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Emergency and Acute Medicine – Alcoholic ketoacidosis
Basics description
Alcoholic ketoacidosis is caused by increased ketone body production resulting from dehydration due to nausea and vomiting with inhibition of antidiuretic hormone, leading to elevated stress hormone release and ketogenesis. Hepatic glycogen stores are depleted because of malnutrition or reduced carbohydrate intake. Ethanol metabolism increases the NADH/NAD ratio, promoting free fatty acid production and favoring β-hydroxybutyrate over acetoacetate as the predominant ketone.
Etiology
Alcoholic ketoacidosis typically occurs in malnourished chronic alcohol users following a recent episode of heavy alcohol consumption. Nausea, vomiting, or abdominal pain lead to abrupt cessation of alcohol intake. Presentation usually occurs within 12–72 hours.
Diagnosis signs and symptoms
Dehydration is common. Fever is usually absent unless infection is present. Tachycardia frequently occurs due to hypovolemia with orthostatic changes and concurrent alcohol withdrawal. Tachypnea is common, often with deep, rapid Kussmaul respirations. Nausea, vomiting, and abdominal pain are the most frequent symptoms and are usually diffuse with nonspecific tenderness; epigastric pain is common. Rebound tenderness, abdominal distension, and hypoactive bowel sounds are uncommon and should prompt evaluation for alternative pathology. Urine output is decreased due to hypovolemia. Mental status is typically minimally altered; significant alteration requires evaluation for head injury, cerebrovascular accident, intracranial hemorrhage, hypoglycemia, alcohol withdrawal, encephalopathy, or toxic ingestion. Visual disturbances may occur.
History often reveals chronic alcohol use with a recent binge followed by abrupt cessation. Physical examination commonly shows dehydration, ketotic breath odor, Kussmaul respirations, and palmar erythema.
Essential workup
An increased anion gap metabolic acidosis due to ketone accumulation should be identified. Toxic alcohol ingestion and other causes of anion gap metabolic acidosis must be excluded.
Diagnosis tests and interpretation
Laboratory findings demonstrate increased anion gap metabolic acidosis as the hallmark. Mixed acid–base disorders are common and may include respiratory alkalosis, metabolic alkalosis from vomiting, hyperchloremic acidosis, and mild lactic acidosis related to dehydration and ethanol metabolism. Severe lactic acidosis suggests alternative pathology such as hypoxia, seizures, or shock. Urine and serum nitroprusside tests are positive but underestimate severity because β-hydroxybutyrate predominates and is not detected; results may paradoxically increase during treatment. Electrolyte abnormalities include low bicarbonate, hypokalemia, hypocalcemia, hypophosphatemia, and hypomagnesemia. Glucose levels are usually normal or mildly elevated, though hypoglycemia may occur. Alcohol levels may be negative. BUN and creatinine are mildly elevated due to dehydration. CBC may show mild leukocytosis, anemia, and thrombocytopenia related to chronic alcohol use. Urinalysis shows ketonuria without glucosuria. Amylase and lipase may be elevated with pancreatitis. Liver enzymes may be mildly elevated. The osmolal gap may be increased; values greater than 20 mOsm/kg warrant evaluation for methanol or ethylene glycol ingestion, correcting for ethanol by dividing the ethanol level by 4.6.
Chest radiography is indicated if pneumonia is suspected. Abdominal imaging is considered for acute abdomen. CT of the head is required with trauma or unexplained altered mental status.
Differential diagnosis
Causes of elevated anion gap metabolic acidosis include alcoholic ketoacidosis, toxic ingestions, acetaminophen toxicity, fulminant hepatic failure, antiretroviral toxicity, toluene, methanol, metformin, uremia, diabetic ketoacidosis, paraldehyde, iron, isoniazid, lactic acidosis, ethylene glycol, salicylates, and starvation ketosis. Other considerations include hypovolemia from GI bleeding or sepsis and abdominal pain from pancreatitis, gastritis, hepatitis, perforated ulcer, alcohol withdrawal, viral illness, or bowel obstruction.
Treatment pre hospital
Provide supportive care with IV access, 0.9% normal saline, oxygen, and cardiac monitoring. Evaluate for toxic ingestion, diabetic history, and coexisting illness such as gastrointestinal bleeding.
Initial stabilization therapy
Initiate cardiac monitoring and supplemental oxygen. Administer naloxone, thiamine, and dextrose if mental status is altered. Begin IV normal saline with a 500 mL–1 L bolus and continue resuscitation as needed to promote renal ketone clearance.
Ed treatment procedures
Administer antiemetics and benzodiazepines for alcohol withdrawal. Begin dextrose-containing fluids such as D5NS, which resolve metabolic abnormalities more rapidly than saline alone by restoring glycogen stores and stimulating endogenous insulin. Avoid dextrose if significant hyperglycemia is present. Administer IV thiamine before glucose to prevent Wernicke encephalopathy. Sodium bicarbonate is rarely indicated and reserved for severe acidosis with cardiovascular compromise. Anticipate and correct electrolyte shifts, particularly hypokalemia, hypophosphatemia, and hypomagnesemia. Insulin is not indicated and may cause hypoglycemia.
Medication
Dextrose 50%: 25 g IV
Lorazepam: 2 mg IV, titrate to effect
Naloxone: 2 mg IV
Ondansetron: 4–8 mg IV
Prochlorperazine: 5–10 mg IV slowly
Promethazine: 12.5–25 mg IV
Thiamine: 100 mg IV
Follow up disposition
Admission is indicated for persistent metabolic acidosis, hypovolemia, ongoing vomiting, unclear abdominal pain, comorbid illness, or electrolyte abnormalities requiring monitoring. Many patients can be managed in an observation unit for 12–24 hours if tolerating oral intake, metabolic abnormalities resolve, and no additional illness is present.
Follow up recommendations
Provide counseling and referral for alcohol cessation.
Pearls and pitfalls
Aggressive volume resuscitation with dextrose-containing fluids is essential. Always administer thiamine before glucose. Monitor electrolytes and glucose closely. Evaluate unexplained elevated osmolal gaps. Continuous cardiac monitoring is required due to the risk of dysrhythmias, electrolyte disturbances, and alcoholic cardiomyopathy.
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Emergency and Acute Medicine – Alcohol Poisoning
BASICS DESCRIPTION
Alcohol is the most commonly abused recreational agent among emergency department patients. Alcohol is frequently associated with traumatic injuries.
ETIOLOGY
Alcohol intoxication: Directly depresses CNS function. Blood alcohol levels drop by 15–40 mg/dL/hr depending on individual variables and chronicity of alcohol use.
Alcohol withdrawal: Occurs in chronic alcohol abusers after partial or complete alcohol abstinence. May occur despite a serum alcohol level >100 mg/dL (e.g., “intoxicated”). Primarily due to loss of chronic CNS inhibition: profound CNS excitation with increased catecholamine release and adrenergic tone.
DIAGNOSIS SIGNS AND SYMPTOMS
Acute alcohol intoxication: CNS effects occur on a spectrum including relaxation, euphoria, sedation, memory loss, impaired judgment, ataxia, slurred speech, obtundation, or coma. May also cause GI upset.
Alcohol withdrawal syndrome:
Early or minor withdrawal: <8 hr after last drink—symptoms of hangover, headache, nausea />omiting. At 12 hr—mild tremors/anxiety, anorexia, nausea, vomiting, weakness, myalgias, vivid dreams/nightmares.
12–36 hr after last drink—irritability/agitation, tachycardia/HTN, tremors in hands and tongue.
24–48 hr—alcoholic hallucinosis with visual hallucinations most common (bug crawling) and auditory hallucinations (buzzing, clicks).
Alcohol withdrawal seizures: 8–12 hr after last drink; brief, spontaneously abating tonic–clonic activity; often precede delirium tremens (DTs).
Late or major withdrawal: ≥48 hr after last drink—DTs characterized by clouded consciousness, confusion, agitation/combativeness, tachycardia/HTN, hyperpyrexia, and diaphoresis.
History is often provided by EMS, family, or friends. Beware the “frequent flyer” in the ED, as other causes of AMS may coexist, including hepatic encephalopathy, postictal state, hypoglycemia, head injury, or intracranial bleeding.
Physical exam: Vital signs—acute intoxication usually normal or depressed; withdrawal usually elevated. Mental status—acute intoxication presents with somnolence or coma; withdrawal presents with hyperalert agitation. Signs of hepatic injury include jaundice, icterus, spider angiomata, asterixis, and hepatomegaly. Signs of malnutrition include alopecia, poor dentition, poor muscle mass, abdominal wasting, and temporal wasting.
ESSENTIAL WORKUP
Obtain accurate alcohol ingestion and abstinence history. Investigate life-threatening causes of seizures including hypoglycemia (rapid bedside glucose), intracranial hemorrhage, CNS infection, and electrolyte abnormalities. Evaluate for occult trauma. Monitor vital signs frequently; hyperthermia predicts poorer outcomes.
DIAGNOSTIC TESTS & INTERPRETATION
Labs: Alcohol level if abnormal mental status; urine toxicology for coingestants; electrolytes, BUN, creatinine, glucose; CBC; magnesium, calcium, phosphate; PT/INR if coagulopathy suspected; LFTs if liver disease suspected; ammonia if hepatic encephalopathy suspected; urinary ketones or serum acetone if alcoholic ketoacidosis suspected.
Imaging: CT head if mental status is disproportionate to alcohol level, head trauma suspected, focal neurologic findings, signs of increased ICP, new-onset seizure, or deterioration. EEG differentiates alcohol withdrawal seizures from epilepsy. Chest radiograph if aspiration or pneumonia suspected.
DIFFERENTIAL DIAGNOSIS
Acute intoxication: Hypoglycemia, CO₂ narcosis, mixed-drug overdose, ethylene glycol, methanol, isopropanol poisoning, hepatic encephalopathy, psychosis, severe vertigo, psychomotor seizure.
Withdrawal/seizures: Sedative–hypnotic withdrawal, carbon monoxide poisoning, isoniazid toxicity, amphetamines, anticholinergics, cocaine.
Secondary seizure disorders: Infection, meningitis, encephalitis, brain abscess, trauma, intracranial hemorrhage, CVA, tumor, anticonvulsant noncompliance, thyroid disease.
TREATMENT PRE HOSPITAL
Administer benzodiazepines for seizures. Give naloxone, oxygen, and dextrose for comatose patients. Intubate as needed for airway protection. Immobilize cervical spine if trauma suspected.
INITIAL STABILIZATION/THERAPY
Airway, breathing, circulation (ABCs). Evaluate cervical spine. Initiate IV rehydration with 0.9% NS, then D5 0.45 NS. Administer naloxone, thiamine, and glucose (or Accu-Chek) if altered mental status. Treat seizures with benzodiazepines, often requiring large doses.
Pediatric considerations: Young children have decreased hepatic glycogen reserves and may not mount an adequate glucose response. Rapid bedside glucose is essential; administer dextrose with D5 (10 mL/kg), D10 (5 mL/kg), or D25 (2 mL/kg) depending on age and size.
ED TREATMENT/PROCEDURES
Alcohol intoxication: IV rehydration and correction of electrolyte abnormalities including magnesium, potassium, folate, thiamine, and multivitamins.
Alcoholic ketoacidosis: Aggressive rehydration with D5 0.9 NS; exclude other causes of anion-gap metabolic acidosis.
Alcohol withdrawal syndrome: Use CIWA-Ar scale to assess severity and guide symptom-triggered therapy. Benzodiazepines are first-line; large, frequent doses may be required. Phenobarbital may be used for severe or refractory withdrawal. Propofol is indicated for intubated patients with refractory seizures. β-blockers and α-agonists may normalize vital signs but do not treat CNS complications. Phenytoin is not indicated unless seizures are unrelated to withdrawal.
MEDICATION
Dextrose: D50W 1 amp (50 mL or 25 g); peds D25W 2–4 mL/kg IV.
Diazepam: 5–10 mg IV q5–10 min until calm.
Lorazepam: 0.5–4 mg IV/IM q5–10 min until calm.
Naloxone: 0.4–2 mg IV/IM (peds 0.1 mg/kg).
Phenobarbital: 10–20 mg/kg IV loading dose.
Phenytoin: 15–18 mg/kg (max 25 mg/min); fosphenytoin 15–20 mgPE/kg.
Propofol: 25–75 µg/kg/min loading, then 5–50 µg/kg/min maintenance.
Thiamine: 100 mg IV/IM (peds 50 mg).
FOLLOW-UP DISPOSITION
Admission criteria: Uncontrolled seizures or withdrawal, hepatic failure, infection, dehydration, malnutrition, cardiovascular collapse, dysrhythmia, trauma, hallucinations, abnormal vital signs, severe agitation, Wernicke encephalopathy, confusion, or delirium.
Discharge criteria: Clinically sober and seizure-free for 6 hr with negative workup if first seizure.
FOLLOW-UP RECOMMENDATIONS
Substance abuse referral for patients with recurrent alcohol intoxication or use.
PEARLS AND PITFALLS
Do not attribute AMS solely to alcohol in chronic users. Serum alcohol should fall by 15–40 mg/dL/hr; lack of improvement warrants further evaluation. Inadequate benzodiazepine dosing is common—massive doses may be required. Hypoglycemia frequently mimics intoxication and is common in chronic alcoholics and children.
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Emergency and Acute Medicine – Airway Management
Overview
Airway management encompasses techniques used to ensure adequate oxygenation and ventilation in critically ill or injured patients. It is a core skill in emergency medicine and includes basic airway maneuvers, airway adjuncts, definitive intubation, and surgical airway access. The priority is oxygenation and ventilation rather than intubation alone.
Basic Airway Adjuncts
Oral and nasopharyngeal airways lift the tongue off the hypopharynx and facilitate bag-valve-mask ventilation. Oropharyngeal airways require an absent gag reflex, whereas nasopharyngeal airways may be used when the gag reflex is intact.
Rapid Sequence Intubation (RSI)
RSI is the preferred ED method for oral intubation because it minimizes aspiration risk and optimizes intubating conditions through rapid induction and paralysis. It is contraindicated when paralysis is unsafe or when a difficult airway is anticipated without a reliable rescue plan. A preformulated backup strategy is essential.
Awake and Assisted Intubation Techniques
Awake oral intubation uses sedation without paralysis and is indicated when neuromuscular blockade is contraindicated. Ketamine is commonly used, often with benzodiazepines. A gum elastic bougie is helpful when vocal cords are poorly visualized, with tracheal placement suggested by tactile contact with tracheal rings.
Alternative Airway Devices
Extraglottic devices are inserted blindly into the oropharynx for rapid airway control. Laryngeal mask airways form a seal around glottic structures but provide less aspiration protection than endotracheal tubes. Intubating LMAs allow endotracheal tube placement. Esophageal–tracheal tubes such as the Combitube or King LT ventilate the hypopharynx while occluding the esophagus.
Advanced Visualization Techniques
Video laryngoscopes and fiberoptic devices improve visualization of the airway and are useful in patients with anatomic limitations or cervical spine instability. These techniques are less effective when blood or secretions obscure the airway and are contraindicated when immediate airway control is required.
Nasotracheal Intubation
Nasotracheal intubation is useful when oral access is impaired, oral intubation fails, or paralysis is contraindicated. Absolute contraindication is apnea. Relative contraindications include anticoagulation, massive facial trauma, upper airway abscess, epiglottitis, and penetrating neck injury.
Surgical Airways
Cricothyrotomy is the definitive rescue airway for failed intubation and ventilation. It is indicated in crash airways, massive facial trauma, or complete upper airway obstruction. Percutaneous translaryngeal ventilation may provide temporary oxygenation while preparing for cricothyrotomy.
Indications for Airway Intervention
Airway intervention is required when patients cannot maintain or protect the airway, develop hypoxia or ventilatory failure, or are expected to deteriorate. Common indications include altered mental status, status epilepticus, severe trauma, and the need for controlled ventilation during procedures.
Airway Assessment
A difficult airway should be anticipated using structured assessment such as the LEMON approach, evaluating external anatomy, mouth opening, mandibular and thyromental distance, Mallampati class, obstruction, and neck mobility. Early recognition guides appropriate technique selection and backup planning.
Verification of Tube Placement
Direct visualization of the tube passing through the vocal cords is the gold standard. End-tidal CO₂ monitoring is the most reliable bedside confirmation. Auscultation, chest rise, tube condensation, and pulse oximetry trends are supportive but less reliable. Chest radiography confirms depth and complications but does not exclude esophageal intubation.
Emergency Department Management
RSI requires thorough preparation, preoxygenation, appropriate positioning, and rapid confirmation of tube placement. Adequate postintubation sedation and, if needed, continued paralysis are essential. Failed attempts require immediate transition to alternative airway devices or surgical airway access.
Disposition
Most intubated patients require ICU admission. Rarely, selected patients intubated briefly for airway protection or diagnostic procedures may be extubated in the ED after observation and discharged safely.
Pearls and Pitfalls
Failure to ventilate is immediately life-threatening. Always assess for a difficult airway and establish a backup plan before intervention. Prioritize oxygenation and ventilation over intubation, and escalate early to alternative or surgical airway techniques when standard approaches fail.
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Emergency and Acute Medicine – Airway Adjuncts
Overview and Purpose
Airway adjuncts are devices used to support and maintain upper airway patency when normal airway reflexes or anatomy compromise ventilation and oxygenation. In emergency and acute care, they are frequently used as rescue techniques when standard endotracheal intubation is difficult or when effective bag-mask ventilation cannot be achieved. Their primary goal is to ensure adequate oxygenation and ventilation while a definitive airway is established.
Types of Airway Adjuncts
Airway adjuncts include oral and nasopharyngeal airways as well as extraglottic devices. Oral and nasopharyngeal airways function by lifting the tongue away from the posterior pharynx, relieving obstruction. These devices are typically used in conjunction with proper patient positioning. Nasopharyngeal airways may be used when the gag reflex is intact, whereas oropharyngeal airways require an absent gag reflex to avoid vomiting or aspiration.
Extraglottic Airway Devices
Extraglottic devices are divided into supraglottic and retroglottic or infraglottic devices. Supraglottic devices sit above and surround the glottis, while retroglottic or infraglottic devices ventilate at the level of the hypopharynx and occlude the esophagus. These devices are usually inserted blindly using device-specific techniques. Although they have high success rates and allow rapid airway control, they offer less protection from aspiration than endotracheal tubes.
Epidemiology and Clinical Context
Most emergency department airway interventions are successful with the first selected method, with overall intubation success approaching 98%. Difficult airways account for a small but clinically significant proportion of cases, underscoring the importance of airway adjuncts within a structured airway management plan.
Assessment of the Difficult Airway
Airway assessment is essential prior to intervention. Predictors of difficult bag-mask ventilation include poor mask seal, obesity or airway obstruction, advanced age, edentulous state, and reduced chest wall compliance. Predictors of difficult laryngoscopy and intubation include abnormal external anatomy, limited mouth opening, short mandibular or thyromental distance, higher Mallampati class, airway obstruction, and limited neck mobility. Early recognition guides appropriate selection of adjuncts and backup strategies.
Confirmation of Airway Placement
Effective airway management should result in stable or improving oxygen saturation. End-tidal capnography is the most reliable bedside method to confirm correct airway placement. Physical examination findings such as chest rise, auscultation, and tube condensation are commonly used but are less reliable. Chest radiography is helpful after endotracheal intubation to confirm tube depth and identify complications, but it does not exclude esophageal intubation.
Prehospital and Initial Emergency Management
Prehospital airway options vary by system and may include bag-valve-mask ventilation with adjuncts, endotracheal intubation, extraglottic device placement, or surgical airway access. Initial emergency department management prioritizes oxygenation, cervical spine protection when indicated, and vascular access for resuscitation and medication administration.
Emergency Department Airway Management
Rapid sequence intubation is a cornerstone of definitive airway control. Preparation includes assembling suction, oxygen delivery systems, primary and rescue airway devices, and medications. Preoxygenation, optimal positioning, and postintubation confirmation are critical. If intubation fails, clinicians must promptly transition to alternative airway adjuncts or surgical airway techniques rather than persisting with repeated unsuccessful attempts.
Disposition and Follow-Up
Nearly all patients requiring advanced airway management, particularly intubation, require admission to an intensive care unit or operating room for ongoing care. Rarely, selected patients may be extubated in the emergency department after observation and safely discharged.
Pearls and Pitfalls
Failure to ventilate is immediately life-threatening. Every patient should be assessed for potential airway difficulty, and a backup plan must always be in place. The priority is effective oxygenation and ventilation rather than intubation alone. Early transition to airway adjuncts or surgical airway techniques is essential when conventional methods fail, especially in pediatric patients where anatomical considerations are critical.
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Emergency and Acute Medicine – Agitation
Overview and Definition
Agitation is a state of extreme restlessness marked by increased verbal activity, motor activity, or both. It represents a broad clinical spectrum ranging from excessive talkativeness to aggressive, threatening, or violent behavior. Agitation may be the presenting feature of numerous medical (organic) or psychiatric (functional) conditions and therefore requires careful and systematic evaluation in the emergency setting.
Clinical Significance and Special Forms
Agitation varies widely in severity and includes life-threatening entities such as excited delirium syndrome. This condition is characterized by severe agitation, metabolic acidosis, and hyperadrenergic autonomic dysfunction, and is associated with a risk of sudden cardiac death, particularly following prolonged physical struggle or restraint. Early recognition and intervention are critical to reduce morbidity and mortality.
Epidemiology
Behavioral disturbances account for approximately 6% of all emergency department visits, translating to an estimated 1.7 million visits annually in the United States. Agitated patients frequently require significant ED resources and pose safety challenges for staff and other patients.
Etiology
Agitation has a wide differential diagnosis. Medical causes include infections such as meningitis, encephalitis, and sepsis-related delirium; metabolic disturbances including hypoglycemia, electrolyte abnormalities, renal or hepatic failure, and acid–base disorders; endocrine emergencies such as thyroid storm; pulmonary causes including hypoxia and hypercapnia; toxicologic causes such as intoxication or withdrawal states; and neurologic disorders including stroke, intracranial hemorrhage, postictal states, or brain tumors. Psychiatric causes include mood disorders (mania or agitated depression), psychotic disorders such as schizophrenia, and severe anxiety disorders.
History and Clinical Assessment
A detailed history and physical examination are essential in distinguishing organic from functional causes of agitation. The history of present illness alone has high sensitivity for detecting underlying medical illness in patients presenting with psychiatric symptoms. When the patient is unable to provide a reliable history, collateral information should be obtained from family, friends, emergency medical services, or caregivers. Key historical points include trauma, recent infection, medication use, substance exposure, psychiatric history, and neurologic symptoms.
Physical Examination
A comprehensive physical examination is mandatory. Abnormal vital signs should prompt an aggressive search for medical causes. Hyperthermia may suggest infection, neuroleptic malignant syndrome, serotonin syndrome, or excited delirium. A toxidrome-oriented examination should include pupillary size, skin findings, sweating patterns, and urinary retention. A focused but thorough neurologic examination is critical, as focal deficits mandate evaluation for structural or metabolic disease. Cognitive testing is particularly important, as impaired attention, memory, or orientation suggests delirium rather than a purely psychiatric disorder.
Diagnostic Evaluation
The extent of diagnostic testing should be guided by clinical suspicion. At a minimum, all agitated patients require a full set of vital signs, a complete physical and neurologic examination, and bedside blood glucose testing. Additional laboratory studies, imaging, or procedures should be tailored to suspected etiologies. Head CT imaging is indicated in patients with trauma or neurologic deficits, while lumbar puncture should be considered when CNS infection is suspected and no source is otherwise identified.
Prehospital and Initial Management
Prehospital providers should follow established protocols for physical and chemical restraint and provide advance notification to the receiving facility. Initial emergency department management focuses on airway, breathing, and circulation, with prompt treatment of any life-threatening conditions. Severely agitated patients may pose immediate danger and should be placed in a controlled environment, changed into hospital attire, and searched for weapons to ensure safety.
Management of Agitation
Treatment should be directed at the underlying cause whenever possible. Verbal de-escalation techniques are first-line therapy for mild to moderate agitation. When pharmacologic intervention is required, benzodiazepines are preferred for alcohol withdrawal, while antipsychotics are first-line for agitation due to primary psychiatric disorders. Combination therapy may be necessary for severe agitation. Physical restraints should be used only when necessary and always in conjunction with chemical sedation to minimize complications.
Disposition and Follow-Up
Disposition depends on the etiology and resolution of agitation. Admission is indicated when an underlying medical or psychiatric condition requires inpatient management. Discharge should be reserved for patients whose agitation has resolved and who can be safely managed as outpatients. Appropriate psychiatric or substance-use referrals should be arranged, and follow-up tailored to the underlying diagnosis.
Pearls and Pitfalls
Clinicians must maintain a high index of suspicion for medical causes of agitation, particularly in patients with new onset after age 45, abnormal vital signs, focal neurologic deficits, acute onset, visual hallucinations, or impaired cognition. Common pitfalls include failure to undress and search patients for weapons, inadequate sedation, prolonged or poorly monitored restraint use, and insufficient documentation of clinical decision-making and restraint justification.
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Emergency And Acute Medicine – Ankle Fracture/Dislocation
Basics – Description
Common mechanisms and injury patterns of the ankle include inversion, eversion, external rotation, combined mechanisms (e.g., Maisonneuve fracture), and inversion with dorsiflexion (snowboarder’s fracture). These mechanisms result in predictable patterns of malleolar, fibular, syndesmotic, or talar injuries. Most ankle fractures involve the malleoli and are common in young males and women aged 50–70 years. Risk factors include cigarette use and elevated BMI. Pediatric ankle fractures frequently involve the physis and may result in growth disturbances.
Diagnosis – Signs And Symptoms
Patients typically present with a history of trauma, ankle pain, swelling, deformity, and inability to bear weight. Soft tissue swelling, ecchymosis, skin tenting, or blanching may be present. Neurovascular compromise should be assessed carefully, including capillary refill and dorsalis pedis/posterior tibial pulses. A detailed history should determine the position of the ankle at injury, ability to bear weight afterward, and any audible “pop” or “snap.”
Physical Examination
The Ottawa Ankle Rules are highly sensitive for determining the need for imaging and are reliable in children older than 5 years. Examination should include inspection of the skin, assessment of distal neurovascular status, palpation of the proximal fibula when indicated, and evaluation of motor and sensory function.
Diagnosis – Tests And Interpretation
Radiographs should include AP, lateral, and mortise views, with additional tibia/fibula views if a Maisonneuve fracture is suspected. Post-reduction imaging is required for unstable fractures or dislocations. CT or MRI may be used to further evaluate tibial plafond or ligamentous injury
Treatment
Prehospital Care
Immobilize the ankle to limit pain, bleeding, and further injury. Avoid traction devices and do not attempt reduction of protruding bone.
Initial Stabilization And Therapy
Non–weight bearing, ice, compression, and elevation are essential.
ED Treatment And Procedures
All ankle fractures and dislocations require orthopedic referral. Open fractures require antibiotics, tetanus prophylaxis, and emergent consultation. Closed dislocations should be reduced promptly and immobilized with appropriate splinting. Stable injuries may be managed conservatively, while unstable injuries often require operative fixation.
Medications
Analgesics are the mainstay for closed fractures. Procedural sedation may be required for reductions. Open fractures require IV antibiotics and tetanus prophylaxis.
Follow-Up And Disposition
Unstable fractures, open injuries, dislocations, or neurovascular compromise require admission. Stable, nondisplaced fractures may be discharged with splinting and close orthopedic follow-up.
Key Clinical Insights And Common Errors
When reducing a dislocated ankle, partial flexion of the knee helps relax the Achilles tendon and decreases resistance during manipulation. Careful examination is necessary to differentiate ankle fractures from subtalar injuries, as subtalar dislocations are uncommon and often difficult to reduce. Clinicians should remain vigilant for associated injuries, including trauma to the lumbar spine, hip, tibia, fibula—especially the proximal fibular neck—and the foot, which may otherwise be overlooked.
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Emergency And Acute Medicine – Angioedema
Core Description
Angioedema is a nonpruritic, well-demarcated, nonpitting swelling of the deeper dermis and subcutaneous tissues caused by increased vascular permeability. It results from inflammatory mediator release, either mast cell mediated or kinin mediated through bradykinin and complement pathways. Unlike urticaria, angioedema affects deeper tissues with fewer mast cells and nerve endings, leading to minimal itching. In addition to the skin, angioedema may involve the gastrointestinal tract and upper airway, and it may occur with or without associated urticaria.
Pathophysiologic Mechanisms
Hereditary and acquired forms of angioedema are related to quantitative or functional deficiencies of C1 esterase inhibitor (C1-INH), resulting in unregulated bradykinin activity. Hereditary angioedema is an autosomal dominant disorder with multiple genetic variants, while acquired forms are associated with lymphoproliferative or autoimmune disease. Angiotensin-converting enzyme inhibitor–related angioedema is common in emergency settings and may occur early or years after initiation of therapy.
Underlying Causes
Kinin-mediated etiologies include hereditary angioedema, acquired C1-INH deficiency, and ACE inhibitor–associated reactions. Mast cell–mediated causes include food allergies, medication reactions, insect stings, and physical triggers such as exercise, temperature changes, or trauma. Idiopathic recurrent angioedema and autoimmune-associated forms are also recognized.
Clinical Features
Patients typically present with sudden, asymmetric swelling of the lips, eyelids, face, tongue, or extremities. Lesions are large, nonpitting, and nonpruritic. Abdominal involvement may cause severe pain, nausea, vomiting, or diarrhea. Airway involvement involving the pharynx or larynx is the most dangerous manifestation and may progress rapidly. Attacks of hereditary angioedema are notably not associated with urticaria or itching.
History And Physical Assessment
A careful history should assess family history, recurrent episodes, recent medication use (especially ACE inhibitors), food exposures, and prior similar events. Emotional stress or minor trauma may precipitate attacks. Physical examination focuses on identifying airway compromise, facial and oropharyngeal swelling, and abdominal tenderness. Lesions typically spare gravity-dependent areas.
Diagnostic Approach
Angioedema is primarily a clinical diagnosis. A family history may be absent, as new mutations account for a significant proportion of hereditary cases. Laboratory testing may support the diagnosis but is not required acutely.
Laboratory And Specialized Testing
Basic studies may include a complete blood count and inflammatory markers. Complement levels such as C4 are often reduced during attacks in hereditary and acquired forms. Measurement of C1-INH levels and function confirms hereditary angioedema but is rarely available in the emergency department. Skin biopsy is rarely required.
Differential Considerations
Conditions that may mimic angioedema include superior vena cava syndrome, heart failure, nephrotic syndrome, facial cellulitis, contact dermatitis, autoimmune connective tissue diseases, hypothyroidism, and facial lymphedema.
Emergency Management Principles
Early airway protection is the priority in all cases. Intravenous access and close monitoring are essential. Epinephrine, antihistamines, and corticosteroids are commonly used when mast cell–mediated angioedema is suspected, though response may be limited in bradykinin-mediated disease. Early intubation should be strongly considered if there is progressive airway involvement.
Targeted Therapy
Hereditary and acquired angioedema may require C1-INH replacement, bradykinin receptor antagonists, or kallikrein inhibitors. Fresh frozen plasma may be used when specific agents are unavailable, though caution is advised. ACE inhibitor–induced angioedema requires immediate discontinuation of the offending drug.
Disposition And Follow-Up
Patients with airway involvement or persistent systemic symptoms require admission and monitored care. Those with mild, nonprogressive symptoms may be discharged after observation with antihistamines, steroids, and clear return precautions. Referral to an allergist or immunologist is recommended for recurrent, hereditary, or unexplained cases.
Clinical Pearls And Pitfalls
Airway compromise can evolve rapidly and unpredictably, necessitating early intervention. Standard allergic therapies may be ineffective in bradykinin-mediated angioedema. Recognition of hereditary angioedema and ACE inhibitor–related cases is critical to avoid delayed or ineffective treatment.
Core Description
Angioedema is a nonpruritic, well-demarcated, nonpitting swelling of the deeper dermis and subcutaneous tissues caused by increased vascular permeability. It results from inflammatory mediator release, either mast cell mediated or kinin mediated through bradykinin and complement pathways. Unlike urticaria, angioedema affects deeper tissues with fewer mast cells and nerve endings, leading to minimal itching. In addition to the skin, angioedema may involve the gastrointestinal tract and upper airway, and it may occur with or without associated urticaria.
Pathophysiologic Mechanisms
Hereditary and acquired forms of angioedema are related to quantitative or functional deficiencies of C1 esterase inhibitor (C1-INH), resulting in unregulated bradykinin activity. Hereditary angioedema is an autosomal dominant disorder with multiple genetic variants, while acquired forms are associated with lymphoproliferative or autoimmune disease. Angiotensin-converting enzyme inhibitor–related angioedema is common in emergency settings and may occur early or years after initiation of therapy.
Underlying Causes
Kinin-mediated etiologies include hereditary angioedema, acquired C1-INH deficiency, and ACE inhibitor–associated reactions. Mast cell–mediated causes include food allergies, medication reactions, insect stings, and physical triggers such as exercise, temperature changes, or trauma. Idiopathic recurrent angioedema and autoimmune-associated forms are also recognized.
Clinical Features
Patients typically present with sudden, asymmetric swelling of the lips, eyelids, face, tongue, or extremities. Lesions are large, nonpitting, and nonpruritic. Abdominal involvement may cause severe pain, nausea, vomiting, or diarrhea. Airway involvement involving the pharynx or larynx is the most dangerous manifestation and may progress rapidly. Attacks of hereditary angioedema are notably not associated with urticaria or itching.
History And Physical Assessment
A careful history should assess family history, recurrent episodes, recent medication use (especially ACE inhibitors), food exposures, and prior similar events. Emotional stress or minor trauma may precipitate attacks. Physical examination focuses on identifying airway compromise, facial and oropharyngeal swelling, and abdominal tenderness. Lesions typically spare gravity-dependent areas.
Diagnostic Approach
Angioedema is primarily a clinical diagnosis. A family history may be absent, as new mutations account for a significant proportion of hereditary cases. Laboratory testing may support the diagnosis but is not required acutely.
Laboratory And Specialized Testing
Basic studies may include a complete blood count and inflammatory markers. Complement levels such as C4 are often reduced during attacks in hereditary and acquired forms. Measurement of C1-INH levels and function confirms hereditary angioedema but is rarely available in the emergency department. Skin biopsy is rarely required.
Differential Considerations
Conditions that may mimic angioedema include superior vena cava syndrome, heart failure, nephrotic syndrome, facial cellulitis, contact dermatitis, autoimmune connective tissue diseases, hypothyroidism, and facial lymphedema.
Emergency Management Principles
Early airway protection is the priority in all cases. Intravenous access and close monitoring are essential. Epinephrine, antihistamines, and corticosteroids are commonly used when mast cell–mediated angioedema is suspected, though response may be limited in bradykinin-mediated disease. Early intubation should be strongly considered if there is progressive airway involvement.
Targeted Therapy
Hereditary and acquired angioedema may require C1-INH replacement, bradykinin receptor antagonists, or kallikrein inhibitors. Fresh frozen plasma may be used when specific agents are unavailable, though caution is advised. ACE inhibitor–induced angioedema requires immediate discontinuation of the offending drug.
Disposition And Follow-Up
Patients with airway involvement or persistent systemic symptoms require admission and monitored care. Those with mild, nonprogressive symptoms may be discharged after observation with antihistamines, steroids, and clear return precautions. Referral to an allergist or immunologist is recommended for recurrent, hereditary, or unexplained cases.
Clinical Pearls And Pitfalls
Airway compromise can evolve rapidly and unpredictably, necessitating early intervention. Standard allergic therapies may be ineffective in bradykinin-mediated angioedema. Recognition of hereditary angioedema and ACE inhibitor–related cases is critical to avoid delayed or ineffective treatment.
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Emergency And Acute Medicine – Anemia
Core Definition
Anemia refers to a reduction below normal in total red blood cell (RBC) mass. It is most commonly identified by decreased hemoglobin concentration, hematocrit, or RBC count. Normal reference values vary with age, sex, altitude, and physiologic state. Because hemoglobin and hematocrit reflect concentrations, values may fall due to reduced RBC mass or increased plasma volume. Importantly, anemia is never a normal variant and always signifies an underlying disorder or deficiency that requires evaluation.
Causative Mechanisms
The most common cause of anemia is excessive blood loss, including trauma, gastrointestinal hemorrhage, and menstruation. Increased RBC destruction (hemolysis) may occur due to hypersplenism, autoimmune processes, mechanical injury, toxins, infections, or inherited membrane and enzyme defects. Reduced RBC production results from impaired bone marrow function or deficiencies and is commonly classified by RBC size into microcytic, macrocytic, or normocytic patterns.
Clinical Presentation
Symptoms depend on the severity, chronicity, and speed of onset. Acute anemia may produce hypovolemia, whereas chronic mild anemia may be asymptomatic. Common complaints include fatigue, reduced exercise tolerance, dyspnea on exertion, chest pain, syncope, and signs of bleeding. Physical findings may include pallor, tachycardia, murmurs, orthostatic hypotension, jaundice, splenomegaly, neurologic deficits, or nail and skin changes that reflect the underlying cause.
Initial Evaluation
A focused history should assess bleeding, chronic disease, nutritional status, medication use, and family history. Vital signs and orthostatic measurements are essential. The primary goals are to determine whether anemia is due to blood loss, hemolysis, or impaired RBC production and to assess hemodynamic stability.
Laboratory Assessment
Initial testing includes a complete blood count with RBC indices, reticulocyte count, and peripheral smear. Reticulocyte response helps distinguish between underproduction and increased destruction or loss. Additional studies may include iron studies, vitamin B12 and folate levels, renal function tests, hemolysis markers, stool occult blood testing, and specialized assays such as hemoglobin electrophoresis when indicated.
Diagnostic Considerations
Patterns of anemia guide further evaluation. Microcytic anemia suggests iron deficiency or thalassemia; macrocytic anemia raises concern for vitamin deficiencies, liver disease, or marrow disorders; normocytic anemia may indicate acute blood loss, chronic disease, renal failure, or marrow suppression. Bone marrow biopsy is reserved for selected cases involving suspected marrow pathology.
Differential Diagnoses
Important considerations include acute blood loss, anemia of chronic disease, hemolysis, malignancy, nutritional deficiencies, bone marrow failure, and dilutional anemia. Age-specific factors apply in pediatric, pregnant, and elderly populations.
Emergency Management
Immediate treatment is dictated by severity and stability. Patients with ongoing hemorrhage or hemodynamic compromise require airway support, oxygen, IV access, crystalloid resuscitation, and transfusion when indicated. Most chronic anemias identified in the emergency department do not require urgent intervention.
Definitive Therapy
Management targets the underlying cause. Iron supplementation is used for iron deficiency, erythropoietin for renal failure–associated anemia, corticosteroids or immunosuppression for autoimmune hemolysis, vitamin replacement for nutritional deficiencies, and disease-specific therapies for hematologic malignancies or hemoglobinopathies.
Disposition And Follow-Up
Admission is required for unstable patients, those with symptomatic or severe anemia, ongoing blood loss, or need for transfusion. Stable patients may be discharged with clear outpatient follow-up for diagnostic evaluation and treatment. Newly diagnosed anemia always warrants further investigation.
Clinical Insights And Common Errors
Anemia is a sign, not a diagnosis, and its cause must be identified. Life-threatening cases require rapid correction, while most emergency department presentations represent chronic disease. Failure to recognize occult bleeding or hemolysis and assuming anemia is benign are frequent pitfalls.
Core Definition
Anemia refers to a reduction below normal in total red blood cell (RBC) mass. It is most commonly identified by decreased hemoglobin concentration, hematocrit, or RBC count. Normal reference values vary with age, sex, altitude, and physiologic state. Because hemoglobin and hematocrit reflect concentrations, values may fall due to reduced RBC mass or increased plasma volume. Importantly, anemia is never a normal variant and always signifies an underlying disorder or deficiency that requires evaluation.
Causative Mechanisms
The most common cause of anemia is excessive blood loss, including trauma, gastrointestinal hemorrhage, and menstruation. Increased RBC destruction (hemolysis) may occur due to hypersplenism, autoimmune processes, mechanical injury, toxins, infections, or inherited membrane and enzyme defects. Reduced RBC production results from impaired bone marrow function or deficiencies and is commonly classified by RBC size into microcytic, macrocytic, or normocytic patterns.
Clinical Presentation
Symptoms depend on the severity, chronicity, and speed of onset. Acute anemia may produce hypovolemia, whereas chronic mild anemia may be asymptomatic. Common complaints include fatigue, reduced exercise tolerance, dyspnea on exertion, chest pain, syncope, and signs of bleeding. Physical findings may include pallor, tachycardia, murmurs, orthostatic hypotension, jaundice, splenomegaly, neurologic deficits, or nail and skin changes that reflect the underlying cause.
Initial Evaluation
A focused history should assess bleeding, chronic disease, nutritional status, medication use, and family history. Vital signs and orthostatic measurements are essential. The primary goals are to determine whether anemia is due to blood loss, hemolysis, or impaired RBC production and to assess hemodynamic stability.
Laboratory Assessment
Initial testing includes a complete blood count with RBC indices, reticulocyte count, and peripheral smear. Reticulocyte response helps distinguish between underproduction and increased destruction or loss. Additional studies may include iron studies, vitamin B12 and folate levels, renal function tests, hemolysis markers, stool occult blood testing, and specialized assays such as hemoglobin electrophoresis when indicated.
Diagnostic Considerations
Patterns of anemia guide further evaluation. Microcytic anemia suggests iron deficiency or thalassemia; macrocytic anemia raises concern for vitamin deficiencies, liver disease, or marrow disorders; normocytic anemia may indicate acute blood loss, chronic disease, renal failure, or marrow suppression. Bone marrow biopsy is reserved for selected cases involving suspected marrow pathology.
Differential Diagnoses
Important considerations include acute blood loss, anemia of chronic disease, hemolysis, malignancy, nutritional deficiencies, bone marrow failure, and dilutional anemia. Age-specific factors apply in pediatric, pregnant, and elderly populations.
Emergency Management
Immediate treatment is dictated by severity and stability. Patients with ongoing hemorrhage or hemodynamic compromise require airway support, oxygen, IV access, crystalloid resuscitation, and transfusion when indicated. Most chronic anemias identified in the emergency department do not require urgent intervention.
Definitive Therapy
Management targets the underlying cause. Iron supplementation is used for iron deficiency, erythropoietin for renal failure–associated anemia, corticosteroids or immunosuppression for autoimmune hemolysis, vitamin replacement for nutritional deficiencies, and disease-specific therapies for hematologic malignancies or hemoglobinopathies.
Disposition And Follow-Up
Admission is required for unstable patients, those with symptomatic or severe anemia, ongoing blood loss, or need for transfusion. Stable patients may be discharged with clear outpatient follow-up for diagnostic evaluation and treatment. Newly diagnosed anemia always warrants further investigation.
Clinical Insights And Common Errors
Anemia is a sign, not a diagnosis, and its cause must be identified. Life-threatening cases require rapid correction, while most emergency department presentations represent chronic disease. Failure to recognize occult bleeding or hemolysis and assuming anemia is benign are frequent pitfalls.
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Emergency And Acute Medicine – Anaphylaxis
Clinical Overview
Anaphylaxis is an acute, life-threatening systemic hypersensitivity reaction that develops rapidly after exposure to an antigen in a sensitized individual. It represents a form of distributive shock caused by widespread mediator release, leading to vasodilation, increased vascular permeability, smooth-muscle contraction, and excessive glandular secretion. These physiologic changes result in reduced systemic vascular resistance, decreased venous return and cardiac output, and intravascular volume depletion. Anaphylaxis accounts for hundreds of deaths annually in the United States and thousands of emergency department visits each month.
Underlying Causes
IgE-mediated reactions are most commonly triggered by antibiotics (particularly penicillins), insect venoms, foods such as peanuts, shellfish, and tree nuts, latex, vaccines, and monoclonal antibody therapies. Non–IgE-mediated reactions may occur with iodine-based contrast agents, opiates, and vancomycin.
Special Considerations In Children: Food allergens—especially milk, egg, wheat, soy, and peanuts—are the most frequent triggers, and even trace exposures may provoke severe reactions.
Clinical Manifestations
Symptoms typically begin within minutes of antigen exposure. Skin and mucosal involvement is present in the vast majority of cases, with urticaria, erythema, pruritus, and angioedema being common. Patients may report an early sense of impending doom. Respiratory findings range from nasal congestion to bronchospasm and upper airway edema. Cardiovascular involvement may include hypotension, arrhythmias, or myocardial ischemia. Gastrointestinal symptoms such as nausea, vomiting, and diarrhea may occur, along with ocular irritation, neurologic symptoms including seizures, and, rarely, hematologic abnormalities such as coagulopathy.
Key Historical Features
Diagnosis is clinical. A focused history should identify prior allergic reactions, known triggers, and recent exposures to foods, medications, or environmental allergens.
Physical Examination Focus
Findings usually involve two or more organ systems, commonly the skin, respiratory tract, gastrointestinal tract, or cardiovascular system. Airway compromise or hypotension may not be present initially but can develop rapidly.
Essential Clinical Assessment
Anaphylaxis is diagnosed on clinical grounds, and early recognition is critical. Ancillary testing should not delay treatment. ECG monitoring is advised in patients with cardiac history, ischemic symptoms, or advanced age.
Diagnostic Evaluation
Laboratory studies are generally not useful in the acute setting. Serum tryptase levels may aid retrospective confirmation. Chest radiography may show hyperinflation in cases with bronchospasm.
Alternative Diagnoses To Consider
Conditions that may mimic anaphylaxis include pulmonary embolism, acute coronary syndromes, asthma, airway obstruction, vasovagal syncope, hereditary angioedema, systemic mastocytosis, hypoglycemia, carcinoid syndrome, and foreign body aspiration.
Prehospital Care Principles
Early airway assessment, oxygen supplementation, IV access, and continuous monitoring are essential. Intramuscular epinephrine should be administered promptly, even before IV access is obtained. Progressive laryngeal edema may necessitate early airway intervention.
Immediate Stabilization Measures
Airway protection and adequate ventilation take priority. Orotracheal intubation is preferred when airway compromise is anticipated. Advanced airway techniques may be required in the presence of significant edema. Epinephrine may be administered via IM, IV, or endotracheal routes, along with aggressive fluid resuscitation.
Emergency Department Management
Continuous cardiac and vital-sign monitoring is required. Persistent bronchospasm is treated with inhaled β2-agonists. Hypotension is addressed with IV fluids and vasopressors if needed. Antihistamines reduce histamine-mediated effects, corticosteroids help prevent biphasic reactions, and glucagon is indicated for epinephrine-resistant anaphylaxis in patients taking β-blockers.
Pharmacologic Therapy
First-line therapy includes intramuscular epinephrine, H1 antihistamines, corticosteroids, and inhaled bronchodilators. Second-line agents include racemic epinephrine, H2 blockers, and glucagon when indicated. Special caution is required in patients receiving β-blockers.
Disposition Planning
Patients requiring intubation or ongoing respiratory or hemodynamic support should be admitted to an intensive care setting. Those with persistent or severe reactions warrant inpatient observation due to the risk of biphasic reactions. Patients with complete symptom resolution may be discharged after a period of observation.
Post-Discharge Follow-Up
All patients should receive early outpatient follow-up, ideally with an allergist. Education regarding trigger avoidance and prescription of self-injectable epinephrine are essential. Patients should be instructed on proper auto-injector use and advised to carry it at all times.
Clinical Pearls And Pitfalls
Delayed recognition of anaphylaxis can result in rapid airway compromise and cardiovascular collapse. Early administration of epinephrine is the single most critical intervention. Patients with a prior history of anaphylaxis require education on avoidance strategies and prompt self-treatment to prevent fatal outcomes.
Clinical Overview
Anaphylaxis is an acute, life-threatening systemic hypersensitivity reaction that develops rapidly after exposure to an antigen in a sensitized individual. It represents a form of distributive shock caused by widespread mediator release, leading to vasodilation, increased vascular permeability, smooth-muscle contraction, and excessive glandular secretion. These physiologic changes result in reduced systemic vascular resistance, decreased venous return and cardiac output, and intravascular volume depletion. Anaphylaxis accounts for hundreds of deaths annually in the United States and thousands of emergency department visits each month.
Underlying Causes
IgE-mediated reactions are most commonly triggered by antibiotics (particularly penicillins), insect venoms, foods such as peanuts, shellfish, and tree nuts, latex, vaccines, and monoclonal antibody therapies. Non–IgE-mediated reactions may occur with iodine-based contrast agents, opiates, and vancomycin.
Special Considerations In Children: Food allergens—especially milk, egg, wheat, soy, and peanuts—are the most frequent triggers, and even trace exposures may provoke severe reactions.
Clinical Manifestations
Symptoms typically begin within minutes of antigen exposure. Skin and mucosal involvement is present in the vast majority of cases, with urticaria, erythema, pruritus, and angioedema being common. Patients may report an early sense of impending doom. Respiratory findings range from nasal congestion to bronchospasm and upper airway edema. Cardiovascular involvement may include hypotension, arrhythmias, or myocardial ischemia. Gastrointestinal symptoms such as nausea, vomiting, and diarrhea may occur, along with ocular irritation, neurologic symptoms including seizures, and, rarely, hematologic abnormalities such as coagulopathy.
Key Historical Features
Diagnosis is clinical. A focused history should identify prior allergic reactions, known triggers, and recent exposures to foods, medications, or environmental allergens.
Physical Examination Focus
Findings usually involve two or more organ systems, commonly the skin, respiratory tract, gastrointestinal tract, or cardiovascular system. Airway compromise or hypotension may not be present initially but can develop rapidly.
Essential Clinical Assessment
Anaphylaxis is diagnosed on clinical grounds, and early recognition is critical. Ancillary testing should not delay treatment. ECG monitoring is advised in patients with cardiac history, ischemic symptoms, or advanced age.
Diagnostic Evaluation
Laboratory studies are generally not useful in the acute setting. Serum tryptase levels may aid retrospective confirmation. Chest radiography may show hyperinflation in cases with bronchospasm.
Alternative Diagnoses To Consider
Conditions that may mimic anaphylaxis include pulmonary embolism, acute coronary syndromes, asthma, airway obstruction, vasovagal syncope, hereditary angioedema, systemic mastocytosis, hypoglycemia, carcinoid syndrome, and foreign body aspiration.
Prehospital Care Principles
Early airway assessment, oxygen supplementation, IV access, and continuous monitoring are essential. Intramuscular epinephrine should be administered promptly, even before IV access is obtained. Progressive laryngeal edema may necessitate early airway intervention.
Immediate Stabilization Measures
Airway protection and adequate ventilation take priority. Orotracheal intubation is preferred when airway compromise is anticipated. Advanced airway techniques may be required in the presence of significant edema. Epinephrine may be administered via IM, IV, or endotracheal routes, along with aggressive fluid resuscitation.
Emergency Department Management
Continuous cardiac and vital-sign monitoring is required. Persistent bronchospasm is treated with inhaled β2-agonists. Hypotension is addressed with IV fluids and vasopressors if needed. Antihistamines reduce histamine-mediated effects, corticosteroids help prevent biphasic reactions, and glucagon is indicated for epinephrine-resistant anaphylaxis in patients taking β-blockers.
Pharmacologic Therapy
First-line therapy includes intramuscular epinephrine, H1 antihistamines, corticosteroids, and inhaled bronchodilators. Second-line agents include racemic epinephrine, H2 blockers, and glucagon when indicated. Special caution is required in patients receiving β-blockers.
Disposition Planning
Patients requiring intubation or ongoing respiratory or hemodynamic support should be admitted to an intensive care setting. Those with persistent or severe reactions warrant inpatient observation due to the risk of biphasic reactions. Patients with complete symptom resolution may be discharged after a period of observation.
Post-Discharge Follow-Up
All patients should receive early outpatient follow-up, ideally with an allergist. Education regarding trigger avoidance and prescription of self-injectable epinephrine are essential. Patients should be instructed on proper auto-injector use and advised to carry it at all times.
Clinical Pearls And Pitfalls
Delayed recognition of anaphylaxis can result in rapid airway compromise and cardiovascular collapse. Early administration of epinephrine is the single most critical intervention. Patients with a prior history of anaphylaxis require education on avoidance strategies and prompt self-treatment to prevent fatal outcomes.
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Emergency And Acute Medicine – Anal Fissure
Basics Description
Hard stool passage causes a linear tear in the anoderm. The fissure typically extends from the dentate line to the anoderm, most commonly in the posterior midline (95%) and less often in the anterior midline (5%). Externally, a skin tag or sentinel pile may form; internally, a hypertrophied anal papilla can be present. Chronic fissures may expose fibers of the internal sphincter with an associated sentinel pile.
Etiology
Increased anal sphincter tone and stress lead to local ischemia of the posterior anoderm. Diarrhea or passage of hard stool can tear the anoderm. Local trauma, including anal intercourse or sexual abuse, may also be causative. Lateral fissures suggest underlying systemic disease such as Crohn disease, anal cancer, leukemia, syphilis, or prior anal surgery.
Diagnosis – Signs And Symptoms
Patients commonly report bright red blood per rectum, usually noted on toilet paper. Pain is sharp, cutting, throbbing, or burning during bowel movements and may persist for hours afterward. Constipation is frequent due to pain-related stool avoidance, often with hard, nondeformable stools.
History
Key historical features include recent constipation or passage of hard stool, episodes of diarrhea, and bright red blood on toilet paper.
Physical Examination
Inspection is performed by gently retracting the buttocks and asking the patient to bear down to visualize the fissure. Severe pain often precludes manual or digital rectal examination; topical anesthetics such as lidocaine jelly or ELA-Max5 may be applied prior to examination. It is important to exclude abscess or tumor.
Pediatric Considerations: A clear test tube may be used as an improvised anoscope to visualize the anal canal and fissure.
Essential Workup
A careful rectal examination is the primary diagnostic step.
Diagnostic Tests And Interpretation
Laboratory testing may include hematocrit if there is a history of severe bleeding. CT pelvis is indicated to exclude anorectal abscess or tumor if a palpable mass is identified.
Differential Diagnosis
Consider Crohn disease, chronic ulcerative colitis, anorectal carcinoma, perirectal abscess, thrombosed hemorrhoid, sexual abuse, tuberculosis, syphilis, lymphoma, leukemia, and prior anal surgery.
Treatment – Prehospital
Establish IV access in patients with significant rectal bleeding.
Initial Stabilization And Therapy
Provide analgesia for patients with significant pain.
Emergency Department Treatment And Procedures
Pain control may include IV, IM, or oral NSAIDs and acetaminophen. Muscle relaxants to relieve sphincter spasm include cyclobenzaprine, diazepam, topical diltiazem 2% ointment, or nifedipine 0.3% ointment. Topical anesthetics such as ELA-Max5 or 2% lidocaine jelly may be used. Sitz baths with warm water help reduce sphincter spasm.
Dietary management includes a high-fiber diet (approximately 20 g/day), psyllium supplementation, and increased oral hydration (10–12 glasses of water daily).
Medications
Common options include cyclobenzaprine, diazepam, diltiazem 2% ointment, docusate sodium, ELA-Max5, ibuprofen, nifedipine 0.3% ointment, and nitroglycerin 0.2% ointment as outlined above.
Follow-Up Disposition
Admission is indicated for severe abdominal pain or distention due to fecal impaction. Most acute fissures are managed conservatively as outpatients; chronic fissures require operative referral.
Follow-Up Recommendations
Colorectal surgery or gastroenterology follow-up is recommended for symptomatic fissures.
Clinical Pearls And Common Pitfalls
A meticulous rectal examination is essential to identify fissures and exclude alternative pathology. Optimal management combines pain control with sphincter relaxation. Discharge instructions should emphasize constipation prevention to reduce recurrence.
Basics Description
Hard stool passage causes a linear tear in the anoderm. The fissure typically extends from the dentate line to the anoderm, most commonly in the posterior midline (95%) and less often in the anterior midline (5%). Externally, a skin tag or sentinel pile may form; internally, a hypertrophied anal papilla can be present. Chronic fissures may expose fibers of the internal sphincter with an associated sentinel pile.
Etiology
Increased anal sphincter tone and stress lead to local ischemia of the posterior anoderm. Diarrhea or passage of hard stool can tear the anoderm. Local trauma, including anal intercourse or sexual abuse, may also be causative. Lateral fissures suggest underlying systemic disease such as Crohn disease, anal cancer, leukemia, syphilis, or prior anal surgery.
Diagnosis – Signs And Symptoms
Patients commonly report bright red blood per rectum, usually noted on toilet paper. Pain is sharp, cutting, throbbing, or burning during bowel movements and may persist for hours afterward. Constipation is frequent due to pain-related stool avoidance, often with hard, nondeformable stools.
History
Key historical features include recent constipation or passage of hard stool, episodes of diarrhea, and bright red blood on toilet paper.
Physical Examination
Inspection is performed by gently retracting the buttocks and asking the patient to bear down to visualize the fissure. Severe pain often precludes manual or digital rectal examination; topical anesthetics such as lidocaine jelly or ELA-Max5 may be applied prior to examination. It is important to exclude abscess or tumor.
Pediatric Considerations: A clear test tube may be used as an improvised anoscope to visualize the anal canal and fissure.
Essential Workup
A careful rectal examination is the primary diagnostic step.
Diagnostic Tests And Interpretation
Laboratory testing may include hematocrit if there is a history of severe bleeding. CT pelvis is indicated to exclude anorectal abscess or tumor if a palpable mass is identified.
Differential Diagnosis
Consider Crohn disease, chronic ulcerative colitis, anorectal carcinoma, perirectal abscess, thrombosed hemorrhoid, sexual abuse, tuberculosis, syphilis, lymphoma, leukemia, and prior anal surgery.
Treatment – Prehospital
Establish IV access in patients with significant rectal bleeding.
Initial Stabilization And Therapy
Provide analgesia for patients with significant pain.
Emergency Department Treatment And Procedures
Pain control may include IV, IM, or oral NSAIDs and acetaminophen. Muscle relaxants to relieve sphincter spasm include cyclobenzaprine, diazepam, topical diltiazem 2% ointment, or nifedipine 0.3% ointment. Topical anesthetics such as ELA-Max5 or 2% lidocaine jelly may be used. Sitz baths with warm water help reduce sphincter spasm.
Dietary management includes a high-fiber diet (approximately 20 g/day), psyllium supplementation, and increased oral hydration (10–12 glasses of water daily).
Medications
Common options include cyclobenzaprine, diazepam, diltiazem 2% ointment, docusate sodium, ELA-Max5, ibuprofen, nifedipine 0.3% ointment, and nitroglycerin 0.2% ointment as outlined above.
Follow-Up Disposition
Admission is indicated for severe abdominal pain or distention due to fecal impaction. Most acute fissures are managed conservatively as outpatients; chronic fissures require operative referral.
Follow-Up Recommendations
Colorectal surgery or gastroenterology follow-up is recommended for symptomatic fissures.
Clinical Pearls And Common Pitfalls
A meticulous rectal examination is essential to identify fissures and exclude alternative pathology. Optimal management combines pain control with sphincter relaxation. Discharge instructions should emphasize constipation prevention to reduce recurrence.
