Emergency and Acute Medicine: Vitreous Hemorrhage




Vitreous Hemorrhage is the presence of blood within the vitreous cavity of the eye and is considered a secondary diagnosis, meaning that identifying the underlying cause is essential for proper management. It most commonly results from retinal vessel disruption due to vitreous separation, trauma, or spontaneous bleeding from neovascularization, particularly in patients with diabetes mellitus.


The causes of vitreous hemorrhage are varied and include both traumatic and nontraumatic conditions. Trauma may be blunt or penetrating, leading to direct vessel rupture. Nontraumatic causes include proliferative retinopathies (especially diabetic retinopathy), retinal tears or detachments, retinal vein occlusion, sickle cell disease, and age-related macular degeneration. Less common causes include intraocular tumors and intracranial hemorrhage such as Terson syndrome. In pediatric patients, important considerations include prematurity, congenital retinal disorders, and nonaccidental trauma such as shaken-baby syndrome.


Clinically, patients typically present with sudden, painless, unilateral visual disturbance, ranging from mild blurring to significant vision loss. They often describe floaters, cobwebs, or a hazy visual field, sometimes accompanied by flashing lights if there is associated retinal traction. On examination, a key finding is loss of the red reflex and inability to visualize the fundus, which strongly suggests vitreous hemorrhage. A mild afferent pupillary defect may also be present depending on severity.


Evaluation requires a thorough ocular examination, including slit-lamp assessment, tonometry, and dilated fundoscopic examination. When the fundus cannot be visualized, B-scan ultrasonography is essential to assess for serious underlying pathology such as retinal detachment or intraocular tumor. Additional laboratory tests, such as complete blood count and coagulation studies, may be performed if a systemic cause is suspected. Imaging like CT may be necessary in cases of trauma to exclude intraocular foreign bodies.


Management in the emergency setting is primarily supportive. Patients should be advised to rest with the head of the bed elevated to allow blood to settle inferiorly and improve vision. Activities that increase intraocular pressure, such as heavy lifting or straining (Valsalva), should be avoided. Medications that impair clotting, such as NSAIDs and anticoagulants, should also be avoided unless medically necessary. There are no specific emergency medications required for vitreous hemorrhage itself; treatment is directed at the underlying cause.


Definitive management is guided by ophthalmology and may include laser photocoagulation or cryotherapy for proliferative vascular disease, surgical repair for retinal detachment, or vitrectomy if the hemorrhage does not resolve or is associated with complications such as neovascularization or glaucoma. Urgent ophthalmologic consultation within 24–48 hours is essential, even in seemingly mild cases, to prevent missed vision-threatening conditions.


A critical point is that vitreous hemorrhage may mimic or coexist with other serious conditions such as retinal detachment or vascular occlusions. Therefore, prompt evaluation and follow-up are necessary to prevent permanent visual impairment.

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Emergency and Acute Medicine: Vaginal Bleeding in Pregnancy




Vaginal bleeding in pregnancy is a major cause of maternal and fetal morbidity and mortality. It is categorized into early pregnancy bleeding (≤20 weeks), which occurs in up to 30% of pregnancies and results in spontaneous abortion in about half of cases, and late pregnancy bleeding (>20 weeks), which occurs in 3–5% of pregnancies. Risk factors include advanced maternal age, substance abuse, pelvic inflammatory disease, prior cesarean section, previous pregnancy loss or procedures, multiple gestations, hypertension, trauma, and assisted reproductive technology. A significant proportion of miscarriages (50–60%) are due to chromosomal abnormalities.


The etiology of bleeding may arise from vaginal, cervical, uterine, uteroplacental, or hematologic sources. In early pregnancy, important causes include implantation bleeding, spontaneous abortion (threatened, incomplete, complete, inevitable, missed), Ectopic pregnancy, gestational trophoblastic disease, subchorionic hemorrhage, and infection. In late pregnancy, the most critical diagnoses are Placenta previa and Placental abruption, along with vasa previa, uterine rupture, and labor-related bleeding.


Clinical presentation varies but key historical features include the amount and duration of bleeding, passage of clots or tissue, associated pain, and gestational age. Pain patterns can help differentiate causes: crampy diffuse pain suggests spontaneous abortion, sharp unilateral pelvic pain suggests ectopic pregnancy, painless bright red bleeding is typical of placenta previa, and painful dark bleeding is more consistent with placental abruption. Importantly, life-threatening conditions may present with minimal bleeding. Associated symptoms such as syncope, fever, or prior obstetric complications should also be assessed.


On examination, vital signs may show tachycardia or hypotension, although these can be masked by increased blood volume in pregnancy. Fetal heart activity is an important marker, detectable by transvaginal ultrasound at approximately 5–6 weeks and by Doppler after 10 weeks, with a normal rate of 120–160 beats per minute. Abdominal examination assesses uterine size and tenderness; a firm, tender uterus in late pregnancy suggests abruption. Pelvic examination is appropriate only in early pregnancy to evaluate the cervical os and source of bleeding. In late pregnancy, pelvic examination must be avoided until placenta previa or vasa previa is excluded by ultrasound due to risk of catastrophic hemorrhage.


The essential workup includes a complete blood count, blood type and Rh status, and quantitative β-hCG in early pregnancy. Ultrasound, particularly transvaginal ultrasound, is the most important diagnostic tool. It can confirm intrauterine pregnancy, identify ectopic pregnancy, detect retained products of conception, and visualize placental abnormalities. β-hCG levels help guide interpretation, though correlation is imperfect. Additional testing such as coagulation studies may be required in suspected disseminated intravascular coagulation, especially with placental abruption.


Management begins with stabilization. Patients with significant bleeding or instability require airway management, oxygen, cardiac monitoring, and two large-bore IV lines for fluid resuscitation and blood transfusion as needed. In late pregnancy, positioning the patient in the left lateral position helps reduce inferior vena cava compression and improve circulation. Continuous fetal monitoring is indicated in viable pregnancies.


Treatment depends on the underlying diagnosis. All early pregnancy bleeding must be evaluated for ectopic pregnancy. Unstable patients with suspected ectopic pregnancy require immediate surgical intervention, while stable patients may be candidates for methotrexate therapy. Threatened abortion is managed expectantly with close follow-up, while incomplete or septic abortion requires urgent obstetric consultation and possible uterine evacuation. Septic abortion also requires broad-spectrum antibiotics.


In late pregnancy, bleeding is an obstetric emergency requiring immediate consultation and hospital admission. Placental abruption may necessitate urgent delivery and management of coagulopathy, while placenta previa often requires careful monitoring and possible cesarean delivery. Any signs of disseminated intravascular coagulation must be treated aggressively with blood products.


Rh-negative patients must receive anti-D immunoglobulin to prevent alloimmunization. Failure to check Rh status and administer prophylaxis is a critical pitfall.


Disposition depends on stability and diagnosis. All patients with late pregnancy bleeding require admission. Early pregnancy patients may be discharged if stable with diagnoses such as threatened abortion or small, unruptured ectopic pregnancy after specialist consultation, but they require strict follow-up within 48 hours with repeat β-hCG testing and reassessment.


Key clinical pearls include always ruling out ectopic pregnancy in early bleeding, avoiding pelvic examination in late pregnancy until placenta previa is excluded, and recognizing that even minimal bleeding can represent a life-threatening condition.

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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: 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: Vaginal Bleeding


Vaginal bleeding is a common emergency department presentation with causes ranging from benign to life-threatening. A critical principle is that any woman of reproductive age must be assumed pregnant until proven otherwise, regardless of menstrual or sexual history. The differential diagnosis is broad and is best approached by categorizing causes into pregnancy-related and nonpregnancy-related conditions.


In pregnancy, causes vary by gestational age. In early pregnancy, serious conditions include Ectopic pregnancy, which occurs in about 2% of pregnancies and can be life-threatening, as well as various forms of abortion (threatened, incomplete, complete, missed, inevitable, or septic). Other causes include molar pregnancy and trauma. In later pregnancy, vaginal bleeding may be due to Placenta previa, Placental abruption, labor, or trauma. In the immediate postpartum period, life-threatening causes include postpartum hemorrhage, uterine inversion, retained placenta, and infection such as endometritis.


In nonpregnant patients, vaginal bleeding is most commonly due to dysfunctional uterine bleeding (DUB), often related to anovulation. Structural causes include uterine fibroids (leiomyomas), cervical or endometrial polyps, and pelvic tumors. Postmenopausal bleeding is particularly concerning and most commonly due to endometrial atrophy, though malignancy must always be considered. Less common causes include bleeding disorders such as Von Willebrand disease, infections, trauma, or foreign bodies.


Patients may present with symptoms of blood loss such as lightheadedness, fatigue, weakness, or syncope. A detailed history should assess the duration and quantity of bleeding, last menstrual period, pregnancy status, prior ectopic pregnancy, and passage of clots or tissue. Estimating blood loss can be aided by noting that a tampon holds about 5 mL and a pad 5–15 mL. Physical examination should include vital signs to assess hemodynamic stability, abdominal exam for masses or tenderness, and a pelvic exam to identify the source of bleeding and determine whether the cervical os is open or closed. Altered mental status may indicate severe blood loss.


The essential workup begins with a pregnancy test in all women of childbearing potential. In early pregnancy, evaluation includes quantitative β-hCG, ultrasound to confirm intrauterine pregnancy, hematocrit, and blood type with Rh status. Ultrasound findings must be interpreted in the context of β-hCG levels, using the discriminatory zone (≈1,000–1,500 mIU/mL for transvaginal ultrasound). In later pregnancy, fetal heart tones, ultrasound, and coagulation studies may be required, especially in suspected placental abruption. In postpartum patients, ultrasound helps identify retained products of conception.


Management priorities focus on stabilization. Patients with significant bleeding or hypotension require immediate resuscitation with oxygen, cardiac monitoring, and two large-bore IV lines for fluid resuscitation. Blood transfusion may be necessary if instability persists. In pregnant patients, positioning in the left lateral decubitus position helps prevent vena cava compression.


Treatment depends on the underlying cause. In early pregnancy, confirmed ectopic pregnancy may be managed with methotrexate or surgery depending on stability. Threatened miscarriage with confirmed intrauterine pregnancy can often be managed outpatient with close follow-up. Incomplete or septic abortions require obstetric consultation, with septic cases needing IV antibiotics and admission. In later pregnancy, placenta previa and placental abruption require urgent obstetric management and possible delivery. Postpartum hemorrhage may require uterine massage, removal of retained placenta, or surgical intervention.


In nonpregnant patients, treatment of DUB may include hormonal therapy such as medroxyprogesterone or combined oral contraceptives. Severe bleeding may be treated with intravenous conjugated estrogens. Structural causes require gynecologic evaluation, imaging, and sometimes surgical management.


Disposition depends on stability and diagnosis. Admission is required for unstable patients, ectopic pregnancy not meeting outpatient criteria, placental abruption, septic abortion, postpartum hemorrhage, or significant comorbidities. Stable patients with confirmed intrauterine pregnancy or mild nonpregnancy-related bleeding may be discharged with close follow-up, typically within 48 hours.


Key clinical pearls include always ruling out ectopic pregnancy in first-trimester bleeding, recognizing that menstrual history does not exclude pregnancy, and maintaining a high index of suspicion for life-threatening causes. Clear return precautions are essential, including worsening bleeding, abdominal pain, fever, dizziness, or syncope.

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: 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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