25.2 Testicular Torsion, Priapism & Acute Urinary Retention

Testicular Torsion: Pathoanatomy, Diagnosis & Emergency Surgical Salvage

Testicular torsion is a true urologic surgical emergency characterized by the twisting of the spermatic cord and its vascular pedicle, compromising venous outflow and arterial inflow to the testis. Without rapid intervention, testicular ischemia progresses to irreversible hemorrhagic infarction, parenchymal necrosis, and permanent loss of spermatogenesis and endocrine function.

Anatomy & Pathophysiology: The Bell-Clapper Deformity

• Congenital Etiology: In normal anatomical development, the tunica vaginalis lines only the anterior and lateral aspects of the testis, while the posterior surface of the testis and epididymis is firmly anchored to the posterolateral scrotal wall via the gubernaculum testis.
• The 'Bell-Clapper' Anomaly: In approximately 12% of males, an abnormally high termination of the parietal tunica vaginalis completely surrounds the testis, epididymis, and distal spermatic cord. This prevents posterior anchoring, leaving the testis suspended freely within the tunica vaginalis cavity like the clapper inside a bell. This allows the testis to rotate freely around the vertical axis of the spermatic cord.
• Bilateral Vulnerability: The bell-clapper deformity is a congenital anatomical defect that is bilateral in 50% to 80% of affected individuals. Consequently, any patient with unilateral torsion is at high risk for future contralateral torsion, establishing the absolute requirement for bilateral orchiopexy during surgical repair.
• Ischemic Cascade: Rotation of the spermatic cord first compresses the thin-walled, low-pressure testicular veins and pampiniform venous plexus. Venous outflow obstruction causes progressive interstitial edema, swelling, and rapid elevation of intracompartmental pressure within the non-compliant tunica albuginea. When intracompartmental pressure exceeds testicular arterial diastolic and systolic pressures, arterial thrombosis and parenchymal infarction ensue.

Epidemiology & Clinical Presentation

• Age Distribution: Demonstrates a classic bimodal distribution: a minor peak occurs in neonates (typically extravaginal torsion, where the entire spermatic cord twists outside the tunica vaginalis during testicular descent), and a major peak occurs in adolescents aged 12 to 18 years (intravaginal torsion, related to rapid testicular growth and pubertal surges).
• Clinical Presentation:
  • Sudden, abrupt onset of severe, excruciating unilateral scrotal pain, frequently awakening the patient from sleep or occurring during vigorous athletic activity.
  • Pain commonly radiates along the spermatic cord into the ipsilateral inguinal canal, lower abdomen, and flank.
  • Nausea and vomiting occur in up to 30% to 50% of patients due to intense autonomic stimulation of the celiac ganglion via common sympathetic innervation (T10-T11 spinal cord levels).
  • Absence of systemic infectious symptoms: fever is typically absent early, and dysuria, frequency, and urethral discharge are distinctly absent.

Physical Examination: Cremasteric Reflex & Prehn Sign

Physical examination provides the cornerstone of clinical diagnosis. The key physical findings include:

1. Scrotal Inspection & Palpation: The affected testis is enlarged, exquisitely tender, and retracted upward into a high-riding position with a transverse (horizontal) lie (Brunzel's sign) caused by shortening of the twisted spermatic cord. Early on, the epididymis may be palpable anteriorly rather than in its normal posterior location.
2. The Cremasteric Reflex (The Most Sensitive Sign):
   • Technique: Lightly stroke or pinch the skin of the ipsilateral upper inner thigh (L1-L2 genitofemoral nerve sensory territory).
   • Normal Response: Immediate contraction of the cremaster muscle, elevating the ipsilateral testis by at least 0.5 cm.
   • Diagnostic Significance: The cremasteric reflex is ABSENT in >95% to 99% of patients with acute testicular torsion. The presence of a normal, brisk cremasteric reflex makes acute testicular torsion highly improbable (negative predictive value >95%), though rare exceptions exist.
3. Prehn's Sign:
   • Technique: Gentle manual elevation of the affected hemiscrotum toward the symphysis pubis.
   • Significance: Classically, in acute epididymitis, scrotal elevation relieves tension on the epididymal cord and relieves pain (Positive Prehn sign). In testicular torsion, scrotal elevation does NOT relieve pain and may exacerbate it (Negative Prehn sign).
   • Board Pearl: Prehn's sign is notoriously unreliable and must never be used in isolation to exclude testicular torsion.

Scrotal Ultrasound & The Whirlpool Sign

• Urgent Color Doppler Scrotal Ultrasonography: The imaging modality of choice, demonstrating sensitivity of 85-90% and specificity of 95-99% in experienced hands.
• Hallmark Ultrasonographic Findings:
  • Markedly diminished or completely absent intratesticular arterial and venous blood flow on color and spectral Doppler imaging (compared to the normal contralateral testis);
  • High-resistance arterial waveforms with reversed diastolic flow in early or partial torsion;
  • The 'Whirlpool Sign': Direct visualization of the twisting, spiraling loops of the spermatic cord at the external inguinal ring or within the scrotal neck (near 100% specific for torsion);
  • Heterogeneous, hypoechoic parenchymal echotexture: indicates advanced ischemia, parenchymal necrosis, and impending non-viability.

The Golden Window & Emergency Surgical Mandate

                  TESTICULAR SALVAGE BY TIME WINDOW

  Time from Pain Onset          Testicular Salvage Rate
  ─────────────────────────────────────────────────────────
  < 6 hours                     > 90% - 95%  (Golden Window)
  6 to 12 hours                 ~ 50%
  12 to 24 hours                10% - 20%
  > 24 hours                    < 10% (Orchiectomy typically required)

• CRITICAL BOARD & CLINICAL MANDATE: If clinical suspicion for testicular torsion is high, NEVER DELAY EMERGENCY SURGICAL EXPLORATION TO OBTAIN AN ULTRASOUND!
• If ultrasound equipment is not instantly available, or if sonographic findings are equivocal or report 'normal flow' in a patient with an absent cremasteric reflex and agonizing pain, immediate urologic surgical exploration takes absolute precedence. Operative exploration is both the definitive diagnostic gold standard and definitive therapy.

Manual Detorsion: The 'Open Book' Maneuver

When emergency urologic consultation is requested but operative transport involves unavoidable delay, bedside manual detorsion should be attempted immediately:

• Direction of Torsion: In approximately two-thirds of cases, the testis torses inward (medially) toward the median scrotal raphe.
• The 'Open Book' Technique:
  • The physician stands facing the supine patient's feet;
  • Grasp the affected testis between thumb and index finger;
  • Rotate the testis from medial to lateral—analogous to opening the pages of a book:
    • Right Testis: Rotate counter-clockwise (toward the patient's right thigh);
    • Left Testis: Rotate clockwise (toward the patient's left thigh);
  • Most torsions involve 180 to 720 degrees (one to two full rotations) of twisting. Successful detorsion is indicated by immediate, dramatic relief of pain, elongation of the spermatic cord with normal low-riding vertical testicular lie, and restoration of palpable pulses or Doppler flow;
  • Caveat: In ~30% of cases, the testis torses laterally. If gentle medial-to-lateral rotation increases patient resistance and exacerbates pain, immediately rotate in the opposite direction.
• SURGICAL RULE: Manual detorsion NEVER eliminates the need for emergency surgery. Even if manual detorsion is completely successful, residual partial torsion often persists, and orchiopexy is mandatory to prevent recurrent torsion.

Operative Management & Mandatory Bilateral Orchiopexy

1. Scrotal Exploration: Midline raphe or transverse hemiscrotal incision, opening the dartos and tunica vaginalis.
2. Detorsion & Viability Assessment: Untwist the spermatic cord and place the ischemic testis in warm, saline-moistened gauze sponges for 15 to 20 minutes with high-fraction supplemental oxygen.
3. Orchiopexy vs. Orchiectomy:
   • If the testis regains pink coloration, demonstrates arterial bleeding upon surface needle puncture, and Doppler flow returns: the testis is preserved and secured via three-point suture fixation using non-absorbable monofilament sutures (e.g., 3-0/4-0 polypropylene) anchoring the tunica albuginea to the scrotal dartos fascia (orchiopexy).
   • If the testis remains black, necrotic, and cold without arterial bleeding after 20 minutes of rewarming: an orchiectomy is performed to prevent ischemic auto-immunization and anti-sperm antibody formation that could impair fertility in the contralateral testis.
4. Mandatory Contralateral Orchiopexy: The contralateral hemiscrotum must be explored and secured to the dartos fascia during the same operative session to eliminate the risk of contralateral torsion secondary to bilateral bell-clapper anomaly.

Differential Diagnosis of the Acute Scrotum

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Priapism: Ischemic vs. Non-Ischemic Emergencies

Priapism is defined as a prolonged, persistent, involuntary penile erection lasting greater than 4 hours that is unrelated to or persists beyond sexual stimulation. Priapism is fundamentally divided into two distinct clinical entities with vastly different urgencies:

                         PRIAPISM CLASSIFICATION

  FEATURE              ISCHEMIC (Low-Flow)          NON-ISCHEMIC (High-Flow)
  ──────────────────────────────────────────────────────────────────────────
  Pathophysiology      Veno-occlusive; impaired     Arterial fistula; unregulated
                       venous outflow; compartment  cavernosal arterial inflow
                       syndrome of penis
  Urgency              TRUE UROLOGIC EMERGENCY     Elective; non-emergent
  Clinical Symptoms    Exquisitely painful; rigid   Painless (or mild discomfort);
                       corpora; FLACCID GLANS       semi-rigid, tumescent penis
  Etiologies           Sickle cell disease,         Perineal or penile blunt trauma
                       PDE-5i, trazodone, neuro-    (laceration of cavernosal
                       leptics, intracavernosal Rx  artery)
  Cavernosal Blood     DARK venous blood            BRIGHT RED arterial blood
  Cavernosal Gas       pH < 7.25, pO2 < 30 mmHg,    pH > 7.40, pO2 > 90 mmHg,
                       pCO2 > 60 mmHg (Hypoxic)     pCO2 < 40 mmHg (Arterial)
  Initial Management   Corporal aspiration, saline  Observation, ice; elective
                       irrigation, Phenylephrine    embolization if persistent

Etiologic Triggers of Ischemic Priapism

• Hematologic: Sickle Cell Disease (SCD) accounts for up to 65% of pediatric priapism and 25% of adult cases. Deoxygenation in the venous sinusoids induces sickling of erythrocytes, vascular sludging, and venous outflow obstruction. Other triggers include leukemia, polycythemia vera, and multiple myeloma.
• Medications (Most Common Adult Etiology):
  • Phosphodiesterase Type 5 (PDE-5) Inhibitors: Sildenafil, tadalafil, vardenafil (especially when combined with alcohol, cocaine, or recreational intracavernous agents);
  • Intracavernosal Vasoactive Injections: Alprostadil (PGE1), papaverine, phentolamine;
  • Antidepressants: Trazodone (classic board association, secondary to potent peripheral alpha-1 adrenergic antagonism) and selective serotonin reuptake inhibitors (SSRIs);
  • Antipsychotics: Typical and atypical neuroleptics (chlorpromazine, haloperidol, quetiapine, risperidone) via alpha-adrenergic blockade;
  • Antihypertensives: Prazosin, terazosin, hydralazine;
  • Recreational Substances: Cocaine, amphetamines, ethanol.

Corporal Blood Gas Analysis: Low-Flow vs. High-Flow

When a patient presents with an erection lasting >4 hours, immediate corporal aspiration confirms the diagnosis and differentiates ischemic from non-ischemic priapism:

• Aspiration Technique: Using a 19- or 21-gauge butterfly needle inserted into the lateral corpus cavernosum at the 2 o'clock or 10 o'clock position (avoiding the dorsal neurovascular bundle at 12 o'clock and the urethra at 6 o'clock), aspirate 1 to 2 mL of blood for blood gas analysis.
• Ischemic Profile: Blood appears thick and dark/black; blood gas reveals marked acidosis (pH <7.25), profound hypoxia (pO2 <30 mmHg), and hypercapnia (pCO2 >60 mmHg).
• Non-Ischemic Profile: Blood appears bright red; blood gas reveals normal room air arterial parameters (pH >7.40, pO2 >90 mmHg, pCO2 <40 mmHg).

Stepwise Emergency Management of Ischemic Priapism

Ischemic priapism untreated for >12 to 24 hours results in irreversible smooth muscle necrosis, corporal fibrosis, and permanent refractory erectile dysfunction. Management follows a strict stepwise protocol:

                 ISCHEMIC PRIAPISM ESCALATION PROTOCOL

  ┌─────────────────────────────────────────────────────────────┐
  │ STEP 1: Penile Anesthesia                                   │
  │ Dorsal penile nerve block or circumferential ring block      │
  │ using 1% plain lidocaine (WITHOUT epinephrine)              │
  └──────────────────────────────┬──────────────────────────────┘
                                 ▼
  ┌─────────────────────────────────────────────────────────────┐
  │ STEP 2: Corporal Aspiration & Decompression                 │
  │ Insert 19-gauge butterfly needle at 2 or 10 o'clock         │
  │ Aspirate 20-30 mL of dark, viscous sludged blood           │
  │ Relieves high compartmental pressure; resolves pain          │
  └──────────────────────────────┬──────────────────────────────┘
                                 ▼
  ┌─────────────────────────────────────────────────────────────┐
  │ STEP 3: Intracavernosal Normal Saline Irrigation            │
  │ Irrigate corpora with sterile isotonic saline until bright   │
  │ red oxygenated blood is aspirated                           │
  └──────────────────────────────┬──────────────────────────────┘
                                 ▼
  ┌─────────────────────────────────────────────────────────────┐
  │ STEP 4: Intracavernosal Phenylephrine Injection              │
  │ • Selective alpha-1 adrenergic agonist                      │
  │ • Dilute: 100-500 mcg/mL in normal saline                   │
  │ • Inject 100-200 mcg every 3 to 5 minutes (max 1,000 mcg)    │
  │ • Requires continuous ECG and blood pressure monitoring     │
  └──────────────────────────────┬──────────────────────────────┘
                                 ▼
  ┌─────────────────────────────────────────────────────────────┐
  │ STEP 5: Emergent Surgical Shunt (If Refractory >1 Hour)     │
  │ Distal percutaneous shunt (Winter, Ebbehoj) or proximal     │
  │ open shunt (Quackels cavernosum-spongiosum shunt)           │
  └─────────────────────────────────────────────────────────────┘

Step 1: Penile Anesthesia

Perform a dorsal penile nerve block at the base of the penis (at the 10 and 2 o'clock positions deep to Buck's fascia) or a subcutaneous circumferential ring block using 10 mL of 1% or 2% plain lidocaine (never use epinephrine for local anesthesia in the penis).

Step 2: Corporal Aspiration & Decompression

Insert a 19-gauge butterfly needle into the mid-shaft of the lateral corpus cavernosum at the 2 o'clock or 10 o'clock position, perpendicular to the skin. Aspirate 20 to 30 mL of sludged, hypoxic blood. Because intercavernous communications bridge the two corpora, aspirating one side decompresses both corpora. Aspiration alone achieves detumescence in approximately 30% of cases.

Step 3: Normal Saline Irrigation

If detumescence is not achieved with aspiration, irrigate the corpora with sterile normal saline (injecting and re-aspirating in 10-20 mL aliquots) until bright red, oxygenated blood returns.

Step 4: Intracavernosal Phenylephrine Administration

• Mechanism: Phenylephrine is a pure, potent selective alpha-1 adrenergic agonist. Binding to alpha-1 receptors on cavernous smooth muscle induces smooth muscle contraction, terminating the erection by constricting sinusoidal inflow and opening venous emissary outflow channels.
• Preparation: Dilute phenylephrine with normal saline to a final concentration of 100 to 500 mcg/mL.
• Administration: Inject 100 to 200 mcg (0.5 to 1.0 mL of a 200 mcg/mL solution) directly into the corpus cavernosum every 3 to 5 minutes, up to a maximum cumulative dose of 1,000 mcg (1 mg) within a 1-hour period, gently compressing the puncture site between injections.
• CRITICAL MONITORING MANDATE: Due to systemic absorption through open venous channels, phenylephrine can cause acute severe hypertension, reflex bradycardia, coronary vasospasm, and fatal ventricular arrhythmias. Continuous non-invasive blood pressure monitoring and cardiac telemetry are mandatory throughout the procedure.

Step 5: Emergent Surgical Shunts

If corporal aspiration, irrigation, and maximal phenylephrine dosing fail to achieve detumescence after 1 hour, emergency urologic operative intervention is indicated:

• Distal Percutaneous Shunts: A large-bore biopsy needle (Tru-Cut) or scalpel is introduced through the glans penis to puncture the distal tip of the tunica albuginea, creating a fistula between the corpus cavernosum and the glans (Winter or Ebbehoj shunt);
• Proximal Open Shunts: Creation of a surgical anastomosis between the corpus cavernosum and corpus spongiosum (Quackels shunt) or saphenous vein (Grayhack shunt).

Special Consideration: Sickle Cell Disease Priapism

In patients with sickle cell disease presenting with acute ischemic priapism:

• Immediately initiate systemic supportive therapy: high-flow oxygen, aggressive intravenous hydration with hypotonic or isotonic crystalloids, intravenous analgesia (opioids), and alkalinization.
• Board Rule: Never delay local urologic intervention (corporal aspiration and phenylephrine injection) while awaiting systemic therapies or blood transfusions!
• If refractory, perform an urgent automated red blood cell exchange transfusion to reduce hemoglobin S (HbS) concentrations to <30% without raising total hematocrit >30% (avoiding hyperviscosity syndrome).

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Acute Urinary Retention (AUR): Etiology, Catheterization & Post-Obstructive Diuresis

Acute Urinary Retention is defined as the sudden, painful inability to voluntarily micturate despite a fully distended urinary bladder. It represents the most frequent urologic emergency, carrying substantial risks of detrusor myogenic injury, acute kidney injury, sepsis, and bladder rupture.

Pathophysiology & Clinical Assessment

• Clinical Presentation: Severe, agonizing suprapubic pain, lower abdominal fullness, restlessness, diaphoresis, and a palpable, exquisitely tender, dull-to-percussion suprapubic abdominal mass.
• Bedside Ultrasound Assessment: A bedside ultrasound bladder scanner is the non-invasive diagnostic standard. A documented Post-Void Residual (PVR) volume >300 to 400 mL establishes the diagnosis of urinary retention (retained volumes frequently exceed 800 to 1,500 mL in severe acute presentations).

Etiologic Classification of AUR

1. Outflow Obstruction (Mechanical):
   • Men: Benign Prostatic Hyperplasia (BPH) is responsible for >50% of all cases in men >60 years. Other mechanical causes include prostate cancer, urethral stricture disease, bladder calculi, blood clot retention, and acute bacterial prostatitis.
   • Women: Pelvic organ prolapse (cystocele, uterine prolapse), pelvic masses (uterine leiomyomas, ovarian neoplasms), or retroverted gravid uterus (typically between 12 and 16 weeks gestation).
2. Pharmacologic Inhibition (Most Frequent Reversible Trigger):
   • Anticholinergics: Diphenhydramine, hydroxyzine, oxybutynin, tolterodine, scopolamine (inhibit detrusor muscarinic M2/M3 receptors, eliminating bladder contractility);
   • Sympathomimetics: Pseudoephedrine, ephedrine, phenylephrine (stimulate alpha-1 receptors at the bladder neck and prostatic urethra, increasing outflow resistance);
   • Tricyclic Antidepressants: Amitriptyline, nortriptyline (possess potent anticholinergic activity);
   • Opioids: Morphine, hydromorphone, oxycodone (decrease bladder sensation and inhibit parasympathetic sacral motor output);
   • Calcium Channel Blockers & First-Generation Antipsychotics.
3. Neurologic Impairment (Neurogenic Bladder):
   • Cauda Equina Syndrome: Spinal cord compression at L1-S5 secondary to massive central herniated disc, epidural abscess, hematoma, or malignancy. Accompanied by saddle anesthesia, bilateral lower extremity weakness, and loss of anal sphincter tone. AUR is the single most sensitive finding (>90%) for cauda equina syndrome;
   • Acute spinal cord injury, transverse myelitis, multiple sclerosis, and diabetic autonomic cystopathy;
   • Genital herpes simplex virus (HSV-2) lumbosacral radiculopathy (Elsberg syndrome).
4. Infectious & Inflammatory:
   • Acute bacterial prostatitis: characteristically presents with fever, perineal pain, dysuria, and retention. Rectal exam reveals a boggy, exquisitely tender prostate (avoid vigorous prostatic massage to prevent bacteremia).

Emergency Decompression & Catheterization Techniques

Immediate decompression of the distended bladder via urethral catheterization is the mandatory primary intervention.

Foley vs. Coudé Catheterization

• Standard Initial Attempt: Insert a standard 14-French or 16-French silicone or latex Foley catheter using copious sterile 2% lidocaine lubricant gel instillation into the urethra (10 mL syringe).
• Encountering Resistance at the Prostatic Urethra:
  • In men with enlarged prostates (BPH), a standard flexible catheter tip frequently impacts against an elevated, hypertrophied median prostatic lobe or narrow urethral angle.
  • The Coudé-Tip Catheter: If standard catheterization encounters firm resistance, switch immediately to a 16-French Coudé catheter.
  • Technique: The Coudé catheter features an angled, semi-rigid olive or tapered tip. Insert the catheter with the angled tip oriented anteriorly toward the 12 o'clock position (indicated by the raised ridge or line on the catheter funnel). This anterior orientation allows the catheter tip to smoothly navigate over the elevated posterior median prostatic lobe and enter the bladder lumen.
• SURGICAL SAFETY MANDATE: Never use excessive force against resistance. Forcing a catheter risks creating a false urethral tract, tearing the urethral mucosa, and inducing severe hemorrhage or sepsis.

Difficult Catheterization & Suprapubic Cystostomy

If Coudé catheterization fails:

• Obtain emergent urologic consultation for bedside flexible cystoscopy-assisted guidewire catheterization;
• If urology is unavailable and catheterization fails: perform an emergent percutaneous suprapubic cystostomy under real-time ultrasound guidance (visualizing the distended bladder at least 2 to 3 cm above the symphysis pubis to avoid transfixing overlying loops of small bowel).

Complications of Acute Decompression: Post-Obstructive Diuresis (POD)

Following rapid decompression of severe or chronic urinary retention, patients are susceptible to Post-Obstructive Diuresis:

• Definition: Prolonged, severe polyuria defined as urine output >200 mL/hour for two consecutive hours, or >3 to 4 liters of urine in 24 hours.
• Pathophysiology: Rapid release of high intravesical pressure triggers an abrupt fall in medullary interstitial hypertonicity ('medullary washout'), tubular unresponsiveness to antidiuretic hormone (ADH), and osmotic diuresis driven by accumulated blood urea nitrogen and retained natriuretic factors.
• Clinical Monitoring Protocol:
  • Any patient with acute decompression of retained volumes >1,000 mL, baseline renal impairment (elevated BUN/creatinine), or severe peripheral edema must be monitored in an acute care setting for at least 4 to 6 hours;
  • Monitor strict hourly urine output, orthostatic blood pressure, and serial serum electrolytes (sodium, potassium, bicarbonate), BUN, and creatinine every 6 to 12 hours.
• Hydration Strategy:
  • Self-Limiting (Physiological) POD: If the patient is alert, hemodynamically stable, and drinking fluids voluntarily, encourage oral fluid intake matching thirst. Avoid unnecessary intravenous fluids, which perpetuate an iatrogenic polyuric cycle.
  • Pathological POD: If urine output remains massive and the patient develops postural hypotension, tachycardia, hyponatremia, or hypokalemia: administer intravenous 0.45% normal saline replacing 50% to 75% of the preceding hour's urine output (never replace 100% of urine output, as this sustains osmotic polyuria).

Outpatient Medical Optimization & Trial Without Catheter (TWOC)

• Immediate Pharmacotherapy: In men with AUR secondary to suspected or confirmed BPH, initiate a selective alpha-1 adrenergic antagonist immediately upon catheter placement:
  • Tamsulosin 0.4 mg PO once daily, or Alfuzosin 10 mg PO once daily;
  • Mechanism: Rapidly relaxes smooth muscle tone in the prostate stroma and bladder neck, reducing dynamic outflow resistance.
• Catheter Maintenance & TWOC Protocol:
  • Leave the indwelling Foley catheter in place connected to a leg bag for 3 to 7 days to permit detrusor muscle recovery and allow the alpha-blocker to achieve steady-state therapeutic receptor blockade;
  • The Trial Without Catheter (TWOC): The patient returns to the outpatient clinic in 3 to 7 days. The catheter is removed in the early morning, the patient is encouraged to consume fluids, and spontaneous voiding is evaluated over the next 4 to 6 hours.
  • Evidence: Initiating an alpha-1 blocker prior to TWOC doubles the rate of successful spontaneous voiding (approximately 60% vs. 30% with placebo) and significantly reduces the need for emergency recatheterization.