, infections, neurologic disorders, and sequelae of head injury. Acquired tracheoesophageal fistula may occur after disk battery or caustic ingestion or prior surgery. Life-threatening pediatric causes include epiglottitis, retropharyngeal abscess, central nervous system infection, botulism, esophageal perforation, and diphtheria.
Diagnosis Signs And Symptoms
Symptoms include difficulty initiating swallowing, sensation of food sticking after swallowing, coughing or choking after eating, impaired gag reflex, dysphonia, drooling, dysarthria, and chest pain.
History
Determine whether dysphagia occurs with solids, liquids, or both. Difficulty with both solids and liquids suggests a neuromuscular disorder, whereas solids alone or progression from solids to liquids suggests mechanical obstruction. Immediate symptoms indicate oropharyngeal dysphagia, while delayed symptoms suggest esophageal involvement. Intermittent symptoms suggest rings or webs, whereas progressive symptoms raise concern for peptic or malignant strictures. Acute onset is concerning for life-threatening causes, with food impaction being the most common. Associated symptoms such as nasal regurgitation, choking, heartburn, or weight loss should be elicited.
Physical-Exam
Findings are often subtle or normal. Perform careful oropharyngeal inspection, pulmonary and cardiac auscultation, and a complete neurologic examination with emphasis on cranial nerves V, VII, IX, X, and XII.
Essential Workup
Ensure adequate airway evaluation and perform a thorough neurologic examination.
Diagnosis Tests And Interpretation
Electrocardiogram should be obtained when chest discomfort raises concern for cardiac etiology. No routine laboratory studies are indicated. Chest radiograph may show dilated esophagus in achalasia, aspiration pneumonitis, or extrinsic compression. Lateral neck radiograph may be helpful in selected cases. Modified barium swallow or videofluoroscopy assesses anatomy and function but should not be performed if endoscopy is anticipated. CT or MRI of the head is indicated for new-onset neuromuscular dysphagia. Upper endoscopy allows relief of obstruction, direct visualization, and biopsy when indicated. Esophageal manometry and fiberoptic nasopharyngeal laryngoscopy are usually performed in the outpatient setting.
Differential Diagnosis
Oropharyngeal causes include infections such as botulism and central nervous system infections, mechanical causes including congenital abnormalities and malignancy, medication-induced injury, and neuromuscular disorders such as stroke, amyotrophic lateral sclerosis, Guillain–Barré syndrome, myasthenia gravis, Parkinson disease, multiple sclerosis, and traumatic brain injury. Esophageal causes include mechanical obstruction from diverticula, webs, foreign bodies, neoplasms, strictures, rings, radiation injury, and postsurgical changes; motility disorders such as achalasia and diffuse esophageal spasm; inflammatory conditions including eosinophilic or pill esophagitis; and extrinsic compression from cardiovascular or mediastinal abnormalities.
Treatment Pre Hospital
Maintain vigilant airway monitoring and position the patient comfortably with suction readily available.
Initial Stabilization And Therapy
Maintain airway vigilance and keep the patient NPO. Administer intravenous fluids with 0.9% normal saline for dehydration. Evaluate urgently for life-threatening causes including retropharyngeal abscess or hematoma, epiglottitis, foreign body, upper airway obstruction, and cardiovascular etiologies.
Emergency Department Treatment And Procedures
Nitroglycerin may be used for esophageal spasm. Glucagon may be attempted for food impaction. Treat complications such as airway obstruction, aspiration pneumonia, dehydration, and malnutrition. Endoscopy is indicated when obstruction persists. Dietary modifications include thickened liquids for neuromuscular disorders and thin liquids for mechanical causes.
Medication
Glucagon 1 mg IV may be administered for food impaction, with a second 1 mg dose after 5 minutes if no improvement; pediatric dosing is 0.02–0.03 mg/kg, not exceeding 0.5 mg. Calcium channel blockers and nitrates may be considered for esophageal motility disorders such as achalasia.
Follow-Up And Disposition
Admission is required for persistent esophageal obstruction, inability to protect the airway, inability to tolerate secretions, or compromised hydration or nutrition. Patients who are stable and well hydrated may be discharged with urgent referral to neurology, otolaryngology, or gastroenterology.
Issues For Referral
Next-day follow-up with primary care, ENT, or gastroenterology is recommended.
Follow-Up Recommendations
Clear liquid diet until specialist evaluation. Return immediately for shortness of breath, chest pain, or inability to tolerate secretions.
Pearls And Pitfalls
Always consider foreign body aspiration in children. Dysphagia is a common presentation of stroke and should be considered in patients with recurrent pneumonia. Life-threatening causes must be excluded before deferring evaluation to the outpatient setting.
Basics Description
Dysphagia is defined as difficulty swallowing and may result from neuromuscular or mechanical causes. It can involve impairment at the oropharyngeal or esophageal level, and careful clinical distinction is essential because etiologies, workup, and urgency differ significantly.
Etiology
Oropharyngeal (transfer) dysphagia is characterized by difficulty initiating a swallow and impaired transfer of food from the mouth to the proximal esophagus. Patients often swallow solids more easily than liquids and develop symptoms immediately upon swallowing. Associated features include nasal or oral regurgitation, coughing, choking, drooling, and aspiration. This form is usually due to neuromuscular disorders causing bulbar muscle weakness or impaired coordination.
Esophageal (transport) dysphagia results from failure of normal transit through the esophagus and is associated with a retrosternal sticking sensation occurring seconds after swallowing. Patients may experience nocturnal regurgitation, aspiration, or regurgitation of undigested food, which is characteristic of esophageal obstruction. Causes include motility disorders and mechanical obstruction.
Functional dysphagia is a diagnosis of exclusion after a full evaluation shows no mechanical or neuromuscular pathology, with symptoms lasting longer than 12 weeks.
Odynophagia refers to pain with swallowing and is a separate but often related condition. Pain localization is generally poor; upper esophageal pain is better localized due to somatic innervation, while lower esophageal visceral pain is poorly localized and may mimic acute coronary syndrome.
Pediatric Considerations
In infants and newborns, common causes include prematurity, congenital malformations, neuromuscular disease, infection such as candidiasis, and inflammation. Foreign body aspiration must always be considered. Other pediatric causes include caustic ingestions, infections, neurologic disorders, and sequelae of head injury. Acquired tracheoesophageal fistula may occur after disk battery or caustic ingestion or prior surgery. Life-threatening pediatric causes include epiglottitis, retropharyngeal abscess, central nervous system infection, botulism, esophageal perforation, and diphtheria.
Diagnosis Signs And Symptoms
Symptoms include difficulty initiating swallowing, sensation of food sticking after swallowing, coughing or choking after eating, impaired gag reflex, dysphonia, drooling, dysarthria, and chest pain.
History
Determine whether dysphagia occurs with solids, liquids, or both. Difficulty with both solids and liquids suggests a neuromuscular disorder, whereas solids alone or progression from solids to liquids suggests mechanical obstruction. Immediate symptoms indicate oropharyngeal dysphagia, while delayed symptoms suggest esophageal involvement. Intermittent symptoms suggest rings or webs, whereas progressive symptoms raise concern for peptic or malignant strictures. Acute onset is concerning for life-threatening causes, with food impaction being the most common. Associated symptoms such as nasal regurgitation, choking, heartburn, or weight loss should be elicited.
Physical-Exam
Findings are often subtle or normal. Perform careful oropharyngeal inspection, pulmonary and cardiac auscultation, and a complete neurologic examination with emphasis on cranial nerves V, VII, IX, X, and XII.
Essential Workup
Ensure adequate airway evaluation and perform a thorough neurologic examination.
Diagnosis Tests And Interpretation
Electrocardiogram should be obtained when chest discomfort raises concern for cardiac etiology. No routine laboratory studies are indicated. Chest radiograph may show dilated esophagus in achalasia, aspiration pneumonitis, or extrinsic compression. Lateral neck radiograph may be helpful in selected cases. Modified barium swallow or videofluoroscopy assesses anatomy and function but should not be performed if endoscopy is anticipated. CT or MRI of the head is indicated for new-onset neuromuscular dysphagia. Upper endoscopy allows relief of obstruction, direct visualization, and biopsy when indicated. Esophageal manometry and fiberoptic nasopharyngeal laryngoscopy are usually performed in the outpatient setting.
Differential Diagnosis
Oropharyngeal causes include infections such as botulism and central nervous system infections, mechanical causes including congenital abnormalities and malignancy, medication-induced injury, and neuromuscular disorders such as stroke, amyotrophic lateral sclerosis, Guillain–Barré syndrome, myasthenia gravis, Parkinson disease, multiple sclerosis, and traumatic brain injury. Esophageal causes include mechanical obstruction from diverticula, webs, foreign bodies, neoplasms, strictures, rings, radiation injury, and postsurgical changes; motility disorders such as achalasia and diffuse esophageal spasm; inflammatory conditions including eosinophilic or pill esophagitis; and extrinsic compression from cardiovascular or mediastinal abnormalities.
Treatment Pre Hospital
Maintain vigilant airway monitoring and position the patient comfortably with suction readily available.
Initial Stabilization And Therapy
Maintain airway vigilance and keep the patient NPO. Administer intravenous fluids with 0.9% normal saline for dehydration. Evaluate urgently for life-threatening causes including retropharyngeal abscess or hematoma, epiglottitis, foreign body, upper airway obstruction, and cardiovascular etiologies.
Emergency Department Treatment And Procedures
Nitroglycerin may be used for esophageal spasm. Glucagon may be attempted for food impaction. Treat complications such as airway obstruction, aspiration pneumonia, dehydration, and malnutrition. Endoscopy is indicated when obstruction persists. Dietary modifications include thickened liquids for neuromuscular disorders and thin liquids for mechanical causes.
Medication
Glucagon 1 mg IV may be administered for food impaction, with a second 1 mg dose after 5 minutes if no improvement; pediatric dosing is 0.02–0.03 mg/kg, not exceeding 0.5 mg. Calcium channel blockers and nitrates may be considered for esophageal motility disorders such as achalasia.
Follow-Up And Disposition
Admission is required for persistent esophageal obstruction, inability to protect the airway, inability to tolerate secretions, or compromised hydration or nutrition. Patients who are stable and well hydrated may be discharged with urgent referral to neurology, otolaryngology, or gastroenterology.
Issues For Referral
Next-day follow-up with primary care, ENT, or gastroenterology is recommended.
Follow-Up Recommendations
Clear liquid diet until specialist evaluation. Return immediately for shortness of breath, chest pain, or inability to tolerate secretions.
Pearls And Pitfalls
Always consider foreign body aspiration in children. Dysphagia is a common presentation of stroke and should be considered in patients with recurrent pneumonia. Life-threatening causes must be excluded before deferring evaluation to the outpatient setting.
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Emergency And Acute Medicine – Dysfunctional Uterine Bleeding
Basics Description
Abnormal uterine bleeding refers to an alteration in the pattern or volume of normal menses. Typical menstrual blood loss is 30–80 mL, with a normal cycle interval of 28 ± 7 days. Abnormal uterine bleeding is classified into dysfunctional uterine bleeding (DUB) and organic uterine bleeding. Dysfunctional uterine bleeding is hormonally mediated, divided into anovulatory and ovulatory categories, is not due to organic or iatrogenic causes, and is therefore a diagnosis of exclusion. Organic uterine bleeding is related to systemic illness or disease of the reproductive tract.
Etiology
Anovulatory bleeding, the most common cause, results from unopposed estrogen stimulation of the proliferative endometrium. Neuroendocrine dysfunction may be associated with polycystic ovarian syndrome, very low-calorie diets, rapid weight changes, intense exercise, anorexia, psychological stress, obesity, medications, hypothyroidism, or primary hypothalamic dysfunction. Ovulatory bleeding is caused by inadequate uterine prostaglandin F2α, increased uterine contractility, or excessive prostacycline production, which diminishes platelet function and increases uterine vasodilation.
Pediatric Considerations
Anovulatory bleeding is common during adolescence due to immaturity of the hypothalamic–pituitary–ovarian axis.
Diagnosis Signs And Symptoms
Patients present with abnormal uterine bleeding in the absence of systemic or structural disease. It is most common in perimenarcheal and perimenopausal women and is typically painless. Anovulatory patterns include metrorrhagia with irregular bleeding between periods, menorrhagia with regular cycles and excessive flow greater than 80 mL or lasting more than 7 days, oligomenorrhea with cycles longer than 35 days, and menometrorrhagia with heavy and irregular bleeding.
History
History focuses on bleeding pattern, duration, volume, associated symptoms, medication use, and risk factors for pregnancy or systemic disease.
Physical-Exam
Acne, hirsutism, and obesity suggest polycystic ovarian syndrome. Pelvic examination typically reveals mild to moderate bleeding. Pallor, tachycardia, hypotension, and orthostasis indicate severe blood loss. Evaluate for trauma or foreign bodies.
Alert
Hemodynamic instability is rare in dysfunctional uterine bleeding; if present, consider ectopic pregnancy or another cause of acute hemorrhage.
Essential Workup
A pregnancy test is mandatory.
Diagnosis Tests And Interpretation
Laboratory evaluation includes pregnancy test, complete blood count, and coagulation studies. Iron studies, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, prolactin, and cervical cultures are typically deferred for outpatient follow-up. Pelvic ultrasound may identify uterine, tubal, or ovarian pathology and help exclude organic causes. Dilation and curettage may be required for heavy bleeding unresponsive to therapy. Endometrial biopsy is recommended for patients older than 35 years.
Differential Diagnosis
Pregnancy-related causes include threatened, incomplete, or spontaneous abortion, ectopic pregnancy, and molar pregnancy. Infectious causes include vaginitis, cervicitis, and pelvic inflammatory disease. Coagulopathies include von Willebrand disease, idiopathic thrombocytopenic purpura, platelet disorders, and thalassemia. Medication-related causes include warfarin, aspirin, oral contraceptives, tricyclic antidepressants, and antipsychotics. Systemic illnesses include adrenal, hepatic, renal, thyroid disease, diabetes, and other endocrinopathies. Anatomic causes include fibroids, endometriosis, polyps, endometrial hyperplasia, malignancy, intrauterine devices, and trauma.
Treatment Pre Hospital
Administer intravenous crystalloids as needed for hypotension or tachycardia secondary to heavy bleeding.
Initial Stabilization And Therapy
Follow ABCs. Transfuse packed red blood cells for significant bleeding unresponsive to crystalloid resuscitation.
Emergency Department Treatment And Procedures
Observation is usually sufficient for mild bleeding. Administer intravenous fluids or packed red blood cells for continued bleeding or hemodynamic instability. Obtain gynecology consultation for severe bleeding unresponsive to medical therapy. Dilation and curettage may be necessary for instability. Endometrial ablation or hysterectomy is reserved for refractory cases.
Medication
Conjugated estrogen is indicated for heavy bleeding with hemodynamic instability at 2.5 mg orally every 6 hours or 25 mg intravenously, repeatable after 3 hours if needed. Ibuprofen 400–800 mg orally every 8 hours reduces prostaglandin synthesis. Medroxyprogesterone acetate 5–10 mg orally daily is added once bleeding subsides. Combined oral contraceptives containing ethinyl estradiol 35 μg and norethindrone 1 mg may be given four times daily for one week. Tranexamic acid 1,300 mg orally three times daily for five days may be used, though limited by gastrointestinal side effects and allergy risk. Medications may be deferred in mild cases with outpatient gynecology referral.
Follow-Up And Disposition
Admission is required for significant blood loss, continued bleeding, or hemodynamic instability requiring aggressive resuscitation or operative intervention. Most patients may be discharged once bleeding is controlled and vital signs are stable, with gynecology follow-up arranged.
Issues For Referral
Endometrial biopsy is indicated for patients older than 35 years. Follow-up with gynecology or primary care is essential to evaluate for ongoing blood loss or malignancy.
Pearls And Pitfalls
Dysfunctional uterine bleeding is a diagnosis of exclusion. Only 2% of endometrial carcinomas occur before age 40. Hemodynamic instability makes DUB an unlikely primary diagnosis.
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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 – Dizziness
Basics
Description
Patient descriptions of dizziness (vertigo, lightheadedness, disequilibrium, or nonspecific terms) are often unreliable and should not guide decision making. A safer approach emphasizes associated symptoms, timing, and triggers, followed by a focused physical examination for diagnostic clues. Dizziness is categorized using a “timing and triggers” framework. Acute vestibular syndrome presents with abrupt onset of persistent dizziness. Episodic vestibular syndrome consists of spontaneous episodes lasting minutes to hours. Positional vestibular syndrome causes very brief episodes, typically 20–50 seconds, triggered by head or body position changes. Chronic vestibular syndrome has a gradual onset and persists for weeks to months or longer.
Etiology
General medical causes account for nearly half of cases and include arrhythmias, hypoglycemia and other metabolic disturbances, hypovolemia, sepsis, infections, and low cardiac output states. Otologic or vestibular causes represent about one third and include benign paroxysmal positional vertigo, labyrinthitis, and vestibular neuritis. Neurologic causes include stroke, transient ischemic attack, and vestibular migraine. Psychiatric causes such as anxiety and depression account for a smaller proportion.
Diagnosis
Signs and symptoms
History should define the timing and trigger pattern and assess for red flags. Key questions address onset, persistence versus intermittence, duration of episodes, positional triggers, associated hearing or neurologic symptoms, recent head injury, and new medications. Review of systems should focus on clues to serious disease, including headache suggesting stroke or dissection, ear pain suggesting otitis or mastoiditis, hearing changes suggesting Ménière disease or labyrinthitis, neck pain suggesting vertebral dissection, fever suggesting infection, dyspnea suggesting pulmonary embolism or anemia, chest pain suggesting acute coronary syndrome, fluid losses suggesting hypovolemia, and pregnancy-related complications.
Exacerbation with head motion occurs in both central and peripheral causes; however, dizziness only with head motion in an otherwise asymptomatic patient suggests a peripheral etiology.
Physical examination
Vital signs are assessed, including orthostatic testing. Otoscopic examination, cardiac examination, and a complete neurologic examination are essential. Cranial nerves II–XII should be evaluated with special attention to nystagmus. Gait observation and cerebellar testing are performed. The Dix–Hallpike maneuver is reserved for intermittent symptoms.
The HINTS examination is used only in patients with acute vestibular syndrome and consists of head impulse testing, nystagmus assessment, and testing for skew deviation. In the first 48 hours of symptoms, this exam can be more sensitive than MRI for detecting stroke. A normal head impulse test without corrective saccade suggests a central cause, whereas a corrective saccade suggests a peripheral cause. Direction-changing, vertical, or torsional nystagmus suggests a central etiology, while direction-fixed nystagmus suggests a peripheral cause. A vertical corrective saccade on alternate cover testing indicates a central process. Any concerning component should prompt concern for stroke.
Essential workup
History and physical examination are mandatory and often sufficient. Triage focuses on abnormal vital signs, altered mentation, or focal deficits. The evaluation is guided by timing, triggers, and telltale signs such as HINTS findings in acute dizziness.
Diagnosis tests and interpretation
Laboratory testing may include serum glucose, hematocrit if anemia is suspected, electrolytes, renal function tests, venous blood gas when carbon monoxide or hypercapnia is considered, urinalysis for infection, and toxicology screening when exposure is suspected.
Imaging includes noncontrast head CT when acute hemorrhage is suspected, recognizing limited sensitivity for posterior circulation ischemia. MRI is indicated when no alternative etiology is found and the HINTS exam is concerning.
Diagnostic procedures may include Dix–Hallpike testing, head thrust testing, and skew deviation assessment. Electrocardiography is used to detect arrhythmia or myocardial ischemia. Lumbar puncture is considered for unexplained headache or infectious signs.
Differential diagnosis
Acute vestibular syndrome includes benign causes such as vestibular neuritis and labyrinthitis and dangerous causes such as cerebellar or brainstem stroke. Episodic vestibular syndrome includes vestibular migraine and transient ischemic attack. Positional vestibular syndrome includes benign paroxysmal positional vertigo and, rarely, central paroxysmal positional vertigo from posterior fossa mass. Chronic vestibular syndrome includes psychiatric causes, medication effects, and rarely posterior fossa tumors.
Treatment
Initial stabilization and therapy
Stabilization is directed by abnormal vital signs or associated systemic illness. Management depends on classification of dizziness and suspected etiology.
Emergency department treatment and procedures
Symptomatic control is provided while evaluation proceeds. If benign paroxysmal positional vertigo is suspected, the Epley maneuver should be performed.
Medication
Symptomatic medications include ondansetron, diazepam, diphenhydramine, meclizine for short-term use only, and promethazine. Response to these agents does not establish etiology.
Follow-up and disposition
Admission criteria
Admission decisions depend on the underlying cause and associated symptoms, particularly concern for stroke, cardiac disease, or systemic illness.
Discharge criteria
Patients with isolated dizziness, normal neurologic and oculomotor examinations, and ability to function safely at home may be discharged with instructions.
Issues for referral
Outpatient referral may be to primary care, otolaryngology, or neurology depending on the suspected cause.
Follow-up recommendations
Patients should avoid driving or operating machinery while symptomatic and rise slowly from sitting or lying positions. They should seek immediate care for new neurologic deficits, signs of infection, acute cardiopulmonary symptoms, or significant fluid losses.
Pearls and pitfalls
The timing-and-triggers approach improves diagnostic accuracy. Advanced age and vascular risk factors increase stroke likelihood. Noncontrast CT is insensitive for acute cerebellar stroke, and cerebellar infarction may present with isolated dizziness. A negative head impulse test is concerning for central pathology. The treatment for benign paroxysmal positional vertigo is the Epley maneuver, not vestibular suppressants.
Basics
Description
Patient descriptions of dizziness (vertigo, lightheadedness, disequilibrium, or nonspecific terms) are often unreliable and should not guide decision making. A safer approach emphasizes associated symptoms, timing, and triggers, followed by a focused physical examination for diagnostic clues. Dizziness is categorized using a “timing and triggers” framework. Acute vestibular syndrome presents with abrupt onset of persistent dizziness. Episodic vestibular syndrome consists of spontaneous episodes lasting minutes to hours. Positional vestibular syndrome causes very brief episodes, typically 20–50 seconds, triggered by head or body position changes. Chronic vestibular syndrome has a gradual onset and persists for weeks to months or longer.
Etiology
General medical causes account for nearly half of cases and include arrhythmias, hypoglycemia and other metabolic disturbances, hypovolemia, sepsis, infections, and low cardiac output states. Otologic or vestibular causes represent about one third and include benign paroxysmal positional vertigo, labyrinthitis, and vestibular neuritis. Neurologic causes include stroke, transient ischemic attack, and vestibular migraine. Psychiatric causes such as anxiety and depression account for a smaller proportion.
Diagnosis
Signs and symptoms
History should define the timing and trigger pattern and assess for red flags. Key questions address onset, persistence versus intermittence, duration of episodes, positional triggers, associated hearing or neurologic symptoms, recent head injury, and new medications. Review of systems should focus on clues to serious disease, including headache suggesting stroke or dissection, ear pain suggesting otitis or mastoiditis, hearing changes suggesting Ménière disease or labyrinthitis, neck pain suggesting vertebral dissection, fever suggesting infection, dyspnea suggesting pulmonary embolism or anemia, chest pain suggesting acute coronary syndrome, fluid losses suggesting hypovolemia, and pregnancy-related complications.
Exacerbation with head motion occurs in both central and peripheral causes; however, dizziness only with head motion in an otherwise asymptomatic patient suggests a peripheral etiology.
Physical examination
Vital signs are assessed, including orthostatic testing. Otoscopic examination, cardiac examination, and a complete neurologic examination are essential. Cranial nerves II–XII should be evaluated with special attention to nystagmus. Gait observation and cerebellar testing are performed. The Dix–Hallpike maneuver is reserved for intermittent symptoms.
The HINTS examination is used only in patients with acute vestibular syndrome and consists of head impulse testing, nystagmus assessment, and testing for skew deviation. In the first 48 hours of symptoms, this exam can be more sensitive than MRI for detecting stroke. A normal head impulse test without corrective saccade suggests a central cause, whereas a corrective saccade suggests a peripheral cause. Direction-changing, vertical, or torsional nystagmus suggests a central etiology, while direction-fixed nystagmus suggests a peripheral cause. A vertical corrective saccade on alternate cover testing indicates a central process. Any concerning component should prompt concern for stroke.
Essential workup
History and physical examination are mandatory and often sufficient. Triage focuses on abnormal vital signs, altered mentation, or focal deficits. The evaluation is guided by timing, triggers, and telltale signs such as HINTS findings in acute dizziness.
Diagnosis tests and interpretation
Laboratory testing may include serum glucose, hematocrit if anemia is suspected, electrolytes, renal function tests, venous blood gas when carbon monoxide or hypercapnia is considered, urinalysis for infection, and toxicology screening when exposure is suspected.
Imaging includes noncontrast head CT when acute hemorrhage is suspected, recognizing limited sensitivity for posterior circulation ischemia. MRI is indicated when no alternative etiology is found and the HINTS exam is concerning.
Diagnostic procedures may include Dix–Hallpike testing, head thrust testing, and skew deviation assessment. Electrocardiography is used to detect arrhythmia or myocardial ischemia. Lumbar puncture is considered for unexplained headache or infectious signs.
Differential diagnosis
Acute vestibular syndrome includes benign causes such as vestibular neuritis and labyrinthitis and dangerous causes such as cerebellar or brainstem stroke. Episodic vestibular syndrome includes vestibular migraine and transient ischemic attack. Positional vestibular syndrome includes benign paroxysmal positional vertigo and, rarely, central paroxysmal positional vertigo from posterior fossa mass. Chronic vestibular syndrome includes psychiatric causes, medication effects, and rarely posterior fossa tumors.
Treatment
Initial stabilization and therapy
Stabilization is directed by abnormal vital signs or associated systemic illness. Management depends on classification of dizziness and suspected etiology.
Emergency department treatment and procedures
Symptomatic control is provided while evaluation proceeds. If benign paroxysmal positional vertigo is suspected, the Epley maneuver should be performed.
Medication
Symptomatic medications include ondansetron, diazepam, diphenhydramine, meclizine for short-term use only, and promethazine. Response to these agents does not establish etiology.
Follow-up and disposition
Admission criteria
Admission decisions depend on the underlying cause and associated symptoms, particularly concern for stroke, cardiac disease, or systemic illness.
Discharge criteria
Patients with isolated dizziness, normal neurologic and oculomotor examinations, and ability to function safely at home may be discharged with instructions.
Issues for referral
Outpatient referral may be to primary care, otolaryngology, or neurology depending on the suspected cause.
Follow-up recommendations
Patients should avoid driving or operating machinery while symptomatic and rise slowly from sitting or lying positions. They should seek immediate care for new neurologic deficits, signs of infection, acute cardiopulmonary symptoms, or significant fluid losses.
Pearls and pitfalls
The timing-and-triggers approach improves diagnostic accuracy. Advanced age and vascular risk factors increase stroke likelihood. Noncontrast CT is insensitive for acute cerebellar stroke, and cerebellar infarction may present with isolated dizziness. A negative head impulse test is concerning for central pathology. The treatment for benign paroxysmal positional vertigo is the Epley maneuver, not vestibular suppressants.
- 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.
