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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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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 – 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 - 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 - 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 – Disseminated Intravascular Coagulation
Basics
Description
Normal coagulation consists of a localized series of reactions involving blood vessels, platelets, and clotting factors. Disseminated intravascular coagulation is a systemic activation of coagulation and fibrinolysis triggered by an underlying disease process. Widespread activation leads to circulation of thrombin and plasmin.
Thrombin activation occurs through tissue factor and factor VIIIa via the extrinsic pathway, resulting in fibrinogen conversion to fibrin monomers that polymerize into fibrin clots within the circulation. These clots cause microvascular and macrovascular thrombosis, leading to peripheral ischemia and end-organ damage. Platelets are consumed within clots, producing thrombocytopenia.
Plasmin activity results in degradation of fibrinogen into fibrin degradation products, which interfere with fibrin polymerization and impair platelet function, worsening bleeding.
Failure of physiologic anticoagulation is necessary for DIC to occur, with impairment of antithrombin III, the protein C system, and tissue factor pathway inhibitor.
Acute DIC represents an uncompensated state where clotting factors are consumed faster than they are replaced, making hemorrhage the dominant feature. Chronic DIC is a compensated state in which factor production keeps pace with consumption, and thrombosis predominates.
Etiology
DIC may be precipitated by numerous conditions. Obstetric causes include retained fetus, amniotic fluid embolism, placental abruption, abortion, eclampsia, and HELLP syndrome. Sepsis is a major trigger and may be caused by gram-negative bacteria through endotoxin, gram-positive organisms through mucopolysaccharides, or other microorganisms including viruses and parasites. Trauma-related causes include crush injury, severe burns, severe head injury, and fat embolism. Malignancy-associated DIC may occur with solid tumors, metastatic disease, or hematologic malignancies such as leukemia. Intravascular hemolysis from transfusion reactions or massive transfusion, organ destruction from severe pancreatitis or hepatic failure, vascular abnormalities such as Kasabach–Merritt syndrome or large aneurysms, and hematologic disorders such as thrombotic thrombocytopenic purpura or immune thrombocytopenic purpura may also precipitate DIC. Miscellaneous causes include snake envenomation and recreational drug use.
Diagnosis
Signs and symptoms
Bleeding manifestations include petechiae, purpura, hemorrhagic bullae, wound bleeding, oozing from venipuncture or arterial lines, epistaxis, hemoptysis, and gastrointestinal bleeding. Thrombotic manifestations include large-vessel thrombosis, microvascular thrombosis with end-organ dysfunction involving the heart, lungs, kidneys, liver, and central nervous system, thrombophlebitis, pulmonary embolism, nonbacterial thrombotic endocarditis, gangrene, and ischemic infarcts of the kidney, liver, bowel, or brain.
Acute DIC is characterized predominantly by hemorrhagic complications, whereas chronic DIC is dominated by thrombotic events.
History should assess prior bleeding disorders, pregnancy status, recent obstetric events, malignancy, and immunocompromised states.
Physical examination may reveal altered mental status, hypotension, tachycardia, tachypnea, pulmonary crackles, gastrointestinal bleeding, abdominal distension, oliguria, hematuria, petechiae, purpura, jaundice, or skin necrosis.
Essential workup
Evaluation depends on the precipitating illness. The diagnosis is often not definitively established in the emergency department and evolves with serial assessment.
Diagnosis tests and interpretation
Laboratory findings typically include a falling platelet count, often below 100,000/mm³, though it may be normal in chronic DIC. Prothrombin time and partial thromboplastin time are usually prolonged but may be normal in chronic disease. Fibrinogen levels are decreased in most acute cases but may remain normal, limiting sensitivity. Fibrin degradation products and D-dimer levels are elevated. Peripheral smear may show schistocytes and thrombocytopenia, particularly in chronic DIC. Renal dysfunction may be reflected by elevated BUN and creatinine, and arterial blood gases assess oxygenation and acid–base status.
The ISTH scoring system incorporates the presence of an underlying disorder, platelet count, fibrin markers, PT prolongation, and fibrinogen level. A score greater than five indicates overt DIC and is associated with increased mortality.
Imaging may include chest radiography for suspected pneumonia, head CT for altered mental status, and obstetric ultrasound in pregnant patients.
Differential diagnosis
Consider inherited factor deficiencies, anticoagulant or drug-induced coagulopathy, hepatic disease, vitamin K deficiency, massive blood loss, platelet dysfunction, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, heparin-induced thrombocytopenia, and immune thrombocytopenic purpura.
Treatment
Initial stabilization and therapy
Management focuses on airway protection, hemodynamic resuscitation, control of bleeding, intravenous access, and restoration of circulating volume. Prompt treatment of the underlying cause is essential, including antibiotics for sepsis, evacuation of retained products of conception, chemotherapy for malignancy, or surgical debridement for trauma.
Emergency department treatment and procedures
Specific therapy for DIC is controversial and should be individualized based on age, hemodynamic status, severity of bleeding, and degree of thrombosis. Early consultation with the admitting service is recommended.
Replacement of depleted blood components may include fresh frozen plasma for prolonged coagulation times, platelet transfusion for severe thrombocytopenia or active bleeding, and cryoprecipitate for severe hypofibrinogenemia. Recombinant factor VIIa has been reported in selected cases, though benefit and safety remain uncertain.
Heparin use is controversial and may be considered when thrombosis predominates, such as in purpura fulminans, acute promyelocytic leukemia, or chronic DIC with large-vessel thrombosis. Activated protein C and antithrombin supplementation have not demonstrated mortality benefit. Antifibrinolytic agents such as aminocaproic acid or tranexamic acid should be reserved for extreme cases with documented excessive fibrinolysis and refractory bleeding.
Medication
Definitive DIC-directed pharmacologic therapy is rarely initiated in the emergency department. Management emphasizes treatment of the underlying cause. Low-dose heparin infusion may be considered when thrombosis predominates.
Follow-up and disposition
Admission criteria
Patients with severe precipitating illness and DIC require intensive care unit admission.
Discharge criteria
There are no discharge criteria for patients with active DIC.
Follow-up recommendations
Ongoing management includes close monitoring of platelet counts, coagulation parameters, and organ function.
Pearls and pitfalls
DIC should be suspected as a complication of severe, life-threatening illness. Early recognition is critical, as the consequences can be catastrophic. Always address and treat the underlying cause, even when bleeding or thrombotic manifestations dominate the clinical presentation.
Basics
Description
Normal coagulation consists of a localized series of reactions involving blood vessels, platelets, and clotting factors. Disseminated intravascular coagulation is a systemic activation of coagulation and fibrinolysis triggered by an underlying disease process. Widespread activation leads to circulation of thrombin and plasmin.
Thrombin activation occurs through tissue factor and factor VIIIa via the extrinsic pathway, resulting in fibrinogen conversion to fibrin monomers that polymerize into fibrin clots within the circulation. These clots cause microvascular and macrovascular thrombosis, leading to peripheral ischemia and end-organ damage. Platelets are consumed within clots, producing thrombocytopenia.
Plasmin activity results in degradation of fibrinogen into fibrin degradation products, which interfere with fibrin polymerization and impair platelet function, worsening bleeding.
Failure of physiologic anticoagulation is necessary for DIC to occur, with impairment of antithrombin III, the protein C system, and tissue factor pathway inhibitor.
Acute DIC represents an uncompensated state where clotting factors are consumed faster than they are replaced, making hemorrhage the dominant feature. Chronic DIC is a compensated state in which factor production keeps pace with consumption, and thrombosis predominates.
Etiology
DIC may be precipitated by numerous conditions. Obstetric causes include retained fetus, amniotic fluid embolism, placental abruption, abortion, eclampsia, and HELLP syndrome. Sepsis is a major trigger and may be caused by gram-negative bacteria through endotoxin, gram-positive organisms through mucopolysaccharides, or other microorganisms including viruses and parasites. Trauma-related causes include crush injury, severe burns, severe head injury, and fat embolism. Malignancy-associated DIC may occur with solid tumors, metastatic disease, or hematologic malignancies such as leukemia. Intravascular hemolysis from transfusion reactions or massive transfusion, organ destruction from severe pancreatitis or hepatic failure, vascular abnormalities such as Kasabach–Merritt syndrome or large aneurysms, and hematologic disorders such as thrombotic thrombocytopenic purpura or immune thrombocytopenic purpura may also precipitate DIC. Miscellaneous causes include snake envenomation and recreational drug use.
Diagnosis
Signs and symptoms
Bleeding manifestations include petechiae, purpura, hemorrhagic bullae, wound bleeding, oozing from venipuncture or arterial lines, epistaxis, hemoptysis, and gastrointestinal bleeding. Thrombotic manifestations include large-vessel thrombosis, microvascular thrombosis with end-organ dysfunction involving the heart, lungs, kidneys, liver, and central nervous system, thrombophlebitis, pulmonary embolism, nonbacterial thrombotic endocarditis, gangrene, and ischemic infarcts of the kidney, liver, bowel, or brain.
Acute DIC is characterized predominantly by hemorrhagic complications, whereas chronic DIC is dominated by thrombotic events.
History should assess prior bleeding disorders, pregnancy status, recent obstetric events, malignancy, and immunocompromised states.
Physical examination may reveal altered mental status, hypotension, tachycardia, tachypnea, pulmonary crackles, gastrointestinal bleeding, abdominal distension, oliguria, hematuria, petechiae, purpura, jaundice, or skin necrosis.
Essential workup
Evaluation depends on the precipitating illness. The diagnosis is often not definitively established in the emergency department and evolves with serial assessment.
Diagnosis tests and interpretation
Laboratory findings typically include a falling platelet count, often below 100,000/mm³, though it may be normal in chronic DIC. Prothrombin time and partial thromboplastin time are usually prolonged but may be normal in chronic disease. Fibrinogen levels are decreased in most acute cases but may remain normal, limiting sensitivity. Fibrin degradation products and D-dimer levels are elevated. Peripheral smear may show schistocytes and thrombocytopenia, particularly in chronic DIC. Renal dysfunction may be reflected by elevated BUN and creatinine, and arterial blood gases assess oxygenation and acid–base status.
The ISTH scoring system incorporates the presence of an underlying disorder, platelet count, fibrin markers, PT prolongation, and fibrinogen level. A score greater than five indicates overt DIC and is associated with increased mortality.
Imaging may include chest radiography for suspected pneumonia, head CT for altered mental status, and obstetric ultrasound in pregnant patients.
Differential diagnosis
Consider inherited factor deficiencies, anticoagulant or drug-induced coagulopathy, hepatic disease, vitamin K deficiency, massive blood loss, platelet dysfunction, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, heparin-induced thrombocytopenia, and immune thrombocytopenic purpura.
Treatment
Initial stabilization and therapy
Management focuses on airway protection, hemodynamic resuscitation, control of bleeding, intravenous access, and restoration of circulating volume. Prompt treatment of the underlying cause is essential, including antibiotics for sepsis, evacuation of retained products of conception, chemotherapy for malignancy, or surgical debridement for trauma.
Emergency department treatment and procedures
Specific therapy for DIC is controversial and should be individualized based on age, hemodynamic status, severity of bleeding, and degree of thrombosis. Early consultation with the admitting service is recommended.
Replacement of depleted blood components may include fresh frozen plasma for prolonged coagulation times, platelet transfusion for severe thrombocytopenia or active bleeding, and cryoprecipitate for severe hypofibrinogenemia. Recombinant factor VIIa has been reported in selected cases, though benefit and safety remain uncertain.
Heparin use is controversial and may be considered when thrombosis predominates, such as in purpura fulminans, acute promyelocytic leukemia, or chronic DIC with large-vessel thrombosis. Activated protein C and antithrombin supplementation have not demonstrated mortality benefit. Antifibrinolytic agents such as aminocaproic acid or tranexamic acid should be reserved for extreme cases with documented excessive fibrinolysis and refractory bleeding.
Medication
Definitive DIC-directed pharmacologic therapy is rarely initiated in the emergency department. Management emphasizes treatment of the underlying cause. Low-dose heparin infusion may be considered when thrombosis predominates.
Follow-up and disposition
Admission criteria
Patients with severe precipitating illness and DIC require intensive care unit admission.
Discharge criteria
There are no discharge criteria for patients with active DIC.
Follow-up recommendations
Ongoing management includes close monitoring of platelet counts, coagulation parameters, and organ function.
Pearls and pitfalls
DIC should be suspected as a complication of severe, life-threatening illness. Early recognition is critical, as the consequences can be catastrophic. Always address and treat the underlying cause, even when bleeding or thrombotic manifestations dominate the clinical presentation.
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Emergency and Acute Medicine – Diverticulitis
Basics
Description
Diverticulitis results from micro- or macroscopic perforation of a colonic diverticulum. The condition is classified as uncomplicated in approximately 75% of cases and complicated in the remainder. Its incidence is increasing worldwide, and obesity is a recognized risk factor.
Etiology
Fecal material may become trapped within a diverticulum and harden to form a fecalith, leading to increased intraluminal pressure. Progressive erosion of the diverticular wall causes inflammation, focal necrosis, and eventual perforation.
Microperforation leads to uncomplicated diverticulitis, characterized by colonic wall thickening and surrounding inflammatory changes, such as fat stranding on computed tomography.
Macroperforation results in complicated diverticulitis, which may include abscess formation, bowel obstruction, fistula formation after recurrent attacks, and peritonitis. Colovesical fistula is the most common fistula type and presents with dysuria, urinary frequency, urgency, pneumaturia, and fecaluria.
Diagnosis
Signs and symptoms
Symptoms typically evolve over several days, and nearly half of patients report prior similar episodes. Left lower quadrant abdominal pain occurs in about 70% of cases in Western populations, whereas right lower quadrant pain is more common in Asian patients. Pain is often initially vague before localizing. Associated symptoms include nausea, vomiting, constipation, diarrhea, and urinary complaints.
On examination, patients may have low-grade fever and left lower quadrant tenderness, with an occasional palpable mass representing a phlegmon. Abdominal distension and variable bowel sounds may be present. Rectal tenderness with heme-positive stool can occur, although massive rectal bleeding is rare. Peritoneal signs suggest perforation. Elderly, immunocompromised patients, or those on corticosteroids may have minimal findings.
Essential workup
Initial evaluation includes complete blood count and urinalysis. Blood cultures and lactate levels are obtained if sepsis is suspected. Computed tomography of the abdomen and pelvis is the preferred diagnostic modality, as it confirms diverticulitis, assesses severity, and identifies alternative diagnoses. Intravenous and oral or rectal contrast enhance diagnostic accuracy, while barium contrast should be avoided when perforation is suspected. Plain abdominal and chest radiographs may identify free air or obstruction.
Diagnosis tests and interpretation
Leukocytosis is common but not universal. Urinalysis may reveal sterile pyuria, and the presence of colonic bacteria suggests a colovesical fistula. Imaging findings on CT include colonic wall thickening greater than 5 mm, pericolic fat inflammation, and abscess formation. CT-guided percutaneous drainage of localized abscesses may avoid surgery. Endoscopy is not required during the acute phase, though rigid sigmoidoscopy may help exclude alternative diagnoses. Ultrasonography can identify wall thickening or abscesses but is operator dependent. Barium enema is reserved for post-resolution evaluation to exclude malignancy or fistula.
Differential diagnosis
Consider colon carcinoma with perforation, ischemic or infectious colitis, appendicitis, inflammatory bowel disease, irritable bowel syndrome, gynecologic pathology, pancreatic disease, pelvic inflammatory disease, peptic ulcer disease, and renal colic.
Treatment
Prehospital care
Initial management includes intravenous fluid administration.
Initial stabilization and therapy
Resuscitate with isotonic fluids, institute bowel rest with nothing by mouth or clear liquids, and place a nasogastric tube if persistent vomiting or bowel obstruction is suspected.
Emergency department treatment and procedures
Uncomplicated diverticulitis is usually managed medically, though up to 30% of patients may eventually require surgery. Complicated diverticulitis often requires percutaneous drainage or surgical intervention. Analgesia may include anticholinergics such as dicyclomine for colonic spasm or opioids for severe pain, avoiding opioids in unstable patients.
Antibiotics should cover gram-negative aerobic and anaerobic organisms. Mild uncomplicated cases may be treated as outpatients with oral regimens such as amoxicillin-clavulanate or trimethoprim-sulfamethoxazole plus metronidazole. Inpatient regimens include third-generation cephalosporins with metronidazole, beta-lactam/beta-lactamase inhibitor combinations, or carbapenems for severe disease.
Emergent surgery is indicated for generalized peritonitis due to perforation. Elective surgery may be considered after recurrent attacks, fistula formation, obstruction, or failure of medical therapy. Percutaneous drainage is appropriate for well-circumscribed abscesses.
Medication
Common agents include amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, ciprofloxacin, metronidazole, third-generation cephalosporins, beta-lactam/beta-lactamase inhibitors, and carbapenems, selected according to disease severity and patient factors.
Follow-up and disposition
Admission criteria
Hospitalization is indicated for intractable pain or vomiting, high fever, peritonitis, failure of outpatient therapy, severe disease on imaging, significant leukocytosis, immunocompromised status, recurrent episodes, major comorbidities, extremes of age, or diagnostic uncertainty.
Discharge criteria
Patients with mild disease, minimal comorbidities, and ability to tolerate oral intake may be discharged with close follow-up.
Follow-up recommendations
Patients should begin with clear liquids and advance diet as symptoms improve, usually within three days. They should seek care for worsening pain, fever, or inability to tolerate oral intake. Colonoscopy or contrast studies are recommended after recovery to exclude malignancy. Avoidance of seeds and nuts is not required.
Pearls and pitfalls
Computed tomography distinguishes uncomplicated from complicated diverticulitis and guides management. Most uncomplicated cases do not progress to complicated disease, and multiple attacks do not necessarily predict worsening severity. Severe findings on initial imaging are associated with higher risk of treatment failure and complications.
Basics
Description
Diverticulitis results from micro- or macroscopic perforation of a colonic diverticulum. The condition is classified as uncomplicated in approximately 75% of cases and complicated in the remainder. Its incidence is increasing worldwide, and obesity is a recognized risk factor.
Etiology
Fecal material may become trapped within a diverticulum and harden to form a fecalith, leading to increased intraluminal pressure. Progressive erosion of the diverticular wall causes inflammation, focal necrosis, and eventual perforation.
Microperforation leads to uncomplicated diverticulitis, characterized by colonic wall thickening and surrounding inflammatory changes, such as fat stranding on computed tomography.
Macroperforation results in complicated diverticulitis, which may include abscess formation, bowel obstruction, fistula formation after recurrent attacks, and peritonitis. Colovesical fistula is the most common fistula type and presents with dysuria, urinary frequency, urgency, pneumaturia, and fecaluria.
Diagnosis
Signs and symptoms
Symptoms typically evolve over several days, and nearly half of patients report prior similar episodes. Left lower quadrant abdominal pain occurs in about 70% of cases in Western populations, whereas right lower quadrant pain is more common in Asian patients. Pain is often initially vague before localizing. Associated symptoms include nausea, vomiting, constipation, diarrhea, and urinary complaints.
On examination, patients may have low-grade fever and left lower quadrant tenderness, with an occasional palpable mass representing a phlegmon. Abdominal distension and variable bowel sounds may be present. Rectal tenderness with heme-positive stool can occur, although massive rectal bleeding is rare. Peritoneal signs suggest perforation. Elderly, immunocompromised patients, or those on corticosteroids may have minimal findings.
Essential workup
Initial evaluation includes complete blood count and urinalysis. Blood cultures and lactate levels are obtained if sepsis is suspected. Computed tomography of the abdomen and pelvis is the preferred diagnostic modality, as it confirms diverticulitis, assesses severity, and identifies alternative diagnoses. Intravenous and oral or rectal contrast enhance diagnostic accuracy, while barium contrast should be avoided when perforation is suspected. Plain abdominal and chest radiographs may identify free air or obstruction.
Diagnosis tests and interpretation
Leukocytosis is common but not universal. Urinalysis may reveal sterile pyuria, and the presence of colonic bacteria suggests a colovesical fistula. Imaging findings on CT include colonic wall thickening greater than 5 mm, pericolic fat inflammation, and abscess formation. CT-guided percutaneous drainage of localized abscesses may avoid surgery. Endoscopy is not required during the acute phase, though rigid sigmoidoscopy may help exclude alternative diagnoses. Ultrasonography can identify wall thickening or abscesses but is operator dependent. Barium enema is reserved for post-resolution evaluation to exclude malignancy or fistula.
Differential diagnosis
Consider colon carcinoma with perforation, ischemic or infectious colitis, appendicitis, inflammatory bowel disease, irritable bowel syndrome, gynecologic pathology, pancreatic disease, pelvic inflammatory disease, peptic ulcer disease, and renal colic.
Treatment
Prehospital care
Initial management includes intravenous fluid administration.
Initial stabilization and therapy
Resuscitate with isotonic fluids, institute bowel rest with nothing by mouth or clear liquids, and place a nasogastric tube if persistent vomiting or bowel obstruction is suspected.
Emergency department treatment and procedures
Uncomplicated diverticulitis is usually managed medically, though up to 30% of patients may eventually require surgery. Complicated diverticulitis often requires percutaneous drainage or surgical intervention. Analgesia may include anticholinergics such as dicyclomine for colonic spasm or opioids for severe pain, avoiding opioids in unstable patients.
Antibiotics should cover gram-negative aerobic and anaerobic organisms. Mild uncomplicated cases may be treated as outpatients with oral regimens such as amoxicillin-clavulanate or trimethoprim-sulfamethoxazole plus metronidazole. Inpatient regimens include third-generation cephalosporins with metronidazole, beta-lactam/beta-lactamase inhibitor combinations, or carbapenems for severe disease.
Emergent surgery is indicated for generalized peritonitis due to perforation. Elective surgery may be considered after recurrent attacks, fistula formation, obstruction, or failure of medical therapy. Percutaneous drainage is appropriate for well-circumscribed abscesses.
Medication
Common agents include amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, ciprofloxacin, metronidazole, third-generation cephalosporins, beta-lactam/beta-lactamase inhibitors, and carbapenems, selected according to disease severity and patient factors.
Follow-up and disposition
Admission criteria
Hospitalization is indicated for intractable pain or vomiting, high fever, peritonitis, failure of outpatient therapy, severe disease on imaging, significant leukocytosis, immunocompromised status, recurrent episodes, major comorbidities, extremes of age, or diagnostic uncertainty.
Discharge criteria
Patients with mild disease, minimal comorbidities, and ability to tolerate oral intake may be discharged with close follow-up.
Follow-up recommendations
Patients should begin with clear liquids and advance diet as symptoms improve, usually within three days. They should seek care for worsening pain, fever, or inability to tolerate oral intake. Colonoscopy or contrast studies are recommended after recovery to exclude malignancy. Avoidance of seeds and nuts is not required.
Pearls and pitfalls
Computed tomography distinguishes uncomplicated from complicated diverticulitis and guides management. Most uncomplicated cases do not progress to complicated disease, and multiple attacks do not necessarily predict worsening severity. Severe findings on initial imaging are associated with higher risk of treatment failure and complications.
- Published on
Emergency and Acute Medicine – Disulfiram Reaction
Basics
Description
Disulfiram inhibits multiple enzymatic pathways, and its active metabolites contribute additional toxic effects. The classic disulfiram–ethanol reaction usually occurs 8–12 hours after drug ingestion and is not expected beyond 24 hours after dosing. Disulfiram competitively and irreversibly inhibits aldehyde dehydrogenase, blocking ethanol metabolism and causing accumulation of acetaldehyde. Acetaldehyde triggers histamine release, leading to vasodilation and hypotension. Severe reactions may occur at ethanol levels as low as 50–100 mg/dL, and severity correlates with the amount of ethanol consumed.
Disulfiram also inhibits dopamine β-hydroxylase, reducing conversion of dopamine to norepinephrine. Excess dopamine may contribute to behavioral changes, while norepinephrine depletion may worsen hypotension. Its metabolite, carbon disulfide, interferes with pyridoxal-5-phosphate, reducing pyridoxine availability for γ-aminobutyric acid synthesis and potentially lowering the seizure threshold. Carbon disulfide is additionally cardiotoxic, hepatotoxic, inhibits CYP2E1, chelates essential metals, and may cause dose- and duration-dependent peripheral neuropathy.
Etiology
Disulfiram is prescribed as a deterrent for chronic alcohol use disorder, and many patients wear medical alert identification. Disulfiram-like reactions may also occur with other agents, including metronidazole; certain cephalosporins with an N-methylthiotetrazole side chain such as cefoperazone, cefotetan, and cefmetazole; nitrofurantoin; sulfonylurea hypoglycemics; industrial exposures such as carbon disulfide and hydrogen sulfide; and mushrooms including Coprinus atramentarius and Clitocybe clavipes.
Diagnosis
Signs and symptoms
Disulfiram–ethanol reactions commonly present with hypotension, tachycardia, tachypnea, flushing of the face, neck, and torso, pruritus, diaphoresis, warmth, nausea, vomiting, abdominal pain, diarrhea, headache, ataxia, confusion, anxiety, and dizziness. Severe cases may involve dyspnea, pulmonary edema, chest pain, dysrhythmias, and myocardial infarction.
Disulfiram overdose is uncommon with ingestions under 3 g, while doses of 10–30 g may be fatal. Presentations may mimic shock or sepsis and include tachycardia, hypotension, tachypnea, abdominal pain, diarrhea, garlic- or rotten-egg breath, agitation, irritability, ataxia, dysarthria, hallucinations, lethargy, coma, seizures, flaccidity, or parkinsonian features.
History of disulfiram use, ingestion of causative agents, or ethanol exposure—including alcohol-containing foods, medications, or mouthwash—is key. Physical examination often reveals hemodynamic instability, flushing, diaphoresis, pulmonary edema, diffuse abdominal tenderness, altered mental status, cerebellar signs, or seizures.
Essential workup
Suspect a disulfiram–ethanol reaction when characteristic symptoms occur in a patient treated for alcohol use disorder with recent ethanol exposure.
Diagnosis tests and interpretation
Laboratory evaluation includes ethanol level, electrolytes, renal function, glucose, and liver function tests if hepatitis is suspected. Creatine phosphokinase should be checked if seizures or agitation raise concern for rhabdomyolysis. Urinalysis may detect myoglobin. Serum drug levels are not clinically useful.
Electrocardiography evaluates ischemia or dysrhythmias. Neuroimaging is indicated for altered mental status or seizures, as basal ganglia ischemia has been reported. EEG may show diffuse slowing in severe toxicity.
Differential diagnosis
Consider sepsis, meningitis or encephalitis, cardiogenic shock from acute coronary syndrome, anaphylactoid or anaphylactic reactions, gastroenteritis or pancreatitis with dehydration, and ethanol withdrawal.
Treatment
Prehospital care
Initial management includes airway assessment, intravenous access, fluid resuscitation if pulmonary edema is absent, and rapid glucose testing.
Initial stabilization and therapy
Provide airway protection as needed, supplemental oxygen, mechanical ventilation if required, aggressive isotonic fluid resuscitation for hypotension, and vasopressor support with norepinephrine for refractory shock.
Emergency department treatment and procedures
Management is primarily supportive, as no specific antidote exists. Activated charcoal may be considered after disulfiram overdose if the airway is protected and vomiting is controlled; gastric lavage and whole-bowel irrigation are not indicated. Flushing may be treated with antihistamines and prostaglandin inhibitors. Antiemetics are used for persistent vomiting. Seizures are treated with benzodiazepines, and pyridoxine supplementation is recommended.
Fomepizole is not indicated for routine reactions but may improve hemodynamics in severe overdoses. Hemodialysis may be considered after massive ingestion with refractory hypotension, though evidence of benefit is limited.
Medication
Commonly used agents include benzodiazepines for seizures, antihistamines for flushing and pruritus, antiemetics for nausea and vomiting, norepinephrine for refractory hypotension, and intravenous pyridoxine.
Follow-up and disposition
Admission criteria
Intensive care admission is required for coma, mechanical ventilation, refractory hypotension needing vasopressors, cardiac ischemia, uncontrolled seizures, severe agitation, persistent gastrointestinal symptoms, or in elderly patients and those with cardiac disease.
Discharge criteria
Patients with mild reactions that resolve after 8–12 hours of observation may be discharged. Ethanol abstinence is required for at least two weeks after the last dose of disulfiram or related agents, as reactions may recur for up to 7–10 days.
Follow-up recommendations
Psychiatric follow-up is indicated for intentional overdose, and detoxification or addiction follow-up is recommended after disulfiram–ethanol reactions to monitor for hepatic or neurologic sequelae.
Pearls and pitfalls
Patients prescribed disulfiram or drugs with disulfiram-like effects must avoid all alcohol sources, including mouthwash, hand sanitizers, aftershaves, cough syrups, and elixir-based medications. Abstinence should continue for several days beyond completion of therapy to minimize reaction risk.
Basics
Description
Disulfiram inhibits multiple enzymatic pathways, and its active metabolites contribute additional toxic effects. The classic disulfiram–ethanol reaction usually occurs 8–12 hours after drug ingestion and is not expected beyond 24 hours after dosing. Disulfiram competitively and irreversibly inhibits aldehyde dehydrogenase, blocking ethanol metabolism and causing accumulation of acetaldehyde. Acetaldehyde triggers histamine release, leading to vasodilation and hypotension. Severe reactions may occur at ethanol levels as low as 50–100 mg/dL, and severity correlates with the amount of ethanol consumed.
Disulfiram also inhibits dopamine β-hydroxylase, reducing conversion of dopamine to norepinephrine. Excess dopamine may contribute to behavioral changes, while norepinephrine depletion may worsen hypotension. Its metabolite, carbon disulfide, interferes with pyridoxal-5-phosphate, reducing pyridoxine availability for γ-aminobutyric acid synthesis and potentially lowering the seizure threshold. Carbon disulfide is additionally cardiotoxic, hepatotoxic, inhibits CYP2E1, chelates essential metals, and may cause dose- and duration-dependent peripheral neuropathy.
Etiology
Disulfiram is prescribed as a deterrent for chronic alcohol use disorder, and many patients wear medical alert identification. Disulfiram-like reactions may also occur with other agents, including metronidazole; certain cephalosporins with an N-methylthiotetrazole side chain such as cefoperazone, cefotetan, and cefmetazole; nitrofurantoin; sulfonylurea hypoglycemics; industrial exposures such as carbon disulfide and hydrogen sulfide; and mushrooms including Coprinus atramentarius and Clitocybe clavipes.
Diagnosis
Signs and symptoms
Disulfiram–ethanol reactions commonly present with hypotension, tachycardia, tachypnea, flushing of the face, neck, and torso, pruritus, diaphoresis, warmth, nausea, vomiting, abdominal pain, diarrhea, headache, ataxia, confusion, anxiety, and dizziness. Severe cases may involve dyspnea, pulmonary edema, chest pain, dysrhythmias, and myocardial infarction.
Disulfiram overdose is uncommon with ingestions under 3 g, while doses of 10–30 g may be fatal. Presentations may mimic shock or sepsis and include tachycardia, hypotension, tachypnea, abdominal pain, diarrhea, garlic- or rotten-egg breath, agitation, irritability, ataxia, dysarthria, hallucinations, lethargy, coma, seizures, flaccidity, or parkinsonian features.
History of disulfiram use, ingestion of causative agents, or ethanol exposure—including alcohol-containing foods, medications, or mouthwash—is key. Physical examination often reveals hemodynamic instability, flushing, diaphoresis, pulmonary edema, diffuse abdominal tenderness, altered mental status, cerebellar signs, or seizures.
Essential workup
Suspect a disulfiram–ethanol reaction when characteristic symptoms occur in a patient treated for alcohol use disorder with recent ethanol exposure.
Diagnosis tests and interpretation
Laboratory evaluation includes ethanol level, electrolytes, renal function, glucose, and liver function tests if hepatitis is suspected. Creatine phosphokinase should be checked if seizures or agitation raise concern for rhabdomyolysis. Urinalysis may detect myoglobin. Serum drug levels are not clinically useful.
Electrocardiography evaluates ischemia or dysrhythmias. Neuroimaging is indicated for altered mental status or seizures, as basal ganglia ischemia has been reported. EEG may show diffuse slowing in severe toxicity.
Differential diagnosis
Consider sepsis, meningitis or encephalitis, cardiogenic shock from acute coronary syndrome, anaphylactoid or anaphylactic reactions, gastroenteritis or pancreatitis with dehydration, and ethanol withdrawal.
Treatment
Prehospital care
Initial management includes airway assessment, intravenous access, fluid resuscitation if pulmonary edema is absent, and rapid glucose testing.
Initial stabilization and therapy
Provide airway protection as needed, supplemental oxygen, mechanical ventilation if required, aggressive isotonic fluid resuscitation for hypotension, and vasopressor support with norepinephrine for refractory shock.
Emergency department treatment and procedures
Management is primarily supportive, as no specific antidote exists. Activated charcoal may be considered after disulfiram overdose if the airway is protected and vomiting is controlled; gastric lavage and whole-bowel irrigation are not indicated. Flushing may be treated with antihistamines and prostaglandin inhibitors. Antiemetics are used for persistent vomiting. Seizures are treated with benzodiazepines, and pyridoxine supplementation is recommended.
Fomepizole is not indicated for routine reactions but may improve hemodynamics in severe overdoses. Hemodialysis may be considered after massive ingestion with refractory hypotension, though evidence of benefit is limited.
Medication
Commonly used agents include benzodiazepines for seizures, antihistamines for flushing and pruritus, antiemetics for nausea and vomiting, norepinephrine for refractory hypotension, and intravenous pyridoxine.
Follow-up and disposition
Admission criteria
Intensive care admission is required for coma, mechanical ventilation, refractory hypotension needing vasopressors, cardiac ischemia, uncontrolled seizures, severe agitation, persistent gastrointestinal symptoms, or in elderly patients and those with cardiac disease.
Discharge criteria
Patients with mild reactions that resolve after 8–12 hours of observation may be discharged. Ethanol abstinence is required for at least two weeks after the last dose of disulfiram or related agents, as reactions may recur for up to 7–10 days.
Follow-up recommendations
Psychiatric follow-up is indicated for intentional overdose, and detoxification or addiction follow-up is recommended after disulfiram–ethanol reactions to monitor for hepatic or neurologic sequelae.
Pearls and pitfalls
Patients prescribed disulfiram or drugs with disulfiram-like effects must avoid all alcohol sources, including mouthwash, hand sanitizers, aftershaves, cough syrups, and elixir-based medications. Abstinence should continue for several days beyond completion of therapy to minimize reaction risk.
- Published on
Emergency And Acute Medicine - Eczema / Atopic Dermatitis
Core Overview
Atopic dermatitis is the most frequent cause of eczema, and the terms are commonly used interchangeably. It is strongly associated with other atopic conditions, including asthma and allergic rhinitis. The term eczema refers to spongiosis, a process in which microscopic vesicles form within the epidermis and subsequently rupture, producing erythema, edema, crusting, and oozing. Intense pruritus is a hallmark feature. Repeated rubbing and scratching lead to skin breakdown with weeping and crust formation, while chronic disease results in epidermal hyperplasia and hyperkeratosis. Approximately 90% of patients are colonized with Staphylococcus aureus, predisposing them to recurrent secondary infections.
Predisposing Factors
Genetic susceptibility plays a major role, particularly a family history of atopic disease such as asthma or allergic rhinitis. Mutations in the filaggrin protein, a key component of the epidermal barrier, are strongly associated with disease development.
Underlying Mechanism
Atopic dermatitis arises from impaired epidermal barrier function, allowing allergens and irritants to penetrate the skin and trigger immune-mediated inflammation.
Clinical Features
Patients typically report a pruritic rash and a personal or family history of atopy. Diagnostic criteria emphasize pruritus plus additional features such as flexural involvement, history of asthma or allergic rhinitis, chronically dry skin, onset before two years of age, and visible flexural dermatitis. Other commonly reported findings include recurrent skin infections, itching with sweating, intolerance to wool or lipid solvents, and symptom exacerbation during periods of stress.
Physical Examination Findings
Dermatitis is commonly located in areas of friction or movement, including flexural surfaces, hands, and feet. Skin findings reflect barrier disruption with dryness, weeping, oozing, and crusting, along with inflammatory changes such as maculopapular erythema and edema. Chronic scratching leads to excoriations, fissuring, lichenification, and hyperkeratosis. Additional characteristic signs may include ichthyosis, palmar hyperlinearity, keratosis pilaris, hand or foot dermatitis, nipple involvement, cheilitis, Dennie–Morgan infraorbital folds, periocular darkening, facial pallor or erythema, pityriasis alba, perifollicular accentuation, and white dermographism or delayed blanching.
Special Pediatric Considerations
Most cases begin early in life, with approximately 70% presenting within the first five years. Only a small proportion begin in adulthood. A significant percentage of affected children later develop asthma or allergic rhinitis. In infants, lesions classically involve the face, scalp, and extensor surfaces.
Essential Evaluation
Diagnosis is primarily clinical and based on history and physical examination.
Diagnostic Testing Considerations
Laboratory studies are generally unnecessary in the emergency setting. Although IgE levels are often elevated, routine testing is not required. Specialized testing such as allergen-specific IgE assays or patch testing is typically reserved for outpatient evaluation, particularly when allergic contact dermatitis is suspected.
Conditions To Differentiate From
Important alternative diagnoses include seborrheic dermatitis, lichen simplex chronicus, allergic or irritant contact dermatitis, psoriasis, dyshidrotic eczema, ichthyosis, and scabies.
Emergency Department Management
Mild disease or involvement of the head and neck is treated with low-potency topical corticosteroids such as hydrocortisone and regular emollient application. Moderate to severe disease affecting the trunk or extremities may require mid- to high-potency topical corticosteroids. Severe head and neck involvement is best managed with topical calcineurin inhibitors such as tacrolimus or pimecrolimus. First-generation antihistamines may be used to reduce pruritus, though their efficacy is limited. Supportive measures include avoiding excessive bathing, using tepid water and mild soaps, and applying emollients frequently. Suspected bacterial superinfection should prompt treatment with appropriate antibiotics, with consideration for methicillin-resistant Staphylococcus aureus.
Pharmacologic Options
Emollients such as petrolatum-based ointments are foundational therapy. Topical corticosteroids are selected based on disease severity and location. Calcineurin inhibitors are useful alternatives for sensitive areas such as the face. Antihistamines may aid symptom control. Antibiotics are indicated when secondary infection is present.
Disposition And Referral Planning
Patients with refractory or severe disease should be referred for dermatology follow-up.
Ongoing Care Guidance
Patients should be counseled regarding potential adverse effects of therapy. Prolonged use of high-potency topical corticosteroids can lead to skin atrophy. Calcineurin inhibitors may cause transient stinging during initial use, and long-term safety considerations should be discussed.
Key Clinical Insights And Common Errors
Always consider secondary bacterial infection, as colonization with S. aureus is common. Use topical calcineurin inhibitors preferentially for moderate to severe disease of the face and neck. Lotions may worsen dryness due to low lipid content; thick creams or ointments are preferred. Avoid using medium- or high-potency topical corticosteroids on the face or eyelids to prevent complications.
Core Overview
Atopic dermatitis is the most frequent cause of eczema, and the terms are commonly used interchangeably. It is strongly associated with other atopic conditions, including asthma and allergic rhinitis. The term eczema refers to spongiosis, a process in which microscopic vesicles form within the epidermis and subsequently rupture, producing erythema, edema, crusting, and oozing. Intense pruritus is a hallmark feature. Repeated rubbing and scratching lead to skin breakdown with weeping and crust formation, while chronic disease results in epidermal hyperplasia and hyperkeratosis. Approximately 90% of patients are colonized with Staphylococcus aureus, predisposing them to recurrent secondary infections.
Predisposing Factors
Genetic susceptibility plays a major role, particularly a family history of atopic disease such as asthma or allergic rhinitis. Mutations in the filaggrin protein, a key component of the epidermal barrier, are strongly associated with disease development.
Underlying Mechanism
Atopic dermatitis arises from impaired epidermal barrier function, allowing allergens and irritants to penetrate the skin and trigger immune-mediated inflammation.
Clinical Features
Patients typically report a pruritic rash and a personal or family history of atopy. Diagnostic criteria emphasize pruritus plus additional features such as flexural involvement, history of asthma or allergic rhinitis, chronically dry skin, onset before two years of age, and visible flexural dermatitis. Other commonly reported findings include recurrent skin infections, itching with sweating, intolerance to wool or lipid solvents, and symptom exacerbation during periods of stress.
Physical Examination Findings
Dermatitis is commonly located in areas of friction or movement, including flexural surfaces, hands, and feet. Skin findings reflect barrier disruption with dryness, weeping, oozing, and crusting, along with inflammatory changes such as maculopapular erythema and edema. Chronic scratching leads to excoriations, fissuring, lichenification, and hyperkeratosis. Additional characteristic signs may include ichthyosis, palmar hyperlinearity, keratosis pilaris, hand or foot dermatitis, nipple involvement, cheilitis, Dennie–Morgan infraorbital folds, periocular darkening, facial pallor or erythema, pityriasis alba, perifollicular accentuation, and white dermographism or delayed blanching.
Special Pediatric Considerations
Most cases begin early in life, with approximately 70% presenting within the first five years. Only a small proportion begin in adulthood. A significant percentage of affected children later develop asthma or allergic rhinitis. In infants, lesions classically involve the face, scalp, and extensor surfaces.
Essential Evaluation
Diagnosis is primarily clinical and based on history and physical examination.
Diagnostic Testing Considerations
Laboratory studies are generally unnecessary in the emergency setting. Although IgE levels are often elevated, routine testing is not required. Specialized testing such as allergen-specific IgE assays or patch testing is typically reserved for outpatient evaluation, particularly when allergic contact dermatitis is suspected.
Conditions To Differentiate From
Important alternative diagnoses include seborrheic dermatitis, lichen simplex chronicus, allergic or irritant contact dermatitis, psoriasis, dyshidrotic eczema, ichthyosis, and scabies.
Emergency Department Management
Mild disease or involvement of the head and neck is treated with low-potency topical corticosteroids such as hydrocortisone and regular emollient application. Moderate to severe disease affecting the trunk or extremities may require mid- to high-potency topical corticosteroids. Severe head and neck involvement is best managed with topical calcineurin inhibitors such as tacrolimus or pimecrolimus. First-generation antihistamines may be used to reduce pruritus, though their efficacy is limited. Supportive measures include avoiding excessive bathing, using tepid water and mild soaps, and applying emollients frequently. Suspected bacterial superinfection should prompt treatment with appropriate antibiotics, with consideration for methicillin-resistant Staphylococcus aureus.
Pharmacologic Options
Emollients such as petrolatum-based ointments are foundational therapy. Topical corticosteroids are selected based on disease severity and location. Calcineurin inhibitors are useful alternatives for sensitive areas such as the face. Antihistamines may aid symptom control. Antibiotics are indicated when secondary infection is present.
Disposition And Referral Planning
Patients with refractory or severe disease should be referred for dermatology follow-up.
Ongoing Care Guidance
Patients should be counseled regarding potential adverse effects of therapy. Prolonged use of high-potency topical corticosteroids can lead to skin atrophy. Calcineurin inhibitors may cause transient stinging during initial use, and long-term safety considerations should be discussed.
Key Clinical Insights And Common Errors
Always consider secondary bacterial infection, as colonization with S. aureus is common. Use topical calcineurin inhibitors preferentially for moderate to severe disease of the face and neck. Lotions may worsen dryness due to low lipid content; thick creams or ointments are preferred. Avoid using medium- or high-potency topical corticosteroids on the face or eyelids to prevent complications.
- Published on
Emergency and Acute Medicine – Diplopia
Basics
Description
Diplopia is double vision with simultaneous perception of two images. The images may be oriented horizontally, vertically, or diagonally. Diplopia most often results from abnormal movement of the extraocular muscles, which are innervated by three cranial nerves. Cranial nerve III innervates the superior, inferior, and medial rectus muscles and the inferior oblique. Cranial nerve IV innervates the superior oblique muscle, and cranial nerve VI innervates the lateral rectus muscle. Brainstem lesions may damage cranial nerve nuclei or their connections, particularly the medial longitudinal fasciculus, resulting in internuclear ophthalmoplegia. Cranial nerve dysfunction may occur due to compression along the subarachnoid space or venous sinuses, inflammation, or altered cerebrospinal fluid pressure, with elevated or reduced pressure commonly causing cranial nerve VI palsy. Disorders affecting the orbits or bony skull may mechanically restrict movement of one or both eyes or extraocular muscles.
Etiology
Traumatic diplopia may result from orbital fractures, contusions, or hematomas, and rarely from brainstem contusion or hematoma. Monocular diplopia is almost always due to intrinsic ocular pathology such as corneal surface disease including keratoconus, lens subluxation, structural defects within the eye, or functional disorders such as conversion disorder, factitious disorder, or somatization.
Nontraumatic binocular diplopia may arise from brain or brainstem dysfunction, including stroke and multiple sclerosis. Cortical causes such as migraine are rare. Cranial nerve dysfunction may be due to posterior communicating artery aneurysm causing cranial nerve III palsy, chronic lymphocytic meningitis with multiple cranial nerve involvement, pseudotumor cerebri causing cranial nerve VI palsy, or spontaneous intracranial hypotension also affecting cranial nerve VI. Disorders of the bony skull and orbits include tumors, thyroid eye disease, and inflammatory conditions such as Tolosa–Hunt syndrome. Neuromuscular junction disorders affecting extraocular muscles include myasthenia gravis.
Diagnosis
Signs and symptoms
History should establish whether diplopia followed head injury, whether it is constant or intermittent, and its duration. It is essential to determine whether diplopia is monocular or binocular and to ask about headache or other neurologic or visual symptoms. Clarify whether the images are separated horizontally, vertically, or diagonally.
On physical examination, monocular diplopia persists when one eye is covered and indicates pathology within the affected eye. Binocular diplopia resolves when either eye is covered and suggests misalignment. Traumatic and nontraumatic causes should be distinguished.
Monocular diplopia requires a careful ocular examination including visual acuity assessment. Binocular diplopia requires full eye examination for ptosis, anisocoria, extraocular movement limitation, proptosis, or exophthalmos, and assessment of visual acuity. Cranial nerve III palsy with pupil involvement typically causes diagonal diplopia with ptosis and a dilated pupil, whereas pupil-sparing cranial nerve III palsy causes diagonal diplopia with normal pupils and eyelids. Cranial nerve IV palsy produces vertical or diagonal diplopia and is the least common. Cranial nerve VI palsy produces horizontal diplopia that worsens with lateral gaze toward the affected side.
A complete neurologic examination is required. In traumatic diplopia, look for facial anesthesia, anisocoria, proptosis, or decreased visual acuity. Patients may appear well, so a systematic examination is critical to localize the lesion. Pupil-involving cranial nerve III palsy should prompt concern for aneurysm, whereas pupil-sparing palsy is usually microvascular. Facial numbness with diplopia suggests cavernous sinus or superior orbital fissure pathology. Decreased vision raises concern for orbital or superior orbital fissure syndrome.
Essential workup
A careful history and physical examination are the cornerstones of diagnosis, with particular attention to trauma history. In spontaneous cases, determine whether diplopia is isolated, which cranial nerve is involved, and whether additional neurologic deficits are present to aid localization. Cerebral angiography using CTA, MRA, or DSA is indicated for cranial nerve III palsy with a dilated pupil.
Diagnosis tests and interpretation
Laboratory testing is generally not useful in the emergency department, though thyroid function tests may occasionally be helpful. Serologic testing for myasthenia gravis is not required in the acute setting.
Diagnostic procedures may include an edrophonium or ice test if myasthenia gravis is suspected. Lumbar puncture is indicated when considering subarachnoid hemorrhage, chronic lymphocytic meningitis, or abnormal cerebrospinal fluid pressure states. Brain and cerebrovascular imaging should be obtained when evaluating for mass lesions, aneurysm, stroke, or multiple sclerosis, with specific tests guided by the suspected diagnosis.
Differential diagnosis
Post-traumatic diplopia includes orbital fracture or hematoma with direct cranial nerve injury or mechanical restriction, and rarely brainstem contusion affecting cranial nerve nuclei or the medial longitudinal fasciculus.
Monocular diplopia may be caused by nearly any ocular disorder involving the cornea, lens, iris, retina, or refractive system, and rarely bilateral monocular diplopia from cortical dysfunction.
Binocular diplopia may result from brainstem stroke or multiple sclerosis, Wernicke encephalopathy, rare cortical causes such as migraine, botulism, cranial nerve palsies due to stretch, ischemia, inflammation, or pressure abnormalities, cavernous sinus pathology, internuclear ophthalmoplegia, orbital infiltrative disorders, myasthenia gravis, or botulism.
Treatment
Initial stabilization and therapy
Most patients with diplopia do not require immediate stabilization. Management is guided by the underlying etiology.
Emergency department treatment and procedures
Lumbar puncture should be performed when lymphocytic meningitis, pseudotumor cerebri, or spontaneous intracranial hypotension is suspected, with mandatory measurement of opening pressure. An edrophonium test may be considered for suspected myasthenia gravis. Eye patching may be offered for symptomatic relief in patients discharged from the emergency department.
Special considerations
Pediatric patients share the same differential diagnosis. In pregnancy, hyperemesis gravidarum may lead to Wernicke encephalopathy or orbital hemorrhage presenting with diplopia. Postpartum diplopia may occur due to cavernous sinus thrombosis, post–dural puncture headache, or orbital hemorrhage.
Follow-up and disposition
Admission criteria
Admission depends on the underlying cause. Many patients require admission to expedite evaluation for serious etiologies, including advanced neuroimaging and specialty consultation.
Discharge criteria
Patients with monocular diplopia or traumatic diplopia with a clearly established, nonurgent cause may be safely discharged.
Follow-up recommendations
All discharged patients with diplopia require follow-up, typically with neurology or ophthalmology.
Pearls and pitfalls
Diplopia may be described as blurred vision if image separation is minimal. Never assume diplopia is an isolated cranial neuropathy without a thorough neurologic examination. Always assess pupils to avoid missing an aneurysmal cranial nerve III palsy, which may occur with normal CT and lumbar puncture. Myasthenia gravis often presents with intermittent diplopia and normal pupils. Facial sensory loss with diplopia localizes pathology to the cavernous sinus or superior orbital fissure. Decreased visual acuity with diplopia suggests orbital or superior orbital fissure disease and may represent a surgical emergency.
Basics
Description
Diplopia is double vision with simultaneous perception of two images. The images may be oriented horizontally, vertically, or diagonally. Diplopia most often results from abnormal movement of the extraocular muscles, which are innervated by three cranial nerves. Cranial nerve III innervates the superior, inferior, and medial rectus muscles and the inferior oblique. Cranial nerve IV innervates the superior oblique muscle, and cranial nerve VI innervates the lateral rectus muscle. Brainstem lesions may damage cranial nerve nuclei or their connections, particularly the medial longitudinal fasciculus, resulting in internuclear ophthalmoplegia. Cranial nerve dysfunction may occur due to compression along the subarachnoid space or venous sinuses, inflammation, or altered cerebrospinal fluid pressure, with elevated or reduced pressure commonly causing cranial nerve VI palsy. Disorders affecting the orbits or bony skull may mechanically restrict movement of one or both eyes or extraocular muscles.
Etiology
Traumatic diplopia may result from orbital fractures, contusions, or hematomas, and rarely from brainstem contusion or hematoma. Monocular diplopia is almost always due to intrinsic ocular pathology such as corneal surface disease including keratoconus, lens subluxation, structural defects within the eye, or functional disorders such as conversion disorder, factitious disorder, or somatization.
Nontraumatic binocular diplopia may arise from brain or brainstem dysfunction, including stroke and multiple sclerosis. Cortical causes such as migraine are rare. Cranial nerve dysfunction may be due to posterior communicating artery aneurysm causing cranial nerve III palsy, chronic lymphocytic meningitis with multiple cranial nerve involvement, pseudotumor cerebri causing cranial nerve VI palsy, or spontaneous intracranial hypotension also affecting cranial nerve VI. Disorders of the bony skull and orbits include tumors, thyroid eye disease, and inflammatory conditions such as Tolosa–Hunt syndrome. Neuromuscular junction disorders affecting extraocular muscles include myasthenia gravis.
Diagnosis
Signs and symptoms
History should establish whether diplopia followed head injury, whether it is constant or intermittent, and its duration. It is essential to determine whether diplopia is monocular or binocular and to ask about headache or other neurologic or visual symptoms. Clarify whether the images are separated horizontally, vertically, or diagonally.
On physical examination, monocular diplopia persists when one eye is covered and indicates pathology within the affected eye. Binocular diplopia resolves when either eye is covered and suggests misalignment. Traumatic and nontraumatic causes should be distinguished.
Monocular diplopia requires a careful ocular examination including visual acuity assessment. Binocular diplopia requires full eye examination for ptosis, anisocoria, extraocular movement limitation, proptosis, or exophthalmos, and assessment of visual acuity. Cranial nerve III palsy with pupil involvement typically causes diagonal diplopia with ptosis and a dilated pupil, whereas pupil-sparing cranial nerve III palsy causes diagonal diplopia with normal pupils and eyelids. Cranial nerve IV palsy produces vertical or diagonal diplopia and is the least common. Cranial nerve VI palsy produces horizontal diplopia that worsens with lateral gaze toward the affected side.
A complete neurologic examination is required. In traumatic diplopia, look for facial anesthesia, anisocoria, proptosis, or decreased visual acuity. Patients may appear well, so a systematic examination is critical to localize the lesion. Pupil-involving cranial nerve III palsy should prompt concern for aneurysm, whereas pupil-sparing palsy is usually microvascular. Facial numbness with diplopia suggests cavernous sinus or superior orbital fissure pathology. Decreased vision raises concern for orbital or superior orbital fissure syndrome.
Essential workup
A careful history and physical examination are the cornerstones of diagnosis, with particular attention to trauma history. In spontaneous cases, determine whether diplopia is isolated, which cranial nerve is involved, and whether additional neurologic deficits are present to aid localization. Cerebral angiography using CTA, MRA, or DSA is indicated for cranial nerve III palsy with a dilated pupil.
Diagnosis tests and interpretation
Laboratory testing is generally not useful in the emergency department, though thyroid function tests may occasionally be helpful. Serologic testing for myasthenia gravis is not required in the acute setting.
Diagnostic procedures may include an edrophonium or ice test if myasthenia gravis is suspected. Lumbar puncture is indicated when considering subarachnoid hemorrhage, chronic lymphocytic meningitis, or abnormal cerebrospinal fluid pressure states. Brain and cerebrovascular imaging should be obtained when evaluating for mass lesions, aneurysm, stroke, or multiple sclerosis, with specific tests guided by the suspected diagnosis.
Differential diagnosis
Post-traumatic diplopia includes orbital fracture or hematoma with direct cranial nerve injury or mechanical restriction, and rarely brainstem contusion affecting cranial nerve nuclei or the medial longitudinal fasciculus.
Monocular diplopia may be caused by nearly any ocular disorder involving the cornea, lens, iris, retina, or refractive system, and rarely bilateral monocular diplopia from cortical dysfunction.
Binocular diplopia may result from brainstem stroke or multiple sclerosis, Wernicke encephalopathy, rare cortical causes such as migraine, botulism, cranial nerve palsies due to stretch, ischemia, inflammation, or pressure abnormalities, cavernous sinus pathology, internuclear ophthalmoplegia, orbital infiltrative disorders, myasthenia gravis, or botulism.
Treatment
Initial stabilization and therapy
Most patients with diplopia do not require immediate stabilization. Management is guided by the underlying etiology.
Emergency department treatment and procedures
Lumbar puncture should be performed when lymphocytic meningitis, pseudotumor cerebri, or spontaneous intracranial hypotension is suspected, with mandatory measurement of opening pressure. An edrophonium test may be considered for suspected myasthenia gravis. Eye patching may be offered for symptomatic relief in patients discharged from the emergency department.
Special considerations
Pediatric patients share the same differential diagnosis. In pregnancy, hyperemesis gravidarum may lead to Wernicke encephalopathy or orbital hemorrhage presenting with diplopia. Postpartum diplopia may occur due to cavernous sinus thrombosis, post–dural puncture headache, or orbital hemorrhage.
Follow-up and disposition
Admission criteria
Admission depends on the underlying cause. Many patients require admission to expedite evaluation for serious etiologies, including advanced neuroimaging and specialty consultation.
Discharge criteria
Patients with monocular diplopia or traumatic diplopia with a clearly established, nonurgent cause may be safely discharged.
Follow-up recommendations
All discharged patients with diplopia require follow-up, typically with neurology or ophthalmology.
Pearls and pitfalls
Diplopia may be described as blurred vision if image separation is minimal. Never assume diplopia is an isolated cranial neuropathy without a thorough neurologic examination. Always assess pupils to avoid missing an aneurysmal cranial nerve III palsy, which may occur with normal CT and lumbar puncture. Myasthenia gravis often presents with intermittent diplopia and normal pupils. Facial sensory loss with diplopia localizes pathology to the cavernous sinus or superior orbital fissure. Decreased visual acuity with diplopia suggests orbital or superior orbital fissure disease and may represent a surgical emergency.
