- Published on
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.
- Published on
Emergency and Acute Medicine: Urinary Tract Infections (Adult)
Urinary tract infections (UTIs) are caused by colonization of urine with uropathogens and subsequent invasion of the genitourinary tract. They are defined by the presence of urinary symptoms along with significant bacterial counts (typically ≥10²–10⁵ CFU/mL) and pyuria. UTIs are extremely common, particularly in women, with a lifetime risk exceeding 50%. They are broadly classified into uncomplicated and complicated infections, as well as lower tract infections (cystitis) and upper tract infections (pyelonephritis).
Uncomplicated cystitis typically occurs in otherwise healthy, nonpregnant women aged 13–50 years who present with short-duration symptoms such as dysuria, urinary frequency, and urgency, without systemic features like fever or flank pain. In contrast, complicated cystitis includes infections in men, pregnant women, immunocompromised individuals, or those with structural or functional abnormalities of the urinary tract, recent instrumentation, or resistant organisms. Pyelonephritis represents infection of the renal parenchyma and presents with systemic symptoms such as fever, chills, flank pain, nausea, and vomiting, often accompanied by costovertebral angle tenderness. Severe cases may involve urosepsis or septic shock.
The pathogenesis usually involves ascending infection, where organisms colonize the periurethral area and ascend into the bladder and possibly the kidneys. The most common pathogen is Escherichia coli, responsible for 80–85% of infections. Other organisms include Staphylococcus saprophyticus, as well as Klebsiella, Proteus, Enterobacter, and Pseudomonas aeruginosa. Risk factors include sexual activity, use of spermicides or diaphragms, postmenopausal changes, incomplete bladder emptying, urinary incontinence, and instrumentation such as catheterization.
Clinically, lower urinary tract infections present with dysuria, urgency, frequency, hesitancy, suprapubic pain, and sometimes hematuria. Upper tract infections add systemic features such as fever, chills, flank pain, nausea, vomiting, and leukocytosis. Elderly patients may present atypically with altered mental status, anorexia, or functional decline rather than classic urinary symptoms.
Diagnosis relies primarily on urinalysis. Dipstick testing for leukocyte esterase and nitrites is a rapid and useful screening tool, with nitrites having high specificity for bacterial infection. Microscopy showing ≥10 white blood cells per mm³ supports the diagnosis. Urine culture is not always necessary in uncomplicated cases but is indicated in complicated infections, pyelonephritis, recurrent infections, treatment failure, or suspected resistant organisms.
The differential diagnosis includes appendicitis, diverticulitis, nephrolithiasis, pelvic inflammatory disease, prostatitis, urethritis, epididymitis, and vulvovaginitis. These should be considered particularly when symptoms are atypical or when patients do not respond to standard therapy.
Management depends on severity and classification. Stable patients with uncomplicated cystitis are typically treated with short-course oral antibiotics, usually for 3 days. First-line agents include nitrofurantoin, trimethoprim–sulfamethoxazole, and fluoroquinolones, although resistance patterns must be considered. Nitrofurantoin is often preferred due to lower resistance rates. Symptomatic relief can be provided with agents such as phenazopyridine for dysuria. For pyelonephritis, initial management may include intravenous fluids, analgesia, and parenteral antibiotics such as ceftriaxone or gentamicin, followed by oral therapy if the patient improves.
Pregnancy requires special consideration. Asymptomatic bacteriuria should be treated due to the high risk of progression to pyelonephritis and adverse pregnancy outcomes. Safe options include nitrofurantoin (avoiding first trimester if possible), amoxicillin, and fosfomycin. Trimethoprim–sulfamethoxazole should be avoided in early and late pregnancy, and fluoroquinolones are contraindicated.
Disposition depends on clinical stability. Patients who are well-appearing, able to tolerate oral therapy, and have no significant comorbidities may be discharged with follow-up. Admission is indicated for those with severe illness, inability to tolerate oral medications, unstable vital signs, immunosuppression, urinary obstruction, or failure of outpatient therapy.
Important clinical pearls include recognizing that asymptomatic bacteriuria is common in elderly patients and usually should not be treated unless symptomatic, except in specific populations such as pregnant women or those undergoing urologic procedures. Recurrent UTIs may require prophylactic strategies. Additionally, antibiotic resistance is increasing, making local resistance patterns important in guiding therapy.
- Published on
Emergency and Acute Medicine: Urinary Tract Fistula
Urinary tract fistulas are abnormal connections between any part of the urinary system and adjacent structures such as the gastrointestinal tract, reproductive organs, skin, or even thoracic or abdominal cavities. These fistulas can significantly impact quality of life and often present in emergency settings due to complications such as infection or continuous urine leakage.
The etiology varies depending on the type of fistula. Colovesical fistulas most commonly arise as complications of gastrointestinal diseases, particularly diverticular disease, but may also result from Crohn’s disease or colon carcinoma. Iatrogenic causes, such as surgery or radiation therapy, are also important contributors. In contrast, vesicovaginal fistulas are the most common acquired urinary fistulas and are typically due to surgical injury, pelvic pathology, or radiation exposure in developed countries, while obstructed labor and obstetric trauma are the leading causes in developing regions. Ureterovaginal and urethrovaginal fistulas are often associated with recent pelvic surgery, especially complicated hysterectomy. Trauma, including urethral disruption, is another possible cause, particularly in males.
Clinical presentation depends on the type of fistula. Colovesical fistulas often present with recurrent urinary tract infections, suprapubic pain, and characteristic findings such as pneumaturia (air in urine), fecaluria, hematuria, foul-smelling urine, or debris in the urine. Vesicovaginal fistulas typically present with painless, continuous leakage of urine from the vagina, often beginning one to three weeks after pelvic surgery or after catheter removal. Urethrovaginal fistulas may cause continuous or intermittent leakage depending on size and location. Ureterovaginal fistulas often present with intermittent vaginal urine leakage along with flank pain, fever, or ileus if associated with obstruction or urinoma formation.
A thorough history is essential, including past surgical, obstetric, and medical history, as well as the timing and characteristics of urinary leakage. Continuous leakage generally suggests a vesicovaginal fistula, whereas intermittent or positional leakage may suggest a ureterovaginal origin. On physical examination, findings may be minimal, but speculum examination in females may reveal pooling of urine in the vaginal vault or a small area of granulation tissue at the fistula site. In colovesical fistulas, physical findings are often related to the underlying gastrointestinal condition.
The diagnostic workup focuses on identifying associated complications such as infection or obstruction. Urinalysis may reveal white blood cells, bacteria, and debris. Renal function tests may be abnormal if obstruction is present. Imaging is typically not emergent but can be useful in defining the fistula. CT scan of the abdomen and pelvis with contrast is commonly used for suspected colovesical fistula. For genitourinary fistulas, cystoscopy with retrograde pyelography or intravenous pyelography may be used. Special diagnostic techniques include the charcoal test for colovesical fistula and the double-dye test to differentiate between vesicovaginal, ureterovaginal, and urethrovaginal fistulas based on the pattern of dye staining.
The differential diagnosis includes recurrent urinary tract infection and other causes of pneumaturia, such as infections with gas-forming organisms. Vaginal urine leakage must be distinguished from urinary incontinence, vaginitis, or normal vaginal discharge.
Management in the emergency setting is primarily supportive and focused on identifying and treating complications. Urosepsis, although uncommon, should be treated promptly with intravenous fluids, vasopressors if needed, and broad-spectrum antibiotics. If a urinary tract infection is present, appropriate antibiotics should be initiated. Placement of a urinary catheter may help reduce leakage in some cases. Definitive management usually requires surgical repair, so early referral to urology or gynecology is essential.
Most patients can be discharged if they are stable, have no evidence of sepsis, and can tolerate oral antibiotics if needed. Admission is required for patients with sepsis, inability to tolerate oral therapy, or complications related to the underlying disease such as malignancy or severe gastrointestinal pathology.
All patients require follow-up with a urologist or gynecologist for definitive evaluation and management. Important clinical pearls include maintaining a high index of suspicion in patients with recent pelvic surgery or recurrent urinary tract infections and recognizing that urine leakage from the vagina is often misdiagnosed as simple urinary incontinence. Additionally, malignancy should always be considered as an underlying cause in patients with urinary tract fistulas.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
Emergency and Acute Medicine: Tularemia
Tularemia is an acute febrile zoonotic illness caused by Francisella tularensis, a highly infectious, small aerobic gram-negative intracellular coccobacillus. It is notable for its extreme infectivity—very few organisms are required to cause disease—and lack of person-to-person transmission. Humans acquire infection through environmental exposure, including bites from infected ticks, deerflies, or mosquitoes; direct contact with infected animal tissue (especially rabbits); ingestion of contaminated food or water; or inhalation of aerosolized organisms (e.g., during lawn mowing or farming activities).
There are multiple subspecies of the organism, with Francisella tularensis subspecies tularensis (type A) being more virulent and common in North America, and Francisella tularensis subspecies holartica (type B) causing milder disease. Natural reservoirs include rabbits, rodents, and various wild and domestic animals, while vectors include ticks, biting flies, and mosquitoes. Due to its high virulence and ability to be aerosolized, tularemia has historically been studied as a potential biologic weapon.
Tularemia primarily affects individuals with outdoor exposure in endemic regions, such as farmers, hunters, forestry workers, and those handling animal carcasses. It is most common in the northern hemisphere and peaks during warmer months (June to October). Although relatively rare, it carries a mortality rate of 5–15% if untreated, which decreases to about 1% with appropriate therapy. Pediatric cases account for approximately 25% of infections.
Clinical presentation varies depending on the route of entry, with an incubation period typically of 3–5 days. The most common form is ulceroglandular tularemia, accounting for 70–80% of cases. It begins as a papule at the inoculation site that progresses to a painful ulcer, followed by regional lymphadenopathy and systemic symptoms such as fever, chills, headache, and myalgias. Glandular tularemia presents similarly but without a visible skin lesion. Oculoglandular tularemia occurs when the organism enters through the eye, causing conjunctivitis, chemosis, and regional lymphadenopathy. Pharyngeal tularemia results from ingestion of contaminated material and presents with severe exudative pharyngitis and lymphadenitis.
Pneumonic tularemia arises from inhalation and presents with fever, dry cough, pleuritic chest pain, and potentially severe pneumonia. Typhoidal tularemia is the most severe form, characterized by systemic illness without a clear entry site, often progressing to sepsis, multiorgan failure, and potentially death—particularly with type A strains.
Diagnosis is often challenging due to nonspecific laboratory findings and the absence of rapid diagnostic tests. Routine labs may be normal or show mild inflammatory changes. Blood cultures are often negative due to the organism’s fastidious growth requirements. Definitive diagnosis relies on serology, with antibody titers typically becoming diagnostic only after 10–14 days. Polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) are available in specialized laboratories. Imaging, such as chest radiography, may reveal pneumonia, pleural effusions, or hilar adenopathy in pulmonary cases.
Management in the emergency setting focuses on supportive care and early antibiotic therapy. Initial stabilization includes airway, breathing, and circulation (ABCs), oxygen supplementation for hypoxia, and intravenous fluids for dehydration or septic shock. First-line antimicrobial therapy consists of aminoglycosides, particularly gentamicin or streptomycin, administered for approximately 10 days. Alternative agents include ciprofloxacin or doxycycline, though these are bacteriostatic and associated with higher relapse rates. Importantly, β-lactam antibiotics and carbapenems are ineffective against F. tularensis.
Disposition depends on disease severity. Patients with severe illness, hemodynamic instability, hypoxemia, or typhoidal tularemia require ICU admission. Mild cases may be managed as outpatients with close follow-up and appropriate antibiotic therapy. Infectious disease consultation is recommended, particularly in severe or unclear cases.
Key clinical pearls include maintaining a high index of suspicion in patients presenting with fever and regional lymphadenopathy—especially when accompanied by a skin ulcer or conjunctivitis—and considering epidemiologic exposure history. Diagnosis is often delayed due to reliance on serology, and early empiric treatment is crucial. Tularemia remains a category A bioterrorism agent due to its high infectivity and potential for aerosol dissemination.
- Published on
Emergency and Acute Medicine – Trigeminal Neuralgia
Trigeminal neuralgia is a distinct facial pain syndrome involving the trigeminal nerve, which provides sensory innervation to the face, oral cavity, nasal mucosa, and cornea. Also known as tic douloureux, the condition is characterized by brief, recurrent episodes of severe facial pain. It most commonly affects individuals over 50 years of age and occurs more frequently in women.
The disorder is divided into two forms. Classical trigeminal neuralgia occurs without an identifiable structural lesion and is typically caused by vascular compression of the nerve root, most often by the superior cerebellar artery. This compression leads to focal demyelination and abnormal nerve firing. Symptomatic trigeminal neuralgia presents with similar clinical features but is caused by an identifiable pathology such as multiple sclerosis, tumors (e.g., cerebellopontine angle tumors), aneurysms, or arteriovenous malformations.
Clinically, patients describe sudden, severe, “electric shock–like” pain affecting one or more divisions of the trigeminal nerve. The maxillary (V2) division is most commonly involved, followed by the mandibular (V3) and ophthalmic (V1) divisions. Pain is usually unilateral and may occur spontaneously or be triggered by light stimuli such as talking, chewing, brushing teeth, shaving, or even gentle touch. Episodes last from a fraction of a second up to 2 minutes and can occur multiple times per day. Between episodes, patients are typically pain-free, although chronic cases may develop a persistent dull ache.
The diagnosis is primarily clinical and based on a characteristic history. Physical examination is usually normal; the presence of neurologic deficits or atypical features—such as bilateral symptoms, prolonged pain, or abnormal cranial nerve findings—should prompt evaluation for secondary causes. Trigger points that reproduce the pain are considered highly suggestive of the diagnosis.
Imaging is not always required in classic cases but is recommended when atypical features are present or when secondary causes are suspected. MRI of the brain is particularly useful for identifying structural lesions such as tumors or demyelinating disease like multiple sclerosis.
Management focuses on pain control. First-line therapy is carbamazepine, an anticonvulsant that is highly effective in reducing symptoms. Alternative or adjunctive medications include gabapentin, oxcarbazepine, lamotrigine, phenytoin, and valproic acid, particularly in refractory cases.
Patients who do not respond to medical therapy may require referral for procedural or surgical interventions. These include percutaneous nerve blocks, radiofrequency ablation, or microvascular decompression, which can provide long-term relief in a significant proportion of patients.
Disposition depends on severity and associated findings. Patients with typical features and good response to treatment can be managed as outpatients with follow-up by a primary care physician or neurologist. Admission is indicated if there are focal neurologic deficits, concerning imaging findings, or refractory pain requiring advanced intervention.
Key clinical points include recognizing the classic presentation of unilateral, paroxysmal, shock-like facial pain and identifying trigger points. It is essential to exclude secondary causes, particularly in younger patients or those with abnormal neurologic findings. Carbamazepine remains the cornerstone of therapy, and early treatment can significantly improve quality of life.
