Medical School · Year 3 · Emergency Medicine · includes a quiz and discussion video

Seminar 13: Genitourinary Emergencies

Emergency Medicine Clerkship

Learning Objectives

By the end of this seminar, students will be able to:

1. Diagnose testicular torsion based on clinical presentation and absent cremasteric reflex, and initiate emergent urologic consultation for surgical exploration within the six-hour salvage window
2. Evaluate nephrolithiasis using non-contrast computed tomography, manage pain with nonsteroidal anti-inflammatory drugs as first-line therapy, and recognize obstructed infected kidney as a urologic emergency
3. Identify the causes of acute urinary retention, perform appropriate catheterization techniques, and manage complications including post-obstructive diuresis and failed catheterization
4. Classify hematuria as glomerular or non-glomerular and determine appropriate emergency department workup, management, and disposition based on clinical severity
5. Diagnose ischemic priapism as a urologic emergency requiring aspiration and phenylephrine injection, and differentiate it from non-ischemic priapism that does not require emergent intervention
6. Recognize penile fracture, paraphimosis, and Fournier gangrene as time-sensitive urologic emergencies requiring prompt intervention to prevent permanent morbidity

Seminar Outline

Section 1: Testicular Torsion

Testicular torsion is a true urologic emergency that occurs when the spermatic cord twists, occluding venous and subsequently arterial blood flow to the testicle, resulting in ischemia and infarction if not promptly corrected. The presentation is characterized by the sudden onset of severe, unilateral scrotal pain, often accompanied by nausea and vomiting from visceral afferent stimulation. The age distribution is bimodal, with peaks in the neonatal period (due to the bell-clapper deformity that has not yet resolved) and during adolescence between 12 and 18 years of age, corresponding to the period of rapid testicular growth. On examination, the affected testicle is high-riding within the scrotum and assumes a horizontal (transverse) lie rather than the normal vertical orientation. The cremasteric reflex, tested by stroking the inner thigh and observing for ipsilateral testicular elevation, is the most specific physical finding and is characteristically absent in torsion. The critical time window for testicular salvage is less than 6 hours from the onset of pain.

The differential diagnosis of acute scrotal pain includes several conditions that must be distinguished from testicular torsion because of the vastly different management implications. Epididymitis, the most common cause of acute scrotal pain in adults, presents with a more gradual onset, positive Prehn sign (pain relief with testicular elevation), and may be accompanied by fever and urinary symptoms. Torsion of the appendix testis, a vestigial embryologic remnant, presents with localized tenderness at the upper pole of the testicle and may produce the pathognomonic blue dot sign, a small blue-black discoloration visible through the scrotal skin. Inguinal hernia presents with a reducible scrotal mass and may be associated with bowel symptoms. Hydrocele, an accumulation of fluid within the tunica vaginalis, characteristically transilluminates when a light source is placed behind the scrotum and is generally painless.

Diagnosis of testicular torsion may be clinical in cases with a classic presentation, and imaging should not delay surgical exploration when clinical suspicion is high. Scrotal ultrasound with color Doppler is the primary imaging modality when the diagnosis is uncertain, demonstrating decreased or absent blood flow to the affected testicle compared with the contralateral side. The sensitivity of ultrasonography ranges from 82 to 100 percent and the specificity from 98 to 100 percent, though false-negative results can occur in early or intermittent torsion where partial flow may be preserved. The decision to proceed directly to surgical exploration without imaging should be made when the clinical presentation is classic, particularly in an adolescent male with sudden-onset unilateral scrotal pain, a high-riding testicle, and an absent cremasteric reflex. Any delay for imaging in such cases may compromise testicular viability.

Management of testicular torsion involves both temporizing measures and definitive surgical treatment. Manual detorsion may be attempted as a bedside maneuver while awaiting surgical consultation; the technique involves rotating the affected testicle laterally (the "open the book" maneuver), as the most common direction of torsion is medial. Successful detorsion is indicated by pain relief and return of the testicle to a normal position. However, manual detorsion does not eliminate the need for surgical exploration, as the underlying anatomic predisposition (bell-clapper deformity) persists. Emergent surgical exploration with bilateral orchiopexy (fixation of both testicles to the scrotal wall) is the definitive treatment, as the contralateral testicle shares the same anatomic predisposition in approximately 80 percent of cases. The salvage rate is approximately 100 percent when surgery occurs within 6 hours, drops to approximately 20 percent at 12 hours, and approaches 0 percent when torsion has been present for more than 24 hours. Urology should be consulted immediately upon clinical suspicion.

<image>Panel A: Anatomical illustration comparing normal testicular anatomy with the bell-clapper deformity showing the horizontal lie and high tunica vaginalis attachment that predisposes to torsion, alongside a photograph of a high-riding testicle with horizontal lie. Panel B: Scrotal Doppler ultrasound images comparing normal testicular blood flow on the unaffected side with absent flow on the torsed side. Panel C: Demonstration of the manual detorsion technique showing the lateral "open the book" rotation of the affected testicle. Panel D: Testicular salvage rate graph showing near 100 percent salvage at less than 6 hours declining to near 0 percent at greater than 24 hours, with the decision algorithm from clinical assessment through imaging and surgical exploration.</image>

Section 2: Nephrolithiasis

Nephrolithiasis is one of the most common causes of acute flank pain presenting to the emergency department, affecting approximately 10 percent of the population over a lifetime. The classic presentation is acute, colicky flank pain that radiates from the costovertebral angle anteriorly and inferiorly toward the ipsilateral groin, reflecting the course of the ureter. The pain is typically severe and fluctuating in intensity as the stone migrates and causes intermittent ureteral obstruction and spasm. Hematuria, either microscopic or gross, is present in approximately 85 percent of cases but its absence does not exclude the diagnosis. Nausea and vomiting are common from shared autonomic innervation. The presence of fever in a patient with suspected nephrolithiasis is a critical finding that suggests concurrent infection and transforms the management from outpatient to emergent. Patients with renal colic characteristically are restless and unable to find a comfortable position, in contrast to patients with peritoneal irritation who lie motionless.

The composition of renal stones determines their radiographic appearance, recurrence risk, and potential for medical dissolution. Calcium oxalate stones are the most common type, comprising 70 to 80 percent of all stones, and are radiopaque on plain radiography and clearly visible on computed tomography. Calcium phosphate stones account for 10 to 15 percent and are similarly radiopaque. Uric acid stones comprise 5 to 10 percent and are notably radiolucent on plain radiographs, though they are detectable on CT; they are the only common stone type amenable to medical dissolution through urinary alkalinization. Struvite (magnesium ammonium phosphate) stones account for 5 to 10 percent and are associated with urease-producing organisms such as Proteus, forming large staghorn calculi that fill the renal collecting system. Cystine stones are rare (1 to 2 percent) and occur in patients with the hereditary condition cystinuria.

Non-contrast computed tomography of the abdomen and pelvis is the gold standard imaging modality for nephrolithiasis, with a sensitivity exceeding 95 percent for detecting stones of all compositions and sizes. Ultrasound is the preferred first-line imaging modality in pregnant patients and in those where radiation exposure should be minimized, though it primarily detects hydronephrosis as an indirect sign of obstruction rather than directly visualizing ureteral stones. Plain radiography (KUB) has limited utility, as it misses radiolucent stones and has poor sensitivity for small stones, but may be useful for monitoring known radiopaque stones. Stone size is the primary determinant of spontaneous passage probability: stones smaller than 5 millimeters pass spontaneously in approximately 90 percent of cases, stones between 5 and 10 millimeters have a decreasing probability of passage, and stones larger than 10 millimeters are unlikely to pass without intervention.

Pain management is the initial priority in nephrolithiasis. Nonsteroidal anti-inflammatory drugs, particularly intravenous ketorolac, are the first-line analgesic and are superior to opioids for renal colic because they reduce ureteral spasm and inflammation in addition to providing analgesia. Opioid analgesics are added for pain refractory to NSAIDs. Intravenous hydration is provided for patients who are unable to tolerate oral fluids due to nausea and vomiting, though aggressive fluid loading has not been shown to accelerate stone passage. Medical expulsive therapy with tamsulosin, an alpha-1 adrenergic antagonist that relaxes ureteral smooth muscle, may facilitate passage of stones between 4 and 10 millimeters in the distal ureter. The critical clinical scenario is the obstructed, infected kidney, which represents a urologic emergency requiring emergent decompression and is discussed in the following section. Urology consultation is also required for obstruction of a solitary kidney, bilateral obstruction, stones unlikely to pass spontaneously, and intractable symptoms.

<image>Panel A: Illustration of the urinary tract showing the typical path of stone migration from the renal pelvis through the ureter with the three physiologic narrowing points (ureteropelvic junction, crossing of iliac vessels, ureterovesical junction) where stones most commonly become impacted. Panel B: Non-contrast CT images demonstrating stones of various sizes and locations within the ureter, with associated hydronephrosis and perinephric stranding. Panel C: Stone composition comparison showing calcium oxalate, calcium phosphate, uric acid, struvite, and cystine stones with their relative frequencies, radiographic characteristics, and appearance. Panel D: Pain management algorithm from NSAID administration (ketorolac first-line) through opioid rescue, medical expulsive therapy with tamsulosin, and criteria for urology consultation and emergent intervention.</image>

Section 3: Obstructed Infected Kidney

The obstructed infected kidney represents one of the most dangerous urologic emergencies, as the combination of urinary tract obstruction and active infection creates a closed-space infection that can rapidly progress to sepsis, multi-organ failure, and death. The clinical presentation typically consists of the triad of obstruction, infection, and fever: the patient develops flank pain from ureteral obstruction (often from an impacted stone), signs and symptoms of urinary tract infection including dysuria and urinary frequency, and systemic manifestations of infection including fever, rigors, and hemodynamic instability. Laboratory evaluation reveals leukocytosis, pyuria, and positive urine or blood cultures. Imaging with computed tomography demonstrates hydronephrosis with an obstructing stone and surrounding inflammatory changes including perinephric fat stranding. This condition must be recognized as a urologic emergency requiring intervention within hours.

Management of the obstructed infected kidney requires simultaneous resuscitation and emergent decompression. Hemodynamic resuscitation should follow standard sepsis protocols with aggressive crystalloid fluid administration and vasopressor initiation if hypotension persists. Broad-spectrum intravenous antibiotics should be administered immediately; appropriate empiric choices include ceftriaxone or piperacillin-tazobactam, with broader coverage for patients with healthcare-associated risk factors. The critical intervention is emergent decompression of the obstructed collecting system, which can be accomplished by two methods: retrograde ureteral stent placement performed by urology in the operating room or cystoscopy suite, or percutaneous nephrostomy tube placement performed by interventional radiology under imaging guidance. The choice between these approaches depends on local expertise and availability, but the procedure should not be delayed while awaiting operating room availability if the patient is septic.

The complications of untreated obstructed infected kidney are severe and progressive. Sepsis develops rapidly as bacteria proliferate within the closed, obstructed collecting system and enter the bloodstream through pyelovenous and pyelolymphatic backflow pathways. Pyonephrosis, the accumulation of purulent material within the renal pelvis and collecting system, indicates advanced infection and may require prolonged drainage. Perinephric abscess may develop when infection extends beyond the renal capsule into the perinephric fat and may require separate percutaneous or surgical drainage. Permanent renal damage with loss of function in the affected kidney occurs when obstruction and infection persist, as the combination of elevated pressure and infection destroys nephrons more rapidly than either insult alone.

Disposition for patients with urinary tract obstruction depends on the presence or absence of concurrent infection. Obstructed urinary tracts with active infection universally require hospital admission and emergent decompression, as described above. Obstruction without infection may be observed in select cases if the patient has adequate pain control, can tolerate oral fluids, and has reliable follow-up with urology. Non-obstructing stones that are small (less than 5 millimeters) and not associated with infection may be managed as outpatients with analgesics, medical expulsive therapy, a urine strainer to capture passed stones for composition analysis, and urology follow-up within 1 to 2 weeks. Patients should be instructed to return immediately for fever, persistent vomiting, or uncontrolled pain.

<image>Panel A: CT images demonstrating the spectrum of obstructive uropathy from mild hydronephrosis to severe hydronephrosis with an impacted ureteral stone and perinephric stranding indicating inflammation. Panel B: Management algorithm showing simultaneous resuscitation (fluids, antibiotics, vasopressors) and emergent decompression pathways (retrograde ureteral stent versus percutaneous nephrostomy), with decision factors for each approach. Panel C: Illustration of retrograde ureteral stent placement via cystoscopy alongside percutaneous nephrostomy tube placement under fluoroscopic guidance. Panel D: Disposition algorithm showing emergent admission and decompression for obstructed infected kidney, observation criteria for obstruction without infection, and outpatient management criteria for non-obstructing stones.</image>

Section 4: Acute Urinary Retention

Acute urinary retention is the sudden inability to void despite a full bladder and represents a common urologic emergency, particularly in older men. The causes are broadly categorized into obstructive, neurologic, pharmacologic, infectious, and post-operative etiologies. Obstructive causes are the most common and include benign prostatic hyperplasia (the single most common cause in men), urethral stricture from prior instrumentation or sexually transmitted infection, prostatic or bladder malignancy, and impacted urinary stones. Neurologic causes include spinal cord compression, diabetic autonomic neuropathy, multiple sclerosis, and cauda equina syndrome, the latter of which must be excluded in any patient with acute urinary retention accompanied by back pain and lower extremity weakness or saddle anesthesia. Medications that predispose to urinary retention include anticholinergics, opioids, and sympathomimetics. Acute prostatitis may cause retention through prostatic edema and inflammation. Post-operative retention commonly occurs after general or spinal anesthesia.

The presentation of acute urinary retention is typically straightforward, with patients reporting a complete inability to void accompanied by suprapubic pain and distension. On examination, the bladder is palpable as a firm, rounded suprapubic mass that is dull to percussion. Overflow incontinence, in which small volumes of urine leak as intravesical pressure exceeds urethral sphincter pressure, may occur and can be mistaken for normal voiding. In elderly patients, particularly those with cognitive impairment, acute urinary retention may present primarily as delirium or agitation, and the distended bladder may be discovered only on careful examination. A thorough neurologic examination including assessment of lower extremity strength, sensation in the perineal (saddle) distribution, and rectal tone should be performed to evaluate for neurogenic causes.

Management of acute urinary retention centers on bladder decompression through catheterization. A standard Foley catheter or intermittent straight catheterization provides immediate relief. The historical concern about rapid decompression causing hemorrhage (ex vacuo hematuria) has not been supported by evidence, and there is no benefit to gradual decompression over rapid drainage. Post-obstructive diuresis, defined as urine output exceeding 200 milliliters per hour for two or more consecutive hours after decompression, may occur in patients with prolonged obstruction and bilateral hydronephrosis; these patients require close monitoring of urine output and intravenous fluid replacement of approximately half the urinary losses to prevent dehydration and electrolyte abnormalities. An alpha-1 adrenergic blocker such as tamsulosin should be initiated before any planned trial of voiding without a catheter, as it relaxes prostatic smooth muscle and improves the likelihood of successful voiding. Outpatient urology follow-up should be arranged for voiding trial and evaluation of the underlying cause.

Failed catheterization is a common challenge in the emergency department and requires a systematic approach. Urethral stricture may be overcome by using a smaller-caliber catheter or a filiform and follower technique. Prostatic enlargement may be better navigated with a coude-tipped catheter, which has a curved tip designed to negotiate the prostatic urethra. If the catheter cannot be advanced, the clinician should never force it, as this risks creating a false passage with urethral perforation, bleeding, and potential abscess formation. When standard catheterization techniques fail, urology consultation for placement of a suprapubic catheter is indicated. Suprapubic catheterization involves percutaneous placement of a catheter directly into the bladder through the anterior abdominal wall above the pubic symphysis, performed under ultrasound guidance. This approach bypasses the entire urethra and is the definitive option for patients in whom urethral catheterization is impossible.

<image>Panel A: Anatomical illustration showing the common causes of urinary retention including benign prostatic hyperplasia compressing the prostatic urethra, urethral stricture, and bladder outlet obstruction from stone or tumor. Panel B: Physical examination findings in acute urinary retention showing the suprapubic mass on inspection and palpation, dullness to percussion, and point-of-care ultrasound demonstrating a markedly distended bladder. Panel C: Catheterization techniques showing standard Foley insertion, coude-tipped catheter navigation of the prostatic urethra, and ultrasound-guided suprapubic catheterization. Panel D: Post-obstructive diuresis monitoring diagram showing urine output thresholds, fluid replacement calculation (replace half of urinary losses), electrolyte monitoring protocol, and indications for intravenous fluid replacement.</image>

Section 5: Hematuria

Hematuria is classified as either gross (visible to the naked eye) or microscopic (detected only on urinalysis, defined as more than 3 red blood cells per high-power field on centrifuged urine microscopy). Further classification as glomerular or non-glomerular is essential because it determines the diagnostic approach and underlying etiology. Glomerular hematuria, identified by the presence of dysmorphic red blood cells and red blood cell casts on urine microscopy, indicates intrinsic renal parenchymal disease. Non-glomerular hematuria demonstrates normal (isomorphic) red blood cells and suggests a urologic source within the collecting system, ureters, bladder, or urethra. Pseudohematuria, in which urine appears discolored without true red blood cells, may result from myoglobinuria, hemoglobinuria, certain medications (rifampin, phenazopyridine), and dietary pigments.

The causes of hematuria span a broad differential that can be organized by anatomic location and mechanism. Urologic causes include nephrolithiasis, urologic malignancy (renal cell carcinoma, transitional cell carcinoma of the bladder or ureter, prostate cancer), urinary tract infection, and trauma. Glomerular causes include IgA nephropathy (Berger disease, the most common glomerulonephritis worldwide), post-infectious glomerulonephritis, lupus nephritis, and other glomerulonephritides. Vascular causes include renal vein thrombosis, renal infarction, and arteriovenous malformations. Coagulopathy from therapeutic anticoagulation or inherited bleeding disorders may cause hematuria, though anticoagulation-associated hematuria should still prompt evaluation for an underlying structural lesion. Blunt or penetrating trauma to the kidneys, ureters, or bladder is an important cause in the emergency department setting.

The emergency department workup for hematuria includes urinalysis to confirm the presence of red blood cells and evaluate for concurrent infection, a basic metabolic panel to assess renal function, and coagulation studies when a bleeding disorder is suspected. Urine microscopy, when available, can distinguish glomerular from non-glomerular hematuria through red blood cell morphology assessment. Computed tomography is indicated when trauma, nephrolithiasis, or a renal mass is suspected. Cystoscopy is the definitive evaluation for bladder pathology but is performed as an outpatient procedure rather than in the emergency department for non-traumatic presentations. Patients over age 35 with unexplained hematuria, particularly gross hematuria, should be referred for urologic evaluation including cystoscopy and upper tract imaging to exclude malignancy.

Emergency department management of hematuria depends on the clinical scenario and severity. Minor, asymptomatic microscopic hematuria in a hemodynamically stable patient requires outpatient follow-up for complete urologic or nephrologic evaluation but does not require emergent intervention. Gross hematuria with clot retention requires bladder irrigation, which may necessitate placement of a three-way catheter (triple-lumen Foley) for continuous bladder irrigation to prevent further clot formation and acute urinary obstruction. Hematuria in the setting of therapeutic anticoagulation that is hemodynamically significant may require reversal of anticoagulation, though this decision must balance the bleeding risk against the indication for anticoagulation. Traumatic hematuria should be evaluated and managed according to trauma protocols with imaging and surgical consultation as indicated. All patients with unexplained gross hematuria should receive urology follow-up for comprehensive evaluation.

<image>Panel A: Urine microscopy images comparing normal (isomorphic) red blood cells indicating non-glomerular hematuria with dysmorphic red blood cells and red blood cell casts indicating glomerular hematuria. Panel B: Anatomic diagram showing potential sources of hematuria organized by location: kidney (stone, mass, glomerulonephritis), ureter (stone, tumor), bladder (infection, tumor, trauma), and urethra (trauma, infection). Panel C: CT images demonstrating common causes of non-glomerular hematuria including a renal mass, ureteral stone with hydronephrosis, and bladder tumor with intraluminal filling defect. Panel D: Emergency department management algorithm from hemodynamic assessment through clot retention management with three-way catheter irrigation, anticoagulation reversal decision, and outpatient referral pathways for urology and nephrology evaluation.</image>

Section 6: Epididymitis and Orchitis

Epididymitis is the most common cause of acute scrotal pain in adults and presents with gradual onset of unilateral scrotal pain and swelling, in contrast to the sudden onset characteristic of testicular torsion. On examination, the epididymis is tender and swollen, located posterolateral to the testis. Prehn sign, pain relief with testicular elevation, is classically positive in epididymitis but unreliable as a distinguishing feature. The microbiology varies with age: in sexually active men younger than 35 years, Chlamydia trachomatis and Neisseria gonorrhoeae are the predominant organisms. In men older than 35 years and in those who are not sexually active, Escherichia coli and other urinary pathogens are more common, and epididymitis is frequently associated with concurrent urinary tract infection or prostatic disease. Scrotal ultrasound with Doppler demonstrates increased blood flow to the affected epididymis, in contrast to the decreased or absent flow seen in torsion.

Orchitis is inflammation of the testis itself and most commonly occurs in conjunction with epididymitis as epididymo-orchitis. Isolated orchitis without epididymal involvement is uncommon in the bacterial setting and more characteristic of viral etiologies, most notably mumps orchitis, which typically develops 4 to 7 days after the onset of parotitis and may lead to testicular atrophy and infertility, particularly when bilateral. Bacterial epididymo-orchitis presents with testicular and epididymal swelling, pain, scrotal erythema, and reactive hydrocele. The distinction from testicular torsion is critical, and when any doubt exists, particularly in younger patients, scrotal ultrasound with Doppler should be obtained promptly. Complications of orchitis include abscess formation requiring drainage, infertility (particularly following bilateral mumps orchitis), chronic orchialgia, and, rarely, progression to Fournier gangrene.

Treatment of epididymitis is guided by the patient's age, sexual history, and most likely causative organisms. For sexually active men younger than 35 years, the recommended regimen is ceftriaxone 500 milligrams intramuscularly as a single dose plus doxycycline 100 milligrams orally twice daily for 10 days, providing coverage for both gonococcal and chlamydial infection. For men older than 35 years or those who are not sexually active, levofloxacin 500 milligrams orally once daily for 10 days provides coverage for enteric gram-negative organisms. Supportive measures include scrotal elevation and support, application of ice for the first 24 to 48 hours, and nonsteroidal anti-inflammatory drugs for pain and inflammation. Sexual partners of patients with sexually transmitted epididymitis should be referred for evaluation and treatment.

Complications of epididymitis and orchitis, while uncommon with appropriate treatment, can be significant. Testicular or epididymal abscess may develop, presenting as a fluctuant mass that may require percutaneous or surgical drainage in addition to antibiotics. Post-infectious infertility may result from damage to the seminiferous tubules, particularly following bilateral orchitis. Chronic epididymitis or orchialgia may develop following acute infection, requiring ongoing pain management and urology follow-up. The rare but life-threatening complication of Fournier gangrene should be suspected when perineal or scrotal pain, erythema, and crepitus develop in the setting of epididymo-orchitis, particularly in diabetic or immunocompromised patients.

<image>Panel A: Anatomical illustration comparing normal scrotal anatomy with epididymitis showing the enlarged, inflamed epididymis posterior to the testicle, and epididymo-orchitis with diffuse testicular and epididymal enlargement. Panel B: Scrotal Doppler ultrasound images comparing epididymitis (increased blood flow to the epididymis) with testicular torsion (absent flow to the testicle). Panel C: Treatment algorithm stratified by age and sexual activity, showing ceftriaxone plus doxycycline for sexually active patients under 35 and levofloxacin for those over 35 or non-sexually active, with supportive care measures. Panel D: Complications spectrum from testicular abscess through infertility to Fournier gangrene, with clinical photographs of each complication and management approaches.</image>

Section 7: Priapism

Priapism is classified into three types based on the underlying hemodynamic mechanism, and this distinction is essential because it determines the urgency and nature of treatment. Ischemic (low-flow, veno-occlusive) priapism is the most common type and constitutes a urologic emergency because prolonged ischemia causes irreversible damage to the corporal smooth muscle and endothelium, leading to permanent erectile dysfunction. Non-ischemic (high-flow, arterial) priapism results from an arterial-lacunar fistula, usually following perineal or penile trauma, and is not an emergency because the corpora are well-oxygenated. Stuttering priapism consists of recurrent episodes of ischemic priapism, often in patients with sickle cell disease, and management focuses on prevention of future episodes. The duration threshold of 4 hours is used to define a priapism episode requiring intervention.

Ischemic priapism presents as a painful, fully rigid erection that persists for more than 4 hours. The most common causes include phosphodiesterase-5 inhibitors (sildenafil, tadalafil), intracavernosal injection therapy for erectile dysfunction, and sickle cell disease with sickling of erythrocytes within the corpora. Examination reveals a rigid penis with the corpora cavernosa fully engorged while the glans and corpus spongiosum remain soft. Aspiration of corporal blood provides both diagnostic and therapeutic information: the blood appears dark (deoxygenated), and corporal blood gas analysis reveals pH below 7.25, pO2 below 30 mmHg, and pCO2 above 60 mmHg, confirming ischemic physiology. The risk of permanent erectile dysfunction increases with the duration of ischemia, with significant damage occurring after 24 to 48 hours.

The management of ischemic priapism follows a stepwise approach beginning with corporal aspiration and progressing to sympathomimetic injection. An 18-gauge needle or butterfly needle is inserted into the lateral aspect of the corpus cavernosum (at the 3 or 9 o'clock position to avoid the dorsal neurovascular bundle), and dark blood is aspirated until the penis becomes detumescent or bright red blood is obtained. If aspiration alone is insufficient, the corpus is irrigated with normal saline followed by injection of phenylephrine, a selective alpha-1 agonist, diluted to a concentration of 100 to 500 micrograms per milliliter and injected in 100 to 500 microgram aliquots every 5 to 10 minutes. The patient's blood pressure and heart rate must be monitored during phenylephrine injection because of the risk of hypertension, reflex bradycardia, and cardiac arrhythmia from systemic sympathomimetic effects. If aspiration and phenylephrine injection fail to achieve detumescence, surgical shunt creation (distal or proximal) is required to establish venous drainage from the corpora.

Sickle cell disease-related priapism warrants additional disease-specific management alongside the standard urologic interventions. Intravenous fluid hydration to reduce blood viscosity and promote hemoglobin S dilution is initiated. Supplemental oxygen is provided to reduce further sickling. Analgesia with opioids addresses the significant pain, and nonsteroidal anti-inflammatory drugs may be used cautiously. Exchange transfusion, which replaces sickle hemoglobin-containing red blood cells with normal donor cells, may be considered for severe or refractory episodes. However, aspiration and phenylephrine injection should not be delayed in favor of medical management, as the ischemic pathophysiology is identical regardless of the underlying cause. Patients with recurrent stuttering priapism may benefit from prophylactic medications including pseudoephedrine, etilefrine, or hormonal therapy.

<image>Panel A: Classification diagram of priapism showing ischemic (low-flow, painful, rigid, emergency) versus non-ischemic (high-flow, painless, partially rigid, non-urgent) types with their respective causes and clinical features. Panel B: Corporal blood gas comparison showing dark, deoxygenated blood (pH below 7.25, pO2 below 30) in ischemic priapism versus bright red, oxygenated blood in non-ischemic priapism. Panel C: Step-by-step procedural illustration of corporal aspiration showing needle insertion at the lateral aspect of the corpus cavernosum, aspiration of dark blood, normal saline irrigation, and phenylephrine injection with hemodynamic monitoring. Panel D: Sickle cell priapism management showing concurrent medical interventions (hydration, oxygen, analgesia, exchange transfusion) alongside standard urologic treatment (aspiration and phenylephrine).</image>

Section 8: Paraphimosis

Paraphimosis is a urologic emergency that occurs when the foreskin of an uncircumcised male becomes retracted behind the glans penis and cannot be returned to its normal position, creating a constricting band that obstructs venous and lymphatic drainage. The result is progressive edema of the glans and distal foreskin, which further impedes reduction and creates a vicious cycle of worsening swelling and ischemia. If untreated, arterial compromise eventually develops, leading to tissue necrosis and gangrene of the glans. The most common iatrogenic cause is failure to replace the foreskin to its anatomic position after Foley catheter insertion or urethral instrumentation. Paraphimosis may also occur during penile examination, intercourse, or in patients with poor hygiene and chronic foreskin inflammation.

The reduction of paraphimosis begins with adequate analgesia, typically achieved through a dorsal penile nerve block using lidocaine without epinephrine injected at the 10 and 2 o'clock positions at the base of the penis. Ice application and gentle sustained compression of the glans for 10 to 15 minutes serves to reduce edema and facilitate manual reduction. The reduction technique involves encircling the glans with both hands, applying firm, sustained circumferential pressure to squeeze edema fluid from the glans while simultaneously using the index fingers to pull the constricting foreskin band distally over the glans. If manual reduction fails due to severe edema, the puncture technique may be employed, in which multiple small punctures are made in the edematous foreskin with a 21-gauge needle to allow drainage of edema fluid, thereby reducing the volume of the swollen tissue. If all manual techniques fail, a dorsal slit, a limited surgical incision through the constricting foreskin band, provides immediate decompression and is performed under local anesthesia.

Prevention of paraphimosis is straightforward and should be part of routine clinical practice. The foreskin must always be replaced to its anatomic position covering the glans after any urethral instrumentation, catheterization, or genital examination. Education of nursing staff and other healthcare providers about this critical step is essential, as iatrogenic paraphimosis is entirely preventable. Patients and caregivers of uncircumcised males should be educated about the importance of replacing the foreskin after retraction for hygiene. Elective circumcision provides definitive prevention and should be discussed with patients who experience recurrent episodes.

Phimosis, in contrast to paraphimosis, is the inability to retract the foreskin over the glans and is generally not an emergency. Physiologic phimosis is normal in young boys and resolves spontaneously in most cases by puberty. Pathologic phimosis in adults results from chronic inflammation, scarring (balanitis xerotica obliterans), or recurrent infection. Treatment options include topical corticosteroid cream applied to the foreskin for 4 to 8 weeks to reduce scarring and allow retraction, gentle manual stretching exercises, and elective circumcision as the definitive surgical option. Phimosis becomes an emergency only when it causes urinary obstruction, preventing the patient from voiding. In this scenario, a dorsal slit or urgent circumcision may be necessary to relieve the obstruction and allow bladder drainage.

<image>Panel A: Anatomical illustration showing normal foreskin position compared with paraphimosis, demonstrating the retracted foreskin forming a constricting band behind the glans with progressive edema and vascular compromise. Panel B: Dorsal penile nerve block technique showing injection sites at the 10 and 2 o'clock positions at the penile base, followed by the manual reduction technique with circumferential compression of the glans and distal traction on the foreskin. Panel C: Alternative techniques for refractory paraphimosis showing the puncture technique with 21-gauge needle drainage of edema fluid and the dorsal slit surgical incision through the constricting band. Panel D: Comparison of paraphimosis (emergency, retracted foreskin behind glans) and phimosis (usually non-emergent, unable to retract foreskin), with their respective treatment approaches and indications for surgical intervention.</image>

Section 9: Penile Fracture

Penile fracture is the traumatic rupture of the tunica albuginea, the tough fibrous covering of the corpus cavernosum, which occurs when the erect penis is subjected to sudden blunt force. The most common mechanism is vigorous sexual intercourse in which the erect penis strikes the partner's pubic symphysis or perineum, bending the shaft and creating a focal area of high pressure that exceeds the tensile strength of the tunica. The patient typically describes an audible popping or cracking sound at the moment of injury, followed by immediate detumescence, severe pain, and rapid swelling. The characteristic "eggplant deformity" develops as blood from the ruptured corpus cavernosum accumulates beneath Buck fascia, producing a large ecchymotic, swollen, and deviated penile shaft that resembles an eggplant in shape and color.

The diagnosis of penile fracture is primarily clinical, based on the classic history of trauma during erection, the audible pop, immediate detumescence, and characteristic physical findings of swelling, ecchymosis, and deviation of the penile shaft away from the side of injury. In most cases, the clinical presentation is sufficiently distinctive that no imaging is required before surgical consultation. Blood at the urethral meatus is a critical finding that suggests concurrent urethral injury and should prompt retrograde urethrography before any urethral instrumentation. When the diagnosis is uncertain, magnetic resonance imaging provides excellent resolution of tunica albuginea defects and corporal hematomas but should not delay treatment in obvious cases. Ultrasound may also demonstrate the tunica defect and associated hematoma.

Emergent surgical repair within 24 hours is the standard of care for penile fracture, as early repair produces significantly better outcomes than delayed repair or conservative management. Operative exploration involves degloving the penis through a circumcoronal or subcoronal incision, identifying the tunica albuginea defect, evacuating the hematoma, and closing the defect with absorbable sutures. Early surgical repair results in lower rates of erectile dysfunction, penile curvature (Peyronie disease), painful erections, and formation of plaque at the injury site. Conservative (non-operative) management with splinting, ice, anti-inflammatory medications, and anti-erection agents has been associated with significantly higher rates of complications including erectile dysfunction in up to 50 percent of patients and penile curvature in up to 35 percent, and is therefore not recommended. Urology should be consulted emergently upon diagnosis.

Concurrent urethral injury accompanies penile fracture in approximately 10 to 20 percent of cases and must be actively evaluated. The clinical sign that raises suspicion for urethral injury is blood at the urethral meatus, though its absence does not completely exclude the diagnosis. When urethral injury is suspected, a retrograde urethrogram should be performed before any attempt at urethral catheterization, as passage of a catheter through a disrupted urethra can convert a partial injury to a complete transection and create false passages. The retrograde urethrogram involves injecting contrast material into the urethral meatus under fluoroscopy to delineate the urethral anatomy and identify the site and extent of injury. Urethral injuries identified in conjunction with penile fracture are repaired simultaneously during the operative exploration.

<image>Panel A: Mechanism of injury illustration showing the erect penis striking the pubic symphysis during intercourse, focal bending force on the tunica albuginea, and rupture of the tunica with corporal blood extravasation. Panel B: Clinical photograph of the characteristic eggplant deformity showing penile swelling, ecchymosis, and deviation, alongside an MRI demonstrating the tunica albuginea defect and surrounding hematoma. Panel C: Surgical repair sequence showing circumcoronal incision, penile degloving, identification of tunica defect with hematoma evacuation, and primary closure with absorbable sutures. Panel D: Retrograde urethrogram technique for evaluating suspected concurrent urethral injury, showing contrast injection at the urethral meatus and fluoroscopic images of normal versus disrupted urethral continuity.</image>

Section 10: Other Urologic Emergencies

Renal trauma is classified by the American Association for the Surgery of Trauma into five grades of increasing severity. Grade I and II injuries represent contusions and subcapsular hematomas without collecting system involvement and are managed conservatively with observation, bed rest, and serial hematocrit monitoring. Grade III injuries involve renal lacerations extending more than 1 centimeter into the parenchyma without collecting system disruption and are generally managed conservatively unless hemodynamic instability develops. Grade IV injuries involve lacerations extending into the collecting system or injury to the main renal artery or vein, requiring close monitoring and potential intervention including angioembolization for active hemorrhage. Grade V injuries represent a shattered kidney or complete avulsion of the renal pedicle and typically require surgical exploration and often nephrectomy. The majority of renal injuries are managed non-operatively, with surgery reserved for hemodynamically unstable patients and grade V injuries.

Bladder injury is classified as either extraperitoneal or intraperitoneal, and this distinction is critical because it determines management. Extraperitoneal bladder rupture, the more common type, is typically associated with pelvic fractures in which bony fragments lacerate the bladder wall, and is managed conservatively with catheter drainage alone for 10 to 14 days followed by confirmatory cystogram. Intraperitoneal bladder rupture occurs when the dome of a full bladder is compressed during blunt trauma, causing a burst injury with spillage of urine into the peritoneal cavity; this injury requires operative surgical repair because urine within the peritoneum causes chemical peritonitis and can progress to sepsis. Diagnosis of bladder injury is made by retrograde cystogram, in which contrast material is instilled into the bladder through a catheter and post-drainage films are obtained to demonstrate extravasation.

Urethral injury should be suspected in any patient with pelvic trauma who presents with blood at the urethral meatus, a high-riding or non-palpable prostate on digital rectal examination, or perineal hematoma (butterfly hematoma). The cardinal rule is that no urethral catheterization should be attempted until urethral integrity has been confirmed by retrograde urethrography. Attempting to pass a catheter through a disrupted urethra can worsen the injury, create false passages, convert a partial tear to a complete disruption, and introduce infection. When retrograde urethrography confirms urethral disruption and the bladder requires drainage, a suprapubic catheter should be placed percutaneously under ultrasound guidance, completely bypassing the injured urethra. Definitive urethral repair may be performed acutely or in a delayed fashion depending on the extent and location of the injury.

Fournier gangrene is the most life-threatening genitourinary soft tissue emergency and is a form of necrotizing fasciitis specifically involving the perineum and external genitalia. Risk factors include diabetes mellitus (present in up to 50 percent of cases), immunocompromise, alcoholism, and local trauma including urologic procedures and perianal abscess. Patients present with rapidly progressive perineal pain, swelling, erythema, and often palpable crepitus from gas-producing organisms. Systemic signs of sepsis including fever, tachycardia, and hypotension develop early and progress rapidly. The mortality rate ranges from 20 to 40 percent and correlates directly with the time from presentation to surgical debridement. Treatment requires emergent, aggressive surgical debridement of all necrotic tissue, broad-spectrum intravenous antibiotics covering gram-positive organisms (including MRSA), gram-negative organisms, and anaerobes, and aggressive hemodynamic resuscitation. Multiple sequential debridements are typically required, followed by skin grafting or flap reconstruction of the resulting tissue defect.

<image>Panel A: Renal trauma grading system showing CT images for Grade I (contusion), Grade III (deep laceration), Grade IV (collecting system involvement with urine leak), and Grade V (shattered kidney with pedicle avulsion), with corresponding management approaches. Panel B: Retrograde cystogram images comparing extraperitoneal bladder rupture (contrast extravasation around the bladder) with intraperitoneal rupture (contrast outlining bowel loops), and their respective management pathways. Panel C: Retrograde urethrogram demonstrating a posterior urethral disruption with contrast extravasation, alongside the suprapubic catheter placement technique bypassing the injured urethra. Panel D: Fournier gangrene clinical presentation showing perineal necrosis with crepitus, CT demonstrating subcutaneous gas, and intraoperative photograph following extensive debridement with exposed structures.</image>

Summary

• Testicular torsion presents with sudden scrotal pain and absent cremasteric reflex; surgery within 6 hours achieves near 100 percent salvage, declining to 0 percent after 24 hours
• Nephrolithiasis is best diagnosed by non-contrast CT; NSAIDs are first-line analgesia; the combination of obstruction plus infection constitutes a urologic emergency requiring emergent decompression
• Obstructed infected kidney requires simultaneous sepsis resuscitation and emergent decompression via ureteral stent or percutaneous nephrostomy
• Acute urinary retention is managed with catheterization; tamsulosin should be started before catheter removal; a coude-tipped catheter navigates prostatic enlargement
• Epididymitis presents with gradual onset and positive Prehn sign; ceftriaxone plus doxycycline is used for patients under 35 with suspected STI
• Ischemic priapism lasting more than 4 hours is a urologic emergency treated with corporal aspiration and phenylephrine injection; surgical shunt is required if refractory
• Paraphimosis requires manual reduction after dorsal penile block and edema reduction; dorsal slit is the surgical rescue for failed manual reduction
• Penile fracture presents with the classic triad of popping sound, immediate detumescence, and eggplant deformity; emergent surgical repair within 24 hours is standard of care
• Urethral injury is suspected when blood is present at the meatus; retrograde urethrography must be performed before catheterization
• Fournier gangrene requires emergent surgical debridement; mortality correlates with time to surgery

Key Terms

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