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.

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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.

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Emergency and Acute Medicine: Tympanic Membrane Perforation




Tympanic membrane (TM) perforation refers to a disruption or hole in the eardrum and can be classified by duration, location, and extent. Acute perforations are defined as those present for less than 3 months, whereas chronic perforations persist beyond this period. Anatomically, perforations may involve the pars tensa or pars flaccida, and the extent may range from small defects confined to one quadrant to total perforations involving the entire membrane.


The most common cause of acute TM perforation is infection, particularly acute otitis media, where increased middle ear pressure leads to rupture. Trauma is another frequent cause and may be blunt, such as a slap to the ear (often seen in assaults or domestic violence), or penetrating, such as injury from cotton swabs (Q-tips). Rapid pressure changes from activities like diving or flying can also cause rupture (barotrauma), as can blast injuries, extreme noise exposure, lightning strikes, and thermal injuries such as slag burns during welding. Less commonly, perforation may result from surgical procedures (e.g., myringotomy or tympanostomy tube placement) or infections like acute necrotizing myringitis.


Patients typically present with mild ear pain, though severe pain or complete hearing loss may indicate more serious associated injury. Other common symptoms include tinnitus, vertigo (especially if injury occurs in water), and partial hearing loss. On physical examination, findings may include visible perforation on otoscopy, decreased hearing, and purulent or bloody discharge from the ear canal. Small perforations may only be detected by decreased mobility of the tympanic membrane during pneumatic otoscopy. Special tests such as the Weber and Rinne tuning fork tests help differentiate conductive from sensorineural hearing loss. The presence of nystagmus or vertigo during pressure testing may suggest a more serious inner ear injury such as a labyrinthine fistula.


Diagnosis is primarily clinical, based on direct visualization of the tympanic membrane and hearing assessment. If discharge is present, culture may be considered. Imaging, particularly CT of the temporal bone, is reserved for cases where a temporal bone fracture or more severe injury is suspected.


Management in the emergency setting focuses on supportive care and prevention of complications. Initial stabilization follows standard trauma principles when indicated. The ear canal should be gently cleared of debris using suction or manual removal, but irrigation must be avoided to prevent forcing contaminants into the middle ear. Routine prophylactic antibiotics are not necessary; however, antibiotics should be prescribed if there is evidence of infection or contamination (e.g., water exposure). Common options include amoxicillin or amoxicillin-clavulanate. Ototopical antibiotics—particularly fluoroquinolone drops such as ciprofloxacin with dexamethasone—are preferred in cases of chronic suppurative otitis media or when contamination is suspected, as they are safer with respect to ototoxicity compared to other agents.


Urgent ENT consultation is indicated in patients with concerning features such as vertigo, sensorineural hearing loss, severe tinnitus, significant bleeding, or facial nerve paralysis. Most patients can be safely discharged with outpatient follow-up. Nearly all tympanic membrane perforations heal spontaneously, especially small ones—many within weeks to months. Surgical repair (e.g., tympanoplasty) is reserved for the minority (10–20%) that fail to heal.


Patients should be given clear discharge instructions to prevent complications. They should keep the ear dry by occluding it during showering, avoid swimming unless protected, and refrain from forceful nose blowing. Prognosis is generally excellent, though complications such as infection, ossicular disruption, perilymph leakage, or cholesteatoma can occur in some cases.


Key clinical pearls include recognizing acute otitis media as the most common cause, avoiding irrigation of the ear, and understanding that most perforations heal without intervention. Proper protection of the ear from water and contaminants is essential to promote healing and prevent infection.

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Emergency and Acute Medicine: Ultraviolet Keratitis




Ultraviolet keratitis is a painful ocular condition caused by corneal epithelial damage following exposure to ultraviolet (UV) light. Also known as photokeratitis, snow blindness, UV conjunctivitis, or welder’s flash, it results from absorption of UV radiation—particularly at wavelengths around 290 nm—by the corneal epithelium. This exposure damages epithelial cells and penetrates to nociceptor nerve endings, leading to intense pain due to subepithelial nerve stimulation.


The condition is commonly associated with occupational exposures such as welding, electrical work, and mechanical tasks, as well as recreational exposures including skiing, snowboarding, water sports, and use of tanning beds. The severity of injury is directly related to the intensity and duration of UV exposure. Importantly, patients are often unaware of the exposure at the time of injury.


Symptoms typically develop with a delay of 6–12 hours after exposure. Patients usually present with bilateral eye pain, photophobia, tearing, and redness. A foreign-body sensation is commonly reported, but purulent discharge is absent. Additional findings may include eyelid edema, facial erythema, and blepharospasm. On examination, visual acuity may be mildly decreased. Conjunctival injection, chemosis, and excessive tearing are typical. Slit-lamp examination with fluorescein staining reveals multiple superficial punctate epithelial lesions across the cornea, which are characteristic of the condition.


Diagnosis is clinical and relies heavily on history and physical examination. A key diagnostic clue is a history of UV exposure several hours prior to symptom onset. Evaluation should include assessment of visual acuity, extraocular movements, and a detailed ocular exam with fluorescein staining. Lid eversion is important to rule out retained foreign bodies, and the anterior chamber should be assessed for signs of inflammation such as cells or flare. Laboratory tests and imaging are generally not required unless other injuries are suspected.


Management is primarily supportive, as ultraviolet keratitis is a self-limited condition. In the emergency setting, topical anesthetics may be used to facilitate examination but should not be prescribed for outpatient use due to the risk of delayed healing and corneal ulceration. Treatment includes oral analgesics such as ibuprofen or acetaminophen (with or without opioids for severe pain), topical antibiotic ointment (e.g., erythromycin) to prevent secondary infection, and short-acting cycloplegic agents to relieve ciliary spasm. Eye patching may provide comfort but does not accelerate healing.


Disposition is generally outpatient, as most cases resolve completely within 24–72 hours. Admission is rarely required but may be considered in cases of severe visual impairment, inability to care for oneself, or when both eyes are patched and functional vision is significantly impaired. Follow-up with an ophthalmologist within 24–48 hours is recommended to ensure proper healing and symptom resolution.


Key clinical pearls include recognizing the delayed onset of symptoms after UV exposure, which is critical for diagnosis, and understanding that the condition, while extremely painful, is typically benign and self-limited. Preventive measures are essential—individuals at risk should use appropriate UV-protective eyewear, as regular glasses or contact lenses do not provide adequate protection.

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Emergency and Acute Medicine – Toxoplasmosis

Emergency and Acute Medicine – Toxoplasmosis


Toxoplasmosis is an infection caused by Toxoplasma gondii, an intracellular protozoan that exists in three forms: tachyzoites (actively replicating), tissue cysts (chronic latent form), and oocysts (shed in cat feces). Transmission occurs primarily through ingestion of undercooked meat containing tissue cysts, ingestion of food or water contaminated with oocysts, or contact with cat feces or contaminated soil. Less common routes include transplacental transmission, blood transfusion, and organ transplantation.


Toxoplasmosis is extremely common worldwide, with approximately 70% of adults demonstrating prior exposure. Most immunocompetent individuals remain asymptomatic. Cats serve as the definitive host, and the incubation period typically ranges from 4 to 21 days.


Clinical manifestations vary depending on the host’s immune status and the type of infection. In immunocompromised patients, particularly those with HIV/AIDS, toxoplasmosis most commonly presents as encephalitis. Symptoms are typically subacute and include headache, fever, altered mental status, seizures, cranial nerve deficits, and focal neurologic signs. Neuropsychiatric symptoms such as psychosis, paranoia, or dementia may also occur. Pulmonary involvement may present as pneumonitis with dyspnea and nonproductive cough.


In immunocompetent individuals, approximately 90% of infections are asymptomatic. When symptoms occur, they usually present as a self-limited mononucleosis-like illness with cervical lymphadenopathy, fever, malaise, sore throat, and occasionally hepatosplenomegaly or rash. Rarely, severe complications such as encephalitis or pneumonitis may occur.


Ocular toxoplasmosis is an important manifestation, often presenting with blurred vision, scotoma, pain, and photophobia. Examination may reveal chorioretinitis with characteristic yellow-white retinal lesions. This form is particularly common in individuals with untreated congenital infection and may lead to long-term visual impairment.


Congenital toxoplasmosis results from maternal infection during pregnancy. Infection during the first trimester is associated with severe outcomes such as miscarriage or stillbirth, while later infections are more likely to be transmitted to the fetus but may present with delayed manifestations. Many affected infants are asymptomatic at birth but later develop neurologic or ocular complications, including blindness, seizures, or developmental delay.


Diagnosis involves a combination of clinical suspicion and laboratory testing. Detection of the organism may be achieved through analysis of blood, cerebrospinal fluid, bronchoalveolar lavage, or amniotic fluid. Serologic testing for IgM and IgG antibodies is commonly used, although interpretation can be challenging due to false positives and negatives. Imaging plays a key role in CNS disease: CT or MRI typically shows multiple bilateral ring-enhancing lesions. Chest radiography may reveal a reticulonodular pattern in pulmonary involvement.


The differential diagnosis includes Cryptococcal meningitis, Primary CNS lymphoma, Pneumocystis pneumonia, Cytomegalovirus retinitis, and mycobacterial infections, particularly in immunocompromised patients.


Management depends on disease severity and host immune status. Immunocompetent patients with mild disease typically require no treatment. Symptomatic or severe cases are treated with a combination of pyrimethamine, sulfadiazine, and folinic acid, or alternatively clindamycin in patients with sulfa allergy.


Immunocompromised patients require prompt and aggressive therapy, often initiated empirically when characteristic brain lesions are present. Treatment typically continues for 4–6 weeks after symptom resolution, and long-term prophylaxis may be necessary, particularly in patients with HIV.


Ocular disease is treated similarly, often with the addition of corticosteroids in cases involving the macula or optic nerve. In pregnancy, management is complex and requires specialist consultation; spiramycin is typically used early in pregnancy to reduce fetal transmission risk.


Patients with severe systemic disease, CNS involvement, or immunocompromise require hospital admission. Immunocompetent patients with mild disease can usually be managed as outpatients with follow-up.


Key clinical pearls include recognizing that toxoplasmosis is often asymptomatic in healthy individuals but can cause life-threatening disease in immunocompromised patients. CNS toxoplasmosis should always be suspected in patients with HIV presenting with focal neurologic deficits and ring-enhancing brain lesions. Prevention, particularly in pregnant women, includes avoiding undercooked meat and exposure to cat litter or contaminated soil.

Emergency and Acute Medicine – Transient Global Amnesia




Transient global amnesia (TGA) is a sudden, temporary episode of memory loss characterized by abrupt onset of profound anterograde amnesia without other focal neurologic deficits. Patients are unable to form new memories during the episode, resulting in repetitive questioning and confusion about recent events. Despite this, personal identity—such as name, birth date, and address—remains intact. After recovery, there is typically a permanent memory gap corresponding to the duration of the episode, while previously stored memories gradually return.


TGA is relatively uncommon, with an incidence of approximately 3–8 cases per 100,000 people, most often affecting individuals between 50 and 70 years of age. It is rare in patients younger than 40. Episodes usually last between 1 and 8 hours, although durations can range from 15 minutes up to 24 hours, and by definition must resolve within that time frame.


The exact cause of TGA remains unclear. Imaging studies such as MRI, SPECT, and PET have demonstrated transient abnormalities in the hippocampus, a brain region critical for memory formation. Proposed mechanisms include transient venous congestion of the hippocampus during Valsalva-like activities, vasoconstriction related to hyperventilation, and migraine-associated phenomena. Importantly, there is no established link between TGA and thromboembolic stroke or other forms of Cerebrovascular disease.


Diagnosis is clinical and relies on strict criteria. The episode must be witnessed, with sudden onset of anterograde amnesia and no alteration in consciousness. There should be no focal neurologic deficits, seizure activity, or recent head trauma. Cognitive function remains intact aside from memory impairment, and the patient retains awareness of self. The episode must resolve within 24 hours, and alternative causes of amnesia must be excluded.


Patients often present after a triggering event such as physical exertion, emotional stress, sexual activity, temperature extremes, or Valsalva maneuvers. They may repeatedly ask questions like “Where am I?” or “How did I get here?” while remaining cooperative and able to follow complex commands. Associated symptoms such as mild headache, dizziness, or nausea may occur at onset.


On examination, patients demonstrate marked anterograde amnesia but are otherwise neurologically normal. They are alert, attentive, and oriented to personal identity. They can perform complex tasks and do not exhibit aphasia, apraxia, or agnosia. Importantly, they are not globally confused, somnolent, or inattentive—features that would suggest alternative diagnoses such as encephalopathy.


In classic cases, no diagnostic testing is required. However, if the diagnosis is uncertain, further evaluation may include laboratory testing to rule out metabolic or toxic causes, imaging such as MRI (which may show transient hippocampal lesions), CT scan for structural pathology, EEG for seizure activity, or lumbar puncture if encephalitis is suspected.


The differential diagnosis includes transient ischemic attack involving posterior circulation, complex partial seizures, psychogenic amnesia, metabolic encephalopathy, and early dementia such as Alzheimer disease. These conditions can usually be distinguished by additional neurologic findings, altered consciousness, shorter or recurrent episodes, or broader cognitive impairment.


Management of TGA is supportive, as the condition is self-limited and benign. Patients should be observed until symptoms resolve, and reassurance should be provided to both the patient and family. No specific pharmacologic treatment is indicated.


Disposition depends on clinical certainty and recovery. Patients with a clear diagnosis and resolving symptoms, along with good social support, can be safely discharged. Admission is appropriate for patients with uncertain diagnosis, incomplete resolution, or inadequate support at home.


The recurrence rate of TGA is relatively low, around 8%. Patients with recurrent episodes should be referred to a neurologist for further evaluation, including possible EEG to exclude seizure disorders.


Key clinical pearls include recognizing TGA as a benign condition characterized by isolated anterograde amnesia with preserved identity and normal neurologic exam. Clinicians must remain vigilant for red flags such as focal deficits, impaired consciousness, or recurrent brief episodes, which may indicate more serious conditions like seizure, encephalitis, or vascular events.

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Emergency and Acute Medicine – Transfusion Complications




Transfusion complications are relatively common clinical events associated with blood product administration, ranging from mild allergic reactions to life-threatening conditions. Approximately 5–6% of hospitalized patients receive transfusions, and about 2% of transfused units result in some type of reaction within 24 hours. Although mortality is rare, complications can be severe, especially with acute hemolytic reactions or pulmonary syndromes.


Noninfectious complications are more common than infectious ones. Febrile nonhemolytic reactions occur in approximately 1 in 500 red blood cell transfusions and are characterized by fever and chills due to antigen–antibody reactions involving leukocytes or cytokines. Allergic reactions are relatively frequent and usually mild, presenting with urticaria or pruritus, while anaphylaxis is rare but potentially fatal. Acute hemolytic transfusion reactions, often due to ABO incompatibility, are uncommon but dangerous, occurring in roughly 1 in 38,000 to 70,000 transfusions. Delayed hemolytic reactions occur days later and are typically less severe.


Transfusion-associated circulatory overload (TACO) is relatively common, particularly in elderly or volume-sensitive patients, and presents with signs of fluid overload such as dyspnea and hypertension. Transfusion-related acute lung injury (TRALI) is a serious complication presenting within 6 hours of transfusion with acute respiratory distress, bilateral pulmonary infiltrates, and normal cardiac function. It is a leading cause of transfusion-related mortality and must be distinguished from TACO and Acute Respiratory Distress Syndrome.


Other important complications include electrolyte disturbances such as hypocalcemia (due to citrate binding calcium) and hyperkalemia (from stored blood breakdown), iron overload with repeated transfusions, and rare but fatal graft-versus-host disease. Infectious complications are now rare due to screening but include transmission of viruses such as HIV, Hepatitis B, and Hepatitis C, as well as bacterial contamination (especially in platelet transfusions), which remains the most common infectious cause of mortality.


Acute intravascular hemolytic transfusion reactions are the most severe form and typically occur immediately due to ABO incompatibility, often from clerical or identification errors. Even small volumes (5–20 mL) can trigger symptoms. These reactions result in rapid destruction of transfused red blood cells, triggering a cascade involving cytokine release, activation of the coagulation system, and potential progression to shock, disseminated intravascular coagulation, renal failure, and respiratory failure.


Clinical manifestations of transfusion reactions vary widely but commonly include fever, chills, urticaria, dyspnea, hypotension, chest pain, nausea, and hemoglobinuria. Severe reactions may present with shock, bleeding, renal failure, or respiratory distress. The classic triad of fever, flank pain, and dark urine in hemolytic reactions is uncommon but highly suggestive when present.


Evaluation begins with immediate recognition of symptoms and verification of patient and blood product identity. Laboratory testing includes CBC, electrolytes, renal function, coagulation studies, bilirubin, and a direct Coombs test. Hemolysis may be indicated by hemoglobinemia or hemoglobinuria. Imaging such as chest x-ray is useful when pulmonary complications like TRALI are suspected, typically showing bilateral infiltrates without cardiomegaly.


Management requires immediate cessation of the transfusion as the first and most critical step. Supportive care follows the ABC approach, including oxygen supplementation and hemodynamic stabilization. Intravenous fluids with normal saline are used for hypotension, while avoiding lactated solutions or dextrose-containing fluids. Maintaining adequate urine output is essential to prevent renal failure, often requiring diuretics such as furosemide or osmotic agents like mannitol.


Febrile reactions are treated with antipyretics, while allergic reactions are managed with antihistamines such as diphenhydramine. Severe allergic or anaphylactic reactions require prompt administration of epinephrine and corticosteroids. In cases of electrolyte disturbances, calcium replacement may be necessary. If disseminated intravascular coagulation develops, it must be treated accordingly.


Patients with severe reactions, including hemolysis, anaphylaxis, pulmonary complications, or sepsis, require ICU admission and close monitoring. Mild febrile or allergic reactions may be managed conservatively and discharged with appropriate follow-up.


Key clinical pearls include the importance of strict patient identification and cross-matching procedures to prevent catastrophic hemolytic reactions. Clinicians should always suspect hemolysis when hypotension, dark urine, or unexplained bleeding occurs during transfusion. Additionally, transfusions should be used judiciously, as they carry significant risks despite their lifesaving potential.

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Emergency and Acute Medicine – Toxic Shock Syndrome (TSS)




Toxic shock syndrome (TSS) is a severe, acute, life-threatening illness caused by toxin-producing bacteria, most commonly Staphylococcus aureus and less commonly Group A Streptococcus (referred to as streptococcal toxic shock syndrome, STSS). These organisms produce exotoxins such as toxic shock syndrome toxin (TSST-1) and streptococcal pyrogenic exotoxins, which act as superantigens. These toxins trigger massive cytokine release, leading to fever, immune dysregulation, and profound vasodilation with capillary leak, ultimately resulting in hypotension and shock.


The etiology of TSS has evolved over time. Initially associated with menstruating women using highly absorbent tampons, modern cases are now frequently nonmenstrual. These include infections related to surgical wounds, postpartum infections, burns, nasal packing, mastitis, osteomyelitis, and soft tissue infections. Many individuals are asymptomatic carriers of S. aureus in areas such as the nasal passages, skin, or genital tract. In streptococcal TSS, infection often follows minor trauma and may present with severe pain even before visible signs of infection appear.


Clinically, TSS is diagnosed using criteria established by the CDC. Patients typically present with high fever (>38.9°C), hypotension, and a diffuse blanching macular erythroderma rash. This rash is followed 1–2 weeks later by desquamation, especially of the palms and soles. Multisystem involvement is a hallmark and includes gastrointestinal symptoms (vomiting, diarrhea), musculoskeletal involvement (severe myalgias or elevated creatine phosphokinase), mucosal hyperemia (conjunctival, oral, or vaginal), renal dysfunction, hepatic involvement, hematologic abnormalities such as thrombocytopenia, and central nervous system symptoms including confusion or hallucinations.


Streptococcal TSS differs slightly in presentation and diagnostic criteria. It requires isolation of Group A Streptococcus from a sterile site, hypotension, and evidence of organ dysfunction such as renal failure, coagulopathy, liver dysfunction, acute respiratory distress syndrome, or soft tissue necrosis. A key distinguishing feature is severe pain, often out of proportion to physical findings, which may indicate deep soft tissue infection such as necrotizing fasciitis.


Laboratory findings are nonspecific but reflect systemic inflammation and organ dysfunction. These may include leukocytosis or leukopenia, elevated creatinine and liver enzymes, thrombocytopenia, electrolyte abnormalities (such as hypocalcemia), and elevated creatine phosphokinase. Cultures from blood or suspected infection sites should be obtained, although blood cultures are not always positive in staphylococcal TSS. Imaging such as chest radiography or CT may help identify the source of infection or complications.


The differential diagnosis includes Kawasaki disease, Scarlet fever, Stevens-Johnson syndrome, Rocky Mountain spotted fever, and meningococcemia. Differentiation is essential because management strategies differ significantly.


Management of TSS is a medical emergency and focuses on rapid stabilization and source control. Prehospital care includes airway management, IV access, and fluid resuscitation. In the emergency department, aggressive management of shock is critical, often requiring large volumes of intravenous fluids (up to 4–20 L in the first 24 hours). If hypotension persists, vasopressors such as norepinephrine or dopamine are initiated.


Identifying and removing the source of infection is essential, such as removing tampons, nasal packing, or infected wound material. Early surgical consultation is necessary if drainage or debridement is required, particularly in cases of suspected necrotizing infection.


Antibiotic therapy should be initiated promptly. Regimens typically include clindamycin or linezolid to suppress toxin production, combined with agents such as vancomycin for broad coverage. For confirmed methicillin-sensitive S. aureus, oxacillin or nafcillin may be used. In streptococcal TSS, broader-spectrum regimens including beta-lactams and clindamycin are recommended. Intravenous immunoglobulin (IVIG) may be considered, particularly in streptococcal TSS or refractory shock.


All patients with TSS require hospital admission, and most require intensive care due to the risk of rapid progression to multiorgan failure.


Key clinical pearls include recognizing the combination of fever, rash, hypotension, and multisystem involvement, and initiating aggressive supportive care immediately. Early antibiotic therapy, toxin suppression, and prompt source control are critical for survival.

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Emergency and Acute Medicine – Transient Ischemic Attack (TIA)




A transient ischemic attack (TIA) is a brief episode of neurologic dysfunction caused by a temporary reduction in blood flow to a region of the central nervous system. Traditionally defined as symptoms lasting less than 24 hours, most TIAs resolve within one hour. Importantly, TIA is a major warning sign for impending stroke, with approximately 12–30% of strokes preceded by a TIA.


The underlying mechanism involves transient cerebral hypoperfusion. Common causes include atherosclerotic thrombosis in large or medium arteries, small vessel disease, and emboli originating from the heart—particularly in conditions such as Atrial fibrillation. Less common causes include arterial dissection, vasculitis, and hypercoagulable states, while in a significant proportion of patients, no clear etiology is identified.


Clinical presentation depends on the vascular territory affected. Large-vessel TIAs produce characteristic focal deficits. For example, involvement of the middle cerebral artery causes contralateral weakness and sensory loss affecting the face and arm more than the leg, often accompanied by aphasia (dominant hemisphere) or neglect (nondominant hemisphere). Posterior circulation TIAs may present with vertigo, ataxia, diplopia, or cranial nerve deficits. Transient monocular blindness, known as amaurosis fugax, reflects involvement of the ophthalmic branch of the internal carotid artery. Small-vessel (lacunar) TIAs typically produce isolated motor or sensory deficits without cortical signs.


The history is critical in diagnosis. TIAs typically have sudden onset, short duration, and produce “negative” neurologic symptoms such as weakness, vision loss, or aphasia due to loss of function. In contrast, gradual onset or “positive” symptoms such as tingling, jerking, or visual scintillations suggest alternative diagnoses like migraine or seizure.


Physical examination should include a detailed neurologic assessment, evaluating strength, sensation, coordination, speech, and visual fields. By definition, neurologic deficits resolve in TIA; persistent deficits indicate an acute Ischemic stroke rather than TIA. Standardized tools such as the NIH Stroke Scale can aid in assessment and monitoring.


Initial evaluation in the emergency setting focuses on excluding mimics and identifying risk factors. A rapid bedside glucose test is essential, as hypoglycemia can mimic focal neurologic deficits. A noncontrast CT scan of the head should be obtained urgently to exclude intracranial hemorrhage. MRI with diffusion-weighted imaging is more sensitive and may reveal infarction in up to 50% of patients initially thought to have TIA. Vascular imaging of the head and neck—via CT angiography, MR angiography, or carotid ultrasound—is important, as nearly half of patients have significant arterial stenosis or occlusion.


Additional workup includes ECG to detect arrhythmias such as atrial fibrillation and echocardiography to evaluate for cardiac sources of emboli. Laboratory tests assess metabolic abnormalities,

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