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Emergency and Acute Medicine: Urinary Tract Infections (Pediatric)
Pediatric urinary tract infections (UTIs) occur when bacteria colonize the urinary tract, most commonly via retrograde spread from rectal or perineal flora. In infants, hematogenous spread can also occur, while in older children, Vesicoureteral reflux is a major predisposing factor. A definitive diagnosis requires a urine culture showing a single organism at >10,000 CFU/mL obtained from a catheterized or suprapubic specimen, as contamination rates are high with other collection methods. UTIs are particularly important in young infants because those aged 0–3 months have up to a 30% risk of associated sepsis.
Several risk factors increase susceptibility, including female sex (due to a shorter urethra), poor perineal hygiene, infrequent voiding, constipation, and sexual activity in adolescents. Lack of male circumcision may also increase risk. UTIs occur in approximately 4–7% of febrile infants. The most common pathogen is Escherichia coli, responsible for about 80% of cases, followed by organisms such as Klebsiella pneumoniae, Staphylococcus aureus, Enterobacter, Proteus, Pseudomonas aeruginosa, and Enterococcus species.
Clinical presentation varies significantly by age and is often nonspecific, especially in younger children. Neonates may present with signs of sepsis such as poor feeding, irritability, lethargy, fever, or even hypothermia. Children aged 1 month to 3 years commonly present with fever, vomiting, diarrhea, abdominal pain, and failure to thrive. In children older than 3 years, symptoms become more typical and include dysuria, urinary frequency, enuresis, abdominal or flank pain, fever, hematuria, and foul-smelling urine. Severe infections may present with systemic toxicity, including high fever, chills, and costovertebral angle tenderness.
Diagnosis can be challenging and requires laboratory confirmation. Urinalysis with microscopy and Gram stain is essential, although it has limited sensitivity in infants, and up to 80% of neonates with confirmed UTI may have a normal urinalysis. Leukocyte esterase suggests pyuria, while nitrites indicate nitrate-reducing bacteria, though false negatives are common. Urine culture remains the gold standard and must be processed promptly. Catheterization is the preferred method for obtaining urine in infants and young children due to high contamination rates with bag or clean-catch specimens. Blood tests, including CBC and blood cultures, are recommended in young or febrile children to evaluate for bacteremia.
Imaging plays an important role in selected cases. Renal and bladder ultrasound is used to detect structural abnormalities and is recommended in children under 2 years with a first febrile UTI, those with recurrent infections, or poor response to treatment. Voiding cystourethrogram (VCUG) may be used to detect vesicoureteral reflux, although its routine use is debated. Additional imaging may be indicated based on clinical severity and recurrence.
The differential diagnosis includes vulvovaginitis, viral cystitis, urethritis (including sexually transmitted infections in adolescents), glomerulonephritis, appendicitis, trauma, nephrolithiasis, diabetes, and possible abuse in certain contexts. Careful evaluation is essential to avoid misdiagnosis.
Management depends on age and severity. Infants younger than 3 months with suspected UTI should be treated empirically for sepsis with intravenous antibiotics such as ampicillin and gentamicin. Older children who are stable may be treated with oral antibiotics for 10–14 days, guided by local resistance patterns. Common options include amoxicillin, amoxicillin-clavulanate, cephalexin, trimethoprim–sulfamethoxazole, and third-generation cephalosporins such as cefixime or cefdinir. Shorter courses (≈5 days) may be considered in older children with uncomplicated, afebrile infections.
Hospital admission is indicated for infants under 3 months, toxic appearance, dehydration, inability to tolerate oral medications, suspected pyelonephritis, urinary obstruction, immunocompromised state, or failure of outpatient therapy. Patients who are stable, hydrated, and able to take oral medications with reliable follow-up may be discharged.
Follow-up is essential to ensure resolution of infection, monitor for recurrence, and evaluate for underlying abnormalities such as reflux or structural anomalies. Long-term complications include recurrent UTIs, renal scarring, hypertension, and chronic kidney disease. Early diagnosis and treatment are critical to reducing these risks.
Key clinical points include recognizing that symptoms are often nonspecific in young children, that laboratory confirmation is essential, and that febrile infants with UTIs are at risk for bacteremia and require careful evaluation and management.
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Emergency and Acute Medicine: Urticaria
Urticaria, commonly known as hives, is a cutaneous reaction caused by activation of mast cells and basophils with release of inflammatory mediators such as histamine. This leads to increased vascular permeability, resulting in pruritic wheals and edema involving the epidermis and superficial dermis. It is more frequently seen in children, young adults, women, and individuals with atopic tendencies. Approximately 40% of patients also develop angioedema, which involves deeper dermal or submucosal tissues and may affect areas such as the lips, eyelids, or airway.
In children, urticaria is often triggered by infections or food-related reactions. Infants may present with more prominent swelling of distal extremities and even acrocyanosis, and occasionally bullae may form in the center of lesions. Acute urticaria lasts less than six weeks and is often idiopathic, although triggers such as medications (including antibiotics, opiates, and vaccines), foods, insect stings, infections (especially viral upper respiratory infections), and environmental allergens are commonly implicated. Physical triggers are also important and include dermographism (skin writing), cholinergic urticaria from heat or exercise, cold exposure, sunlight, and water contact.
Chronic urticaria persists beyond six weeks and is idiopathic in the majority of cases, though it may be associated with autoimmune diseases, immune complex disorders, or occult infections. Conditions such as Hashimoto’s thyroiditis are recognized associations. Chronic forms may also represent unrecognized physical urticaria or underlying systemic illness.
Patients typically present with intensely pruritic, well-circumscribed wheals that vary in size and shape and may appear anywhere on the body, including the palms and soles. Lesions are transient, usually resolving within a few hours, while new ones continue to appear. Associated symptoms such as fever, arthralgia, weight loss, or lymphadenopathy should raise concern for systemic disease. The presence of mucosal swelling, respiratory symptoms, hypotension, or stridor suggests progression to Anaphylaxis, which is life-threatening.
Physical examination should focus on identifying signs of systemic involvement. Airway compromise, wheezing, or hypotension must be rapidly recognized. Dermatologic findings include transient wheals, sometimes with associated edema, petechiae, or purpura. Dermographism can be elicited by lightly scratching the skin to produce a linear wheal, while other forms may require specific provocation tests such as heat, cold, or exercise challenges.
Diagnosis is clinical, based on history and examination. Acute urticaria does not require laboratory testing. In chronic cases, evaluation may include CBC, inflammatory markers, thyroid function tests, and urinalysis to assess for underlying systemic or infectious causes. A skin biopsy is reserved for suspected urticarial vasculitis, particularly when lesions are painful, prolonged, or nonblanching.
Management is primarily symptomatic and begins with removal of any identifiable trigger. The cornerstone of therapy is H1 antihistamines, preferably second-generation agents such as cetirizine or loratadine due to fewer sedative effects. First-generation antihistamines like diphenhydramine may be used as adjuncts. H2 blockers (e.g., famotidine) can be added in refractory cases. Corticosteroids are reserved for severe or persistent symptoms.
In cases with systemic involvement or airway compromise, immediate treatment with intramuscular epinephrine is essential. Bronchospasm should be treated with β-agonists such as albuterol, and hypotension managed with IV fluids and vasopressors as needed. Patients should avoid NSAIDs and opiates, as these may exacerbate symptoms.
Disposition depends on severity. Patients with stable vital signs and no airway involvement can be discharged with antihistamines and follow-up. Admission is indicated for those with anaphylaxis, respiratory compromise, hypotension, or severe refractory symptoms. Follow-up with a primary care physician or specialist is recommended, particularly for chronic urticaria lasting more than six weeks.
Important clinical considerations include the potential for a biphasic reaction in severe cases, with recurrence occurring several hours after initial resolution. Clinicians should maintain vigilance for signs of systemic disease in chronic urticaria and ensure appropriate evaluation when indicated.
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Emergency and Acute Medicine: Uvulitis
Uvulitis refers to inflammation of the uvula and may result from infectious or noninfectious causes. It can range from a mild, self-limited condition to a potentially life-threatening illness if associated with airway compromise. Infectious causes include bacterial, viral, and fungal pathogens, while noninfectious causes include trauma, allergic reactions, chemical irritation, and angioedema. Although once considered rare, uvulitis is likely underrecognized, especially in milder viral cases. It is more commonly seen in children aged 5–15 years due to the prevalence of Group A Streptococcus infections, whereas noninfectious causes are more common in adults.
The most common infectious cause is Group A Streptococcus, followed by Haemophilus influenzae type b and other organisms such as Streptococcus pneumoniae and anaerobes. Viral etiologies, including Herpes simplex virus, Coxsackie virus, varicella-zoster virus, and Epstein–Barr virus, are often responsible for milder presentations. Noninfectious causes include trauma (e.g., instrumentation or thermal injury), inhalation of irritants, vasculitis, and allergic reactions such as Angioedema, which may be hereditary or medication-induced (e.g., ACE inhibitors).
Symptoms typically develop rapidly, often within 4–6 hours. Patients commonly report a foreign-body sensation in the throat, sore throat, dysphagia, and odynophagia. More severe cases may include dyspnea, drooling, muffled “hot-potato” voice, stridor, and respiratory distress. Fever suggests an infectious etiology, while a history of new medication use or prior episodes of swelling points toward angioedema. Associated symptoms such as urticaria or wheezing may indicate an allergic process.
Physical examination findings vary from mild uvular erythema and edema to marked swelling with airway compromise. The uvula may appear erythematous or pale and swollen, sometimes with exudates if infection is present. Cervical lymphadenopathy and pharyngitis may accompany infectious cases. Signs such as hypoxia, stridor, or inability to handle secretions indicate a potential airway emergency. It is critical to assess for other serious conditions such as Epiglottitis, peritonsillar abscess, or retropharyngeal abscess when symptoms are severe.
Diagnosis is primarily clinical but may be supported by targeted testing. Rapid antigen testing for streptococcus and throat cultures can help confirm bacterial infection. Laboratory findings such as leukocytosis suggest infection, while eosinophilia may indicate an allergic cause. Imaging, such as a lateral neck X-ray or CT scan of the neck, is reserved for cases where deeper infection or alternative diagnoses are suspected. Fiberoptic nasopharyngoscopy may be required in severe cases to assess airway involvement.
Management focuses first on airway assessment and stabilization. Patients with signs of airway compromise require immediate intervention, including supplemental oxygen, possible nebulized β-agonists or racemic epinephrine, and preparation for definitive airway management (e.g., intubation or, in extreme cases, cricothyrotomy). Early consultation with otolaryngology is recommended in moderate to severe cases.
Treatment is directed at the underlying cause. Infectious uvulitis is treated with empiric antibiotics targeting common organisms such as streptococcus and Hib, with agents like ceftriaxone or clindamycin. Mild cases may be managed with oral antibiotics such as penicillin or amoxicillin. Noninfectious causes, particularly allergic or angioedema-related uvulitis, are treated with antihistamines, corticosteroids, and epinephrine in severe cases. Patients with hereditary angioedema may require specific therapies such as C1 inhibitor concentrate or bradykinin receptor antagonists.
Disposition depends on severity and response to treatment. Patients with airway compromise, hypoxia, inability to tolerate oral intake, or systemic infection require admission, often to a monitored or intensive care setting. Those with mild symptoms that resolve with treatment may be discharged after observation (typically 4–6 hours) if they remain stable and have reliable follow-up within 24–48 hours.
Key clinical points include recognizing that isolated uvulitis rarely causes severe airway obstruction; significant respiratory distress should prompt evaluation for other serious conditions such as epiglottitis or anaphylaxis. Early airway assessment and readiness for intervention are critical, and treatment should be tailored to the suspected underlying cause.
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Emergency and Acute Medicine: Varicella (Chickenpox)
Varicella is a highly contagious viral illness caused by the varicella-zoster virus (VZV), a DNA virus that establishes lifelong latency in sensory ganglia. It is commonly known as chickenpox and typically affects children, although adults experience more severe disease and have a significantly higher mortality risk. The incidence has decreased substantially due to vaccination.
Transmission occurs via respiratory droplets or direct contact with skin lesions. After primary infection, the virus remains dormant and may reactivate later in life as Herpes zoster. Humans are the only known reservoir. The incubation period ranges from 10 to 21 days, and patients are contagious from about 48 hours before rash onset until all lesions have crusted over.
Clinically, varicella usually begins with a prodrome of low-grade fever, malaise, headache, and anorexia, followed by the characteristic rash. The rash typically starts on the face and spreads to the trunk and extremities. Lesions evolve through stages—papules, vesicles, and crusts—often described as “dew drops on a rose petal.” A key diagnostic feature is the presence of lesions in different stages simultaneously. Mucosal involvement may occur. Pruritus is common, and secondary bacterial infection can complicate the disease.
In adolescents and adults, the disease tends to be more severe, with a higher risk of complications such as pneumonia. Immunocompromised patients (e.g., those with HIV, malignancy, or on immunosuppressive therapy) are at high risk for disseminated disease, hemorrhagic lesions, and prolonged illness. Pregnant patients are also at increased risk of severe complications, including varicella pneumonia, which is a life-threatening emergency. Infection during pregnancy may result in congenital varicella syndrome, characterized by limb hypoplasia, neurologic abnormalities, and ocular defects.
Extracutaneous complications include varicella pneumonitis (more common in adults and smokers), cerebellar ataxia (especially in children), cerebritis, and Reye syndrome, particularly in children given aspirin. Varicella pneumonia typically presents a few days after rash onset with cough, dyspnea, and hypoxia, and may require imaging showing diffuse nodular infiltrates.
Diagnosis is usually clinical based on history and the classic rash. Laboratory confirmation (PCR, viral culture, or direct fluorescent antibody testing) is reserved for atypical or severe cases. Imaging such as chest X-ray is indicated if complications like pneumonia are suspected.
Management in uncomplicated cases is supportive, including antipyretics (acetaminophen) and antipruritic measures. Aspirin should be avoided in children due to the risk of Reye syndrome. Good hygiene and nail care help prevent secondary bacterial infection. Antiviral therapy with acyclovir is recommended for high-risk patients, including adults, adolescents, immunocompromised individuals, and those with chronic medical conditions, ideally within 24 hours of rash onset.
Severe or complicated cases require intravenous antivirals such as acyclovir. Immunocompromised patients often need hospital admission and isolation. Varicella-zoster immune globulin (VZIG) is used for post-exposure prophylaxis in high-risk individuals, including pregnant women without immunity and immunocompromised patients.
Vaccination is highly effective and recommended for all susceptible individuals. Two doses are given in childhood, and unvaccinated adolescents and adults should also receive vaccination unless contraindicated.
Key clinical pearls include recognizing that patients are contagious before rash onset, identifying high-risk groups who require antiviral therapy, and treating varicella pneumonia aggressively, especially in pregnancy.
Emergency and Acute Medicine: Varicella (Chickenpox)
Varicella is a highly contagious viral illness caused by the varicella-zoster virus (VZV), a DNA virus that establishes lifelong latency in sensory ganglia. It is commonly known as chickenpox and typically affects children, although adults experience more severe disease and have a significantly higher mortality risk. The incidence has decreased substantially due to vaccination.
Transmission occurs via respiratory droplets or direct contact with skin lesions. After primary infection, the virus remains dormant and may reactivate later in life as Herpes zoster. Humans are the only known reservoir. The incubation period ranges from 10 to 21 days, and patients are contagious from about 48 hours before rash onset until all lesions have crusted over.
Clinically, varicella usually begins with a prodrome of low-grade fever, malaise, headache, and anorexia, followed by the characteristic rash. The rash typically starts on the face and spreads to the trunk and extremities. Lesions evolve through stages—papules, vesicles, and crusts—often described as “dew drops on a rose petal.” A key diagnostic feature is the presence of lesions in different stages simultaneously. Mucosal involvement may occur. Pruritus is common, and secondary bacterial infection can complicate the disease.
In adolescents and adults, the disease tends to be more severe, with a higher risk of complications such as pneumonia. Immunocompromised patients (e.g., those with HIV, malignancy, or on immunosuppressive therapy) are at high risk for disseminated disease, hemorrhagic lesions, and prolonged illness. Pregnant patients are also at increased risk of severe complications, including varicella pneumonia, which is a life-threatening emergency. Infection during pregnancy may result in congenital varicella syndrome, characterized by limb hypoplasia, neurologic abnormalities, and ocular defects.
Extracutaneous complications include varicella pneumonitis (more common in adults and smokers), cerebellar ataxia (especially in children), cerebritis, and Reye syndrome, particularly in children given aspirin. Varicella pneumonia typically presents a few days after rash onset with cough, dyspnea, and hypoxia, and may require imaging showing diffuse nodular infiltrates.
Diagnosis is usually clinical based on history and the classic rash. Laboratory confirmation (PCR, viral culture, or direct fluorescent antibody testing) is reserved for atypical or severe cases. Imaging such as chest X-ray is indicated if complications like pneumonia are suspected.
Management in uncomplicated cases is supportive, including antipyretics (acetaminophen) and antipruritic measures. Aspirin should be avoided in children due to the risk of Reye syndrome. Good hygiene and nail care help prevent secondary bacterial infection. Antiviral therapy with acyclovir is recommended for high-risk patients, including adults, adolescents, immunocompromised individuals, and those with chronic medical conditions, ideally within 24 hours of rash onset.
Severe or complicated cases require intravenous antivirals such as acyclovir. Immunocompromised patients often need hospital admission and isolation. Varicella-zoster immune globulin (VZIG) is used for post-exposure prophylaxis in high-risk individuals, including pregnant women without immunity and immunocompromised patients.
Vaccination is highly effective and recommended for all susceptible individuals. Two doses are given in childhood, and unvaccinated adolescents and adults should also receive vaccination unless contraindicated.
Key clinical pearls include recognizing that patients are contagious before rash onset, identifying high-risk groups who require antiviral therapy, and treating varicella pneumonia aggressively, especially in pregnancy.
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Emergency and Acute Medicine: Vasculitis
Vasculitis refers to a heterogeneous group of disorders characterized by inflammation of blood vessel walls, leading to ischemia, necrosis, aneurysm formation, or hemorrhage. The underlying mechanisms include immune complex deposition, complement activation, cell-mediated hypersensitivity, and granulomatous inflammation. Because vessels of varying sizes and organs may be involved, vasculitis often presents as a multisystem disease with diverse clinical manifestations.
Vasculitis may be primary (idiopathic) or secondary to infections, drugs, autoimmune diseases, or malignancy. Classification is increasingly based on antineutrophil cytoplasmic antibodies (ANCA), though traditional classification divides vasculitis by vessel size. Large-vessel vasculitides include Giant cell arteritis, typically affecting patients older than 50 years, and Takayasu arteritis, which affects younger individuals. Medium-vessel diseases include Polyarteritis nodosa and Kawasaki disease, the latter primarily affecting children and involving coronary arteries. Small-vessel vasculitides include Granulomatosis with polyangiitis, microscopic polyangiitis, and eosinophilic granulomatosis (Churg–Strauss), often associated with pulmonary and renal involvement.
Clinically, patients often present initially with constitutional symptoms such as fever, fatigue, weight loss, and diffuse myalgias before organ-specific manifestations appear. Signs of arterial insufficiency depend on the vascular territory involved. Neurologic symptoms may include headache, transient ischemic attacks, stroke, or vision loss. Renal involvement may manifest as hypertension, hematuria, or renal failure. Cutaneous findings are common and include palpable purpura, ulcers, nodules, and livedo reticularis. Respiratory symptoms such as sinusitis, epistaxis, and pulmonary hemorrhage may be seen in small-vessel vasculitis. Gastrointestinal ischemia may present with abdominal pain or bleeding.
Diagnosis requires a high index of suspicion, particularly in patients with unexplained multisystem disease. Laboratory evaluation typically reveals elevated inflammatory markers (ESR, CRP), anemia, leukocytosis, and sometimes eosinophilia. Urinalysis may show proteinuria or hematuria, suggesting renal involvement. Autoimmune testing including ANA and ANCA can help guide diagnosis. Imaging studies such as CT, MRI, or angiography may demonstrate vessel abnormalities, while definitive diagnosis often requires tissue biopsy.
Management depends on the specific type and severity of vasculitis and is usually guided by a specialist. Initial emergency care focuses on stabilizing life-threatening complications such as stroke, renal failure, or pulmonary hemorrhage. Corticosteroids are the cornerstone of treatment for many vasculitides, particularly giant cell arteritis, where prompt treatment is critical to prevent vision loss. Immunosuppressive agents such as cyclophosphamide, methotrexate, or azathioprine are used in more severe or refractory cases. Intravenous immunoglobulin (IVIG) is used in conditions like Kawasaki disease, often combined with aspirin to reduce coronary complications.
Patients with severe disease or evidence of end-organ damage require hospital admission. Those with milder symptoms may be managed as outpatients but require urgent referral to a rheumatologist for further evaluation and initiation of definitive therapy. Close follow-up is essential, as untreated vasculitis can lead to irreversible organ damage or death.
Key clinical considerations include recognizing vasculitis as a cause of unexplained systemic illness, avoiding premature immunosuppressive therapy without specialist input, and ruling out mimics such as Infective endocarditis. Early diagnosis and targeted treatment are critical to improving outcomes in these potentially life-threatening conditions.
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Emergency and Acute Medicine: Varices
Esophageal varices develop as a consequence of Portal hypertension, where increased portal venous pressure leads to the formation of portal–systemic collateral vessels. At the gastroesophageal junction, these collaterals become fragile submucosal veins prone to rupture, resulting in life-threatening upper gastrointestinal bleeding.
Variceal bleeding accounts for approximately 10–30% of all upper GI hemorrhage and up to 90% of bleeding episodes in patients with cirrhosis. About 30% of cirrhotic patients will experience a variceal hemorrhage, with a mortality rate of around 30% per episode and a high recurrence rate of up to 70%. The most common underlying cause in adults is cirrhosis due to alcohol use or chronic hepatitis, although other causes include metabolic storage diseases such as Wilson disease or hemochromatosis. In certain regions, such as the Middle East, schistosomiasis is a major cause. In children, causes include biliary atresia, cystic fibrosis, and other intrahepatic obstructive disorders.
Patients typically present with signs of acute upper GI bleeding, including hematemesis, melena, or hematochezia (in severe cases). They may also show signs of hypovolemia such as tachycardia, hypotension, cool clammy skin, and altered mental status. Stigmata of chronic liver disease—such as jaundice, ascites, spider angiomata, and hepatosplenomegaly—are often present. In severe cases, patients may lose 20–40% of their total blood volume. Importantly, hematochezia in an unstable patient should be considered an upper GI bleed until proven otherwise.
Diagnosis is primarily clinical, supported by laboratory and endoscopic evaluation. Initial labs should include CBC, coagulation profile, renal function tests, and type and cross-match for transfusion. Hemoglobin may initially be normal despite significant blood loss, so serial measurements are essential. A BUN-to-creatinine ratio greater than 30 suggests significant upper GI bleeding. Definitive diagnosis and treatment are achieved via emergent endoscopy, which allows visualization and intervention.
Management in the emergency setting focuses on rapid stabilization and control of bleeding. Airway protection is critical, and early intubation is often recommended, especially in patients with altered mental status or massive bleeding. Two large-bore IV lines should be established for fluid resuscitation and blood transfusion, with a target hemoglobin around 8 g/dL. Overly aggressive fluid resuscitation should be avoided, as it may increase portal pressure and worsen bleeding.
Pharmacologic therapy should be initiated early. Octreotide is commonly used as first-line therapy (or somatostatin where available) to reduce portal pressure and control bleeding. Prophylactic antibiotics such as ceftriaxone or fluoroquinolones are essential, as they reduce the risk of infection and improve survival. Erythromycin may be given to improve gastric emptying prior to endoscopy.
Endoscopic therapy is the cornerstone of treatment. Endoscopic band ligation is preferred due to fewer complications compared to sclerotherapy. In cases of massive uncontrolled bleeding, balloon tamponade using devices such as the Sengstaken–Blakemore tube may be used as a temporary measure, though it carries significant risks including esophageal rupture. For refractory bleeding, a transjugular intrahepatic portosystemic shunt (TIPS) procedure or surgical intervention may be required.
All patients with active variceal bleeding require ICU admission due to the high risk of rebleeding and mortality. High-risk features include age over 60, renal failure, and low initial hemoglobin. Patients with nonbleeding varices may be managed as outpatients with close gastroenterology follow-up, including surveillance endoscopy and preventive therapy.
Key clinical points include the importance of early airway control, prompt initiation of vasoactive medications and antibiotics, and rapid involvement of gastroenterology for endoscopic management. Recognizing variceal bleeding early and initiating aggressive but targeted therapy significantly improves outcomes in this high-risk population.
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Emergency and Acute Medicine: Valvular Heart Disease
Valvular heart disease refers to dysfunction of one or more heart valves, leading to either obstruction of forward blood flow (stenosis) or backward leakage (regurgitation). The four major conditions commonly encountered in emergency and clinical practice are mitral stenosis, mitral regurgitation, aortic stenosis, and aortic regurgitation. These disorders alter cardiac hemodynamics and may lead to heart failure, arrhythmias, or sudden death.
Mitral stenosis is characterized by obstruction of diastolic blood flow from the left atrium to the left ventricle, most commonly due to rheumatic fever. In contrast, mitral regurgitation results from failure of the mitral valve to close properly, allowing blood to flow backward into the left atrium. Acute mitral regurgitation causes sudden pressure overload leading to pulmonary edema, while chronic disease leads to left ventricular dilation and hypertrophy.
Aortic stenosis involves obstruction of left ventricular outflow, leading to increased systolic pressure and concentric hypertrophy of the left ventricle. It is commonly caused by calcific degeneration or congenital bicuspid valve. Aortic regurgitation, on the other hand, allows backflow of blood from the aorta into the left ventricle during diastole, resulting in volume overload. Acute aortic regurgitation can rapidly lead to pulmonary edema and heart failure, whereas chronic disease leads to progressive ventricular dilation.
Pregnancy significantly increases circulatory demands and may worsen underlying valvular disease, increasing the risk of thromboembolic events. In elderly patients, degenerative changes are the most common cause, particularly affecting the aortic and mitral valves. Surgical valve replacement is frequently required in advanced disease.
Clinically, symptoms vary depending on the valve involved. Mitral stenosis presents with exertional dyspnea, fatigue, orthopnea, and hemoptysis, along with a low-pitched diastolic murmur and opening snap. Mitral regurgitation is associated with dyspnea, atrial fibrillation, and a high-pitched pansystolic murmur radiating to the axilla. Aortic stenosis classically presents with the triad of angina, syncope, and heart failure, along with a harsh systolic murmur radiating to the carotids and delayed pulse upstroke. Aortic regurgitation presents with wide pulse pressure, bounding pulses, and a high-pitched diastolic murmur, along with characteristic peripheral signs such as head bobbing and nail-bed pulsations.
Evaluation includes a thorough history and cardiovascular examination, supported by ECG and chest X-ray findings such as chamber enlargement or pulmonary congestion. Laboratory tests may include blood cultures if Infective endocarditis is suspected. Imaging with echocardiography is essential for assessing valve structure, function, and severity of disease, while CT may be required in suspected aortic dissection.
Management depends on the specific lesion and whether it is acute or chronic. Initial stabilization follows standard resuscitation principles, including oxygen, monitoring, and IV access. Mitral stenosis is treated with diuretics and rate control (e.g., beta-blockers or digoxin), especially in atrial fibrillation. Acute mitral regurgitation requires urgent afterload reduction and may need surgical intervention. Aortic stenosis requires cautious management—vasodilators such as nitrates should be avoided, and gentle fluid management is essential. Aortic regurgitation is managed with afterload reduction and diuretics, with urgent surgery in acute cases.
Disposition depends on severity. Patients with hemodynamic instability, new arrhythmias, pulmonary edema, or acute valve dysfunction require admission. Stable patients with chronic disease may be discharged with close cardiology follow-up.
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Emergency and Acute Medicine: Urethritis
Urethritis is inflammation of the urethra, most commonly caused by infection, and is a frequent presentation in emergency and acute care settings. It typically presents with urethral discharge and dysuria and often develops after exposure to a sexual partner with a sexually transmitted infection (STI), bacterial vaginosis, or urinary tract infection. It may also occur after orogenital contact.
The most common etiologies are sexually transmitted pathogens, particularly Neisseria gonorrhoeae, which accounts for about 35% of cases, and Chlamydia trachomatis, responsible for 25–50%. Other significant causes include Mycoplasma genitalium and Ureaplasma urealyticum. Less commonly, organisms such as Trichomonas vaginalis, Herpes simplex virus, adenovirus, Candida species, and enteric bacteria may be involved. Noninfectious causes such as chemical irritation, alcohol, systemic illness, or foreign bodies are rare.
Symptoms usually develop within 1 to 2 weeks after exposure but may take up to 4 to 6 weeks. Patients commonly report urethral discharge, dysuria, and cloudy first-void urine. Pyuria is often present, and some patients may have inguinal lymphadenopathy. Important historical features include the color and quantity of discharge, associated urinary symptoms, recent sexual history, and risk factors such as multiple partners or unprotected intercourse.
On physical examination, findings may include visible urethral discharge, staining on undergarments, meatal crusting, and sometimes genital lesions. Palpation of the testes, epididymis, and spermatic cord is important to evaluate for complications such as epididymitis. Inguinal lymphadenopathy may also be present.
Diagnosis is typically confirmed using nucleic acid amplification tests (NAATs), such as PCR, performed on first-void urine or urethral swabs, which are highly sensitive for detecting gonorrhea and chlamydia. Urinalysis is useful to rule out urinary tract infection. Because STIs often coexist, patients should also be screened for HIV and syphilis using appropriate serologic tests.
The differential diagnosis includes urinary tract infection, prostatitis, epididymitis, orchitis, pelvic inflammatory disease, reactive arthritis, and chemical irritation from soaps or spermicides. In children, urethritis should raise concern for possible abuse.
Management in the emergency setting is largely empirical, with treatment directed at both gonorrhea and chlamydia regardless of confirmed results. Standard therapy includes ceftriaxone for gonorrhea and either azithromycin or doxycycline for chlamydia. In pregnant patients, azithromycin is preferred, as doxycycline and fluoroquinolones are contraindicated.
Most patients can be discharged after treatment with appropriate follow-up arranged. Patients should be advised to abstain from sexual activity until symptoms resolve and for at least one week after completing treatment. All sexual partners should be evaluated and treated to prevent reinfection. Repeat testing may be recommended, particularly in pregnant patients, to ensure cure.
Complications of untreated urethritis include epididymitis, pelvic inflammatory disease, infertility, reactive arthritis, and ocular complications. Key clinical pearls include always treating for both gonorrhea and chlamydia, recognizing increasing antibiotic resistance, and considering atypical organisms in recurrent cases.
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Emergency and Acute Medicine - Urinary Retention
Urinary retention is the sudden or chronic inability to empty the bladder adequately. Acute urinary retention refers to the abrupt inability to void spontaneously and occurs most often in men older than 60 years. In the emergency department, the most common cause is benign prostatic hyperplasia (BPH).
The causes of urinary retention are broad and include anatomic, neurologic, and medication-related conditions. Anatomic causes may involve the penis, urethra, or prostate and include phimosis, paraphimosis, meatal stenosis, tumors, pelvic masses, pelvic organ prolapse, foreign bodies, urethral calculi, urethritis, strictures, hematoma, vulvar edema after vaginal delivery, benign prostatic hypertrophy, prostate carcinoma, prostatitis, bladder neck contracture, and prostatic infarction. Neurologic causes include motor or paralytic disorders such as spinal shock and spinal cord syndromes, as well as sensory or paralytic disorders such as diabetes, multiple sclerosis, and other spinal cord syndromes. Medications may also precipitate retention, especially antihistamines, anticholinergics, antispasmodics, tricyclic antidepressants, alpha-adrenergic stimulators, narcotics, and NSAIDs.
Patients with acute urinary retention typically present with lower abdominal or suprapubic discomfort and may appear restless or distressed. Chronic urinary retention, in contrast, is often painless. A careful history is essential and should include any prior episodes of urinary retention, history of BPH or prostate cancer, other malignancy, prior radiation treatment, pelvic trauma, signs or symptoms of infection or abscess, symptoms suggesting urinary stones, neurologic complaints, intravenous drug use, back pain, and a complete medication review.
The physical examination should include assessment of vital signs for evidence of infection or shock, an abdominal examination, a rectal examination, and a genitourinary examination. In women, a pelvic examination should be considered. If the presentation suggests a neurologic cause, a thorough neurologic examination is necessary. In trauma patients, special attention should be given to possible urethral injury.
Because urinary retention has many possible causes, the workup is guided by the history and examination. Laboratory testing is usually limited. Renal function tests may be obtained if acute renal insufficiency is suspected, although this is uncommon in isolated acute urinary retention. A PSA test is not useful in the emergency department because it is often elevated in the setting of retention. Urinalysis may be obtained if the history or exam suggests infection. Imaging such as abdominal or pelvic ultrasound or CT may be indicated if there is concern for a mass, abscess, malignancy, bladder calculi, or another structural cause. Neuroimaging or spinal imaging is warranted if an acute neurologic process is suspected. A postvoid residual volume greater than 200 mL is generally considered abnormal.
Management begins with identifying and treating any immediately life-threatening condition. The key initial step is prompt bladder decompression. This is usually attempted with placement of a 14–18 French urinary catheter. If that cannot be passed and there is a history of prior transurethral procedures or known stricture, a smaller 10–12 French catheter may be tried. In men without prior instrumentation, a 20–22 French coudé catheter may be helpful. If catheter placement remains unsuccessful, suprapubic aspiration or suprapubic catheter placement may be required. In trauma patients with suspected urethral injury, such as those with gross hematuria, blood at the meatus, or a high-riding prostate, urethral catheterization should be deferred until a retrograde urethrogram has been performed.
After catheter placement, the bladder should be drained and urine output monitored. Rapid decompression may occasionally cause transient gross hematuria, though this is rarely clinically significant. Postobstructive diuresis is a possible complication after relief of retention, so it is reasonable to observe patients for two to three hours to ensure they do not develop hypotension or significant volume loss. If the catheter is to remain in place, a leg bag should be attached before discharge, and the patient and family should receive instructions on catheter care. Prophylactic antibiotics are not indicated for an indwelling urinary catheter unless there is evidence of infection. If BPH is the cause, starting an alpha-blocker is appropriate. Medications contributing to retention should be discontinued when possible, and constipation should be treated if present.
Common medications used for BPH-related urinary retention include alpha-blockers such as prazosin, tamsulosin, alfuzosin, and terazosin. These agents help improve urinary flow and are often started in the emergency setting when BPH is suspected.
Most patients can be discharged after successful bladder decompression, provided there is no serious underlying cause or complication. Admission is indicated for significant postobstructive diuresis requiring IV fluids or vasopressors, sepsis, retention related to spinal cord compression, obstruction caused by malignancy or a mass, or any condition requiring urgent urologic or surgical intervention.
All patients require follow-up for continued evaluation of the underlying cause, management of the catheter if one remains in place, and further treatment planning. Important pitfalls include failing to recognize a mass or malignancy, overlooking spinal cord compression, and missing a medication-related cause. A careful drug history, including over-the-counter medications, is especially important when no obvious cause is identified.
Urinary retention is the sudden or chronic inability to empty the bladder adequately. Acute urinary retention refers to the abrupt inability to void spontaneously and occurs most often in men older than 60 years. In the emergency department, the most common cause is benign prostatic hyperplasia (BPH).
The causes of urinary retention are broad and include anatomic, neurologic, and medication-related conditions. Anatomic causes may involve the penis, urethra, or prostate and include phimosis, paraphimosis, meatal stenosis, tumors, pelvic masses, pelvic organ prolapse, foreign bodies, urethral calculi, urethritis, strictures, hematoma, vulvar edema after vaginal delivery, benign prostatic hypertrophy, prostate carcinoma, prostatitis, bladder neck contracture, and prostatic infarction. Neurologic causes include motor or paralytic disorders such as spinal shock and spinal cord syndromes, as well as sensory or paralytic disorders such as diabetes, multiple sclerosis, and other spinal cord syndromes. Medications may also precipitate retention, especially antihistamines, anticholinergics, antispasmodics, tricyclic antidepressants, alpha-adrenergic stimulators, narcotics, and NSAIDs.
Patients with acute urinary retention typically present with lower abdominal or suprapubic discomfort and may appear restless or distressed. Chronic urinary retention, in contrast, is often painless. A careful history is essential and should include any prior episodes of urinary retention, history of BPH or prostate cancer, other malignancy, prior radiation treatment, pelvic trauma, signs or symptoms of infection or abscess, symptoms suggesting urinary stones, neurologic complaints, intravenous drug use, back pain, and a complete medication review.
The physical examination should include assessment of vital signs for evidence of infection or shock, an abdominal examination, a rectal examination, and a genitourinary examination. In women, a pelvic examination should be considered. If the presentation suggests a neurologic cause, a thorough neurologic examination is necessary. In trauma patients, special attention should be given to possible urethral injury.
Because urinary retention has many possible causes, the workup is guided by the history and examination. Laboratory testing is usually limited. Renal function tests may be obtained if acute renal insufficiency is suspected, although this is uncommon in isolated acute urinary retention. A PSA test is not useful in the emergency department because it is often elevated in the setting of retention. Urinalysis may be obtained if the history or exam suggests infection. Imaging such as abdominal or pelvic ultrasound or CT may be indicated if there is concern for a mass, abscess, malignancy, bladder calculi, or another structural cause. Neuroimaging or spinal imaging is warranted if an acute neurologic process is suspected. A postvoid residual volume greater than 200 mL is generally considered abnormal.
Management begins with identifying and treating any immediately life-threatening condition. The key initial step is prompt bladder decompression. This is usually attempted with placement of a 14–18 French urinary catheter. If that cannot be passed and there is a history of prior transurethral procedures or known stricture, a smaller 10–12 French catheter may be tried. In men without prior instrumentation, a 20–22 French coudé catheter may be helpful. If catheter placement remains unsuccessful, suprapubic aspiration or suprapubic catheter placement may be required. In trauma patients with suspected urethral injury, such as those with gross hematuria, blood at the meatus, or a high-riding prostate, urethral catheterization should be deferred until a retrograde urethrogram has been performed.
After catheter placement, the bladder should be drained and urine output monitored. Rapid decompression may occasionally cause transient gross hematuria, though this is rarely clinically significant. Postobstructive diuresis is a possible complication after relief of retention, so it is reasonable to observe patients for two to three hours to ensure they do not develop hypotension or significant volume loss. If the catheter is to remain in place, a leg bag should be attached before discharge, and the patient and family should receive instructions on catheter care. Prophylactic antibiotics are not indicated for an indwelling urinary catheter unless there is evidence of infection. If BPH is the cause, starting an alpha-blocker is appropriate. Medications contributing to retention should be discontinued when possible, and constipation should be treated if present.
Common medications used for BPH-related urinary retention include alpha-blockers such as prazosin, tamsulosin, alfuzosin, and terazosin. These agents help improve urinary flow and are often started in the emergency setting when BPH is suspected.
Most patients can be discharged after successful bladder decompression, provided there is no serious underlying cause or complication. Admission is indicated for significant postobstructive diuresis requiring IV fluids or vasopressors, sepsis, retention related to spinal cord compression, obstruction caused by malignancy or a mass, or any condition requiring urgent urologic or surgical intervention.
All patients require follow-up for continued evaluation of the underlying cause, management of the catheter if one remains in place, and further treatment planning. Important pitfalls include failing to recognize a mass or malignancy, overlooking spinal cord compression, and missing a medication-related cause. A careful drug history, including over-the-counter medications, is especially important when no obvious cause is identified.
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Emergency and Acute Medicine: Urethral Trauma
Urethral trauma is a significant genitourinary injury most commonly associated with pelvic fractures and high-energy trauma. Classic clinical findings include blood at the urethral meatus, inability to void, a palpable distended bladder, and/or gross hematuria. It occurs in approximately 14% of pelvic fractures and is strongly associated with bilateral pubic rami (straddle) fractures.
In females, urethral injuries are rare due to the short, mobile, and relatively protected urethra, though risk is higher in younger patients with more flexible pelvic anatomy. When injuries do occur, the bladder neck is most commonly affected. In males, urethral trauma is more common and anatomically divided into anterior and posterior injuries. Posterior urethral injuries—affecting the prostatic and membranous urethra—account for about 90% of cases and are typically associated with pelvic fractures. These injuries are classified as stretching (type 1), partial or complete disruption with intact urogenital diaphragm (type 2), or complete disruption both proximal and distal to the diaphragm (type 3). Anterior urethral injuries (bulbar or penile) are less common and are typically associated with straddle injuries or penetrating trauma.
Etiologies differ by sex and mechanism. In males, pelvic fractures, straddle injuries, penetrating trauma, and instrumentation are common causes. In females, causes include pelvic trauma, childbirth, surgical injury, or sexual trauma. A history of pelvic or perineal trauma is often present.
Clinically, males may present with blood at the urethral meatus (seen in about 50% of cases), gross hematuria, and urinary retention. In females, blood may be seen in the vaginal vault. Physical examination during trauma assessment may reveal pelvic tenderness and bladder distention. The classic triad—blood at the meatus, inability to void, and a palpable bladder—is highly suggestive. A “high-riding prostate” on digital rectal exam has low sensitivity and should not be relied upon. Bedside ultrasound (FAST) may demonstrate fluid around the bladder.
Diagnosis requires a high index of suspicion. The essential rule in suspected urethral injury is to avoid blind Foley catheter placement until urethral integrity is confirmed. The gold standard diagnostic test is retrograde urethrography (RUG), in which contrast is injected into the urethra to assess for extravasation. Complete tears show no contrast entering the bladder, while partial tears allow some contrast passage with leakage. Because up to 40% of urethral injuries are associated with bladder injuries, cystography is also recommended.
Management prioritizes overall trauma stabilization (ABCs) before addressing the urethral injury. Early urologic consultation is essential. Bladder decompression is a key step; if urethral catheterization is unsafe or unsuccessful, suprapubic catheter placement or cystostomy is performed. Definitive management depends on the severity of injury: partial tears are typically managed with catheter drainage, while complete disruptions often require surgical repair or delayed reconstruction.
Patients with associated injuries, hemodynamic instability, or severe urethral damage require admission, often to a surgical or ICU setting. Isolated injuries may be managed on an outpatient basis after appropriate urinary diversion and with close urologic follow-up.
Important clinical pearls include recognizing blood at the urethral meatus as a red flag for urethral injury and avoiding catheter insertion until imaging is performed. Failure to diagnose urethral trauma can result in long-term complications such as urinary incontinence, urethral stricture, and sexual dysfunction.
