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Infectious Disease and Microbiology – Septic Bursitis
Bursitis refers to inflammation of a bursa, one of more than 150 sac-like structures in the body that cushion soft tissues over bony prominences. Bursitis may result from infection (pyogenic), crystal deposition due to trauma or gout, or inflammatory arthritis such as rheumatoid arthritis. Septic bursitis most commonly involves superficial bursae and frequently affects the olecranon, prepatellar, subdeltoid, ischial, and trochanteric bursae.
The most important predisposing factor for septic bursitis is trauma, which accounts for approximately 70% of cases. Repetitive microtrauma is common in certain activities and occupations. Specific associations include ischial bursitis in individuals with spinal cord injuries, malleolar bursitis in ice skaters, and subdeltoid bursitis following injections. Additional risk factors include diabetes mellitus, alcohol abuse, chronic skin conditions, intravenous drug use, and invasive procedures such as acupuncture or joint injections, which have been associated with outbreaks of methicillin-resistant Staphylococcus aureus (MRSA).
The most common causative organism is Staphylococcus aureus. Streptococcal species account for 5–30% of cases. Gram-negative bacteria and fungi are rare causes. Prototheca wickerhamii, an environmental algae, has been reported in immunocompromised individuals. In endemic regions, brucellosis should be considered in the differential diagnosis, and tuberculous bursitis may occur as part of disseminated disease.
Clinically, septic bursitis presents with localized painful swelling, erythema, warmth, and tenderness over the affected bursa. Fever may be present. Overlying cellulitis may extend beyond the bursa. Deep bursal infections are more likely to be associated with systemic signs of infection and bacteremia.
Aspiration of bursal fluid is the diagnostic procedure of choice. Fluid analysis typically shows elevated white blood cell counts, often below 20,000 cells/mm³ in septic bursitis. Gram stain positivity varies widely, and culture of aspirated fluid has high sensitivity and specificity. Use of liquid media may improve culture yield. Crystal analysis should be performed, as crystal-induced bursitis can coexist with infection. Laboratory blood tests may show inflammatory markers, but they are nonspecific.
Imaging may support the diagnosis. Plain radiographs can demonstrate soft tissue swelling and subcutaneous edema. Ultrasound is useful in identifying fluid collections and guiding aspiration. MRI may show a fluid-filled bursa with rim enhancement after gadolinium administration, while surrounding structures are typically spared unless there is extension of infection.
The differential diagnosis includes cellulitis, fasciitis, acute monoarthritis, gout, pseudogout, and traumatic injury.
Management includes repeated needle aspiration, often daily, until the bursa is no longer fluctuant. Empiric antibiotic therapy should cover staphylococci and streptococci. For methicillin-sensitive Staphylococcus aureus, intravenous oxacillin or nafcillin is recommended. For MRSA, vancomycin is indicated. Antibiotic therapy is generally continued for at least 14 days, although shorter courses (7 days) may be sufficient in selected non-immunocompromised patients with severe infection requiring hospitalization. The choice between intravenous and oral therapy depends on severity and systemic involvement. Immobilization of the affected joint is advised during acute treatment.
If medical therapy fails, or if there is persistent swelling, pain, or loculated infection, surgical incision and drainage may be necessary. In chronic or recurrent cases, excision of the bursa may be required.
Follow-up care includes rehabilitation to prevent limitation of joint movement and ensure restoration of function.
Bursitis refers to inflammation of a bursa, one of more than 150 sac-like structures in the body that cushion soft tissues over bony prominences. Bursitis may result from infection (pyogenic), crystal deposition due to trauma or gout, or inflammatory arthritis such as rheumatoid arthritis. Septic bursitis most commonly involves superficial bursae and frequently affects the olecranon, prepatellar, subdeltoid, ischial, and trochanteric bursae.
The most important predisposing factor for septic bursitis is trauma, which accounts for approximately 70% of cases. Repetitive microtrauma is common in certain activities and occupations. Specific associations include ischial bursitis in individuals with spinal cord injuries, malleolar bursitis in ice skaters, and subdeltoid bursitis following injections. Additional risk factors include diabetes mellitus, alcohol abuse, chronic skin conditions, intravenous drug use, and invasive procedures such as acupuncture or joint injections, which have been associated with outbreaks of methicillin-resistant Staphylococcus aureus (MRSA).
The most common causative organism is Staphylococcus aureus. Streptococcal species account for 5–30% of cases. Gram-negative bacteria and fungi are rare causes. Prototheca wickerhamii, an environmental algae, has been reported in immunocompromised individuals. In endemic regions, brucellosis should be considered in the differential diagnosis, and tuberculous bursitis may occur as part of disseminated disease.
Clinically, septic bursitis presents with localized painful swelling, erythema, warmth, and tenderness over the affected bursa. Fever may be present. Overlying cellulitis may extend beyond the bursa. Deep bursal infections are more likely to be associated with systemic signs of infection and bacteremia.
Aspiration of bursal fluid is the diagnostic procedure of choice. Fluid analysis typically shows elevated white blood cell counts, often below 20,000 cells/mm³ in septic bursitis. Gram stain positivity varies widely, and culture of aspirated fluid has high sensitivity and specificity. Use of liquid media may improve culture yield. Crystal analysis should be performed, as crystal-induced bursitis can coexist with infection. Laboratory blood tests may show inflammatory markers, but they are nonspecific.
Imaging may support the diagnosis. Plain radiographs can demonstrate soft tissue swelling and subcutaneous edema. Ultrasound is useful in identifying fluid collections and guiding aspiration. MRI may show a fluid-filled bursa with rim enhancement after gadolinium administration, while surrounding structures are typically spared unless there is extension of infection.
The differential diagnosis includes cellulitis, fasciitis, acute monoarthritis, gout, pseudogout, and traumatic injury.
Management includes repeated needle aspiration, often daily, until the bursa is no longer fluctuant. Empiric antibiotic therapy should cover staphylococci and streptococci. For methicillin-sensitive Staphylococcus aureus, intravenous oxacillin or nafcillin is recommended. For MRSA, vancomycin is indicated. Antibiotic therapy is generally continued for at least 14 days, although shorter courses (7 days) may be sufficient in selected non-immunocompromised patients with severe infection requiring hospitalization. The choice between intravenous and oral therapy depends on severity and systemic involvement. Immobilization of the affected joint is advised during acute treatment.
If medical therapy fails, or if there is persistent swelling, pain, or loculated infection, surgical incision and drainage may be necessary. In chronic or recurrent cases, excision of the bursa may be required.
Follow-up care includes rehabilitation to prevent limitation of joint movement and ensure restoration of function.
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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.
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.
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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.
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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.
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.
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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.
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.
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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.
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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.
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Emergency And Acute Medicine – Radiation Injury
Radiation injury refers to damage caused by ionizing radiation. Types include alpha particles, which are helium nuclei that do not penetrate skin; beta particles, which are electrons that penetrate a few centimeters into tissue; gamma rays, which are highly penetrating photons; and neutrons, which are very penetrating and not detected by standard Geiger counters, though neutron sources usually emit gamma radiation as well. A radionuclide is a radioactive element that emits radiation from its nucleus; radioactivity cannot be destroyed, only relocated or shielded, and radioactive elements retain their usual chemical properties, including heavy metal toxicity.
Exposure or irradiation means a patient has been in the presence of ionizing radiation, affecting part or all of the body. Contamination refers to radioactive material being present where it is not desired, either externally on skin, hair, or clothing, or internally within the body, such as in the lungs. Radiation dose is the amount of energy absorbed by tissue and is measured in gray (Gy) or sievert (Sv); 1 Gy equals 100 rad, and for beta and gamma radiation, 1 Gy equals 1 Sv. If a radiation incident is suspected, regional or federal authorities should be contacted immediately for guidance.
Ionizing radiation causes cellular injury and vascular damage, leading to endarteritis and impaired blood supply. Rapidly dividing tissues such as bone marrow and gastrointestinal epithelium are highly sensitive, whereas skin and nerve tissue are less sensitive. Acute radiation syndrome (ARS) follows whole-body exposure and progresses through stages. The prodromal phase occurs within 0–48 hours and includes nausea, vomiting, and inflammation. The latent phase may last up to two weeks, during which symptoms temporarily improve. The manifest illness phase involves organ failure, particularly hematopoietic, gastrointestinal, or neurovascular systems, depending on dose. Recovery or death, often from infection, follows. Sources include medical and industrial devices, therapeutic radiation, nuclear weapons, and radiologic dispersal devices.
Clinical manifestations depend on dose. Whole-body exposure resembles high-dose chemotherapy toxicity. Nausea and vomiting within 3–6 hours suggest exposure greater than 100 rad, while vomiting within 1 hour suggests potentially lethal exposure exceeding 600 rad. Confusion and weakness may occur with doses above 200 rad. Fever may reflect early inflammation or later infection. Hair loss, hemorrhage, and diarrhea occur with higher doses. Local radiation injury initially resembles a thermal burn with erythema, later progressing to blistering, ischemia, and necrosis. Suspicion should arise if multiple patients present with ARS symptoms, burns without thermal history, or unusual ischemic ulcers.
Assessment includes radiation survey with a Geiger counter. The probe should be covered with a glove to prevent contamination and moved slowly 1-2 cm from the skin at 2-3 cm per second. Background radiation should be measured first. Contamination is defined as greater than twice background levels. Palms, soles, and hair must be examined. Absolute lymphocyte count is the most useful laboratory indicator of ARS severity; counts below 1,000/mm³ suggest moderate exposure (200-600 rad), and below 500/mm³ suggest severe exposure (>600 rad). Serial complete blood counts every 4–6 hours during the first 24 hours are recommended. Cytogenetic analysis at 24 hours postexposure provides more accurate dose estimation but requires specialized facilities.
Management prioritizes airway, breathing, and circulation. Removal of clothing eliminates approximately 80% of external contamination. Emergency care takes precedence over decontamination, as no documented case shows a contaminated patient posing immediate life-threatening radiation risk to providers. Staff should use particulate respirators such as N-95 masks, gowns, gloves, and protective covers; radiography lead aprons do not protect against most gamma radiation. Decontamination focuses first on wounds, then mucous membranes, then intact skin. Gentle washing with soap and water is recommended, avoiding abrasion. Runoff should be collected and monitored. If contamination persists, the area should be covered to prevent spread.
Symptomatic treatment includes antiemetics such as ondansetron and intravenous fluids for dehydration. Potassium iodide is useful only for preventing thyroid uptake of radioactive iodine and must be given within four hours of exposure; adult dosing is 130 mg orally daily, with weight-based pediatric dosing. Cytokines and transfusions may be required for significant bone marrow suppression. Internal contamination requires radionuclide-specific decorporation therapy in consultation with radiation experts such as REAC/TS.
Admission is indicated for lymphocyte counts below 1,000/mm³ at 24–48 hours, a 50% decline in lymphocyte count, suspected exposure above 200 rad, significant trauma, or uncontrolled vomiting. Discharge may be considered if there is no residual contamination, no evidence of significant exposure, and the patient tolerates oral intake. All patients with confirmed exposure require dose assessment, counseling, and follow-up.
Children and fetuses are more sensitive to radiation effects. Potassium iodide is particularly important for children in radioactive iodine exposure. Pregnant staff should avoid caring for contaminated patients. Psychological reactions are common and may mimic ARS; a falling lymphocyte count helps distinguish true radiation injury from stress-related symptoms.
Radiation injury refers to damage caused by ionizing radiation. Types include alpha particles, which are helium nuclei that do not penetrate skin; beta particles, which are electrons that penetrate a few centimeters into tissue; gamma rays, which are highly penetrating photons; and neutrons, which are very penetrating and not detected by standard Geiger counters, though neutron sources usually emit gamma radiation as well. A radionuclide is a radioactive element that emits radiation from its nucleus; radioactivity cannot be destroyed, only relocated or shielded, and radioactive elements retain their usual chemical properties, including heavy metal toxicity.
Exposure or irradiation means a patient has been in the presence of ionizing radiation, affecting part or all of the body. Contamination refers to radioactive material being present where it is not desired, either externally on skin, hair, or clothing, or internally within the body, such as in the lungs. Radiation dose is the amount of energy absorbed by tissue and is measured in gray (Gy) or sievert (Sv); 1 Gy equals 100 rad, and for beta and gamma radiation, 1 Gy equals 1 Sv. If a radiation incident is suspected, regional or federal authorities should be contacted immediately for guidance.
Ionizing radiation causes cellular injury and vascular damage, leading to endarteritis and impaired blood supply. Rapidly dividing tissues such as bone marrow and gastrointestinal epithelium are highly sensitive, whereas skin and nerve tissue are less sensitive. Acute radiation syndrome (ARS) follows whole-body exposure and progresses through stages. The prodromal phase occurs within 0–48 hours and includes nausea, vomiting, and inflammation. The latent phase may last up to two weeks, during which symptoms temporarily improve. The manifest illness phase involves organ failure, particularly hematopoietic, gastrointestinal, or neurovascular systems, depending on dose. Recovery or death, often from infection, follows. Sources include medical and industrial devices, therapeutic radiation, nuclear weapons, and radiologic dispersal devices.
Clinical manifestations depend on dose. Whole-body exposure resembles high-dose chemotherapy toxicity. Nausea and vomiting within 3–6 hours suggest exposure greater than 100 rad, while vomiting within 1 hour suggests potentially lethal exposure exceeding 600 rad. Confusion and weakness may occur with doses above 200 rad. Fever may reflect early inflammation or later infection. Hair loss, hemorrhage, and diarrhea occur with higher doses. Local radiation injury initially resembles a thermal burn with erythema, later progressing to blistering, ischemia, and necrosis. Suspicion should arise if multiple patients present with ARS symptoms, burns without thermal history, or unusual ischemic ulcers.
Assessment includes radiation survey with a Geiger counter. The probe should be covered with a glove to prevent contamination and moved slowly 1-2 cm from the skin at 2-3 cm per second. Background radiation should be measured first. Contamination is defined as greater than twice background levels. Palms, soles, and hair must be examined. Absolute lymphocyte count is the most useful laboratory indicator of ARS severity; counts below 1,000/mm³ suggest moderate exposure (200-600 rad), and below 500/mm³ suggest severe exposure (>600 rad). Serial complete blood counts every 4–6 hours during the first 24 hours are recommended. Cytogenetic analysis at 24 hours postexposure provides more accurate dose estimation but requires specialized facilities.
Management prioritizes airway, breathing, and circulation. Removal of clothing eliminates approximately 80% of external contamination. Emergency care takes precedence over decontamination, as no documented case shows a contaminated patient posing immediate life-threatening radiation risk to providers. Staff should use particulate respirators such as N-95 masks, gowns, gloves, and protective covers; radiography lead aprons do not protect against most gamma radiation. Decontamination focuses first on wounds, then mucous membranes, then intact skin. Gentle washing with soap and water is recommended, avoiding abrasion. Runoff should be collected and monitored. If contamination persists, the area should be covered to prevent spread.
Symptomatic treatment includes antiemetics such as ondansetron and intravenous fluids for dehydration. Potassium iodide is useful only for preventing thyroid uptake of radioactive iodine and must be given within four hours of exposure; adult dosing is 130 mg orally daily, with weight-based pediatric dosing. Cytokines and transfusions may be required for significant bone marrow suppression. Internal contamination requires radionuclide-specific decorporation therapy in consultation with radiation experts such as REAC/TS.
Admission is indicated for lymphocyte counts below 1,000/mm³ at 24–48 hours, a 50% decline in lymphocyte count, suspected exposure above 200 rad, significant trauma, or uncontrolled vomiting. Discharge may be considered if there is no residual contamination, no evidence of significant exposure, and the patient tolerates oral intake. All patients with confirmed exposure require dose assessment, counseling, and follow-up.
Children and fetuses are more sensitive to radiation effects. Potassium iodide is particularly important for children in radioactive iodine exposure. Pregnant staff should avoid caring for contaminated patients. Psychological reactions are common and may mimic ARS; a falling lymphocyte count helps distinguish true radiation injury from stress-related symptoms.
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Emergency And Acute Medicine – Rabies
Rabies is a viral infection of the central nervous system affecting mammals and has the highest case fatality rate of any known infectious disease once clinical symptoms develop. It is caused by a negative-stranded RNA virus in the genus Lyssavirus of the family Rhabdoviridae. Worldwide, rabies causes approximately 30,000–70,000 deaths annually, most commonly in Southeast Asia, the Philippines, Africa, South America, and the Indian subcontinent. In the United States, 2–3 human cases occur per year, most related to foreign travel or bat exposure. In the U.S., bats are the most common reservoir; globally, dogs are the primary reservoir. Other reservoirs include raccoons, skunks, foxes, woodchucks, and groundhogs. Small rodents such as squirrels and rats have not been documented to transmit rabies to humans.
Transmission occurs through contact with infected saliva, most commonly via animal bite. Nonbite transmission may occur through saliva exposure to mucous membranes or open wounds. Bat exposures may occur without a visible bite. Organ transplantation represents the only well-documented person-to-person transmission. Casual contact such as petting an animal or contact with blood, urine, or feces is not considered a transmission risk.
After inoculation, the virus replicates locally in muscle tissue and binds to nicotinic acetylcholine receptors, then enters peripheral nerves and travels via retrograde axonal transport toward the CNS at approximately 1–4 inches per day. Once in the CNS, rapid viral replication causes encephalitis. The virus then spreads centrifugally to peripheral nerves and salivary glands.
The disease progresses through five stages: incubation, prodrome, encephalitis, coma, and death (rarely recovery). The incubation period averages 1–3 months but may range from 10 days to 1 year, depending on viral load and proximity of the exposure to the CNS. The prodrome lasts 1–7 days and includes nonspecific symptoms such as fever, headache, malaise, myalgias, nausea, and sore throat. Paresthesias or fasciculations at the bite site are highly suggestive.
The encephalitic (classic) form accounts for approximately 80% of cases. Patients develop anxiety, agitation, hallucinations, confusion, seizures, muscle spasms, and autonomic instability. Hydrophobia—painful pharyngeal spasms triggered by attempts to swallow—and aerophobia—pharyngeal spasms induced by airflow—are pathognomonic. Brainstem involvement may cause diplopia and facial paralysis. Paralytic rabies (about 20%) presents with ascending paralysis resembling Guillain–Barré syndrome. Atypical forms, often associated with bat exposures, may present with neuropathic pain or movement disorders.
Once neurologic symptoms appear, rabies is almost universally fatal. Most patients die within two weeks of symptom onset due to respiratory failure or cardiovascular collapse. Rare survivors typically have significant neurologic deficits.
Diagnosis during life relies on detection of rabies RNA by RT-PCR in saliva, virus isolation, or detection of rabies antibodies in serum (if unvaccinated) or cerebrospinal fluid (CSF). CSF may show mild pleocytosis and elevated protein. Neuroimaging is often normal but may demonstrate cerebral edema. A high index of suspicion is essential, especially in patients with unexplained encephalitis and a history of animal exposure or travel to endemic areas.
Emergency management begins with thorough wound cleansing using soap and water, which significantly reduces viral load. Tetanus immunization should be updated as indicated. Determination of need for postexposure prophylaxis (PEP) should involve consultation with local public health authorities. For domestic animals, a 10-day observation period may be appropriate. For wild animals, the animal should be tested if available. If the animal cannot be tested or exposure is high risk, PEP should be initiated.
PEP consists of both passive and active immunization. Human rabies immune globulin (HRIG) is administered at 20 IU/kg, with as much as possible infiltrated around the wound and the remainder given intramuscularly at a site distant from vaccine administration. Rabies vaccine (1 mL IM in the deltoid in adults or anterolateral thigh in infants) is given on days 0, 3, 7, and 14, with an additional dose on day 28 for immunocompromised patients. Individuals previously vaccinated require only vaccine doses on days 0 and 3 and do not require HRIG. HRIG should not be administered more than 7 days after the first vaccine dose.
Pre-exposure prophylaxis consists of vaccination on days 0, 7, and either 21 or 28 and is recommended for veterinarians, animal handlers, laboratory workers, and travelers to endemic regions. Rabies vaccination and HRIG are considered safe in pregnancy.
Patients with clinical rabies require hospital admission and supportive care. Stable patients receiving PEP may be discharged with arrangements for completion of the vaccine series. Coordination with public health authorities is essential.
The key principle is that postexposure prophylaxis is the only proven effective intervention and must be administered promptly in all high-risk exposures. Once symptoms develop, rabies is almost universally fatal.
Rabies is a viral infection of the central nervous system affecting mammals and has the highest case fatality rate of any known infectious disease once clinical symptoms develop. It is caused by a negative-stranded RNA virus in the genus Lyssavirus of the family Rhabdoviridae. Worldwide, rabies causes approximately 30,000–70,000 deaths annually, most commonly in Southeast Asia, the Philippines, Africa, South America, and the Indian subcontinent. In the United States, 2–3 human cases occur per year, most related to foreign travel or bat exposure. In the U.S., bats are the most common reservoir; globally, dogs are the primary reservoir. Other reservoirs include raccoons, skunks, foxes, woodchucks, and groundhogs. Small rodents such as squirrels and rats have not been documented to transmit rabies to humans.
Transmission occurs through contact with infected saliva, most commonly via animal bite. Nonbite transmission may occur through saliva exposure to mucous membranes or open wounds. Bat exposures may occur without a visible bite. Organ transplantation represents the only well-documented person-to-person transmission. Casual contact such as petting an animal or contact with blood, urine, or feces is not considered a transmission risk.
After inoculation, the virus replicates locally in muscle tissue and binds to nicotinic acetylcholine receptors, then enters peripheral nerves and travels via retrograde axonal transport toward the CNS at approximately 1–4 inches per day. Once in the CNS, rapid viral replication causes encephalitis. The virus then spreads centrifugally to peripheral nerves and salivary glands.
The disease progresses through five stages: incubation, prodrome, encephalitis, coma, and death (rarely recovery). The incubation period averages 1–3 months but may range from 10 days to 1 year, depending on viral load and proximity of the exposure to the CNS. The prodrome lasts 1–7 days and includes nonspecific symptoms such as fever, headache, malaise, myalgias, nausea, and sore throat. Paresthesias or fasciculations at the bite site are highly suggestive.
The encephalitic (classic) form accounts for approximately 80% of cases. Patients develop anxiety, agitation, hallucinations, confusion, seizures, muscle spasms, and autonomic instability. Hydrophobia—painful pharyngeal spasms triggered by attempts to swallow—and aerophobia—pharyngeal spasms induced by airflow—are pathognomonic. Brainstem involvement may cause diplopia and facial paralysis. Paralytic rabies (about 20%) presents with ascending paralysis resembling Guillain–Barré syndrome. Atypical forms, often associated with bat exposures, may present with neuropathic pain or movement disorders.
Once neurologic symptoms appear, rabies is almost universally fatal. Most patients die within two weeks of symptom onset due to respiratory failure or cardiovascular collapse. Rare survivors typically have significant neurologic deficits.
Diagnosis during life relies on detection of rabies RNA by RT-PCR in saliva, virus isolation, or detection of rabies antibodies in serum (if unvaccinated) or cerebrospinal fluid (CSF). CSF may show mild pleocytosis and elevated protein. Neuroimaging is often normal but may demonstrate cerebral edema. A high index of suspicion is essential, especially in patients with unexplained encephalitis and a history of animal exposure or travel to endemic areas.
Emergency management begins with thorough wound cleansing using soap and water, which significantly reduces viral load. Tetanus immunization should be updated as indicated. Determination of need for postexposure prophylaxis (PEP) should involve consultation with local public health authorities. For domestic animals, a 10-day observation period may be appropriate. For wild animals, the animal should be tested if available. If the animal cannot be tested or exposure is high risk, PEP should be initiated.
PEP consists of both passive and active immunization. Human rabies immune globulin (HRIG) is administered at 20 IU/kg, with as much as possible infiltrated around the wound and the remainder given intramuscularly at a site distant from vaccine administration. Rabies vaccine (1 mL IM in the deltoid in adults or anterolateral thigh in infants) is given on days 0, 3, 7, and 14, with an additional dose on day 28 for immunocompromised patients. Individuals previously vaccinated require only vaccine doses on days 0 and 3 and do not require HRIG. HRIG should not be administered more than 7 days after the first vaccine dose.
Pre-exposure prophylaxis consists of vaccination on days 0, 7, and either 21 or 28 and is recommended for veterinarians, animal handlers, laboratory workers, and travelers to endemic regions. Rabies vaccination and HRIG are considered safe in pregnancy.
Patients with clinical rabies require hospital admission and supportive care. Stable patients receiving PEP may be discharged with arrangements for completion of the vaccine series. Coordination with public health authorities is essential.
The key principle is that postexposure prophylaxis is the only proven effective intervention and must be administered promptly in all high-risk exposures. Once symptoms develop, rabies is almost universally fatal.
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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.
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.
