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.

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.

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.

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.

Emergency and Acute Medicine – Digoxin Poisoning


Basics
Description
Acute digitalis toxicity, typically seen with elevated levels in children or intentional overdose, occurs through inhibition of the sodium–potassium ATPase pump in cell membranes. This allows increased intracellular calcium, leading to stronger myocardial contraction, increased extracellular potassium, enhanced vagal tone, slowed atrioventricular (AV) node conduction (vagotonic effect), increased automaticity, prolonged refractory periods, and predominantly bradydysrhythmias.
Chronic digitalis toxicity, usually occurring in elderly patients at therapeutic to toxic levels, also involves sodium–potassium ATPase inhibition with increased intracellular calcium and vagal tone. These patients commonly develop bradydysrhythmias, increased automaticity, tachydysrhythmias, and are often hypokalemic due to concurrent diuretic use.


Etiology
Sources include digoxin and digitoxin pharmaceuticals as well as plants and animals containing cardiac glycosides such as foxglove, oleander (white and yellow), lily of the valley, dogbane, red squill, cane toad, and Colorado River toad.


Diagnosis
Signs and symptoms
Toxicity typically begins about 2 hours after oral ingestion and as early as 15 minutes after intravenous administration. Toxicity may occur at normal digoxin levels in chronic exposure and may be absent despite elevated levels in acute overdose.
Cardiovascular manifestations include a wide range of dysrhythmias: premature ventricular contractions (most common), paroxysmal atrial tachycardia with AV block, nonparoxysmal accelerated junctional tachycardia, atrial fibrillation or flutter, bigeminy, sinus arrhythmia, AV blocks, bradycardia, ventricular tachycardia, ventricular fibrillation, and the pathognomonic bidirectional ventricular tachycardia. Other findings include hypotension, syncope, shock, cardiovascular collapse, and exacerbation of congestive heart failure.
Central nervous system findings include agitation, lethargy, psychosis, and characteristic visual disturbances such as blurred vision, scotomas, photophobia, and green-to-yellow halos.
Gastrointestinal symptoms include anorexia, nausea, vomiting, and abdominal pain.
History may reveal accidental pediatric or adult overdose, intentional acute or chronic overdose, unintentional chronic toxicity due to declining renal clearance or dose escalation, or recent antibiotic use—especially macrolides—that alter gastrointestinal flora and increase digoxin absorption by reducing Eubacterium lentum.


Physical examination
Common findings include altered mental status, bradycardia or tachycardia, irregular rhythm, and hypotension.


Essential workup
Electrocardiography is required to evaluate for dysrhythmias. Serum digoxin level should be obtained, recognizing that steady-state levels are most accurate when measured more than 6 hours after oral ingestion. False elevations may occur with spironolactone use, pregnancy, hyperbilirubinemia, chronic renal failure, liver failure, or congestive heart failure. Levels may be falsely elevated after administration of digoxin-specific Fab fragments.


Diagnosis tests and interpretation
Laboratory studies
Electrolytes, blood urea nitrogen, creatinine, and glucose should be assessed. Hypokalemia predisposes to toxicity, whereas hyperkalemia in acute poisoning correlates more strongly with mortality than digoxin serum levels and should be followed serially. Calcium and magnesium levels should also be measured.
Serum digoxin concentration should not be obtained after digoxin-specific Fab fragments are administered, as results will be inaccurate.


Differential diagnosis
Consider overdoses involving calcium channel blockers, β-blockers, clonidine, organophosphates, quinidine, procainamide, other antidysrhythmics or antihypertensives, primary cardiac dysrhythmias, and acute gastroenteritis.


Treatment
Prehospital care
Establish intravenous access, initiate continuous cardiac monitoring, and apply defibrillation pads. If cardioversion is required for tachydysrhythmias, use low-energy shocks (around 50 J), as higher energy may precipitate refractory arrhythmias.


Initial stabilization
Follow airway, breathing, and circulation principles. Provide oxygen, intravenous fluids if hypovolemic, and administer naloxone, thiamine, and dextrose for altered mental status when indicated.


Emergency department treatment and procedures
Cardiac arrest should be managed according to standard advanced cardiac life support protocols, including defibrillation for ventricular fibrillation or pulseless ventricular tachycardia. Administer digoxin-specific antibody Fab fragments promptly, typically 5–20 vials intravenously as indicated. Magnesium sulfate 2 g IV may be given, and resuscitation should continue for at least 30 minutes after Fab administration.
Supportive care includes activated charcoal for acute ingestion, magnesium repletion, and treatment of hyperkalemia with insulin, dextrose, bicarbonate, or sodium polystyrene sulfonate. Calcium is generally avoided unless life-saving membrane stabilization is required in unstable patients. In hemodynamically stable patients with hyperkalemia from digoxin toxicity, digoxin-specific Fab fragments are the first-line therapy.


Dysrhythmia management
First-line therapy is digoxin-specific antibody Fab fragments (Digibind or DigiFab). Indications include serum digoxin concentration ≥15 ng/mL at any time or ≥10 ng/mL at steady state, ingestion of more than 10 mg in adults or 0.2 mg/kg (or 4 mg) in children, hyperkalemia >5–5.5 mEq/L, hemodynamic instability, or life-threatening dysrhythmias such as ventricular tachycardia, ventricular fibrillation, atrial tachycardia with variable AV block, atropine-resistant bradycardia, or hypotension.
If Fab fragments are unavailable, lidocaine may be used for ventricular dysrhythmias without AV block, atropine or pacing for symptomatic bradycardia, and magnesium sulfate for torsades de pointes. Quinidine and procainamide are contraindicated. Electrical cardioversion is a last resort and should begin at low energy (10–50 J).


Medication
Activated charcoal may be administered at 1 g/kg if within 1 hour of ingestion. Each 40-mg vial of digoxin-specific Fab fragments neutralizes approximately 0.5 mg of digoxin. Dosing may be calculated based on amount ingested, serum concentration, or given empirically (acute toxicity: 5–10 vials; chronic toxicity: 1–2 vials). Additional doses may be required for rebound toxicity. Standard therapies for hyperkalemia and bradycardia should be used, with calcium reserved only when absolutely necessary.


Special populations
In older adults, dosing of Fab fragments is based on weight and serum concentration and does not change with renal or hepatic dysfunction, though rebound toxicity may occur in renal failure. Pediatric dosing follows the same weight-based principles as adults. Digoxin-specific Fab fragments are pregnancy category C.


Follow-up and disposition
Admission criteria
Patients with unstable cardiovascular status from acute or chronic toxicity require intensive care admission. Telemetry admission is appropriate for asymptomatic or mildly symptomatic patients with dysrhythmias or high risk for progression.


Discharge criteria
Patients may be discharged if digoxin levels are below 2 ng/mL, they remain asymptomatic for at least 6 hours, and no ECG abnormalities are present.


Follow-up recommendations
Psychiatric referral is recommended for patients with intentional overdose.


Pearls and pitfalls
In patients known to be taking digoxin who present with cardiovascular instability or hyperkalemia, treatment should begin immediately with digoxin-specific Fab fragments rather than waiting for confirmatory testing.

Emergency And Acute Medicine - Endometriosis


Basic Overview
Endometriosis is defined by the presence of endometrial glands and stroma located outside the uterine cavity. It is an estrogen-dependent, chronic inflammatory condition. The disorder affects approximately 6–10% of women of reproductive age and up to 50–60% of women and adolescents presenting with chronic pelvic pain. Ectopic endometrial tissue is most commonly found within the pelvic cavity, particularly on the ovaries and uterosacral ligaments, likely related to retrograde menstruation. Less commonly, implants may occur at distant sites, including the bowel, diaphragm, and lungs.


Underlying Mechanisms
The exact cause of endometriosis remains unknown.


Risk Factors And Special Populations
Risk factors include early menarche, short menstrual cycles, anatomic obstruction to menstrual outflow, and a suspected genetic predisposition supported by family and twin studies.
In pediatric patients, endometriosis does not occur before menarche.


Clinical Presentation
Symptoms vary widely and are often chronic and cyclical. Dysmenorrhea is the most common complaint, occurring in the majority of patients. Other frequent symptoms include deep pelvic pain, dyspareunia, abnormal uterine bleeding, lower abdominal pain, nausea, abdominal bloating, and infertility, which affects up to half of patients.


Physical Examination Findings
Pelvic examination may reveal focal tenderness, particularly along the uterosacral ligaments, a retroverted uterus, rectovaginal nodularity, or a palpable pelvic mass. Findings depend on the location and extent of ectopic endometrial tissue and may be subtle or absent. Rarely, thoracic involvement may cause catamenial pneumothorax, characterized by recurrent pneumothorax coinciding with menses.


Initial Evaluation Priorities
A pregnancy test is mandatory in all patients of reproductive age. Testing for gonorrhea and chlamydia should be considered. Additional diagnostic studies are guided by the history and physical examination. Endometriosis is rarely definitively diagnosed in the emergency department.


Diagnostic Studies And Interpretation
Laboratory evaluation typically includes pregnancy testing and sexually transmitted infection screening. Hematocrit and type-and-screen testing are indicated if bleeding is significant.
Imaging has limited sensitivity in the acute setting. Ultrasound and CT have low diagnostic yield, while MRI offers higher sensitivity and specificity but is not routinely used emergently. Definitive diagnosis generally requires laparoscopy.


Conditions To Consider
The differential diagnosis includes appendicitis, ectopic pregnancy, pelvic inflammatory disease, tubo-ovarian abscess, ovarian cyst or torsion, inflammatory bowel disease, irritable bowel syndrome, dysfunctional uterine bleeding, and physiologic menstrual pain such as mittelschmerz.


Emergency Management Principles
Prehospital care focuses on stabilization and analgesia as needed.


Initial Stabilization Measures
Patients with hypotension or tachycardia due to blood loss should receive isotonic intravenous fluids. Transfusion with packed red blood cells may be necessary in cases of significant hemorrhage.


Emergency Department Interventions
Management is largely symptomatic and includes pain control. Hormonal therapy, such as oral progestins or gonadotropin-releasing hormone agonists, should be initiated only in consultation with gynecology or the patient’s primary care clinician. Gynecology consultation is indicated for severe pain, heavy bleeding, or suspected complications.


Medication Options
First-line analgesia includes nonsteroidal anti-inflammatory drugs and acetaminophen. Ketorolac may be used for moderate to severe pain, and opioids are reserved for refractory cases.


Disposition And Follow-Up
Hospital admission is warranted for patients with intractable pain, significant bleeding, peritoneal signs, diagnostic uncertainty, or need for further evaluation. Most patients with suspected endometriosis who are clinically stable can be discharged with adequate pain control and outpatient gynecology referral.


Follow-Up Guidance
All suspected cases require referral to a gynecologist for definitive diagnosis and long-term management.


Clinical Insights And Common Errors
Endometriosis affects a substantial proportion of women of reproductive age and commonly presents with cyclical pelvic pain. It is rarely diagnosed during an initial emergency department visit, and delays in diagnosis often span years. Emergency clinicians must exclude other acute and life-threatening conditions, manage symptoms appropriately, and ensure reliable outpatient follow-up. Endometriosis is a chronic disease that requires ongoing care by gynecology or primary care providers.

Emergency And Acute Medicine - Endocarditis


Basic Overview
Endocarditis is an inflammatory condition involving the endothelial lining of the heart. It most commonly affects native cardiac valves but may also involve prosthetic valves, the interventricular septum, chordae tendineae, mural endocardium, or intracardiac devices. The disease is defined by the formation of vegetations, which are thrombotic aggregates of fibrin and platelets that become colonized by microorganisms. Progressive bacterial growth enlarges these vegetations, disrupts normal blood flow, provokes inflammation, and may result in systemic embolization. The condition is almost always infectious in origin, typically bacterial. Rare noninfectious forms include nonbacterial thrombotic (marantic) endocarditis associated with hypercoagulable states and Libman–Sacks endocarditis related to systemic lupus erythematosus, both characterized by small sterile vegetations.


Epidemiologic Features
Endocarditis occurs more frequently in men, with incidence rates significantly higher than in women. Risk increases with advanced age, poor dental hygiene, and comorbid medical conditions. Structural heart disease, including rheumatic heart disease, mitral valve prolapse, aortic valve dysfunction, congenital heart defects, and prosthetic valves, predisposes patients due to altered intracardiac flow. Hemodialysis, diabetes, and indwelling intravascular catheters further increase risk. Intravenous drug use confers a particularly high risk and commonly involves right-sided valves. Septic embolization may lead to neurologic, pulmonary, splenic, renal, hepatic, or coronary complications, as well as mycotic aneurysm formation.


Causative Mechanisms
Most cases are due to bacterial infection. Common pathogens include Staphylococcus aureus, the most frequent cause across all populations and especially prevalent among intravenous drug users. Streptococcus viridans is a typical cause of native valve disease and originates from the oropharynx. Streptococcus bovis is associated with colonic polyps or gastrointestinal malignancy. Streptococcus pneumoniae may cause aggressive valvular destruction and heart failure. Staphylococcus epidermidis is frequently implicated in prosthetic valve infections. Enterococci are often linked to genitourinary or gastrointestinal instrumentation. Fungal causes, such as Candida or Aspergillus, occur primarily in immunocompromised patients or those with prosthetic valves. Culture-negative endocarditis may result from organisms such as Coxiella burnetii, Bartonella, or Brucella.


Clinical Presentation
Fever is the most common symptom, present in the majority of patients, though it may be absent in the elderly, those with chronic renal failure, heart failure, or severe debility. Constitutional symptoms include chills, sweats, rigors, malaise, and flulike illness. Cardiac findings often include a new or changing murmur and signs of heart failure. Embolic phenomena may cause neurologic deficits, stroke, or mycotic aneurysms. Cutaneous manifestations include petechiae, splinter hemorrhages, Osler nodes, and Janeway lesions. Splenomegaly, abdominal or back pain, arthralgias, and myalgias may also be present.


Diagnostic Assessment
Evaluation should focus on identifying risk factors in patients with unexplained fever. Multiple sets of blood cultures obtained before antibiotic administration are essential. Laboratory studies commonly show anemia, leukocytosis, elevated inflammatory markers, and microscopic hematuria. Electrocardiography may reveal arrhythmias or new conduction abnormalities. Chest radiography can demonstrate signs of heart failure or septic pulmonary emboli. Echocardiography is critical for diagnosis, with transesophageal echocardiography offering superior sensitivity for detecting vegetations, abscesses, and valvular dysfunction. Computed tomography may aid in identifying complications.


Differential Considerations
Conditions that may mimic endocarditis include rheumatic fever, atrial myxoma, acute pericarditis, myocardial infarction, aortic dissection with valvular involvement, thrombotic thrombocytopenic purpura, systemic lupus erythematosus, metastatic malignancy, septicemia, and cotton fever.


Initial Management Principles
Patients should be closely monitored for signs of heart failure or embolic complications. Early consultation with cardiology and cardiothoracic surgery is required for patients with severe valvular dysfunction, intracardiac abscess, prosthetic valve instability, persistent infection despite therapy, or large or fungal vegetations. Empiric intravenous bactericidal antibiotics should be initiated after blood cultures are obtained, with regimens tailored based on valve type, risk factors, and local resistance patterns.


Antimicrobial Therapy
Empiric treatment commonly includes combinations of penicillin, nafcillin, gentamicin, or vancomycin, adjusted once culture data are available. Prosthetic valve infections and intravenous drug use often require broader coverage, including rifampin. Resistant organisms may necessitate agents such as daptomycin or quinupristin–dalfopristin. Fungal endocarditis is treated with amphotericin B, and HACEK organisms respond well to ceftriaxone.


Disposition And Follow-Up
All patients with suspected or confirmed endocarditis require hospital admission. Individuals with hemodynamic instability, neurologic complications, or heart failure should be managed in a monitored or intensive care setting. There are no criteria for emergency department discharge.


Clinical Insights And Common Errors
Endocarditis should be strongly considered in any patient with fever and a new or changing murmur, even in the absence of known valvular disease. Health care exposure and indwelling devices are important risk factors. Failure to obtain adequate blood cultures before antibiotics or to recognize embolic and heart failure complications can delay diagnosis and worsen outcomes. All intravenous drug users presenting with fever should be admitted and evaluated for endocarditis.

Emergency And Acute Medicine - Encephalitis

Basics Overview
Encephalitis is an acute inflammatory process involving the brain parenchyma and accounts for approximately 20,000 cases annually in the United States, with an overall mortality near 10%. The inflammatory response leads to neuronal destruction, cerebral edema, and petechial hemorrhages. Central nervous system infection most commonly occurs via hematogenous spread from respiratory or gastrointestinal sources, blood transfusion, or organ transplantation. Certain pathogens, including rabies virus, herpes simplex virus (HSV), and varicella zoster virus (VZV), may reach the CNS through neural migration.

Etiologic Factors
Viral infections represent the most frequent cause, although noninfectious etiologies such as autoimmune, paraneoplastic, and collagen vascular diseases are increasingly recognized. In nearly half of cases, no specific cause is identified. HSV accounts for approximately 10–20% of all encephalitis cases, and early antiviral therapy significantly improves outcomes. Arboviruses cause 10–15% of cases and are transmitted by mosquitoes or ticks during warmer months. Eastern equine encephalitis is notable for its fulminant course and hippocampal involvement, while Western equine encephalitis tends to follow a nonspecific prodrome. Japanese encephalitis, the most common arboviral encephalitis worldwide, often progresses from mild systemic symptoms to severe neurologic dysfunction.

Flaviviruses such as West Nile virus have increased in incidence in North America and are associated with higher morbidity and mortality in elderly patients, with possible flaccid paralysis and respiratory failure. Enteroviruses primarily affect children and usually follow a benign course. Measles-related encephalitis may occur acutely or years after infection and often involves seizures and rapid neurologic decline. HIV-associated encephalitis is linked to low CD4 counts and presents with white matter degeneration, motor spasticity, and dementia. Rabies causes isolated CNS infection without systemic illness.

Nonviral infectious causes include Mycoplasma pneumoniae, Toxoplasma gondii, Rickettsia rickettsii, Mycobacterium tuberculosis, Borrelia burgdorferi, and Bartonella henselae. In immunocompromised patients, pathogens such as Cryptococcus neoformans, CMV, HHV-6, Listeria monocytogenes, and VZV are common. Autoimmune etiologies include anti-LGI1 and anti–NMDA receptor encephalitis.

Clinical Features And Symptoms
Encephalitis often begins after a brief flulike prodrome characterized by fever, headache, myalgias, sore throat, and reduced appetite. Progressive neurologic involvement includes altered mental status ranging from confusion to coma, personality changes, hallucinations, psychosis, agitation, or delirium. Seizures are common, as are focal neurologic deficits such as tremor, ataxia, cranial nerve palsies, and autonomic instability. Rash may accompany certain infectious causes. Papilledema may be present, and the disease course may be indolent or rapidly progressive, potentially resulting in permanent neurologic injury or death.

Diagnostic Evaluation
A lumbar puncture is essential and typically reveals lymphocytic pleocytosis, elevated protein, and normal glucose in viral etiologies. CSF should undergo Gram stain, culture, and targeted antigen or antibody testing based on clinical suspicion. PCR testing of CSF is critical for confirming viral causes, particularly HSV, VZV, enteroviruses, and West Nile virus. Blood studies include CBC, metabolic panel, liver function tests, and blood cultures. Imaging begins with CT to exclude mass lesions or hemorrhage, while MRI is more sensitive for detecting temporal lobe abnormalities typical of HSV encephalitis. EEG is useful in patients with seizures or unexplained altered mental status.

Differential Considerations
Conditions that may mimic encephalitis include meningitis, brain abscess, sepsis, ischemic or hemorrhagic stroke, head trauma, subarachnoid hemorrhage, metabolic encephalopathies, epilepsy, acute disseminated encephalomyelitis, neoplasms, and toxic exposures such as carbon monoxide.

Initial Management And Stabilization
Immediate priorities include airway protection, seizure control, and stabilization of vital functions. Patients with depressed consciousness or absent protective reflexes require intubation. Empiric treatment for altered mental status includes glucose, thiamine, and naloxone when indicated. Signs of increased intracranial pressure warrant hyperventilation and osmotic therapy with mannitol, along with neurosurgical consultation. Intravenous fluids should be administered cautiously to avoid worsening cerebral edema.

Emergency Department Care
Seizures are treated promptly with benzodiazepines, followed by longer-acting antiepileptic agents if recurrent. Although no specific therapy exists for most viral encephalitides, intravenous acyclovir must be initiated immediately when HSV encephalitis is suspected, based on clinical presentation and preliminary CSF or imaging findings. In immunocompromised patients, ganciclovir or foscarnet should be considered for CMV or HHV-6. Broad-spectrum antibiotics should be administered when meningitis cannot be excluded, especially in the presence of rash or systemic toxicity.

Pharmacologic Therapy
Recommended agents include intravenous acyclovir for suspected HSV, benzodiazepines for acute seizure control, fosphenytoin or phenobarbital for seizure prophylaxis, and mannitol for elevated intracranial pressure. Antiviral therapy should not be delayed while awaiting confirmatory testing.

Disposition And Follow-Up
All patients with suspected or confirmed encephalitis require hospital admission for close neurologic monitoring and definitive management.

Clinical Insights And Common Errors
Empiric treatment with acyclovir should be started immediately in any patient with unexplained encephalitis, as delays significantly increase morbidity and mortality. Failure to initiate early antiviral therapy remains one of the most critical and preventable errors in management.

Emergency And Acute Medicine - Electrical Injury


Basics Description
Electricity represents the movement of electrons through a conductor down a gradient from higher to lower concentration. The severity and pattern of electrical injury depend on multiple factors, including voltage, current strength and type, tissue resistance, and duration of contact. According to Ohm’s law, voltage equals current multiplied by resistance, meaning that current increases with higher voltage and decreases with greater resistance. Electrical sources are broadly divided into low- and high-voltage exposures. Household outlets typically supply 110 V, dryers and ranges about 220 V, subway third rails approximately 600 V, residential trunk lines around 7,620 V, and industrial power lines may reach 100,000 V. Some household devices contain internal transformers that increase voltage despite being plugged into low-voltage outlets.


Tissue resistance influences injury patterns. Nerves, muscles, and blood vessels have low resistance and conduct electricity efficiently, while bone, fat, and tendon have higher resistance. Moist skin lowers resistance, whereas calloused skin increases it. Higher resistance generates more heat at the tissue level. Current strength, measured in amperes, determines physiologic effects. Very small currents produce tingling, slightly higher levels cause pain, and increasing currents lead to muscle tetany, respiratory muscle paralysis, ventricular fibrillation, or asystole. Alternating current, used in homes and offices, reverses direction rhythmically and is more dangerous than direct current because it can cause sustained muscle contraction and prolonged contact, increasing the risk of ventricular fibrillation. Direct current, used in defibrillators and industrial sources, tends to cause a single powerful muscle contraction that may throw the victim away from the source, shortening exposure but increasing traumatic injury risk.


Electrical injuries follow a trimodal age distribution, affecting toddlers exposed to outlets and cords, adolescents engaging in risk-taking behaviors, and adults with occupational exposures.


Etiology
Electrical injuries occur through several mechanisms. Direct contact can cause electrothermal burns with coagulation necrosis of skin and deep tissues, often underestimating the true extent of injury. Flame injuries may result from ignition of clothing or surrounding materials. Electrical arcs can produce flash burns when high-voltage current passes through air, usually causing superficial partial-thickness burns. Primary electrical effects include cardiac dysrhythmias and sustained muscle contraction, while secondary injuries result from falls or being thrown due to intense muscle tetany.


Diagnosis Signs And Symptoms
Clinical manifestations vary by organ system. Head and neck involvement is common in high-voltage injuries and may include facial or corneal burns, tympanic membrane perforation, and delayed ocular complications such as cataracts or optic nerve damage. Cardiovascular effects are a leading cause of mortality and include cardiac arrest, ventricular fibrillation, asystole, and transient dysrhythmias. Respiratory compromise may occur from central respiratory inhibition, chest wall tetany, or traumatic lung injury. Neurologic findings range from transient confusion and amnesia to seizures, coma, spinal cord injury, and long-term neuropsychiatric sequelae. Vascular injury can lead to thrombosis, compartment syndrome, and renal failure from myoglobinuria. Musculoskeletal injuries may result from powerful muscle contractions, classically causing vertebral fractures, posterior shoulder dislocations, or femoral neck fractures. Dermatologic findings include entry and exit wounds, commonly on the hands, feet, or head, as well as characteristic “kissing” burns at flexor surfaces.


Essential Workup
Evaluation should include urinalysis to assess for myoglobin, electrocardiography, and cardiac enzymes in patients with high-voltage exposure or cardiorespiratory symptoms. Cardiac monitoring is indicated for patients with loss of consciousness, dysrhythmias, abnormal ECGs, hypoxia, chest pain, known heart disease, or significant associated trauma. Asymptomatic patients with normal ECGs and low-voltage exposure generally do not require prolonged monitoring.


Diagnosis Tests And Interpretation
Laboratory testing is often unnecessary for minor household exposures but should be considered when myoglobinuria or high-voltage injury is suspected. Creatine kinase, electrolytes, renal function tests, and cardiac biomarkers provide baseline assessment and help identify complications such as rhabdomyolysis, metabolic derangements, or myocardial injury. Imaging studies are guided by clinical findings and concern for associated trauma.


Differential Diagnosis
Important considerations include distinguishing deep electrothermal injury from superficial flash burns and separating electrical injury effects from trauma-related instability.


Treatment Prehospital
Scene safety is paramount, with immediate disconnection of the power source. Victims should be assumed to have traumatic injuries if unstable or unconscious, with spinal immobilization as indicated. Early cardiopulmonary resuscitation may be lifesaving in electrical arrest. Burns should be covered with clean, dry dressings, and fractures or dislocations splinted.


Initial Stabilization And Therapy
Management follows standard airway, breathing, and circulation principles. Local wound care, fracture reduction, and immobilization are addressed early.


Emergency Department Treatment And Procedures
Aggressive intravenous fluid resuscitation is often required due to extensive third spacing within injured muscle, targeting urine output of at least 1 mL/kg/hr. Foley catheter placement assists in monitoring. Prevention of renal failure includes maintaining urine flow and alkalinization with sodium bicarbonate to reduce myoglobin toxicity. Diuretics such as furosemide or mannitol may be used selectively. Tetanus prophylaxis and adequate analgesia are essential.


Medication
Therapeutic options include intravenous sodium bicarbonate to alkalinize urine, loop diuretics, and osmotic diuretics when indicated to maintain urine output and prevent renal complications.


Follow-Up Disposition
Admission is required for patients with loss of consciousness, dysrhythmias, abnormal ECGs, suspected deep tissue injury, myoglobinuria, significant burns, major trauma, or pregnancy beyond 20 weeks’ gestation. Patients with minor low-voltage injuries, normal examinations, and no symptoms after observation may be discharged with appropriate instructions.


Follow-Up Recommendations
Patients should receive specialty referral as indicated, including burn care, neurology for delayed neurologic symptoms, obstetrics for pregnant patients, dentistry or reconstructive surgery for pediatric oral burns, and ophthalmology to screen for delayed cataract formation.


Clinical Insights And Common Errors
Routine prolonged cardiac monitoring is unnecessary in asymptomatic patients with normal ECGs after low-voltage exposure. In significant electrical injuries, adequate fluid resuscitation is critical to counteract extensive third spacing and prevent renal failure.

Emergency And Acute Medicine - Elbow Injuries


Overview and injury patterns
Elbow trauma includes both bony and soft tissue injuries and varies by age and mechanism. In children, supracondylar fractures are the most frequent elbow fractures, most often occurring between 5 and 10 years of age and rarely after adolescence. These fractures are commonly extension type injuries caused by a fall on an outstretched hand with the elbow extended or hyperextended. Extension injuries are classified by displacement, ranging from nondisplaced to completely displaced fractures. Flexion type supracondylar fractures are less common and result from a direct blow to a flexed elbow. Radial head fractures typically occur through indirect mechanisms such as a fall on an outstretched hand, where force is transmitted up the forearm into the capitellum.


Soft tissue injuries are also common. Elbow dislocation is the second most frequent large-joint dislocation after the shoulder, with posterior dislocations accounting for the majority. Overuse injuries such as medial and lateral epicondylitis involve repetitive stress at the flexor or extensor tendon insertions and are often seen in individuals whose occupations or sports require repetitive wrist rotation and gripping.


Age specific considerations
In young children, radial head subluxation, commonly referred to as nursemaid’s elbow, accounts for a significant proportion of upper extremity injuries. It most often affects children aged 1 to 4 years and results from sudden longitudinal traction on the pronated forearm. Pediatric patients are also at risk for nonaccidental trauma, which should be considered when the history does not align with the injury pattern.


Mechanisms and causes
Understanding the mechanism of injury is essential, as most elbow injuries are caused by indirect trauma transmitted through the forearm bones, such as falls on an outstretched hand. Direct blows to the elbow are a less common cause of fractures or dislocations.


Clinical presentation and examination features
The manner in which a patient holds the injured arm often provides diagnostic clues. In flexion type supracondylar fractures, patients typically support the forearm with the opposite hand and hold the elbow flexed at 90 degrees. Extension type fractures may present with the arm held at the side in an abnormal configuration. Posterior elbow dislocations produce a prominent olecranon, whereas anterior dislocations cause loss of the normal olecranon contour. Radial head subluxation presents with the elbow slightly flexed and the forearm pronated, with resistance to movement. Epicondylitis develops gradually, with aching pain over the medial or lateral elbow that worsens with grasping or twisting activities.


Essential evaluation steps
Plain radiographs are the cornerstone of evaluation and should include assessment of the wrist and shoulder for associated injuries. A thorough neurovascular examination is mandatory, along with inspection of the skin and assessment for compartment syndrome, which is particularly associated with supracondylar fractures.


Diagnostic studies and interpretation
Routine anteroposterior and lateral radiographs are usually sufficient, with oblique views added when subtle fractures are suspected. The presence of a fat pad sign is an important indicator of intra-articular injury. An elevated anterior fat pad or any visible posterior fat pad suggests joint effusion. In adults, an isolated posterior fat pad sign often indicates a radial head fracture, while in children it is more suggestive of a supracondylar fracture. Pediatric radiographs can be challenging due to unossified cartilage, so alignment lines and comparison views of the unaffected elbow may be helpful.


Conditions to distinguish from elbow trauma
Alternative diagnoses include sprains, strains, effusions, contusions, bursitis, and inflammatory arthritis.


Prehospital and early management principles
Initial care focuses on appropriate splinting and immobilization to prevent further injury during transport and evaluation.


Emergency department management strategies
Immobilization prior to imaging is essential. Orthopedic consultation is recommended for all but stable, nondisplaced fractures. Nondisplaced supracondylar fractures may be managed with posterior splinting and close follow-up, while displaced fractures require urgent orthopedic involvement, especially if vascular compromise is present. Elbow dislocations should be reduced promptly when neurovascular compromise exists, followed by splinting at 90 degrees of flexion. Minimally displaced radial head fractures may be managed with aspiration and immobilization, whereas more complex injuries warrant specialist evaluation. Radial head subluxation can often be reduced with a single supination-flexion maneuver or hyperpronation technique. Overuse injuries are treated conservatively with rest, splinting in severe cases, and anti-inflammatory therapy.


Medication and analgesia considerations
Adequate pain control is important and may include nonsteroidal anti-inflammatory drugs, acetaminophen-opioid combinations, or intravenous opioids for severe pain. Conscious sedation is often required to facilitate reduction of dislocations or displaced fractures.


Disposition and follow-up planning
Admission is indicated for open fractures, vascular injuries, fractures requiring surgical intervention, or significant swelling that raises concern for compartment syndrome. Stable fractures and successfully reduced dislocations may be discharged with splinting and orthopedic follow-up within 24 to 48 hours.


Clinical insights and frequent errors
A posterior fat pad sign should never be dismissed as normal. Neurovascular status must be assessed and documented before and after reduction of any elbow injury. Caregivers of children with supracondylar fractures should be educated on warning signs of compartment syndrome, as delayed recognition can result in serious morbidity.