Emergency And Acute Medicine – Rhabdomyolysis




Rhabdomyolysis is a potentially life-threatening condition characterized by the abnormal systemic release of skeletal muscle cell contents—including creatine phosphokinase (CPK), myoglobin, potassium, phosphate, and urate—into the bloodstream. It results from trauma, toxins, infections, metabolic disturbances, medications, inherited muscle disorders, or extreme exertion. Major complications include acute renal failure (15–50% in adults and about 5% in children), life-threatening hyperkalemia, hypocalcemia, metabolic acidosis, hypovolemia from fluid sequestration into damaged muscle, compartment syndrome (particularly in crush injuries), hepatic dysfunction, and disseminated intravascular coagulation (DIC). Approximately 26,000 cases occur annually in the United States, and disaster situations may produce large numbers of renal failure cases.


The underlying pathophysiology begins with disruption of the sarcolemma, which normally maintains low intracellular calcium levels. Membrane injury allows calcium influx, activating calcium-dependent proteases that destroy muscle fibers. Ischemia and inflammatory mediators further exacerbate damage. Intracellular components such as myoglobin, potassium, phosphate, lactate, and CPK are released into the circulation. Myoglobin contributes to renal injury through direct tubular toxicity in acidic urine, precipitation with proteins causing tubular obstruction, and renal vasoconstriction worsened by hypovolemia. Potassium release may lead to fatal arrhythmias, while calcium binds to phosphate in injured muscle, resulting in systemic hypocalcemia.


The cause is often obvious but not always. Trauma and crush injury are the most common overall causes. Other etiologies include strenuous exertion (such as marathon running or seizures), prolonged immobilization, ischemia from shock or thrombosis, surgery with hypotension, temperature extremes, and massive blood transfusion. Drugs and toxins—such as alcohol, cocaine, amphetamines, opioids, carbon monoxide, and certain medications including statins and antipsychotics—are frequent contributors. Metabolic abnormalities, infections (viral, bacterial, parasitic), inherited myopathies, and autoimmune muscle disorders may also be responsible. In children, viral myositis is a common nontraumatic cause.


Clinical presentation varies widely depending on the underlying cause. Classic symptoms include muscle pain, weakness, and dark “tea-colored” urine, although muscle pain is present in only about half of patients. Decreased urine output may occur. Physical findings can include hypovolemia with tachycardia and hypotension, altered mental status, hypo- or hyperthermia, and signs of compartment syndrome. In children, physical findings may be minimal, and the condition should be suspected in the setting of viral illness with muscle symptoms.


Diagnosis relies primarily on laboratory evaluation, as history and examination may be nonspecific. A serum CPK level greater than 1,000 U/L is considered diagnostic, and levels above 15,000 U/L are associated with a higher risk of renal failure. Urine dipstick testing may show heme positivity without red blood cells, suggesting myoglobinuria; however, myoglobin clears rapidly, and the dipstick may be negative despite significant disease. Electrolytes must be closely monitored, especially potassium, calcium, phosphate, bicarbonate, BUN, and creatinine. An ECG should be obtained early to detect hyperkalemia-related changes. Imaging studies are generally not required for diagnosis but may be used to evaluate complications.


Management centers on early and aggressive intravenous fluid resuscitation to prevent renal failure. In trauma or crush injuries, isotonic saline should be started as early as possible. In the emergency department, adults typically receive 1–1.5 liters per hour, and children receive 10–20 mL/kg per hour, aiming for a urine output of 200–300 mL per hour (3–5 mL/kg per hour in children). Total daily fluid requirements may reach 10–12 liters in severe cases. Urine alkalinization with sodium bicarbonate to maintain a urine pH greater than 6.5 is often recommended, particularly in crush injuries, though evidence is mixed. Hyperkalemia must be treated promptly with standard therapies such as insulin with dextrose and beta-agonists; calcium should be reserved for severe cases with ECG changes. Hypocalcemia should be treated only if symptomatic. Hemodialysis is indicated for refractory hyperkalemia, severe acidosis, fluid overload, or persistent anuria. Compartment syndrome requires urgent surgical evaluation and possible fasciotomy.


All but the most trivial elevations in CPK should prompt hospital admission because complications are unpredictable. Intensive care admission is indicated for severe electrolyte disturbances, very high CPK levels, renal failure, or significant comorbid illness. Prognosis is excellent in patients who do not develop renal failure but worsens significantly when renal failure occurs. Early recognition and aggressive hydration remain the most important interventions to reduce morbidity and mortality.

Emergency And Acute Medicine – Reye Syndrome


Reye syndrome is a rare but potentially fatal, reversible clinicopathologic syndrome characterized by acute noninflammatory encephalopathy and hepatic dysfunction with fatty infiltration. It is believed to involve primary mitochondrial injury leading to impaired oxidative phosphorylation and decreased activity of enzymes involved in the Krebs cycle, gluconeogenesis, and urea synthesis. The result is hyperammonemia, hypoglycemia, and hepatic dysfunction without significant inflammation. Rapid neurologic deterioration is due to cerebral cytotoxic edema and increased intracranial pressure (ICP), with herniation being the most common cause of death. Survivors often recover normal liver and neurologic function.


The condition primarily affects children, with peak incidence between ages 4 and 11 years and an average age of 7 years. It is extremely rare in individuals older than 18 years. Fewer than 10% of cases occur before age 1 year. Incidence is highest in winter and early spring and has historically been associated with antecedent viral infections such as influenza A or B and varicella. Epidemiologic evidence strongly links exposure to salicylates during viral illness as a major risk factor. Genetic susceptibility and other environmental factors may contribute. Reye-like syndromes describe similar presentations due to inborn errors of metabolism or toxic exposures affecting fatty acid oxidation and urea metabolism.


Patients typically present with a biphasic illness. An initial viral prodrome is followed several days later by persistent, profuse vomiting and rapid onset of neurologic symptoms. The patient is usually afebrile at presentation. Early manifestations include lethargy, behavioral changes, irritability, confusion, delirium, and combativeness. As cerebral edema worsens, patients may develop hyperventilation, decorticate or decerebrate posturing, seizures, and coma. Hepatomegaly is present in about 40% of cases. No focal neurologic deficits are typically found. Infants may present atypically with tachypnea, apnea, hypoglycemia, irritability, or seizures.


Laboratory evaluation demonstrates elevated liver transaminases (at least three times normal), elevated serum ammonia, hypoglycemia (particularly in infants), prolonged prothrombin time due to decreased clotting factor synthesis, and elevated blood urea nitrogen. Serum bilirubin is usually normal or only mildly elevated. Ammonia levels often peak 24 to 48 hours after onset of neurologic symptoms; levels greater than 300 μg/dL are associated with poor prognosis. Platelet count and peripheral smear are usually normal. Toxicology screening should be performed to exclude other causes. Head CT may demonstrate diffuse cerebral edema. Lumbar puncture is not contraindicated but typically shows fewer than 8 leukocytes/mm³. Liver biopsy confirms the diagnosis by demonstrating microvesicular fatty infiltration but should not delay treatment.


The differential diagnosis includes inborn errors of metabolism (urea cycle defects, fatty acid oxidation disorders, organic acidemias), toxin exposures, drug intoxications such as acetaminophen or salicylates, hypoglycemia, sepsis, meningitis, encephalitis, and head trauma.


Management is supportive and aimed primarily at controlling intracranial pressure and correcting metabolic derangements. All patients require intensive care admission in a facility capable of ICP monitoring. Airway protection with rapid-sequence intubation is indicated for significant encephalopathy. Supplemental oxygen and cardiorespiratory monitoring are essential. Intravenous glucose should be administered promptly for altered mental status, and serum glucose should be maintained between 125 and 175 mg/dL with careful monitoring. Overhydration should be avoided.


Elevated ICP is managed with head elevation, controlled hyperventilation, osmotic therapy such as mannitol, and, in severe cases, barbiturate coma. Intracranial pressure monitoring via subarachnoid bolt or intraventricular catheter may be required in advanced stages. Vitamin K is administered if prothrombin time is prolonged, and fresh-frozen plasma may be given for severe coagulopathy or bleeding. Diuretics such as furosemide may be used adjunctively. Treatment should be initiated promptly without waiting for liver biopsy confirmation.


All children with suspected Reye syndrome should be admitted to the intensive care unit. Discharge decisions are individualized and depend on stabilization of mental status and laboratory values. Long-term follow-up with hepatology and neurology is recommended, including neuropsychological assessment.


A critical preventive point is the avoidance of aspirin and salicylate-containing products in children and adolescents with viral illnesses. Clinicians must maintain vigilance for alternative diagnoses and aggressively manage intracranial pressure, as neurologic complications are the primary determinant of outcome.

Infectious Disease and Microbiology – Candidiasis


Candida is a yeast that forms part of the normal flora of the skin, gastrointestinal tract, and genitourinary tract. Although often harmless, Candida species can cause both superficial mucocutaneous infections and life-threatening systemic disease, particularly in immunocompromised individuals. Candida has become an increasingly important cause of bloodstream infections in hospitalized patients.


Candidal infections affect individuals of all ages but are more common in infants, elderly patients, and pregnant women. In U.S. hospitals, Candida accounts for approximately 9% of bloodstream infections. While Candida albicans remains the most frequently isolated species, non-albicans species are increasingly encountered, including Candida parapsilosis, Candida glabrata, and Candida tropicalis.


Major risk factors include immunosuppression and neutropenia, malignancy, HIV/AIDS, major burns, prolonged antibiotic use, indwelling intravenous catheters, chemotherapy, solid organ or bone marrow transplantation, total parenteral nutrition, chronic renal failure with hemodialysis, gastrointestinal perforation, diabetes mellitus, pregnancy, and glucocorticoid therapy. Prevention strategies focus on judicious antibiotic use and removal of unnecessary central venous catheters.


Candidemia may arise from disruption of mucosal barriers along the gastrointestinal tract or from colonization of intravascular devices. More than 150 Candida species exist, but clinically significant species include Candida albicans, Candida glabrata, Candida parapsilosis, Candida tropicalis, Candida krusei, Candida guilliermondii, and Candida lusitaniae. Candida albicans accounts for more than half of candidemia cases.


Clinical manifestations vary by site of infection. Vulvovaginal candidiasis presents with pruritus, irritation, dysuria, dyspareunia, and a white “cheesy” discharge. Oropharyngeal candidiasis (thrush) may cause oral discomfort, altered taste, or may be asymptomatic. Candida esophagitis presents with nausea, retrosternal chest pain, odynophagia, and dysphagia. Invasive candidiasis and candidemia may present with fever, hypotension, tachycardia, altered mental status, and signs of severe sepsis, particularly in immunocompromised patients.


Physical findings depend on the affected organ. Vulvovaginal candidiasis shows vulvar or vaginal erythema and characteristic discharge. Oral candidiasis presents with white plaques on the tongue and palate that leave an erythematous base when scraped. Esophageal involvement may occur without oral lesions. Candidemia ranges from isolated fever to septic shock.


Diagnosis of vulvovaginal and oral candidiasis is often clinical, supported by microscopic examination of KOH preparations showing yeast with or without pseudohyphae. Vaginal pH typically remains normal (4–4.5). Esophageal candidiasis may require endoscopy and biopsy, although empiric treatment is often initiated in high-risk patients with suggestive symptoms. Candidemia is diagnosed by positive blood cultures; Candida in blood should never be considered a contaminant. Susceptibility testing is important in serious infections or when there is treatment failure. Imaging may be required to evaluate complications such as endocarditis, central nervous system involvement, hepatosplenic candidiasis, pneumonia, or peritonitis. All patients with candidemia should undergo ophthalmologic examination due to the risk of endophthalmitis.


Treatment depends on the site and severity of infection. Vulvovaginal candidiasis can be treated with topical azoles (e.g., butoconazole cream for 3–7 days) or a single 150 mg oral dose of fluconazole, with longer courses in severe or immunocompromised cases. Oropharyngeal candidiasis is treated with nystatin suspension, clotrimazole troches, or fluconazole 100–200 mg daily until several days after symptom resolution. Candida esophagitis is treated with fluconazole (400 mg loading dose followed by 200–400 mg daily for 7–14 days), given orally or intravenously.


Management of candidemia depends on host factors. Stable, non-neutropenic patients without prior antifungal exposure may receive fluconazole (800 mg loading dose, then 400 mg daily). Unstable patients, neutropenic individuals, or those with prior antifungal exposure should receive an echinocandin (caspofungin, micafungin, or anidulafungin), voriconazole, or lipid-formulation amphotericin B. Therapy should be adjusted based on species identification and susceptibility. Notably, Candida krusei is resistant to fluconazole; Candida glabrata often exhibits azole resistance; Candida parapsilosis may have higher minimum inhibitory concentrations to echinocandins; and Candida lusitaniae may be resistant to amphotericin B. Treatment should continue for at least two weeks after clearance of blood cultures and resolution of symptoms, with removal of infected catheters or other sources.


Infectious disease consultation is recommended for candidemia and neutropenic patients. Pharmacologic monitoring is essential due to potential drug interactions and QT prolongation with triazoles. Daily blood cultures should be obtained until clearance is documented.


Prognosis depends on early recognition and prompt antifungal therapy. Delayed treatment significantly increases mortality, which may exceed 40% when therapy is initiated three or more days after documented candidemia. Complications include renal failure, endocarditis, endophthalmitis, meningitis, peritonitis, pericarditis, abscess formation, esophageal perforation, and death.

Infectious Disease and Microbiology – Brucellosis


Brucellosis is a zoonotic infectious disease affecting both wild and domestic animals, with humans serving as accidental hosts. It produces a systemic illness that may have either an acute or insidious onset. Globally, approximately 500,000 new cases occur annually. Incidence varies widely: fewer than 2 cases per million population in countries such as the United States and the United Kingdom, 2–50 cases per million in many Mediterranean countries, and more than 50 cases per million in parts of the Middle East.


Brucellosis is primarily an occupational disease. High-risk groups include farm and ranch workers, abattoir workers, veterinarians, meat inspectors, and laboratory personnel. In endemic regions, ingestion of unpasteurized milk or dairy products represents the most significant risk factor. Prevention relies on eradication of Brucella species from livestock through vaccination programs and identification of infected animals. Avoidance of unpasteurized dairy products is essential; boiling milk is effective when pasteurization is not available. There is currently no safe vaccine for humans at occupational risk.


The disease is caused by Brucella species, which are small, nonmotile, gram-negative coccobacilli. Species infecting humans include Brucella melitensis, Brucella abortus, Brucella suis, and Brucella canis. After infection, a small number of organisms survive within macrophages, escaping intracellular destruction. The host immune response involves increased γ/δ lymphocytes and interferon-γ production, with altered tumor necrosis factor-alpha responses. This intracellular persistence contributes to chronicity and recurrence.


Clinically, brucellosis presents with nonspecific systemic symptoms such as fever, chills, rigors, malaise, headache, weight loss, profuse sweating, generalized aches, arthralgias, and depression. Physical examination may reveal hepatomegaly, splenomegaly, and lymphadenopathy. Osteoarticular involvement occurs in 20–50% of patients, and spondylodiscitis must be excluded. Orchitis or epididymitis is seen in 5–25% of cases. Brucellosis can involve virtually any organ and may occasionally present as a localized infection such as pneumonia.


Definitive diagnosis is established by isolating the organism from blood, bone marrow, or other tissue cultures. Laboratories should be informed when brucellosis is suspected, as optimal growth may require specific media and 5–10% CO₂. Cultures should be maintained for at least four weeks. Serologic testing using the standard tube agglutination test is useful but must be interpreted carefully due to possible false negatives (prozone phenomenon) and false positives from cross-reacting antibodies. ELISA-based antibody detection is more reliable. Polymerase chain reaction testing can detect Brucella DNA but may remain positive long after clinical cure, requiring cautious interpretation. Imaging studies such as abdominal ultrasound, CT, or MRI may reveal organomegaly or lymphadenopathy, and MRI is valuable in evaluating suspected bone involvement. Liver biopsy in cases of fever of unknown origin may show granulomatous hepatitis.


Brucellosis should be considered in patients from endemic areas presenting with prolonged febrile illness, especially with osteoarticular symptoms. The differential diagnosis includes other infectious causes of fever of unknown origin.


First-line treatment consists of combination therapy to prevent relapse. Streptomycin (1 g intramuscularly daily for 2–3 weeks) combined with doxycycline (100 mg orally every 12 hours for 6 weeks) is recommended. Gentamicin is non-inferior to streptomycin. Triple regimens that include doxycycline, an aminoglycoside, and rifampin may provide superior outcomes. An alternative regimen is doxycycline combined with rifampin for six weeks, though it is less effective in spondylitis, central nervous system involvement, and endocarditis. Quinolone combinations are considered suboptimal. In pregnant women, co-trimoxazole and/or rifampin have been used. Valve replacement is often required in cases of Brucella endocarditis.


Careful follow-up is essential due to the high risk of relapse, which is attributed to intracellular persistence rather than antimicrobial resistance. Renal and hepatic function should be monitored during aminoglycoside and rifampin therapy. Patients should be counseled that rifampin may cause orange discoloration of urine and body secretions. Prognosis is generally excellent, although endocarditis carries a poorer outcome and accounts for most fatalities. The overall case-fatality rate is approximately 2%. Recurrence is common and may require prolonged antibiotic therapy. Occasionally, a Jarisch–Herxheimer–like reaction may occur shortly after initiation of treatment.

Infectious Disease and Microbiology – Bronchitis


Bronchitis is inflammation of the lining of the tracheobronchial tree and is classified as acute or chronic. Acute bronchitis is defined by cough, with or without sputum production, lasting less than three weeks. Chronic bronchitis is clinically defined as a productive cough for at least three months in each of two consecutive years and is a major component of chronic obstructive pulmonary disease (COPD).


Chronic bronchitis affects approximately 9.5 million Americans annually, while around 10 million people seek medical care for acute bronchitis each year. Acute bronchitis occurs in all age groups and affects males and females equally. Chronic bronchitis is most prevalent in individuals older than 50 years and is more common in males.


Risk factors for acute bronchitis include cigarette smoking, exposure to respiratory irritants such as air pollution and gases, recent upper respiratory tract infections, chronic lung disease, older age, and decreased immunity. Chronic bronchitis is strongly associated with long-term smoking and environmental pollutants, as well as recurrent respiratory infections, allergies, and advancing age. Genetic factors have a moderate influence on the development of chronic bronchitis.


Preventive strategies focus on smoking cessation and avoidance of secondhand smoke and environmental irritants. Reducing exposure to individuals with respiratory infections is important. Annual influenza vaccination and pneumococcal vaccination every 5–10 years in individuals aged 65 years or older or those with chronic disease are recommended.


The pathophysiology involves irritation of the bronchial mucosa, leading to hyperemia, edema, and excessive mucus production. Bronchial smooth muscle hyperreactivity results in bronchospasm. Increased airflow resistance can lead to hypoventilation, hypercapnia, and hypoxemia. In chronic bronchitis, goblet cell hyperplasia, mucus plugging, smooth muscle hyperplasia, and persistent inflammatory cell infiltration are characteristic findings.


Acute bronchitis is most commonly viral, caused by influenza A and B viruses, parainfluenza virus, respiratory syncytial virus, coronavirus, adenovirus, and rhinovirus. Atypical bacteria such as Mycoplasma pneumoniae, Chlamydia pneumoniae, and Bordetella pertussis may also be responsible. Chronic bronchitis is primarily caused by smoking and environmental pollutants. Acute exacerbations of chronic bronchitis are frequently associated with Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, viral infections, and, in patients with severe lung impairment, Pseudomonas aeruginosa and Enterobacteriaceae.


Patients with acute bronchitis often report a recent cold or sinus infection, exposure to irritants, or smoking history. Symptoms include cough, mild fever, sore throat, dyspnea on exertion, wheezing, chest tightness, fatigue, and malaise. Chronic bronchitis presents with persistent productive cough. Acute exacerbations are characterized by increased dyspnea, increased sputum production, and increased sputum purulence. On physical examination, fever is uncommon. Findings may include tachypnea, tachycardia, coarse breath sounds, wheezing, and prolonged expiration. Worsening respiratory function is typical during acute exacerbations.


Laboratory evaluation may include a complete blood count and sputum cultures when bacterial infection is suspected. Serum procalcitonin levels may help guide antibiotic therapy decisions. Pulse oximetry and arterial blood gas analysis are useful in more severe cases. Chest radiography is performed to exclude pneumonia. Spirometry is recommended after recovery to assess lung function and airway obstruction, especially in suspected chronic bronchitis.


The differential diagnosis includes asthma, bronchiolitis, pneumonia, pharyngitis, bronchiectasis, chronic sinusitis, pulmonary embolism, congestive heart failure, sarcoidosis, atelectasis, chemical pneumonitis, and gastroesophageal reflux disease.


Management of acute bronchitis is generally supportive, as most cases are viral. Antiviral therapy such as oseltamivir or zanamivir is indicated for confirmed influenza. For Bordetella pertussis infection, azithromycin, erythromycin, or clarithromycin is recommended, with trimethoprim–sulfamethoxazole as a second-line option. Antibiotics are not routinely indicated for uncomplicated acute bronchitis. In acute bacterial exacerbations of chronic bronchitis, antibiotics such as amoxicillin, amoxicillin–clavulanate, trimethoprim–sulfamethoxazole, doxycycline, macrolides, or fluoroquinolones may be prescribed for 5–10 days. Bronchodilators can relieve dyspnea, systemic corticosteroids may be used during exacerbations, and low-flow oxygen therapy is indicated for hypoxemia. Antitussives such as codeine or dextromethorphan may provide short-term symptomatic relief.


Most patients with acute bronchitis have an excellent prognosis. Smoking cessation slows the progression of chronic bronchitis and improves outcomes. Complications may include respiratory failure, pulmonary emphysema, right heart failure, and treatment failure due to advanced disease, incorrect diagnosis, inadequate antibiotic dosing, immunocompromised state, or resistant organisms such as Pseudomonas. Regular follow-up, spirometry in chronic cases, patient education, and environmental modification are essential components of long-term management.

Emergency And Acute Medicine – Ring/Constricting Band Removal




A constricting band occurs when an object encircles an appendage and causes swelling, pain, and potential vascular compromise. A primary constricting band refers to a band that directly causes swelling, such as a hair tightly wrapped around a toddler’s toe. A secondary constricting band occurs when underlying injury or disease leads to swelling that becomes trapped against a tight band, such as a ring on a fractured finger. If untreated, the band may become embedded in tissue, compromise skin integrity, and interrupt distal circulation. When distal tissue injury results from constriction, the condition is referred to as tourniquet syndrome.


In children, especially preverbal infants, a constricting band may be a manifestation of neglect or abuse and should be considered in cases of inconsolable crying. Hair tourniquets are a well-recognized cause of unexplained irritability. In elderly or cognitively impaired patients, such as those with dementia, the inability to communicate pain may delay diagnosis. Tourniquet syndrome may result from a wide variety of conditions, including allergic, dermatologic, infectious, traumatic, endocrinologic, metabolic, malignant, physiologic, or pregnancy-related causes.


Patients typically present with a visible constricting band and distal swelling, most commonly involving a finger. However, other sites include the toe, wrist, ankle, umbilicus, earlobe, nipple, nasal septum, penis, scrotum, labia, vagina, uvula, or tongue. Pain is usually present with manipulation. In nonverbal populations, the history may be limited, and the diagnosis relies heavily on careful physical examination. In any irritable infant or agitated nonverbal adult, fingers, toes, and genitalia must be examined thoroughly.


Diagnosis of a primary constricting band is made clinically with special attention to distal neurovascular status, including capillary refill, sensation, motor function, and pulses if applicable. In secondary constricting bands, evaluation for underlying pathology may require imaging or laboratory studies. Plain radiographs are helpful if fracture or retained foreign body is suspected. Laboratory testing is generally unnecessary in acute management unless investigating an underlying systemic cause.


Management begins with pain control or procedural sedation when necessary. Removal can be attempted either by advancing the band distally off the appendage or by dividing it. Adjunctive techniques may reduce swelling and facilitate removal. Elevation and cooling with ice may decrease edema. Lubrication with soap or mineral oil may assist with sliding the band. A digital nerve block with 1–2% lidocaine without epinephrine can reduce discomfort, although it may temporarily increase swelling.


Edema reduction techniques may be used prior to removal. Self-adherent tape can be wrapped tightly from distal to proximal to compress tissue and create a smoother surface over which the band may be advanced. A Penrose drain or cut glove finger may be stretched over the distal swelling and used to create a cuff to help advance the band. A suture, dental floss, or umbilical tape technique involves tightly wrapping material distal to proximal, tucking the proximal end under the band, and then unwinding it while pulling distally to force the band over the compressed tissue.


If these methods fail, the constricting band must be divided. Hair or fibrous bands may be cut with scissors or a scalpel blade, or treated with a depilatory cream when the hair is obscured by edema. Metallic rings may be removed using handheld wire cutters, bolt cutters, standard ring cutters, or motorized high-speed cutting devices. Softer metals such as gold or silver can often be cut with standard ring cutters, though this may be labor-intensive. Larger or harder rings may require bolt cutters or motorized devices.


When using motorized cutting equipment, safety precautions are essential. Flammable substances should be cleared from the area, and protective eyewear must be worn by all present, including the patient. A thin aluminum splint should be inserted between the ring and skin to protect underlying tissue. The area must be cooled with ice water before and during cutting to prevent thermal injury. Cutting intervals should be brief, with adequate cooling between attempts.


After removal, the affected area should be irrigated thoroughly to remove metallic debris and prevent foreign-body reaction. Tetanus prophylaxis should be administered if indicated. Antibiotics are not routinely required but may be considered in cases with tissue injury or infection risk. Patients with neurovascular compromise, tissue necrosis, infection, or suspected abuse require admission. Successful removal with restoration of circulation and no complications allows for discharge with close follow-up and clear return precautions for increasing pain, numbness, swelling, redness, drainage, or fever.


Early removal of rings and other constricting objects following distal extremity trauma is essential to prevent progression to tourniquet syndrome. Failure to carefully examine digits and genitalia in irritable infants is a common and preventable pitfall. Hair tourniquets may be hidden beneath edematous tissue and visible only as a subtle constricting crease. Prompt recognition and timely intervention are critical to preventing permanent tissue injury.

Emergency And Acute Medicine – Rocky Mountain Spotted Fever




Rocky Mountain spotted fever (RMSF) is a potentially life-threatening rickettsial infection characterized by invasion of small blood vessels, resulting in direct vascular injury and secondary immune-mediated vasculitis. The disease is caused by acute infection with Rickettsia rickettsii, transmitted by tick vectors. In the western United States, the primary vector is Dermacentor andersoni (wood tick), while in the eastern United States it is Dermacentor variabilis (dog tick). Although reported in all states, approximately half of cases occur in North Carolina, South Carolina, Tennessee, Oklahoma, and Arkansas. RMSF is more common from April through September but can occur year-round. It is more frequently seen in males and in individuals between 40 and 64 years of age.


The incubation period ranges from 2 to 14 days, with a median of 7 days. A history of tick bite within 14 days of rash onset is reported in about 60% of patients, though absence of a known tick bite does not exclude the diagnosis. Patients often report outdoor or rural exposure.


The hallmark finding is a characteristic rash that typically appears 3 to 5 days after symptom onset. Initially, the rash consists of small (1–4 mm), red, macular lesions that blanch with pressure. Over hours to days, lesions become darker, papular, and palpable. Within 2 to 3 days, the rash may become petechial or purpuric and may coalesce or ulcerate. In severe cases, necrosis of distal extremities can occur. Classically, the rash begins on the flexor surfaces of the wrists and ankles, spreads to the palms and soles, and then progresses centrally to involve the trunk and face. However, 10% of patients never develop a rash, and early in the illness the rash may be absent or subtle.


Systemic symptoms are common. Pulmonary findings may include nonproductive cough, chest pain, dyspnea, and rales. Gastrointestinal symptoms such as nausea, vomiting, abdominal pain, distention, ileus, and hepatosplenomegaly are frequent and may be associated with more severe disease due to widespread vasculitis. Neurologic involvement occurs in approximately two-thirds of patients and may include severe headache, meningismus, encephalitis, or focal deficits. Additional findings may include generalized edema, dehydration, malaise, myalgia, conjunctivitis, and retinal hemorrhages. Complications can include disseminated intravascular coagulation (DIC), noncardiogenic pulmonary edema, acute renal failure, and cardiovascular dysfunction. Mortality is higher in older adults, males, individuals with chronic alcohol abuse, African Americans, and those with glucose-6-phosphate dehydrogenase deficiency.


RMSF is primarily a clinical diagnosis supported by laboratory findings. Early laboratory abnormalities may include thrombocytopenia, anemia, and hyponatremia (often <130 meq />). Liver enzymes such as aspartate aminotransferase and lactate dehydrogenase may be elevated. White blood cell count is often normal. Coagulation studies may reveal abnormalities if DIC is present. Serologic testing confirms the diagnosis but is often negative in the first few days of illness. A single antibody titer greater than 1:64 or a fourfold rise in titers is diagnostic. Indirect immunofluorescence assay is the reference standard. Polymerase chain reaction testing and immunohistochemical staining of skin biopsy specimens may assist in diagnosis. CSF may show pleocytosis and elevated protein. Imaging such as chest radiography may demonstrate pulmonary edema or pneumonia in severe cases.


The differential diagnosis includes other tick-borne diseases such as ehrlichiosis, Lyme disease, tularemia, babesiosis, and Colorado tick fever, as well as meningococcemia, measles, rubella, varicella, viral exanthems, disseminated gonococcal infection, typhus, secondary syphilis, scarlet fever, Kawasaki disease, toxic shock syndrome, staphylococcal sepsis, allergic vasculitis, thrombotic thrombocytopenic purpura, and heat illness.


Management requires immediate initiation of antibiotic therapy based on clinical suspicion and epidemiologic factors. Treatment must not be delayed for laboratory confirmation, as early therapy significantly reduces mortality. Doxycycline is the drug of choice for both adults and children. The recommended dose is 100 mg orally or intravenously twice daily (2 mg/kg for children weighing less than 45 kg) for 5 to 7 days and continued for at least 2 to 3 days after defervescence. Despite prior concerns about dental staining, short courses of doxycycline are considered safe in children and are preferred due to the severity of untreated disease. Chloramphenicol is reserved for pregnant patients or those with severe allergy to doxycycline. Sulfonamides should be avoided, as they may worsen the infection.


Supportive care includes ABC management, intravenous fluid resuscitation with 0.9% normal saline for dehydration, oxygen therapy for hypoxia, correction of electrolyte abnormalities, and treatment of complications such as DIC, acute respiratory distress syndrome, or heart failure. Acetaminophen may be used for fever control. High-dose corticosteroids have been considered in severe cases with extensive vasculitis or cerebral edema, though their use remains controversial.


Patients with moderate to severe illness require hospital admission. Mild cases identified early and treated promptly may be managed as outpatients with close follow-up. Because cases may cluster and reflect shared environmental exposure, family members should be informed and evaluated if symptomatic.


Early recognition and empiric treatment based on clinical presentation and epidemiologic exposure are critical. Delayed therapy significantly increases morbidity and mortality, making prompt initiation of doxycycline the cornerstone of management.

Emergency And Acute Medicine – Rheumatic Fever


Rheumatic fever is an inflammatory, autoimmune condition that follows infection with group A streptococcus (GAS), also known as Streptococcus pyogenes, most commonly after untreated streptococcal pharyngitis. It is characterized by a constellation of clinical findings defined by the Jones criteria. Although now uncommon in the United States, it remains a major cause of cardiac morbidity and mortality worldwide, accounting for over 230,000 deaths annually. It most commonly affects children between 5 and 15 years of age and is more prevalent in developing nations and in populations living in crowded or resource-limited conditions.


The disease results from an abnormal immune response to GAS infection. Molecular mimicry between streptococcal antigens and human tissues—particularly cardiac, synovial, skin, and neural tissue—leads to cross-reactive antibodies and inflammatory injury. Symptoms typically develop 2 to 4 weeks after the initial streptococcal infection.


Diagnosis requires either two major Jones criteria or one major and two minor criteria, along with evidence of a recent GAS infection. Major manifestations include migratory polyarthritis, carditis, chorea, erythema marginatum, and subcutaneous nodules. Migratory polyarthritis occurs in 60–75% of initial attacks and typically involves large joints such as the knees, ankles, hips, elbows, and wrists, with lower extremities more commonly affected. The arthritis responds well to salicylates. Carditis occurs in one-third to one-half of new cases and may involve the pericardium, myocardium, and endocardium (pancarditis). Clinical signs include a new murmur, tachycardia, gallop rhythm, pericardial friction rub, or congestive heart failure. Valvular involvement—particularly of the mitral and aortic valves—is the most serious long-term complication. Chorea (Sydenham chorea) occurs in about 10% of cases and predominantly affects teenage girls. It is characterized by purposeless, uncoordinated movements that worsen with stress and disappear during sleep. Chorea may be the sole manifestation of the disease. Erythema marginatum is a nonpruritic rash with central clearing and irregular borders, typically seen on the trunk and extremities. Subcutaneous nodules are painless and found over extensor surfaces.


Minor manifestations include fever above 38°C, arthralgia, elevated acute phase reactants (such as ESR or C-reactive protein), and prolonged PR interval on ECG. Evidence of recent GAS infection may include a positive throat culture or rapid antigen test, or elevated or rising antistreptolysin O (ASO) titers.


Patients often report a recent sore throat, fever, joint pain, rash, unusual movements, dyspnea, or edema. Physical examination may reveal pharyngeal erythema, rash consistent with erythema marginatum, subcutaneous nodules, new heart murmurs (commonly mitral regurgitation), or signs of fluid overload and heart failure.


The essential workup includes careful cardiac and joint examination, throat swab for rapid strep testing or culture, ECG, chest radiograph, and echocardiogram. Laboratory studies include CBC, ESR or C-reactive protein, ASO titer, and other serologic tests to exclude alternative rheumatologic conditions. Diagnosis remains clinical, based on meeting the Jones criteria.


The differential diagnosis includes juvenile idiopathic arthritis, infective endocarditis, systemic lupus erythematosus, postgonococcal arthritis, Reiter syndrome, and other infectious causes of arthritis and carditis such as Coxsackie B virus or parvovirus. Rheumatic fever is primarily a pediatric disease, though it can occur in young adults. Testing for streptococcal pharyngitis is generally not recommended in children under 3 years of age in the United States because both strep throat and rheumatic fever are rare in this age group. Women with a history of rheumatic fever should receive prenatal counseling due to increased cardiac risks during pregnancy.


Management focuses on eradication of streptococcal infection, control of inflammation, and treatment of complications. Penicillin is the treatment of choice, administered intramuscularly, intravenously, or orally. Patients allergic to penicillin may receive alternatives such as azithromycin or erythromycin. Aspirin is used for arthritis and carditis, while corticosteroids such as prednisone may be required in severe carditis. Haloperidol may be used for severe chorea. Patients with heart failure may require diuretics such as furosemide and, in some cases, digoxin. Pericardial effusions may require drainage.


Most patients with a new diagnosis should be admitted for evaluation and stabilization, especially if they have congestive heart failure, uncontrolled chorea, pericardial effusion, severe pain, or significant carditis. Discharge is appropriate once pain is controlled, cardiovascular status is stable, and reliable follow-up is ensured. All patients require long-term secondary prophylaxis with monthly intramuscular benzathine penicillin to prevent recurrence, often for years depending on cardiac involvement.


Close follow-up with a cardiologist is essential for echocardiographic monitoring and guidance regarding endocarditis prophylaxis. Infectious disease consultation may be helpful for management of prolonged antibiotic prophylaxis, and rheumatology referral may be considered for persistent joint symptoms.


Although uncommon in the United States, rheumatic fever remains an important preventable cause of valvular heart disease worldwide. Prompt recognition and treatment of streptococcal pharyngitis remain critical to preventing recurrence and long-term cardiac complications.

Emergency And Acute Medicine – Rib Fracture




Rib fractures result from either major or minor thoracic trauma and may be classified as traumatic or pathologic. Most commonly, they occur after blunt thoracic trauma such as falls, motor vehicle collisions, assaults, or cardiopulmonary resuscitation. Penetrating trauma is a less common cause. Ribs typically fracture at the point of impact or at the posterior angle, the structurally weakest portion. Stress fractures may occur in the upper or middle ribs from repetitive high-force activities such as golf, rowing, or throwing, as well as from severe coughing. Pathologic fractures may occur with minimal trauma in patients with osteoporosis, malignancy, or advanced age.


Children are less likely to sustain rib fractures due to the elasticity of their chest wall; therefore, the presence of rib fractures in infants or toddlers without an appropriate mechanism should raise concern for nonaccidental trauma, and a skeletal survey should be considered. Elderly patients are more susceptible not only to fractures but also to complications such as atelectasis, pneumonia, and respiratory failure. Morbidity and mortality in older patients are approximately twice that of younger individuals.


Patients typically present with localized chest wall pain that worsens with deep inspiration, coughing, or movement. Dyspnea and pleuritic chest pain may also be reported. Examination often reveals point tenderness, bony step-off, crepitus, localized edema, ecchymosis (including the “seat belt sign”), and splinting respirations. Breath sounds may be normal or diminished. Segmental paradoxical movement of the chest wall suggests flail chest due to multiple rib fractures. Hypoxia, tachypnea, and respiratory distress may be present in more severe cases.


Diagnosis is initially clinical and confirmed with imaging. Anteroposterior and lateral chest radiographs are commonly used but may miss up to 50% of rib fractures. Imaging is primarily performed to evaluate for associated intrathoracic injuries such as pneumothorax, hemothorax, pulmonary contusion, pneumomediastinum, or widened mediastinum. Pulmonary contusions may not be visible until 6 to 12 hours after injury. CT scanning is more sensitive for detecting rib fractures and internal injuries and may be required when significant trauma is suspected. Fractures of the first three ribs suggest high-energy trauma and possible vascular injury, while fractures of ribs nine through twelve may indicate intra-abdominal injury. Ultrasound is increasingly recognized as a useful diagnostic tool for rib and cartilaginous injuries.


The differential diagnosis includes rib contusion, intercostal muscle strain, pneumothorax, costochondral separation, sternal fracture, and nontraumatic causes of chest pain such as myocardial ischemia, pulmonary embolism, pericarditis, aortic dissection, costochondritis, gastrointestinal disorders, or herpes zoster.


Management focuses on pain control and maintenance of adequate ventilation. In the prehospital setting, airway support, supplemental oxygen, and analgesia are priorities. Most simple fractures require no structural stabilization. Adequate analgesia is essential to prevent splinting, atelectasis, and pneumonia. NSAIDs with or without opioids are first-line therapy, while parenteral opioids may be necessary for severe pain. Care must be taken not to exceed recommended acetaminophen dosing limits. Intercostal nerve blocks using 0.5% bupivacaine provide 6 to 12 hours of effective pain relief and are particularly helpful in patients with severe pain. Incentive spirometry and deep breathing exercises should be encouraged. Chest binders should be avoided because they restrict ventilation and increase the risk of pulmonary complications.


Patients with multiple fractures, advanced age, significant underlying pulmonary disease, or associated injuries may require hospital admission for monitoring, aggressive pulmonary toilet, and possibly thoracic epidural analgesia or patient-controlled analgesia. Endotracheal intubation is indicated in cases of severe hypoxemia or impending respiratory failure. ICU admission is recommended for elderly patients with six or more rib fractures.


Admission is also indicated for intractable pain, inability to clear secretions, compromised pulmonary function, displaced fractures, fractures of the first three ribs, or associated pneumothorax, pulmonary contusion, or intra-abdominal injury. Patients with stable pulmonary function, no associated injuries, and adequate pain control on oral analgesics may be discharged with strict return precautions for worsening shortness of breath, increased pain, fever, or cough.


Most rib fractures heal within approximately six weeks, although patients often resume normal activities sooner. Routine follow-up chest radiographs are not recommended. Clinicians must remain vigilant for underlying intrathoracic and intra-abdominal injuries, as morbidity correlates with the number of fractured ribs, associated injuries, and patient age. Ensuring effective pain control and adequate ventilation is the cornerstone of management.

Emergency And Acute Medicine – QT Syndrome, Prolonged


Prolonged QT syndrome is a disorder of myocardial repolarization characterized by prolongation of the QT interval on electrocardiogram (ECG). It reflects delayed ventricular repolarization and predisposes patients to malignant ventricular arrhythmias, particularly torsades de pointes, ventricular tachycardia, and ventricular fibrillation. These arrhythmias may cause syncope, seizures, or sudden cardiac death.


The underlying pathophysiology involves abnormalities in cardiac sodium, potassium, or calcium ion channels and may also include imbalance in sympathetic innervation. QT prolongation may be “pause-dependent,” often following a short–long–short sequence, or “adrenergic-dependent,” particularly in congenital forms triggered by exercise, emotional stress, or loud auditory stimuli. Nocturnal bradycardia can also lengthen the QT interval, leading to sleep-related events. Prolonged QT is an independent risk factor for sudden cardiac death.


Congenital long QT syndrome is linked to mutations in at least 10 genes affecting cardiac ion channels. The autosomal recessive form associated with congenital deafness is known as Jervell and Lange-Nielsen syndrome, while the autosomal dominant form without deafness is Romano-Ward syndrome. The congenital form occurs in approximately 1 in 3,000–5,000 individuals, with mortality of about 6% by age 40 if untreated. Ten to fifteen percent of gene carriers may have a normal baseline QTc. Sudden death may occur without warning symptoms in some pediatric patients.


Acquired QT prolongation is most commonly drug-induced or secondary to metabolic abnormalities. Medications associated with QT prolongation include class Ia and III antiarrhythmics, certain antibiotics (e.g., erythromycin), antifungals, psychotropic agents (e.g., haloperidol), methadone, and others. Electrolyte abnormalities such as hypokalemia, hypomagnesemia, and hypocalcemia are common causes. Cardiac conditions (bradyarrhythmias, AV block, myocarditis, ischemia), CNS disorders (subarachnoid hemorrhage, stroke), hypothyroidism, hypothermia, anorexia nervosa, and severe fasting may also contribute.


Patients may present with palpitations, lightheadedness, dizziness, syncope, or seizure-like activity. A history of syncope during exercise or emotional stress is suggestive. Family history of sudden death or syncope and congenital deafness are important clues. Medication review is essential.


Diagnosis is based on ECG findings. QTc (corrected QT) is considered prolonged when >0.44 seconds in men and >0.46 seconds in women. The QT interval is measured from the beginning of the QRS complex to the end of the T wave and averaged over several beats. The Bazett formula (QT divided by the square root of the RR interval) is most commonly used for correction. ECG may also show T-wave abnormalities, U waves, increased QT variability, torsades de pointes, or ventricular arrhythmias. Laboratory evaluation should include serum electrolytes, calcium, magnesium, and toxicology screen. Echocardiography may be performed to exclude structural heart disease. Holter monitoring, stress testing, and genetic testing may be considered in suspected congenital cases.


Initial management focuses on stabilization and arrhythmia treatment. Patients should receive supplemental oxygen, IV access, and cardiac monitoring. Hemodynamically unstable patients with torsades de pointes require immediate synchronized cardioversion or defibrillation as indicated.


Magnesium sulfate is first-line therapy for torsades de pointes, even if serum magnesium levels are normal. A typical adult dose is 2 g IV over 2–3 minutes, followed by infusion if needed. Serum potassium should be corrected to high-normal levels (4.5–5.0 mEq/L). In recurrent torsades refractory to magnesium, temporary transvenous pacing at rates of 100–120 bpm may shorten the QT interval. IV isoproterenol may be used in acquired long QT cases associated with bradycardia but is generally ineffective in congenital forms. Offending medications must be discontinued and metabolic abnormalities corrected.


For congenital long QT syndrome, β-blockers reduce the risk of arrhythmic events by approximately 70% and are recommended in symptomatic patients under cardiology guidance. High-risk patients may require pacemaker placement, implantable cardioverter-defibrillator (ICD), or surgical sympathetic denervation.


Admission is indicated for symptomatic patients, those with syncope, ventricular arrhythmias, metabolic abnormalities, or suspected ischemia. Asymptomatic patients with incidental prolonged QT may be discharged after cardiology consultation if no high-risk features are present.


Prolonged QT should be suspected in any patient presenting with unexplained syncope or seizure-like activity. Prompt correction of electrolyte abnormalities and discontinuation of QT-prolonging medications are essential. Magnesium sulfate followed by pacing remains the cornerstone of treatment for torsades de pointes. All patients with newly identified prolonged QT require cardiology follow-up.