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EMERGENCY MEDICINE PRACTICE A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E Male Genitourinary Emergencies: Preserving Fertility And Providing Relief “W HAT was that again, sir? You’ll have to speak up—it’s awfully noisy here in triage. You did what? You’re kidding, right?” Problems that arise with the male genitourinary system range from benign to life- and fertility-threatening. Whether the complaint represents a true emergency or not, it is often of immense concern to the worried patient. This issue of Emergency Medicine Practice discusses the diagnosis and treatment of common penile complaints, the evaluation of the acute scrotum, as well as addressing prostatitis and urinary retention. “Tumescence is the period between pubescence and senescence.”—Robert Byrne Priapism Priapism is a prolonged, usually painful, penile erection not initiated by sexual stimuli.1 It results from a disturbance in the normal regulatory mechanisms that initiate and maintain an erection.1 Priapism results from either a low-flow or high-flow etiology. This distinction is important because the associated treatment and prognosis differ. Low-flow (ischemic) priapism occurs when decreased penile venous outflow produces venous stasis. The subsequent penile ischemia results from arterial compromise.2 Low-flow priapism is a time-sensitive emergency, as irreversible cellular damage and fibrosis occur if treatment is not administered within 24-48 hours.3 Complications include erectile dysfunction and recurrent episodes of priapism.4 High-flow priapism is quite rare and is caused by increased arterial flow into the corpus cavernosa.1 It usually results from direct trauma to the internal pudendal artery producing an arterial to cavernosal shunt. High-flow priapism is not considered as emergent because the penis does not become ischemic.5 Stephen A. Colucciello, MD, FACEP, Assistant Chair, Director of Clinical Services, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC; Associate Clinical Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC. Associate Editor Andy Jagoda, MD, FACEP, Professor of Emergency Medicine; Director, International Studies Program, Mount Sinai School of Medicine, New York, NY. Editorial Board Judith C. Brillman, MD, Residency Director, Associate Professor, Department of Emergency Volume 2, Number 11 Author Lisa Freeman, MD, FACEP Assistant Professor, Department of Emergency Medicine, University of Texas Medical School at Houston, Houston, TX. Peer Reviewers Atilla Üner, MD, FAAEM Assistant Professor of Medicine/Emergency Medicine, UCLA School of Medicine, Los Angeles, CA. Robert E. Schneider, MD Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC. CME Objectives Overview Editor-in-Chief November 2000 Medicine, The University of New Mexico Health Sciences Center School of Medicine, Albuquerque, NM. W. Richard Bukata, MD, Assistant Clinical Professor, Emergency Medicine, Los Angeles County/ USC Medical Center, Los Angeles, CA; Medical Director, Emergency Department, San Gabriel Valley Medical Center, San Gabriel, CA. Francis M. Fesmire, MD, FACEP, Director, Chest Pain—Stroke Center, Erlanger Medical Center; Assistant Professor of Medicine, UT College of Medicine, Chattanooga, TN. Valerio Gai, MD, Professor and Chair, Department of Emergency Medicine, University of Turin, Italy. Michael J. Gerardi, MD, FACEP, Clinical Assistant Professor, Medicine, University of Medicine and Dentistry of New Jersey; Director, Pediatric Emergency Medicine, Children’s Medical Center, Atlantic Health System; Chair, Pediatric Emergency Medicine Committee, ACEP. Michael A. Gibbs, MD, FACEP, Residency Program Director; Medical Director, MedCenter Air, Department of Emergency Medicine, Carolinas Medical Center; Associate Professor of Emergency Medicine, University of North Carolina at Chapel Hill, Charlotte, NC. Gregory L. Henry, MD, FACEP, CEO, Medical Practice Risk Assessment, Inc., Ann Arbor, MI; Clinical Professor, Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor, MI; President, American Physicians Assurance Society, Ltd., Bridgetown, Barbados, West Indies; Past President, ACEP. Jerome R. Hoffman, MA, MD, FACEP, Professor of Medicine/ Upon completing this article, you should be able to: 1. explain important aspects of the history and physical exam in males with genitourinary complaints (excluding problems associated with urinary tract infections and kidney stones); 2. list the indications, advantages, and limitations of imaging studies in patients with scrotal complaints and know which patients need immediate operation; 3. discuss evidence-based methods to evaluate the acute scrotum; and 4. describe treatment regimens for common genitourinary complaints, as well as management of more obscure conditions. Date of original release: November 1, 2000. Date of most recent review: October 31, 2000. See “Physician CME Information” on back page. Emergency Medicine, UCLA School of Medicine; Attending Physician, UCLA Emergency Medicine Center; Co-Director, The Doctoring Program, UCLA School of Medicine, Los Angeles, CA. John A. Marx, MD, Chair and Chief, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC; Clinical Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC. Michael S. Radeos, MD, FACEP, Attending Physician in Emergency Medicine, Lincoln Hospital, Bronx, NY; Research Fellow in Emergency Medicine, Massachusetts General Hospital, Boston, MA; Research Fellow in Respiratory Epidemiology, Channing Lab, Boston, MA. Steven G. Rothrock, MD, FACEP, FAAP, Associate Professor of Emergency Medicine, University of Florida; Orlando Regional Medical Center; Medical Director of Orange County Emergency Medical Service, Orlando, FL. Alfred Sacchetti, MD, FACEP, Research Director, Our Lady of Lourdes Medical Center, Camden, NJ; Assistant Clinical Professor of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA. Corey M. Slovis, MD, FACP, FACEP, Department of Emergency Medicine, Vanderbilt University Hospital, Nashville, TN. Mark Smith, MD, Chairman, Department of Emergency Medicine, Washington Hospital Center, Washington, DC. Thomas E. Terndrup, MD, Professor and Chair, Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL. Epidemiology ines, antihypertensives, anticoagulants, and sildenafil (Viagra).8 Other drug-related causes include inter-cavernosal injections for impotence (papaverine, phentolamine, or prostaglandin E) and drugs of abuse such as alcohol, cocaine, and marijuana.9 Determine whether there is a personal or family history of sickle cell disease or thalassemia. (See Table 1.) Priapism occurs in two age peaks. The first is between ages 5 and 10 years and the second between ages 20 and 50 years. Priapism in children most often results from sickle cell disease—a low-flow state.6 Other causes of priapism in children include leukemias, lymphomas, pelvic tumors, and trauma. In adults, most cases are caused by sickle cell disease, drugs, or are idiopathic.6,7 Physical Examination History When examining the penis, palpate the glans to ascertain whether it is hard or soft. Patients with low-flow priapism usually have a rigid, painful penile shaft with a soft glans. This is because the corpora cavernosa are erect but the corpora spongiosum remains flaccid.10 In patients with highflow priapism, the entire penis is partially rigid and painless; the glans is hard.1 If there is a history of trauma, listen to the penis for a bruit. (Let the patient know this is an accepted medical procedure.) The remainder of the physical exam should focus on a search for precipitating conditions. The history should include the length of time the symptoms have been present, any associated pain, any specific symptoms related to malignancy or hemoglobinopathy, a history of trauma, and any recent medication use. Specific medications associated with priapism include phenothiaz- Table 1. Common Etiologies Of Priapism. Prescription Drugs Psychotropics Antihypertensives Anticoagulants Intra-cavernosal injections Sildenafil (Viagra) Laboratory Evaluation The utility of laboratory studies in the evaluation of priapism remains unknown. Some authorities recommend a complete blood count, a coagulation profile, and possibly Illicit Drugs screening for sickle cell if the patient’s hemoglobinopathy Ethanol status is unknown. A toxicologic screen may be helpful if Cocaine Marijuana the emergency physician suspects drug ingestion, especially in a child. In some centers, gas analysis of aspirated Hematologic intracorporal blood is used to help differentiate low-flow Sickle cell disease (most common etiology in most EDs) from high-flow priapism. A urologist typically aspirates the Leukemia Thalassemia corpus for blood, but the emergency physician can accomplish the procedure if no urologists are available. Prior to Miscellaneous performing corporal aspiration, a dorsal penile nerve block Spinal cord injury is helpful. A dorsal nerve block is easily accomplished by Sources: Mulhall JP, Honig SC. Priapism: etiology and management. injecting 1% lidocaine without epinephrine into the dorsal Acad Emerg Med 1996;3:810; Sur RL, Kane CJ. Sildenafil citrateaspect of the penile base (See Figure 1). Five to 10 cc of the associated priapism. Urology Online 2000;55(6):950. lidocaine is deposited in a subcutaneous ring taking care to Figure 1. Penile Anatomy. avoid intravascular injection. After this is completed, the physician stands to the right of the patient and grasps the penis with the left hand. Palpate the engorged corpora cavernosum bilaterally and, after preparing the skin with Betadine, insert a 21- to 19-gauge butterfly needle into either side at the 10 o’clock or 2 o’clock position. The needle may be placed anywhere from the base of the penis to the distal shaft, avoiding the glans. Avoid deep penetration to minimize risk of injury to the cavernosal artery. Aspirate 20-30 mL of blood while milking the corpus with the other hand. Continue Reproduced with permission: Snell R, Smith M. Emergency Medicine. St. Louis: Mosby; 1993:480. Figure 12-17. aspiration until the egress of dark Emergency Medicine Practice 2 November 2000 Physical Examination blood ceases and bright-red arterial blood is obtained.11 Low-flow priapism is suggested by aspirated blood with a pH of < 7.25, pO2 < 30 mmHg, and pCO2 > 60 mmHg.2 When the foreskin is retracted, the glans and prepuce appear purulent, excoriated, and malodorous. These structures will be tender to palpation. The most common physical findings include redness, swelling, and discharge.16 Balanitis is commonly associated with a partially or completely nonretractable foreskin, but true phimosis (inability to retract the foreskin behind the glans) is usually not present (unless the infection is recurrent). Certain findings may suggest the causative organism. Candidal balanitis will often follow intercourse with an infected partner and manifests as a glazed discharge with satellite pustules.14 Balanitis due to trichomonas may be either superficial or erosive, and trichomonads are usually visible on wet prep. The presence of a thin, purulent discharge within the preputial-glandular sulcus without a true urethral discharge may indicate a streptococcal infection. Other signs of streptococcal disease include pain and significant surrounding erythema. Radiologic Evaluation History and physical examination alone should distinguish between high-flow and low-flow priapism in the vast majority of cases. Occasionally, Doppler ultrasound can also help differentiate between these states. Identification of an arterial-to-cavernosal shunt or of high systolic flow into the cavernosal artery is suggestive of high-flow priapism.1 Treatment The management of priapism varies somewhat, depending on the cause. However, all patients with priapism can be initially treated with terbutaline 0.25-0.5 mg subcutaneously in the deltoid muscle or terbutaline 5 mg PO.9,11 For patients with lowflow priapism likely due to sickle cell disease, several supportive measures are indicated. Analgesia, hydration, oxygen (and occasionally erythrocyte exchange transfusion) are successful in as many as 80% of patients.12 If simple interventions fail, corporal aspiration and injection of a vasoconstrictor are occasionally successful in sickle cell patients.1 The management of low-flow idiopathic priapism includes corporal blood aspiration, as previously described, followed by corporal injection of 200 mcg of phenylephrine (dilute 1 mg of phenylephrine in 9 mL sterile water to achieve a concentration of 1000 100 mcg/mL). If the history and clinical evaluation suggest high-flow priapism, emergent treatment is unnecessary because the risk of permanent sequelae is low.1 Injection of phenylephrine is contraindicated in high-flow priapism because the drug will rapidly leak into the systemic circulation, causing severe hypertension.13 If clinical suspicion is high that priapism is due to malignancy, treatment is usually supportive, but corporal aspiration and injection may be attempted.1 All cases of priapism should be treated in consultation with a urologist, as failure of conservative measures will require more invasive procedures. It may be legally prudent to tell the patient (and document this discussion in the chart) that permanent impotence is a possible consequence of priapism. Diagnosis And Treatment Balanitis or balanoposthitis that appears to have a nonspecific etiology is treated with mild soap, adequate drying, and 0.5% hydrocortisone cream. Prescribe an antifungal cream if candidal infection is suspected. As streptococcal infections may be indistinguishable from nonspecific balanitis, consider a rapid antigen detection test, culture, or empiric therapy. If culturing is deemed necessary, use the secretions or moist surface of the prepuce or glans. An oral penicillin or first-generation cephalosporin is indicated for a streptococcal or other bacterial superinfection. Anaerobic bacteria may produce irritant enzymes that lead to recurrent irritation balanoposthitis. In this case, a short course of a macrolide or penicillin should kill the offending microbe.15 Penile Entrapment Injuries Penile Zipper Entrapment There are two types of zipper entrapment.17 The first is when the zipper has moved past the site of entrapment, catching the skin between the teeth. This is the least common type and is most easily treated by cutting the zipper below the point of entrapment. The second type—the most common—is when the skin is caught in the moveable zipper. This is where precise manipulation is most appreciated by the patient. Tugging at the zipper will only result in tighter entrapment, so choose another approach. One method involves holding the zip teeth at the point of entrapment and applying steady lateral, then inferior traction, in a peeling motion. This will disarticulate the penile skin as the zipper moves inferiorly. This maneuver is facilitated with application of lubricant or mineral oil. While the procedure is usually painless,15 a local anesthetic is a reasonable precaution. If traction fails, the zipper mechanism must be cut apart. The most common way to accomplish this is by cutting the median bar between the faceplates of the zipper with bone cutters.18 An additional method was recently Balanitis And Balanoposthitis Balanitis is an inflammation of the glans, while posthitis is an inflammation of the foreskin. Balanoposthitis refers to the presence of both conditions.14 Etiology And Pathogenesis The etiology of balanitis includes irritation by smegma, urine, friction, trauma, or soaps/detergents. Poor foreskin hygiene and exposure to sexually transmitted organisms are also implicated. Responsible pathogens include various bacteria, yeasts, and fuso-spiral organisms. These commensals become aggressive when there is lowered focal or general host resistance. Chlamydia and mycoplasma can also cause balanoposthitis.14 Recurrent balanitis can be the sole presenting sign of diabetes.11 In children, most cases are nonspecific, usually caused by inadequate hygiene of the genitalia.15 November 2000 3 Emergency Medicine Practice the edematous foreskin distally over the glans. Paraphimosis is a true urologic emergency, because edema and venous engorgement can progress to arterial compromise and gangrene of the glans. The least invasive procedure for paraphimosis reduction does not involve surgical steel. First, snugly wrap the distal penis with an elastic bandage for about 10 minutes to reduce edema. Remove the bandage, and then apply a topical anesthetic lubricant to the inner surface of the foreskin. Grasp the penis with the right hand while using the thumb of the other hand to push the glans through the foreskin, using slow, steady pressure.9 Alternatively, place both thumbs on the meatus and stuff the glans under the foreskin. If arterial compromise is suspected and manual reduction isn’t successful, perform a dorsal slit procedure.11 The procedure begins by injecting plain 1% lidocaine into the dorsal midline of the foreskin just beneath the superficial fascia. (See Figure 2 on page 5.) If adequate anesthesia is not obtained, infiltrate subcutaneous lidocaine (without epinephrine) circumferentially at the base of the penis (“ring” block). This will provide profound distal anesthesia.9 Then use a hemostat to separate any adhesions between the foreskin and the glans. While visualizing the urethral meatus, use the hemostat to crush the anesthetized foreskin. (See Figure 3 on page 5.) Leave the hemostat in place for about five minutes. Remove the hemostat and cut the crushed foreskin with a pair of straight scissors. When the edges of the foreskin separate, each edge can be sutured with absorbable running sutures to maintain hemostasis. Be sure to replace the foreskin to its normal position after the procedure to avoid iatrogenic paraphimosis.9 Once reduction is complete, ensure that the patient can urinate. If not, place a Foley catheter and have the patient follow up with a urologist. described in a child whose foreskin had been caught in a zipper for four days. The swelling was such that the median bar was embedded deeper than the bone cutter could reach. A hemostat was used to stabilize the zipper unit at the handle base while a mini-hacksaw was used to saw through the median bar between the inside and outside faceplates and release the zipper.19 (Despite the ingenuity of this method, consider blindfolding the patient before approaching his penis with a hacksaw.) After removal of the zipper, ensure that the urethra has not been injured and the patient can urinate without difficulty. If so, local wound care is usually all that is required. Follow-up with a urologist is recommended. On occasion, patients presenting with a penile lesion may state, “I think I might have caught my penis in my zipper.” Rest assured that this history is unreliable and the lesion represents a genital ulcer associated with an STD. Catching one’s penis in a zipper is always a certainty— never a hypothesis. Other Entrapment Injuries Other penile entrapment injuries besides zipper entrapment occur when various objects are wrapped around the penis, such as hairs in children. Hair removal creams may be useful if the hair tourniquet is deeply embedded in the penis due to surrounding edema. Urethral integrity and distal arterial integrity should be evaluated when indicated. As in the case of hematuria or persistent cyanosis of the glans, evaluate the urethra with a retrograde urethrogram. Either color-flow Doppler or arteriogram can assess arterial flow.11 If a patient presents with a markedly ecchymotic penis and no explanatory history, he may be too embarrassed to admit to a vacuum-cleaner injury. These injuries are relatively benign, unless the fan blades in the machine slice the penis. The Acute Scrotum: Ruling Out Testicular Torsion Urethral Stricture If the patient’s bladder cannot be cannulated with a 14F or 16F Foley or Coudé catheter, consider urethral stricture, external sphincter spasm, bladder neck contracture, or benign prostatic hypertrophy. Voluntary external sphincter spasm can be overcome by holding the patient’s penis upright and encouraging him to relax his anus and breathe slowly during catheter placement.11 Sometimes a larger, rather than smaller, catheter will provide the added rigidity needed for passage. Liberal use of xylocaine jelly instilled in the urethra 15 minutes before attempting the procedure is helpful. Care should be taken not to apply too much force while placing the catheter, as this could create a false passage. If multiple attempts at catheter placement are unsuccessful, obtain a urology consultation. “Time is testicle.” Overview When a male of any age presents with acute scrotal pain, the first condition the clinician should rule out is testicular torsion. Just as time is myocardium, time is also testicle. Delays associated with diagnostic testing can lead to the very condition you hope to prevent—loss of the testicle. Anatomy The testis normally descends through the inguinal ring and into the scrotum between the 28th week of gestation and birth. The testis drops within an outpouching of the peritoneum, the processus vaginalis, and is suspended by the spermatic cord, which supplies its blood. The processus vaginalis covers the testis and epididymis and fixes them to the posterior scrotal wall. The communication of the processus vaginalis with the peritoneum usually obliterates by the second year of life.20,21 Normally, there is a strong attachment between the testis and epididymis, which is in Phimosis And Paraphimosis Phimosis is the inability to retract the foreskin proximally. Phimosis typically isn’t an emergency unless urinary retention is present. Paraphimosis is the inability to reduce Emergency Medicine Practice 4 November 2000 pre-pubertal age group. Testicular torsion was the most common diagnosis in the pubertal child and adult.28,29 (See Table 2 on page 6.) turn connected to the posterior scrotal wall. This prevents the free rotation of the testis.22 In the so-called “bell-clapper” deformity, the epididymis and the testis become completely surrounded by the processus vaginalis instead of being anchored to the scrotal wall. This allows the testis and epididymis to hang freely within the scrotum, allowing the spermatic cord to twist.23 Autopsy studies show that 10% of the population has an abnormal testicular attachment, although the rate of testicular torsion is much lower.24 The triggering event for torsion is unclear. It is often thought to be due to a forceful contraction of the cremasteric muscle secondary to trauma, physical exertion, an erection, or exposure to an abrupt drop in temperature.22 (See Figure 4 on page 6.) History No single element of the history can reliably distinguish testicular torsion.30 Important historical points to obtain include rapidity of onset and duration of pain, history of previous similar episodes, presence of nausea and vomiting, anorexia, fever, association with erections, urethral discharge, recent urethral instrumentation, voiding symptoms, and recent trauma.30-33 The history should also focus on past genitourinary problems and sexual activity. A prior history of testicular torsion and subsequent orchiopexy doesn’t rule out recurrent torsion, especially if absorbable sutures were used.34,35 Both children and adults may complain only of abdominal pain or minimize their symptoms out of fear or embarrassment. A recent study examined the incidence of various symptoms in 543 patients with an acute scrotum, all of whom had operative confirmation of their diagnosis. Sudden onset of pain was seen in 90% of patients with testicular torsion, in 69% of patients with appendix torsion, in 58% of patients with epididymitis, and in 78% of patients with normal scrotums. Fever was present in 10% of cases of testicular torsion, in 4% of cases of appendix torsion, in 32% of patients with epididymitis, and in 10% of normal patients.36 Nausea, vomiting, and anorexia are fairly specific for testicular torsion; up to 80% of patients with torsion Appendix Testis The testicular appendages are equivalent to the intestinal appendix (and some say hospital administrators) in that they serve no useful purpose and cause pain at random. The appendix testis is a Mullerian duct remnant that is attached to the superior pole of the testicle and rests in the groove between the testis and epididymis. The appendix epididymis is a Wolffian duct remnant that is attached to the head of the epididymis.25 (See Figure 5 on page 6.) Epidemiology The annual incidence of testicular torsion in males under age 25 is estimated to be 1 in 4000. Torsion occurs in every decade of life, from birth to 78 years.26,27 The reported peak incidence is bimodal; the first peak is in the neonate within the first few days of life, and the second peak is in puberty between 12 and 18 years of age.22 Several recent studies show that the incidence of torsion varies by age.28,29 In two studies in which a total of 480 patients with an acute scrotum were surgically evaluated, torsion of a testicular appendage predominated as the cause of scrotal pain in the Figure 3. Treatment Of Phimosis: Crushing the foreskin in preparation for a dorsal slit procedure. Note: The “inside” blade of the hemostat is between the foreskin and the glans, not in the urethra. Figure 2. Anesthesia For Dorsal Slit Procedure. Foreskin “tented up” at coronal sulcus Reproduced with permission of The McGraw-Hill Companies from: Tintinalli JE, Ruiz E, Krome RL, eds. Emergency Medicine: A Comprehensive Study Guide, 5th ed. New York: McGraw-Hill; 2000:881. Figure 73-16. November 2000 Reproduced with permission of The McGraw-Hill Companies from: Tintinalli JE, Ruiz E, Krome RL, eds. Emergency Medicine: A Comprehensive Study Guide, 5th ed. New York: McGraw-Hill; 2000:882. Figure 73-18. 5 Emergency Medicine Practice Start with a visual inspection of the scrotum and penis. Note any scrotal swelling or erythema. Inspect the penis for urethral discharge or rash. The length of the penis may need to be milked to express a discharge. Examine the femoral area for lymphadenopathy.22 The physical exam should include examination of the abdomen and, some believe, the rectum. Assess the cremasteric reflex on each side. The reflex is elicited by gently stroking the inner thigh (a tongue blade is useful) and observing for more than 0.5 cm elevation of the ipsilateral testis.42 Of all physical exam findings, the presence of the cremasteric reflex appears to be one of the most helpful in ruling out torsion. A recent study of 543 patients with an acute scrotum found that the presence of the reflex had a 96% negative predictive value for testicular torsion. The false positives occurred in three infants in report these symptoms. In fact, torsion is occasionally misdiagnosed as gastroenteritis. On the other hand, gastrointestinal complaints are uncommon in epididymitis and appendix torsion.30,31,33 Be wary of a history of trauma or physical exertion prior to the onset of symptoms, as this red herring is present in 10%-20% of those with torsion.30,31,33,37-40 A prior history of similar pain does not rule out torsion. Some patients will spontaneously torse and detorse several times in the weeks or months prior to an ED visit. Nearly half of all adults with surgically proven torsion have had similar episodes in the past.41 Physical Examination The exam should proceed in a manner that respects the patient’s privacy. This is especially important in children. Figure 4. Bell-Clapper Deformity. Figure 5. Torsion Of The Testis vs. Torsion Of The Appendix Testis. Reproduced with permission of The McGraw-Hill Companies from: Knoop KJ, Stack LB, Storm AB, eds. Atlas of Emergency Medicine. New York: McGraw-Hill; 1997:211. Figure 8.2. Reproduced with permission of The McGraw-Hill Companies from: Tintinalli JE, Ruiz E, Krome RL, eds. Emergency Medicine: A Comprehensive Study Guide, 4th ed. New York: McGraw-Hill; 1996:536. Figure 92-7. Table 2. Age Distribution Of Common Causes Of Acute Scrotum Found At Exploration. Source: Watkin NA, Reiger NA, Moisey CU. Is the conservative management of the acute scrotum justified on clinical grounds? Br J Urol 1996;78:623-627. (Retrospective; 209 patients) Age 0-11 years Age 12-16 years Age 17-40 years Testicular Torsion 6.6% 52% 48% Appendix Torsion 62% 32% 5% Epididymitis 6% 3% 27% Source: Ben-Chaim J, Leibovitch I, Ramon J, et al. Etiology of acute scrotum at surgical exploration in children, adolescents and adults. Eur Urol 1992;21:45-47. (Prospective; 171 patients) Age 0-12 years Age 13-21 years Age 22-52 years Testicular Torsion 34% 86% 88% Emergency Medicine Practice Appendix Torsion 47% 9% 6% 6 Normal 11% 5% 6% Epididymitis 4% 0% 0% November 2000 urine.30,33 If infection is suspected, obtain a urine culture. As with most serious emergencies, a white blood cell count is not helpful and is likely to confuse. Leukocytosis (WBC > 10,000/HPF) is seen in torsion as well as epididymitis.29,36 whom the reflex was present, but who were found to have torsion at time of operation, although the testis was not ischemic.36 However, note that the presence of a cremasteric reflex does not always exclude torsion. Palpate the testicle and scrotal contents for localized tenderness and masses. Have the patient stand to note how the testicle lies in the scrotum. The normal testis rests in the vertical axis with the superior pole tipped slightly forward. The epididymis is located above the superior pole in the posterolateral position. (See Table 3.) Prehn reported that elevating the scrotum aggravated torsion of the spermatic cord but relieved the pain of epididymitis. However, “Prehn’s sign” (as this is known) has been found to be extremely unreliable and should not be used— even patients with torsion can feel some relief of pain with this maneuver.27 Most patients with advanced torsion have a diffusely tender and swollen testicle. In contrast, in epididymitis, the tenderness is usually localized to the epididymis at the lower pole of the testis. The operative words here are “most” and “usually.” Up to 10% of patients with testicular torsion have tenderness localized to the epididymis.30 This probably represents inflammation of the twisted spermatic cord. After several hours, torsion usually results in significant scrotal edema and makes palpation of the scrotal contents and determination of how the testicles lie difficult or impossible. Torsion of a testicular appendage will often result in a palpable tender nodule in the testicle near the epididymis. The “blue-dot” sign, which represents an ischemic, torsed testicular appendage, is sometimes visualized through the scrotal skin.43 This finding is difficult to see even through the translucent scrotum of the prepubescent boy, and it is nearly impossible to visualize when the scrotum becomes dark and thickened at puberty. Radiologic Imaging: “Castration Through Procrastination?” Any patient who presents with a classic case of testicular torsion should never see the inside of a radiologic suite. Call the urologist and tell him he has a patient who needs an operation. Radiologic confirmation can be dangerous in a patient with torsion. If a testis can survive for a maximum of 6-10 hours after becoming ischemic, why squander time on a test that may ensure testicular death secondary to surgical delay? How long does it take between the time you order a testicular imaging study until the radiologist will call you with the result? Could this interval damn the testis? This danger associated with diagnostic imaging has been termed “castration through procrastination.”44 Because of the false-negative rate associated with imaging studies and the frequency of torsion in adolescents, some children’s centers suggest immediate surgical exploration for presumed testicular torsion. In one study, radioisotope scanning and Doppler ultrasound were only 86% and 80% sensitive, respectively.32 Torsion is especially likely if the child is 11 years or older, the duration of symptoms is less than 12 hours, and the child has nausea and vomiting.31 This said, some patients with a painful testis present with equivocal history and physical findings. Such patients may require an imaging study. The available tests include nuclear scintigraphy and Doppler ultrasonography. The available literature on this topic is crippled by a very important bias in study design. No large, well-designed study has prospectively performed diagnostic imaging followed by surgical confirmation regardless of the imaging result. Nuclear scintigraphy assesses testicular blood flow by detecting the accumulation of the intravenously administered technetium in the testis. In torsion, little or no isotope collects in the testis. The sensitivity varies from 80%-100%, with an overall accuracy of 95%. Nuclear scintigraphy is rarely available on an immediate basis. The test is timeconsuming, as the radioisotope must be prepared, and the study itself requires at least 20-30 minutes to perform.45-48 Because it provides no anatomic information, scintigraphy cannot differentiate between epididymitis and appendiceal torsion. It is also unable to detect cases in which intermittent torsion or spontaneous detorsion has occurred.22 As a final consideration, some men require convincing that radioactive testicles won’t prune the family tree. Doppler ultrasound has replaced nuclear imaging in many institutions. Color-flow Doppler can detect decreased intratesticular blood flow. It is very sensitive for detecting increased blood flow associated with scrotal inflammation secondary to epididymitis or appendix torsion. However, the sensitivity for torsion ranges from 83%-100%.47,49-51 It appears to be accurate even in those patients who have Laboratory Evaluation Testicular torsion is a clinical, and occasionally radiographic, diagnosis. Do not rely on laboratory tests to either confirm or exclude the diagnosis. If urethral discharge is present, test the patient for chlamydia and gonorrhea. Urinalysis is a reasonable test as long as no decisions are made based on the results. Patients with torsion may have pyuria, and half of all patients with epididymitis have no leukocytes in their Table 3. Physical Findings Strongly Suggestive Of Testicular Torsion. • Abnormal elevation of the affected testicle with shortening of the spermatic cord • Abnormal axis of the affected testicle when the patient is upright (i.e., horizontal lie) • Abnormal position of the epididymis (i.e., anterior rather than posterior) • Abnormal axis of the contralateral testis • Absence of cremasteric reflex (note that presence of cremasteric reflex does not rule out torsion) Adapted from: Knight PJ, Vassy LE. The diagnosis and treatment of acute scrotum in children and adolescents. Ann Surg 1984;200:64. November 2000 7 Emergency Medicine Practice equivocal clinical findings.52 Color-flow Doppler is less specific in small children and especially neonates as it cannot detect blood flow in a testis smaller than 1 mL volume. In neonates, up to 40% of normal testes will show no blood flow.53-55 A recent study compared Doppler ultrasound with scintigraphy in patients with an acute scrotum who presented with equivocal findings. In boys, the two modalities were equally sensitive for torsion but scintigraphy was more specific.52 However, ultrasound has the advantages of being more readily available in most institutions, does not involve ionizing radiation, and, in addition, Doppler can provide anatomic information. The biggest pitfall of either study is the possible delay in scrotal exploration associated with the diagnostic test. In addition, the occasional false-negative study can ensure testicular loss. Doppler ultrasound may demonstrate little or no blood flow in an asymptomatic testis in young children because of the normal “low-flow” state. Furthermore, ultrasound has a higher rate of indeterminate studies when compared to scintigraphy. Both modalities are limited in their ability to detect spontaneous detorsion and intermittent torsion.56 To begin the detorsion attempt, explain to the patient that while local anesthesia of the spermatic cord can reduce the pain of detorsion, it also removes the allimportant endpoint of pain relief. Procedural sedation using a narcotic (possibly combined with a benzodiazepine) may be appropriate. Detorsion is done in a manner similar to opening a book. This means twisting the testicles outward, toward the patient’s thighs. Stand facing the patient and rotate the patient’s right testis in a counterclockwise fashion (from a perspective of looking upward from below the scrotum) or their left testis in a clockwise manner. Relief of pain accompanies successful detorsion. The spermatic cord should lengthen and the testis will develop a more normal lie. Worsening of the pain (and shortening of the cord) indicates that detorsion should be done in the opposite direction. Successful manual detorsion does not preclude an urgent scrotal exploration, as retorsion may occur at any time.11 Most studies report a high viability of the testis—70%100%—if detorsion is achieved within 10 hours. Beyond 10 hours, the salvage rate drops to 20%.59,60 However, there have been reports of testicular salvage after several days of torsion, although the twisting was not as severe61-63 or may have been intermittent. Treatment And Prognosis Of Testicular Torsion The Acute Scrotum: Differential Diagnosis Pitfalls Once torsion is strongly suspected, either clinically or radiographically, call the urologist—quickly. While awaiting his or her arrival, consider manual detorsion. There is no large study that demonstrates which is the best way to untwist the spermatic cord. Manual detorsion is successful in approximately 25% of patients, and counterclockwise twisting seems to be more common.23 Once the physician has ruled out testicular torsion as the cause of acute scrotal pain, a variety of conditions may be considered. (See Table 4.) Epididymitis Epididymitis is fully discussed in a subsequent section. Table 4. Differential Diagnosis Of The Acute Scrotum. Testicular Torsion Epididymitis Appendix Torsion Age >12 years >18 years 0-11 years Onset Acute Gradual more often than acute Acute or gradual Previous similar pain Common Uncommon Occasional Nausea/vomiting Common Uncommon Uncommon Discharge or urinary symptoms Rare Common Rare Fever Uncommon Common Rare Testicular position Abnormal axis Normal Abnormal elevation Contralateral testis abnormal Palpable nodule Blue-dot sign in some patients Tenderness Diffuse Local, then diffuse Local, then diffuse Cremasteric reflex Usually absent Usually present Usually present Pyuria Uncommon Common Uncommon Leukocytosis Common Common Uncommon Perfusion studies Decreased flow Normal or increased flow Normal or increased flow Adapted from: Haynes BE, Beesen HA, Haynes VE. The diagnosis and management of acute scrotal conditions in boys. JAMA 1983;249:2522; Burgher SW. Acute scrotal pain. Emerg Med Clin North Am 1998;16(4):781-809. Emergency Medicine Practice 8 November 2000 Appendix Torsion on physical examination. The appendix testis is the appendage most frequently involved in torsion.27 Pain can begin either suddenly or gradually and ranges from mild to severe. Nausea and vomiting are seldom present. On exam, the “blue-dot” sign is pathognomonic, but it is seen in only 26% of cases.26 Scrotal enlargement is often present due to edema and inflammation. The diagnosis should be confirmed with an imaging study, which should demonstrate normal or increased testicular blood flow. The treatment is supportive; the patient will require pain medications and scrotal support.27 Most torsed appendages will calcify or degenerate in 10-14 days;11 however, some urologists believe that surgery is indicated to resolve the pain. Fournier’s Gangrene A full discussion of this condition follows in a subsequent section. Orchitis Isolated orchitis, or testicular inflammation, is vanishingly rare. It usually occurs in conjunction with other systemic illnesses, such as mumps, various viral illnesses, or syphilis. It is most often seen as an extension of epididymitis (epididymo-orchitis). Orchitis usually presents as bilateral testicular tenderness and swelling of a few days’ duration. Treatment is symptomatic and disease-specific.11 Hernia Epididymitis The presentation of a scrotal hernia will depend upon whether the hernia is reducible, incarcerated, or strangulated. In a strangulated hernia, the patient will give a history consistent with intestinal obstruction. The scrotal contents may be tender, and in the case of advanced pathology, peritoneal signs may be present. In scrotal hernias, there will be inguinal as well as scrotal swelling. A normal testis can usually be palpated below the hernia. Epididymitis is an inflammation of the epididymis that is usually due to infection (most often bacterial). It can also result from sterile urine, which refluxes via the ejaculatory ducts down the vas into the globus minor of the epididymis.64 It is predominately a disease of adult men and is rare in boys and young adolescents. In prepubertal boys, epididymitis is almost always associated with a urinary tract anomaly.65 Idiopathic Scrotal Edema This entity is usually seen in prepubertal males. It presents as erythema and sudden onset of unilateral or bilateral scrotal edema with little or no pain. The patient is afebrile and non-toxic, and the testis and epididymis are non-tender and of normal size. No blood or urine tests are necessary. The condition usually resolves in 2-5 days without therapy,27 although some physicians prescribe H1 and/or H2 blockers in hopes of accelerating resolution. Pathophysiology The etiologic agent responsible for epididymitis is related to age and sexual activity/practices.66,67 In boys, homosexual young men, and men over the age of 35 years, the most common organisms are coliforms, Pseudomonas, and Grampositive cocci.27 The most common organisms in heterosexual young men include Chlamydia trachomatis and Neisseria gonorrhoeae.27 The usual route of infection involves direct extension to the epididymis via the vas deferens.68 Normally, a oneway valve protects the epididymis from urine reflux. Many lower urinary tract anomalies predispose to bacterial invasion of the vas deferens by urinary pathogens. Conditions that lead to epididymitis include prostatic hypertrophy, prostatectomy, urethral stricture, recent urinary tract surgery, or instrumentation. Urinary tract pathology or procedures do not seem to cause epididymitis associated with sexually transmitted diseases.27 Congenital bladder and urethral defects are important considerations in children.65,66,69 Testicular Tumor Acute pain involving a mass is thought to be due to hemorrhage within the tumor. The testis is enlarged, irregular, and tender. A reactive hydrocele is sometimes present.27 Color-flow Doppler is the best means to diagnose this condition. Henoch-Schonlein Purpura Henoch-Schonlein purpura (HSP) is an idiopathic systemic vasculitis characterized by nonthrombocytopenic purpura with skin, joint, and renal involvement. The petechial rash is especially prominent over the buttocks and lower extremities. This is a pediatric disease that usually presents in patients 4-5 years of age. Genitourinary findings include acutely painful scrotal swelling. The scrotum is involved in 2%-38% of cases of HSP but is very rarely the initial presentation.57,58 History Pain usually develops over many hours to days but may be sudden in onset. While the pain associated with epididymitis is usually unilateral, it may present on both sides. Fever occurs in a substantial minority of patients.22 Irritative voiding symptoms are frequent, but nausea, vomiting, and anorexia are rare. Peritonitis Or Intra-abdominal Hemorrhage This is a very rare cause of scrotal pain, but it can be seen in a patient with a patent processus vaginalis. It can occur with appendicitis. Consider ruptured abdominal aortic aneurysm in the differential diagnosis in the older patient. The scrotum and scrotal contents appear normal and non-tender November 2000 Physical Exam Early in the course of the illness, tenderness is localized to Continued on page 12 9 Emergency Medicine Practice Clinical Pathway: Diagnosis And Treatment Of Priapism → History and physical exam Probable high-flow priapism? (Hard glans, history of perineal trauma, penile bruit) Yes → → No Urology consultation (urologist may request corporal blood aspiration and/or penile Doppler) (Class IIa) Probable low-flow priapism → Idiopathic or drug-related → → Neoplastic process → • Corporal blood aspiration after urology consultation (Class IIb) → → Failure Terbutaline 0.25 mg SC; may repeat once (Class IIb) → → • Urology consultation (Class IIa) • Consider terbutaline (see terbutaline pathway) → Sickle cell disease or thalassemia Success • Analgesia (Class IIa) • Terbutaline (see terbutaline pathway) (Class IIb) • Oxygen for sickle cell (Class indeterminate) • Hydration (Class IIb) • Urology consultation (Class IIa) • Admission if persistent priapism (Class IIa) • Telephone urology consultation (Class IIb) • Probable discharge (Class IIb) → • Finalize disposition with urologist (Class IIa) Failure • Finalize disposition with urologist (admit) (Class IIa) → → No Intracorporal injection of phenylephrine 200 mcg; may repeat twice (Class IIb) → Are the results as follows? • pH < 7.25 Yes • pO2 < 30 mmHg → • pCO2 > 60 mmHg Success • Telephone urology consultation (Class IIa) • Probable discharge (Class IIb) The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended. Definitive, excellent evidence provides support. Class IIa: Acceptable and useful. Very good evidence provides support. Class IIb: Acceptable and useful. Fair-to-good evidence provides support. Class III: Not acceptable, not useful, may be harmful. Indeterminate: Continuing area of research. This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care. Copyright 2000 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. Emergency Medicine Practice 10 November 2000 Clinical Pathway: Management Of The Acute Scrotum Are there any of the following? • Abnormal lie (Class IIa) • Absent cremasteric reflex (Class IIa) • Nausea or vomiting (Class IIb) • Tender testicle (Class IIb) Yes → → No Are there at least three of the following? • Gradual onset of symptoms • Dysuria, discharge, or instrumentation • History of genitourinary problems • Fever • Isolated tenderness of epididymis • Pyuria (See Table 5 on page 12) Yes → 1.Call the urologist and advise him or her that there is a patient who may need to go to the OR (see individual findings for Class of evidence) 2.Manual detorsion (Class indeterminate if the duration of symptoms is short and there will be no delay to surgery; Class IIa if symptoms have lasted for more than six hours or there will be a delay in scrotal exploration) 1.If urethral discharge, test for gonorrhea and chlamydia (Class IIb) 2.If prepubertal, consult urology (Class IIa) 3.If postpubertal, treat for epididymitis (a new-generation quinolone, such as ofloxacin or levofloxacin, for 10-14 days will cover nearly every clinical scenario regarding age and sexual practices) (Class IIa) → No Imaging study (If duration of symptoms plus anticipated time to test results is greater than 8-10 hours and torsion is a likely possibility, consult urology before obtaining study) (Class IIa) Equivocal study • Urology consultation (Class IIa) → → → Normal study • Treat for epididymitis or evaluate for other condition (Class IIa) • Urology follow-up (Class IIb) Decreased flow • Emergent urology consultation (Class I) • Consider manual detorsion (Class indeterminate if the duration of symptoms is short and there will be no delay to surgery; Class IIa if symptoms have lasted for more than six hours or there will be a delay in scrotal exploration) The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended. Definitive, excellent evidence provides support. Class IIa: Acceptable and useful. Very good evidence provides support. Class IIb: Acceptable and useful. Fair-to-good evidence provides support. Class III: Not acceptable, not useful, may be harmful. Indeterminate: Continuing area of research. This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care. Copyright 2000 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. November 2000 11 Emergency Medicine Practice Continued from page 9 group is characterized by pyuria, bacteriuria, and a positive culture. These patients should follow up with a urologist. Among the vast majority of males with epididymitis, infection is due to one of two main types of organisms—the coliforms and sexually transmitted diseases. Always suspect chlamydia in sexually active males, as up to one-third of patients will not have a urethral discharge.70 the epididymis. As the infection progresses, a reactive hydrocele may develop and the infection may spread to the testis, resulting in an epididymo-orchitis and generalized testicular tenderness.27 The cremasteric reflex is typically present. Most importantly, the testicular lie should be normal. While urethral discharge is common, it is not necessary to make the diagnosis. No single clinical finding will diagnose epididymitis to the exclusion of torsion, as many signs and symptoms overlap. Homosexual Or Sexually Inactive Males Both homosexuals and sexually inactive males should be presumed to have coliform epididymitis (assuming no urethral discharge is present). In the adult, or teenagers older 17 years, current recommendations include a fluoroquinolone such as ciprofloxacin 500 mg PO BID or ofloxacin 200 mg PO BID for 10-14 days.71 Children or teens younger than 17 years with presumed bacterial disease (secondary to infected urine) may benefit from sulfamethoxazole/trimethoprim or amoxicillin clavulanate, as quinolones are contraindicated in this age group. Laboratory Evaluation If patients have a urethral discharge, test for chlamydia and gonorrhea. If the patient does not report or have a discharge, milk the length of the urethra to express the thin discharge of a chlamydia infection. For patients without a discharge, collect a midstream urine sample and evaluate it for pyuria (≥10 WBC/HPF) and bacteriuria (≥1 Gram-negative rods [GNR]/HPF). These findings, in the appropriate clinical setting, provide evidence for coliform epididymitis.27 Because children have less of an inflammatory response, pyuria in this age group is defined as 3 WBC/HPF or greater.22 Knight and Vassy reviewed the charts of 395 boys 30 days to 17 years old to identify findings suggestive of acute epididymitis. (See Table 5.) In their study, the presence of any three out of six findings was specific for epididymitis. However, a few cases of testicular torsion presented with two findings. While it may help exclude torsion, requiring three findings to make the diagnosis of epididymitis significantly reduces sensitivity. Only about one-third of the patients with this final diagnosis presented with at least three criteria.27,30 Heterosexual Males Younger Than 35 Sexually active males who have epididymitis and present with a urethral discharge should be treated for a sexually transmitted disease regardless of age. There are several accepted strategies, all of which address the likelihood of concomitant chlamydial and gonorrheal infections. Recommended regimens include single-dose ceftriaxone 250 mg IM plus doxycycline 100 mg PO BID for 10 days, or ofloxacin 300 mg PO BID alone for 10 days.71 Single-dose therapy with azithromycin and ofloxacin, while appropriate for simple urethritis, is inadequate in the treatment of epididymitis. Heterosexual Males 35 Or Older, Or Bisexual Males If a sexually active male engages in anal intercourse or is older than 35 years, he may have coliforms, chlamydia, gonorrhea, or some combination. In such cases, a 10-day course of a quinolone such as ofloxacin or levofloxacin will cover “all players.” Ciprofloxacin should not be used in such patients, as it has no activity against chlamydia.71 Treatment Since epididymitis is almost always infectious, antibiotics are generally indicated. One exception includes prepubertal boys, who for the most part have “sterile” epididymitis and do not require antibiotics.67,69 A minority of prepubertal boys will have bacterial epididymitis, usually associated with a urinary tract abnormality. Bacterial epididymitis in this age Supportive Measures Additional supportive measures are important and include oral analgesics, bedrest with scrotal elevation to aid in lymphatic drainage of the epididymis, and scrotal support when ambulatory. A combination of both nonsteroidals and narcotic analgesics may be necessary in those with significant pain. Scrotal elevation is best achieved with the use of a “scrotal bridge.” Instruct the patient to take a folded towel and place it across his upper thighs when he is lying flat. He can then place his aching testes on this bridge to find some relief. Indications for admission include toxic appearance, presence of immunosuppression, or, on occasion, severe bilateral epididymitis. Table 5. Knight-Vassy Criteria For The Diagnosis Of Acute Epididymitis In Children And Adolescents. Three of the following should be present: 1. Gradual onset of pain 2. Dysuria, urethral discharge, recent diagnostic cystoscopy, or indwelling Foley catheter 3. History of urinary tract infection, imperforate anus, an abnormality of bladder emptying, or a hypospadias repair 4. An admission temperature exceeding 101˚F (may indicate epididymo-orchitis or intratesticular abscess) 5. Tenderness and induration localized to the epididymis 6. ≥10 WBC/HPF or ≥10 RBC/HPF in the urinary sediment Fournier’s Gangrene Overview In 1883, Jean Alfred Fournier first described the condition that would later bear his name. Fournier’s gangrene (FG) is Source: Knight PJ, Vassy LE. The diagnosis and treatment of the acute scrotum in children and adolescents. Ann Surg 1984;200:664. Emergency Medicine Practice 12 November 2000 Diagnosis a rapidly progressing necrotizing fasciitis of the perineal, genital, or perianal regions.72 It was originally defined as idiopathic, but it is now known that gastrointestinal or genitourinary lesions play an important role in its development. While Fournier found the disease in young men, FG is not limited to particular age groups, or the male sex.73 An ill-appearing patient with a fever, scrotal pain, and gas in the perineum provides no diagnostic dilemma. The challenge is detecting an early case of FG in hopes of promoting a better outcome. Plain x-rays may or may not reveal soft-tissue air. The modality of choice for early diagnosis is either surgical consultation or, in unclear cases, scrotal ultrasound. Scrotal ultrasound usually reveals diffuse swelling and thickening of the scrotum. It may also detect gas within the scrotal wall.86,87 Computed tomography of the area is only useful to reveal the extent of the infection. Key differential considerations include scrotal cellulitis, scrotal abscess, and hernia. Epidemiology FG is an uncommon, but aggressive, disease. There have been approximately 400 cases reported in the literature in the post-antibiotic era,74,75 but there are no doubt many unreported cases as well. Two recent studies describe the demographics of FG patients. The average age was 54 (range, 20-82).74 Cases even occur in children younger than 3 months.76-78 The most frequent disorders associated with FG include diabetes (40%-60% of patients) and chronic alcoholism (25%-50% of patients).74,79-81 Treatment Once the diagnosis of FG becomes a realistic concern, call a surgeon. Begin aggressive resuscitation with IV fluids (and pressors) if necessary. Parenteral broad-spectrum antibiotics such as a third-generation cepalosporin (or extendedspectrum penicillin/beta-lactamase inhibitor) and an aminoglycoside will cover Gram-positive, Gram-negative, and anaerobic agents. Clindamycin may be useful, as it is effective against anaerobes and can inhibit toxin production.88 Antibiotics are only an adjunct to surgical debridement. After surgery, the patient may benefit from hyperbaric oxygen therapy. Etiology And Pathogenesis FG results when normal flora with low to moderate virulence gain entry into the skin. Colorectal or urogenital diseases provide the portal for most cases. (See Table 6.) The combination of immune suppression and synergistic organisms sparks an infectious conflagration.73 The infection begins near the portal of entry and progresses rapidly through the deep fascial planes. An obliterative endarteritis causes vascular thrombosis and tissue necrosis. This allows the commensal flora to enter previously sterile areas, progressively destroying tissue.73 FG is typically polymicrobial.79,82 Both aerobes and anaerobes are usually present, but the anaerobes are less frequently isolated, probably due to technical difficulties in culturing those organisms.83 The most commonly isolated species include the enterobacteria, especially E. coli, Bacteroides, and streptococcal species. Clostridium is the anaerobe most often identified.84 Prognosis Mortality in FG ranges widely, from 0%-80%.89 Factors that increase mortality include comorbid disease, extremes of age,83,90 primary anorectal infections,91,92 and delay in Table 6. Etiologies Of Fournier’s Gangrene. Colorectal sources Perirectal abscess Incarcerated inguinal hernia Hemorrhoid banding Rectal biopsy Clinical Presentation The most common presenting symptoms are scrotal pain, perineal erythema, and swelling, often associated with fever.84 The patient develops induration, cyanosis, and blistering of the skin as the infection deepens.85 Soft-tissue crepitus may be present. Patients are often critically ill at initial presentation. Even in the early stages, they may display systemic signs of sepsis, disproportionate to the appearance of the scrotal skin.73 The erythema, which is a notable early sign, may be difficult to appreciate in dark-skinned individuals. Many patients are symptomatic for 4-8 days before presentation77,78 and may have already consulted a physician (who might possibly have prescribed an antifungal cream). Patients who are likely to develop FG include chronically ill nursing home patients with decubiti, Foley catheters, diapers, and feeding tubes. Unfortunately, poor hygiene or contractures may discourage completely exposing the perineum. Thus, it is tempting to automatically ascribe fever and “dirty urine” in an elderly male to urosepsis. Such a patient requires a careful examination of the perineal and rectal areas. November 2000 Genitourinary sources Urethral stricture Scrotal carbuncle Scrotal scratches Indwelling catheter Traumatic catheterization Vasectomy Prostate biopsy Sources: Olsofka JN, Carrillo EH, Spain DA, et al. The continuing challenge of Fournier’s gangrene in the 1990s. Am Surg 1999;65:1156-1159; Basoglu M, Gui O, Yildirgan I, et al. Fournier’s gangrene: A review of fifteen cases. Am Surg 1997;1019-1021; Smith GL, Bunker CB, Dinnen MD. Fournier’s gangrene. Br J Urol 1998;81:347-355; Baskin LS, Carroll PR, Caltolica EV, et al. Necrotizing soft tissue infections of the perineum and genitalia: Bacteriology, treatment and risk assessment. Br J Urol 1990;65:524-529; Stephens BJ, Lathrop JC, Rice WT, et al. Fournier’s gangrene: Historic (1764-1978) versus contemporary (1979-1988) differences in etiology and clinical importance. Ann Surg 1993;59:149162; Enriquez JM, Moreno S, Devesa M, et al. Fournier’s syndrome of urogenital and anorectal origin: A retrospective, comparison study. Dis Col Rect 1987;30:33-37; Karim MS. Fournier’s gangrene following urethral necrosis by indwelling Foley catheter. Urology 1984;23:173-175. 13 Emergency Medicine Practice treatment.92 Surprisingly, there has been only minimal improvement in survival rates over the past decades. The mortality before 1945 (before antibiotics) and from 1945 to 1988 remained the same—20%-22%.89 Surgical debridement is key; the latest “gorillacillin” is only an accessory. are susceptible to UTIs and therefore to prostatitis.96 The causative organisms in bacterial prostatitis are similar to those responsible for UTIs—E. coli is the most common, followed by other Enterobacteriaceae species and possibly Gram-positive organisms.98 In some men with CBP, the pathogenic organisms in their prostatic fluid are the same as those found in the vaginal cultures of their female sexual partners. This suggests a possible role for ascending sexually transmitted infection.93,96 The cause and pathogenesis of NBP remain unclear. Possibilities include an unidentified pathogenic organism(s), a non-infectious disease, or a “chemical” prostatitis caused by urine reflux.96 Prostate Problems Anatomy The prostate gland in the normal adult male weighs approximately 20 grams. The prostatic glands produce a complex fluid that constitutes approximately 15%-30% of the typical ejaculate. During ejaculation, the fluid is released through multiple ducts into the prostatic urethra and mixes with the seminal fluid, providing a suitable transport medium for sperm.93 Physical Examination In ABP, the prostate is typically tender, swollen, firm, and warm. The patient may or may not have a urethral exudate. Aggressive palpation of an acutely infected gland may precipitate bacteremia, so palpation should be gentle. The physical findings in a patient with CBP or NBP/prostodynia are often indistinguishable from ABP, although symptoms are typically milder and fever is uncommon.96 The gland is usually tender. During the evaluation of possible prostatitis, the emergency physician should carefully examine the genitalia and abdomen. Incidence Little information concerning the true incidence of prostatitis is available, but it is commonly diagnosed (perhaps overdiagnosed) in adult men while rarely affecting prepubertal boys. Some estimate that half of all men will suffer from symptoms of prostatitis at some point during their lives.94 Types Of Prostatitis Prostatitis is divided into acute bacterial prostatitis (ABP), chronic bacterial prostatitis (CBP), and non-bacterial prostatitis (NBP)/prostodynia. ABP is a febrile illness with an acute onset. Genitourinary signs and symptoms predominate, such as low back pain, perineal pain, urinary frequency, urgency, and dysuria. Acute prostatitis has been likened to sitting on a flaming golf ball. Urinary retention may be present in addition to the constitutional symptoms.95 ABP is relatively rare—a typical urologist may see only two or three cases a year, if that.93 CBP is a more subtle illness, marked by recurrent urinary tract infections (UTIs) with the same pathogen. It may be caused by persistence of the pathogen in the prostatic secretory system despite repeated courses of therapy.95 The organism persists due to poor accumulation of antibiotics within the prostate.96 Most patients complain of irritative voiding symptoms and pain in various sites of the pelvis and genitalia. No physical exam findings are characteristic of CBP.96 Patients with NBP have inflammatory cells in the prostatic secretions but negative cultures. In patients with prostodynia, the patient has a painful prostate but normal prostatic secretions and no history of UTI. In general, treatment of NBP and prostodynia is the same, so they are usually considered together.96 Laboratory Evaluation The most important laboratory test in a patient with suspected ABP is the examination of a clean catch, midstream urine specimen. This will demonstrate pyuria and/ or bacteriuria. Urine culture will identify the pathogenic organism. Although prostatic massage usually produces purulent secretions, bacteremia may result from manipulation of an inflamed gland. Contrary to older recommendations, prostatic massage is unnecessary and should be avoided.96,99 Quantitative bacteriologic culture confirms the diagnosis of bacterial prostatitis. The classic “three-glass” method for localizing infection to the prostate involved prostatic massage and is rarely used in modern practice. Some urologists have the patient with suspected bacterial prostatitis masturbate into a specimen cup and then culture the ejaculate.100 (Like auscultation of the penis, this suggestion may raise a few eyebrows in the ED.) If a urethral discharge is present, test it for chlamydia and gonorrhea. Treatment In the normal host, antibiotics diffuse poorly into the prostate. However, during ABP, the intense inflammatory reaction appears to enhance drug passage from plasma into the prostatic secretory system.96 Antibiotics effective against urinary pathogens also treat ABP, as the organisms are the same. Fluoroquinolones are among the drugs of choice. ABP requires prolonged therapy. Oral doses of ciprofloxacin, norfloxacin, ofloxacin, or enoxacin are generally prescribed for 30 days. If the patient is ill enough to require parenteral medication, consider gentamicin plus ampicillin. An intravenous fluoroquinolone is another good alternative.96 Oral treatment is indicated for CBP, using the same Etiology And Pathogenesis Bacterial prostatitis results from an ascending urethral infection or reflux of infected urine into prostatic ducts. The intraprostatic reflux of urine may play a crucial role in the pathogenesis of bacterial prostatitis.97 Other possible routes of infection include local invasion by rectal bacteria or by lymphatic or hematogenous spread.96 Patients with indwelling urinary catheters and condom catheter drainage systems Emergency Medicine Practice 14 November 2000 Disposition agents as for ABP. Intravenous therapy is rarely, if ever, indicated. For patients with ABP who are younger than 35 years of age, treatment should be directed toward gonorrhea and chlamydia. Remember that ciprofloxacin is not active against chlamydia. For patients over the age of 35 or who have a history of anal intercourse, a fluoroquinolone regimen is necessary.71 As in epididymitis, the newer-generation quinolones such as ofloxacin or levofloxacin will treat gonorrhea, chlamydia, and the urinary pathogens.71 There are multiple therapeutic approaches to NBP and prostodynia, usually directed by a urologist. The emergency physician should make the appropriate referral and control pain with a short course of anti-inflammatory medications or narcotics. When narcotics are given for prostatitis, a stool softener is a useful adjunct to prevent a downward spiral of constipation and tenesmus. Most patients with bacterial prostatitis can be managed on an outpatient basis with urologic referral. Indications for admission include intractable nausea and vomiting, toxic appearance, or the existence of significant comorbidities. Diabetes or other immunosuppressive conditions may predispose to complications. Acute Urinary Retention Acute urinary retention (AUR) manifests as a sudden inability to pass urine. Urinary retention syndromes can range from overt retention to insidious overflow incontinence. The condition is far more common in men than women.13 In one study, benign prostatic hypertrophy was the most common etiology (53%). Other causes include constipation, prostate cancer, urethral stricture, clot reten- Ten Excuses That Don’t Work In Court 1.“I was sure I felt a torsed appendix testis. Besides, the scrotum looked a little blue, so I sent him for follow-up in two days.” The testis was removed several days later; it was the testicle that was blue. To make the diagnosis of torsed appendix testis, have a urologist operate on the scrotum or obtain a timely imaging study. 6.“It was a simple case of urinary retention. He got a Foley and went home!” Actually, it was a simple case of spinal cord compression. The patient had back pain and acute urinary retention. The plaintiff’s attorney made quite a point regarding the lack of a neurologic examination (and no documentation of rectal tone) and the fact that the patient left in a wheelchair as opposed to walking. 2.“I knew it was a torsion, but I had to get an ultrasound to be sure.” You were right about the torsion, but wrong about the imaging study. If it’s any consolation, the pathology report did show a recently deceased testicle. This patient presented at 2 a.m. after seven hours of pain. The ultrasound tech had a flat tire, the Doppler was on the fritz, and the radiologist didn’t realize the study was completed until 8 a.m. Some proponents of mandatory exploration for the acute scrotum suggest imaging studies only if the following caveat is observed: Male emergency physicians must forcefully squeeze their own testicles (and those of the radiologist) every 15 minutes until the test results are back. Female emergency physicians should just be conscientious. 7.“There was nothing wrong with his scrotum. Even though he complained of testicular pain, the testes weren’t tender.” True enough. The testicles are rarely tender in appendicitis, although they may suffer from referred pain. A number of abdominal conditions—most notably, appendicitis, diverticulitis, and abdominal aortic aneurysm—may present with scrotal pain.107 If the testes are non-tender, document a detailed examination of the abdomen. 8.“Little Joey didn’t tell me he had pain in his scrotum. He said his stomach hurt.” This is the converse of excuse #7. Some patients with scrotal pathology may complain only of abdominal pain. This is especially true in children. They may also minimize their symptoms out of fear or embarrassment. Patients with abdominal complaints need a genital exam in most cases (and vice versa). 3.“But I thought his UTI was the source of his fever. The nursing home didn’t mention any scrotal pain.” Don’t miss an early Fournier’s gangrene for lack of a complete examination. Be sure to examine the perineum when looking for the source of a fever—especially in the elderly. 4.“But his Prehn’s sign was positive. That means epididymitis.” Never use this sign to make a diagnostic decision. It is no better than a coin toss. Patients with torsion may develop relief with this maneuver. 9.“He had a penile discharge, so he got single-dose therapy. It always works!” Not if the patient has epididymitis. This patient’s chief complaint was scrotal pain, not dysuria. Patients with epididymitis (even if sexually transmitted) need at least 10-14 days of antibiotic therapy. 5.“But I got the diagnosis right. I knew it was Fournier’s gangrene, so I gave quadruple antibiotics and admitted him to medicine.” Correct diagnosis—wrong disposition. Fournier’s gangrene is a surgical emergency. Antibiotics are a “nice touch,” but the patient needs to go straight to the operating room. 10.“How could it have been torsion? He had white cells in his urine.” Pyuria does not exclude torsion. Age (either very young or very old) does not exclude torsion. Even a normal cremasteric reflex does not exclude torsion. (Hopefully, following the Clinical Pathway on page 11 may exclude torsion.) ▲ November 2000 15 Emergency Medicine Practice able to be discharged without a catheter, compared to only 8% of those with larger residual volumes.106 In patients with chronic retention, post-obstructive diuresis may occur, so the patient should be monitored for a few hours after catheterization.11 Most patients may be discharged with the catheter in place, connected to a leg bag. Instruct the patient and/or his family in how to care for the bag. An indwelling catheter causes bladder spasm with resultant constant urge to void. This can be treated with belladonna and opium (B&O) suppositories. Antibiotics are indicated if a concomitant urinary tract infection is present or for prophylaxis if the catheter is to be left in place for more than a few days.11 However, the evidence behind using prophylactic antibiotics for this indication is admittedly weak (none). The patient should follow up with a urologist in 2-4 days. If an acute neurologic etiology is suspected, obtain urgent consultation in the ED. tion, neurologic disorders, postoperative complications, drugs, and infection.101 In paraplegics, acute overdistention of the bladder can produce autonomic dystonia, characterized by diaphoresis and marked hypertension.102 Among children, cystitis, operations, and voluntary overdistention may all lead to AUR.103 A detailed history, including prescription and over-thecounter medications, may reveal the cause of the urinary retention. Anticholinergics and sympathomimetics are the most common offenders. These agents are often found in over-the-counter medications and in a variety of herbals and health supplements. Physical examination should include a search for meatal stenosis, penile masses, phimosis, and paraphimosis. Examine the abdomen for suprapubic masses. A rectal exam is essential to determine the prostate’s size and consistency. Evaluate anal sphincter tone to help exclude a neurologic problem. The neurologic exam should focus on the sensory and motor exam and the bulbocavernosus reflex to identify neurogenic bladder or spinal cord compression.11 The bulbocavernosus reflex can be elicited by placing a finger in the patient’s rectum. Pinching their glans (gently), or tugging on an inserted Foley catheter, will cause the sphincter to spontaneously contract around the finger in the rectum. Absence of this reflex suggests a neurologic disorder involving the sacral plexus. Treatment of acute urinary retention consists of inserting a straight urinary catheter to decompress the bladder. If the straight catheter will not pass, a Coudé catheter may be used. If resistance is met, take care not to use excessive force, as this could create a false passage. The use of a Coudé catheter or a larger size Foley (which is more rigid) may ensure success. If the catheter cannot be passed, obtain urologic consultation, as filiformes and followers or a suprapubic tube may be required. In the past, there was some concern that rapid decompression of the bladder could lead to complications—most notably, significant hematuria. This led to the practice of clamping the Foley after several hundred ccs of urine were released, waiting some unspecified period of time, and then releasing another aliquot. This practice appears to have no basis in fact. One paper analyzed five studies for complications associated with rapid and complete bladder emptying in patients with acute urinary retention. Hematuria occurred in 2%-16% and was never severe.104 In fact, no patient had significant complications. The authors believe that “quick, complete emptying of the obstructed bladder is safe, simple, and effective and is recommended as the optimal method for decompressing the obstructed urinary bladder.” A prospective study of 300 cases of urinary retention also supports this conclusion.105 Once a patient with acute urinary retention has been treated with a catheter, most emergency physicians send the patient home with the catheter in place. However, this may not be necessary in all cases. In one randomized, controlled trial of 60 males catheterized for AUR, the volume of residual urine correlated with the ability to urinate without a catheter after bladder decompression. Forty-four percent of patients with residual volumes of less than 900 cc were Emergency Medicine Practice Summary Some male genitourinary complaints represent true emergencies. Testicular torsion, Fournier’s gangrene, paraphimosis, and penile entrapment injuries require prompt diagnosis and treatment to save life, penis, or testicle. If testicular torsion is likely, call a urologist. Manual detorsion is another important consideration. In the case of possible torsion, paraphimosis with distal cyanosis, or Fournier’s gangrene, the alacrity of consultation and intervention may prevent a catastrophic outcome. Diagnostic testing may adversely delay necessary treatment. For these reasons, document the time of calls to consultants such as urology and radiology, and chart that you discussed the diagnostic possibilities and proposed management with them. ▲ References Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report. To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. In addition, the most informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference. 1. 2. 3. 4. 16 Harmon WJ, Nehra A. Priapism: Diagnosis and management. Mayo Clin Proc 1997;72:350-355. (Review) Lue TF, Hellstrom WJ, McAninch JW, et al. Priapism: A refined approach to diagnosis and treatment. J Urol 1986;136:104-108. (Case report, review) Broderick GA, Gordon D, Hypolife I, et al. Anoxia and corporal smooth muscle dysfunction: a model for ischemic priapism. J Urol 1994;151:252-262. (Prospective; animal study) Levine FJ, Saenz-de Tejada I, Payton TR, et al. Recurrent prolonged erections and priapism as a sequela of priapism: November 2000 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22.* 23.* 24. 25. 26. 27. 28.* 29.* 30.* 31. Pathophysiology and management. J Urol 1991;145:764-767. (Prospective; 6 patients) Bastuba MD, Saenz-de Tejada I, Dinlenc CZ, et al. Arterial priapism: Diagnosis, treatment and long-term follow-up. J Urol 1994;151:1231-1237. (Longitudinal; 7 patients) Winter CC, McDowell G. Experience with 105 patients with priapism: update, review of all aspects. J Urol 1998;140:980983. (Retrospective) Pohl J, Pott B, Kleinhaus G. Priapism: a three-phase concept of management according to aetiology and prognosis. Br J Urol 1986;58:113-118. (Retrospective; 230 patients) Sur RL, Kane CJ. Sildenafil citrate-associated priapism. Urology Online 2000;55(6):950. (Case) Roberts JR, Hedges JR, eds. Clinical Procedures in Emergency Medicine, 3rd ed. Philadelphia: W.B. Saunders; 1998. (Textbook) O’Brien WM, O’Connor KP, Lynch JH, et al. Priapism: Current concepts. Ann Emerg Med 1989;18:131-134. (Review) Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide, 5th ed. New York: McGraw-Hill; 1999. (Textbook) Tarry WF, Duckett JW Jr, Synder HM III. Urologic complication of sickle cell disease in a pediatric population. J Urol 1987;138:592-594. (Longitudinal; 321 patients) Dawson C, Whitfield H. Urological emergencies in general practice. BMJ 1996;312:838-840. (Review) Vohra S, Badlani G. Balanitis and balanoposthitis. Urol Clin North Am 1992;19(1):143-147. (Review) Schwartz RH, Rushton HG. Acute balanoposthitis in young boys. Pediatr Infect Dis J 1996;15(2):176-177. (Case, review) Escala JM, Rickwood AM. Balanitis. Br J Urol 1989;63:196-197. (Retrospective; 100 children) Wyatt JP, Scobie WG. The management of penile zip entrapment in children. Injury 1994;25:59. (Retrospective; 30 boys) Nolan JF, Stillwell TJ, Sands JP. Acute management of the zipper-entrapped penis. J Emerg Med 1990;8:305-307. (Case) Strait RT. A novel method for removal of penile zipper entrapment. Pediatr Emerg Care 1999;15(6):412-413. (Case) Anderson PA, Giacomantonio JM. The acutely painful scrotum in children: Review of 113 consecutive cases. Can Med Assoc J 1985;132:1153. (Retrospective) Friedman SC, Sheynkin YR. Acute scrotal symptoms due to perforated appendix in children: Case report and review of the literature. Pediatr Emerg Care 1995;11:181. Burgher SW. Acute scrotal pain. Emerg Med Clin North Am 1998;16(4):781-809. (Review) Hawtrey CE. Assessment of acute scrotal symptoms and findings. Urol Clin North Am 1998;25(4):715-723. (Review) Caesar RE, Kaplan GW. Incidence of bell-clapper deformity in an autopsy series. Urology 1994;44:114. (Prospective; 51 males, 101 testes—12% incidence) Johnson JH. The acute scrotum in childhood. Practitioner 1979;223:306. (Review) Haynes BE, Beesen HA, Haynes VE. The diagnosis of testicular torsion. JAMA 1983;249(18):2522-2527. (Review) Edelsberg JS, Surh YS. The acute scrotum. Emerg Med Clin North Am 1988;6(3):521-546. (Review) Ben-Chaim J, Leibovitch I, Ramon J, et al. Etiology of acute scrotum at surgical exploration in children, adolescents and adults. Eur Urol 1992;21:45-47. (Prospective; 171 patients) Watkin NA, Reiger NA, Moisey CU. Is the conservative management of the acute scrotum justified on clinical grounds? Br J Urol 1996;78:623-627. (Retrospective; 209 patients) Knight PJ, Vassy LE. The diagnosis and treatment of the acute scrotum in children and adolescents. Ann Surg 1984;200:664. (Retrospective) Jefferson RH, Perez LM, Joseph DB. Cultural analysis of the clinical presentation of acute scrotum: A 9-year experience at a single institution. J Urol 1997;158:1198-1200. (Retrospective; 115 boys) November 2000 32. Lewis AG, Bukowiski TP, Jarvis PD, et al. Evaluation of the acute scrotum in the emergency department. J Pediatr Surg 1995;30:277-281. (Retrospective; 238 patients) 33. Melekos MD, Asbach HW, Markou SA. Etiology of acute scrotum in 100 boys with regard to age distribution. J Urol 1988;138:1023. (Retrospective) 34. May RE, Thomas WE. Recurrent torsion of the testis following previous surgical fixation. Br J Surg 1980;67:129. (2 cases) 35. Tryfonas G, Violaki A, Tsikopoulos G, et al. Late postoperative results in males treated for testicular torsion during childhood. J Pediatr Surg 1994;29:553. (Longitudinal; 75 patients) 36.* Van Glabeke E, Khairouni A, Larroquet M, et al. Acute scrotal pain in children: Results of 543 surgical explorations. Pediatr Surg Int 1999;15:353-357. (Prospective, pro-exploration) 37. Cos LR, Rabinowitz R. Trauma-induced testicular torsion in children. J Trauma 1982;22:224. (3 cases, review) 38. Manson AL. Traumatic testicular torsion—case report. J Trauma 1989;29:407. (Case, review) 39. Munter DW, Faleski EJ. Blunt scrotal trauma: Emergency department evaluation and management. Am J Emerg Med 1989;7:227. (Review) 40. Rabinowitz R, Hulbert WC. Acute scrotal swelling. Urol Clin North Am 1995;22:101. (Review) 41. Lee LM, Wright JE, McLoughlin MG. Testicular torsion in the adult. J Urol 1983;130(1):93-94. 42.* Rabinowitz R. The importance of the cremasteric reflex in acute scrotal swelling in children. J Urol 1984;132:89. (Retrospective; 245 boys: reflex present—100% correlated with no torsion) 43. Dresner ML. Torsed appendage: Diagnosis and management: blue dot sign. Urology 1973;1:63. (Review) 44. Lindsey D, Stanisic TH. Diagnosis and management of testicular torsion: pitfalls and perils. Am J Emerg Med 1988;6(1):42-46. (Review) 45. Babcock DS. Which is the most sensitive study for testicular nuclear scan? AJR Am J Roentgenol 1995;165:224. (Letter, review) 46. Fenner MN, Roszhart DA, Texter JH. Testicular scanning: Evaluating the acute scrotum in the clinical setting. Urology 1991;38:237. (Retrospective; 128 patients) 47. Melloul M, Paz A, Lask D, et al. The value of radionuclide scrotal imaging in the diagnosis of acute testicular torsion. Br J Urol 1995;76:628-631. (Prospective; 87 patients aged 8-65) 48. Siegel MJ. The acute scrotum. Radiol Clin North Am 1997;35:959. (Review) 49. Fernandez MS, Dominguez C, Sanguesa C, et al. The use of color Doppler sonography of the acute scrotum in children. Cir Pediatr 1997;10:25. (Retrospective; 72 children) 50. Al Mufti RA, Ogedegbe AK, Lafferty K. The use of Doppler ultrasound in the clinical management of acute testicular pain. Br J Urol 1995;76:625-627. (Prospective; 56 patients) 51.* Kass EJ, Stone KT, Cacciarelli AA, et al. Do all children with acute scrotum require exploration? J Urol 1993;150:667-669. (Prospective; 77 children) 52. Paltiel HJ, Connolly LP, Atala A, et al. Acute scrotal symptoms in boys with an indeterminate clinical presentation: Comparison of sonography and scintigraphy. Radiology 1998;297:223231. (Prospective; 41 patients) 53. Atkinson GO Jr, Patrick LE, Ball TI Jr, et al. The normal and abnormal scrotum in children: Evaluation with color Doppler sonography. AJR Am J Roentgenol 1992;158:613. (Prospective; 32 patients) 54. Ingram S, Hollman AS. Colour Doppler sonography of the normal paediatric testis. Clin Radiol 1994;49:266. (Prospective; 50 boys) 55. Middleton WD, Thorne DA, Melson GL. Color Doppler ultrasound of the normal testis. AJR Am J Roentgenol 1989;152:293. (Prospective; 15 patients) 56. Wilbert DM, Schaerfe CW, Stern WD, et al. Evaluation of the acute scrotum by color-coded Doppler ultrasonography. J Urol 1993;149:147. (Prospective; 40 patients) 17 Emergency Medicine Practice 57. Clark WR, Kramer SA. Henoch-Schonlein purpura and the acute scrotum. J Pediatr Surg 1986;211(11):991. (Case report) 58. Turkish VJ, Traisman HS, Belman AB, et al. Scrotal swelling in the Schonlein-Henoch syndrome. J Urol 1976;115:317. (Case report) 59. Donahue RE, Utley WLF. Torsion of the spermatic cord. Urology 1978;11(1):33-36. (Prospective; 198 patients) 60. Skoglund RW, McRoberts JW, Ragde H. Torsion of the spermatic cord: a review of the literature and analysis of 70 new cases. J Urol 1970;104(4):604-607. (Retrospective) 61. Nakielny RA, Thomas WEG, Jackson P, et al. Radionuclide evaluation of acute scrotal disease. Clin Radiol 1984;35:125-129. (Prospective; 106 patients) 62. Riggs, Sanford JP. Viral orchitis. N Engl J Med 1962;266:990993. (Review) 63. Sufrin G. Acute epididymitis. Sex Trans Dis 1981;(Suppl):132139. (Review) 64. Hill DE, Kramer SA. Specific infections of the genitourinary tract. In: Kelalis PP, King LR, Belman AB, eds. Clinical Pediatric Urology, 3rd ed. Philadelphia: W.B. Saunders; 1992:353-355. (Review) 65.* Siegel A, Synder H, Duckett JW. Epididymitis in infants and boys: Underlying urogenital anomalies and efficacy of imaging modalities. J Urol 1987;138(suppl):1100-1103. (Retrospective; 47 patients) 66. Berger RE. Sexually transmitted diseases: the classic diseases (epididymitis). In: Walsh PC, Retik AB, Vaughn ED Jr, et al, eds. Cambell’s Urology, 7th ed. Philadelphia: W.B. Saunders; 1998. (Textbook) 67.* Lau P, Anderson PA, Giacomantonio JM, et al. Acute epididymitis in boys: Are antibiotics indicated? Br J Urol 1997;79:797. (Prospective; 48 boys: no if UA is negative) 68. Rinker JR, Hanock CV, Henderson WD. A statistical study of unilateral prophylactic vasectomy in the prevention of epididymitis: 1029 cases. J Urol 1970;104:303. (Prospective) 69. Anderson PA, Giacomantonio JM, Schwartz RD. Acute scrotal pain in children: Prospective study of diagnosis and management. Can J Surg 1989;32:29. (Prospective; 48 patients) 70. Watson RA. Gonorrhea and acute epididymitis. Milit Med 1979;144:785-787. (Review) 71. Gilbert DN, Moellering RC, Sande MA, eds. The Sanford Guide to Antimicrobial Therapy, 13th ed. Portland, OR: Oregon Health Science University; 2000. 72. Fournier JA. Gangrene foudroyante de la verge. Medecin Pratique 1883;4:589-597. 73.* Smith GL, Bunker CB, Dinnen MD. Fournier’s gangrene. Br J Urol 1998;81:347-355. (Review) 74. Spirnak JP, Resnik MI, Hampel N, et al. Fournier’s gangrene: report of 20 patients. J Urol 1984;131:289-291. (Case series) 75. Fahal AH, Hassan MA. Fournier’s gangrene in Khartoum. Br J Urol 1988;61:451-454. (9 cases) 76. Samm BJ, Dmochowski BR. Urologic emergencies. Postgrad Med 1996;100(4):187-194. (Review) 77. Olsofka JN, Carrillo EH, Spain DA, et al. The continuing challenge of Fournier’s gangrene in the 1990s. Am Surg 1999;65:1156-1159. (Retrospective; 14 patients) 78. Basoglu M, Gui O, Yildirgan I, et al. Fournier’s gangrene: A review of fifteen cases. Am Surg 1997;1019-1021. (Retrospective; 15 patients) 79. Baskin LS, Carroll PR, Caltolica EV, et al. Necrotizing soft tissue infections of the perineum and genitalia: Bacteriology, treatment and risk assessment. Br J Urol 1990;65:524-529. (Retrospective; 29 patients) 80. Lamb R, Juler G. Fournier’s gangrene of the scrotum: A poorly defined condition or misnomer? Arch Surg 1983;118:38. (Retrospective; 12 patients) 81. Clayton MD, Fowler JE Jr, Sharifi R. Causes, presentation and survival of 57 patients with necrotizing fasciitis of the male genitalia. Surg Gynaecol Obstet 1990;170:49-55. (Retrospective; 57 patients) Emergency Medicine Practice 82. 83. 84. 85. 86. 87. 88. 89. 90. 91. 92. 93. 94. 95. 96. 97. 98. 99. 100. 101. 102. 103. 104. 105. 106. 107. 18 Bahlmann JC, Fourie IJ, Arndt TC. Fournier’s gangrene and necrotizing fasciitis of the male genitalia. Br J Urol 1983;55:8588. (Prospective; 9 patients) Laucks SS. Fournier’s gangrene. Surg Clin North Am 1994;74:1339-1359. (Review) Paty R, Smith AD. Gangrene and Fournier’s gangrene. Urol Clin North Am 1992;19:149-162. (Review) Sutherland ME, Meyer AA. Necrotizing soft-tissue infections. Surg Clin North Am 1994;74:591-607. (Review) Biyani CS, Mayor PE, Powell CS. Case report: Fournier’s gangrene—roentgenographic and sonographic findings. Clin Radiol 1995;50:728-729. (Case) Dogra VS, Smeltzer JS, Poblette J. Sonographic diagnosis of Fournier’s gangrene. J Clin Ultrasound 1994;22:571-572. (Case) Stevens DL, Bryant AE, Hackett SP. Antibiotic effects on bacterial viability, toxin production, and host response. Clin Infect Dis 1995;20 Suppl 2:S154-S157. Stephens BJ, Lathrop JC, Rice WT, et al. Fournier’s gangrene: Historic (1764-1978) versus contemporary (1979-1988) differences in etiology and clinical importance. Ann Surg 1993;59:149-162. (Observational) Laor E, Palmer LS, Bhupendra MT, et al. Outcome prediction in patients with Fournier’s gangrene. J Urol 1995;154:89-92. (Retrospective; 30 patients) Enriquez JM, Moreno S, Devesa M, et al. Fournier’s syndrome of urogenital and anorectal origin: A retrospective, comparison study. Dis Col Rect 1987;30:33-37. (Retrospective; 28 patients) Oh C, Lee C, Jacobson J. Neccrotizing fasciitis of perineum. Surgery 1982;91:49-51. (Case) Cooner WH, Roberts RG. Prostate disease. Am Fam Phys 1994;monograph:1-8 (Review) Stamey T. Pathogenesis and Treatment of Urinary Tract Infections. Baltimore: 1980:342-429. (Textbook) Rosen P, Barkin R, eds. Emergency Medicine: Concepts and Clinical Practice, 4th ed. St. Louis, MO: Mosby; 1998. (Textbook) Mears EM: Prostatitis and related disorders. In: Walsh PC, Retik AB, Vaughn ED, et al, eds. Campbell’s Urology, 7th ed. Philadelphia: W.B. Saunders; 1998:604-613. (Review) Kirby RS, Lowe D, Bultitude MI, et al. Intra-prostetic urinary reflux: an aetiological factor in abacteral prostatitis. Br J Urol 1982;54:729-731. (Prospective; 10 cadavers) Domingue GJ, Hellstrom WJ. Prostatitis. Clin Micro Rev 1998;11(4):604-613. (Review) Wilson JD, Braunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine, 12th ed. New York: McGrawHill; 1991. (Textbook) Riedasch G, Mohring K, Ritz E. Do antibody-coated bacteria prove bacterial prostatitis? Infection 1991;19 Suppl 3:S141-S143. Murray K, Massey A, Feneley RC. Acute urinary retention: A urodynamic assessment. Br J Urol 1984;56:468-473. (Prospective; 30 patients) Hart RG, Kanter MC. Acute autonomic neuropathy. Two cases and a clinical review. Arch Intern Med 1990;150(11):23732376. (Review) Choung S, Emberton M. Acute urinary retention. Br J Urol 2000;85:186-201. (Review) Nyman MA, Schwenk NM, Silverstein MD. Management of urinary retention: rapid versus gradual decompression and risk of complications. Mayo Clin Proc 1997;72(10): 951-956. (Review) Glahn BE, Plucnar BJ. Quick complete emptying of the bladder in 300 cases of urinary retention. The occurrence of haematuria. Dan Med Bull 1984;31(1):68-70. (Prospective; 300 patients) Taube M, Gajraj H. Trial without catheter following acute retention of urine. Br J Urol 1989;63(2):180-182. (Randomized, controlled; 60 patients) McGee SR. Referred scrotal pain: case reports and review. J Gen Intern Med 1993;8(12):694-701. November 2000 Physician CME Questions 72. Which statement regarding priapism is false? a. Low-flow or ischemic priapism that is not treated within 24-48 hours can result in erectile dysfunction and recurrent priapism. b. Priapism in children is commonly due to sickle cell disease. c. Dark corporal blood suggests low-flow priapism. d. High-flow priapism is a urologic emergency that requires prompt treatment in the ED. 65. Which statement regarding testicular torsion is correct? a. The bell-clapper deformity is found in less than 5% of the population. b. Testicular torsion does not result from direct scrotal trauma. c. The annual incidence of testicular torsion in males under age 25 is estimated to be 1 in 4000. d. The blue-dot sign is suggestive of testicular torsion. 73. Which of the following signs or symptoms should not be used in the decision-making process when evaluating an acute scrotum? a. Age b. Length of symptoms c. Prehn’s sign d. Testicular lie 66. Which symptom is not commonly seen in epididymitis? a. Scrotal pain b. Nausea and vomiting c. Dysuria d. Gradual onset of pain 74. Which statement about prostatitis is correct? a. Prostatic massage is necessary to produce a diagnostic urinary specimen. b. Fluoroquinolones will treat the majority of organisms responsible for bacterial prostatitis. c. Prostatitis is always infectious. d. It is not necessary to treat for sexually transmitted diseases in patients with prostatitis because gonorrhea and chlamydia do not cause prostatitis. 67. Which physical exam finding is most suspicious for testicular torsion in a patient with scrotal pain? a. Diffuse scrotal tenderness b. Absence of urethral discharge c. Abnormal testicular lie d. Scrotal edema 68. Which of the following statements is true regarding Fournier’s gangrene? a. There is no imaging modality useful in making an early diagnosis. b. It occurs in men only. c. Infection is typically polymicrobial. d. Genitourinary sources carry the highest mortality. 75. A 14-year-old male presents with a one-hour history of scrotal pain and vomiting. There is no fever or urinary symptoms. On exam, his cremasteric reflex is absent and the painful testicle has a horizontal lie. Which of the following is the most appropriate management strategy? a. Immediate urologic consultation for scrotal exploration. b. Order a scrotal ultrasound. c. Order a nuclear perfusion study of the scrotum. d. Order a urinalysis. 69. Which age group is at highest risk for testicular torsion as a cause of acute scrotal pain? a. Newborn and post-pubertal b. Age 35-50 years c. Over age 50 d. Age 5-10 years 76. Which of the following is not a Knight-Vassy criterion for diagnosing acute epididymitis? a. History of sexual activity b. Dysuria or recent urinary tract instrumentation c. An admission temperature exceeding 101˚F d. Tenderness and induration localized to the epididymis 70. Which of the following statements is not characteristic of low-flow priapism? a. The most common causes in adults are related to sickle cell disease, idiopathic causes, and drugs. b. Physical exam reveals a rigid, painful penile shaft with a soft glans. c. It can be treated with intra-cavernosal injections of phenylephrine. d. It often results from trauma. 77. What is the most likely etiology in a patient with balanitis who presents with a thin, purulent discharge that is seen with foreskin retraction, penile pain, and erythema? a. Candida b. Trichomonas c. Irritation d. Streptococcus 71. Which patient is at highest risk for developing Fournier’s gangrene? a. A healthy young male with traumatic brain injury who has a Foley catheter placed in the ED b. An elderly diabetic male with a sacral decubitus ulcer and an indwelling Foley catheter c. An immunocompetent 40-year-old male with a recent vasectomy d. A 3-month-old infant with a history of constipation who had a recent rectal biopsy November 2000 78. Which of the following conditions is considered a urologic emergency? a. Phimosis with no urinary retention b. Paraphimosis c. Urethral stricture without urinary retention d. Balanoposthitis 19 Emergency Medicine Practice Physician CME Information 79. Which of the following is not a common cause of balanitis or balanoposthitis? a. HIV b. Irritation c. Candida d. Trichomonas e. Streptococcus This CME enduring material is sponsored by Mount Sinai School of Medicine and has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education. Credit may be obtained by reading each issue and completing the post-tests administered in December and June. Target Audience: This enduring material is designed for emergency medicine physicians. Needs Assessment: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for emergency physicians. Date of Original Release: This issue of Emergency Medicine Practice was published November 1, 2000. This activity is eligible for CME credit through November 1, 2003. The latest review of this material was October 31, 2000. Discussion of Investigational Information: As part of the newsletter, faculty may be presenting investigational information about pharmaceutical products that is outside Food and Drug Administration approved labeling. Information presented as part of this activity is intended solely as continuing medical education and is not intended to promote off-label use of any pharmaceutical product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice discusses no off-label use of any pharmaceutical product. Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Freeman, Dr. Üner, and Dr. Schneider report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation. Accreditation: Mount Sinai School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to sponsor continuing medical education for physicians. Credit Designation: Mount Sinai School of Medicine designates this educational activity for up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition Award. Each physician should claim only those hours of credit actually spent in the educational activity. Emergency Medicine Practice is approved by the American College of Emergency Physicians for 48 hours of ACEP Category 1 credit (per annual subscription). Earning Credit: Physicians with current and valid licenses in the United States, who read all CME articles during each Emergency Medicine Practice six-month testing period, complete the CME Evaluation Form distributed with the December and June issues, and return it according to the published instructions are eligible for up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition Award (PRA) for each issue. You must complete both the post-test and CME Evaluation Form to receive credit. Results will be kept confidential. CME certificates will be mailed to each participant scoring higher than 70% at the end of the calendar year. 80. Which statement regarding prostatitis is true? a. Acute bacterial prostatitis and chronic bacterial prostatitis are easy to distinguish on physical exam. b. Prostatitis is always infectious. c. Organisms responsible for bacterial prostatitis include those that cause urinary tract infections. d. Intraprostatic reflux of urine is not known to be an important cause of prostatitis. Class Of Evidence Definitions Each action in the clinical pathways section of Emergency Medicine Practice receives an alpha-numerical score based on the following definitions. Class I • Always acceptable, safe • Definitely useful • Proven in both efficacy and effectiveness • Must be used in the intended manner for proper clinical indications Level of Evidence: • One or more large prospective studies are present (with rare exceptions) • Study results consistently positive and compelling Class IIa • Safe, acceptable • Clinically useful • Considered treatments of choice Level of Evidence: • Generally higher levels of evidence • Results are consistently positive Class IIb • Safe, acceptable • Clinically useful • Considered optional or alternative treatments Level of Evidence: • Generally lower or intermediate levels of evidence • Generally, but not consistently, positive results Class III: • Unacceptable • Not useful clinically • May be harmful Level of Evidence: • No positive high-level data • Some studies suggest or confirm harm Indeterminate • Continuing area of research • No recommendations until further research Level of Evidence: • Evidence not available • Higher studies in progress • Results inconsistent, contradictory • Results not compelling Adapted from: The Emergency Cardiovascular Care Committees of the American Heart Association and representatives from the resuscitation councils of ILCOR: How to Develop Evidence-Based Guidelines for Emergency Cardiac Care: Quality of Evidence and Classes of Recommendations; also: Anonymous. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part IX. Ensuring effectiveness of community-wide emergency cardiac care. JAMA 1992;268(16):2289-2295. Publisher: Robert Williford. Vice President/General Manager: Connie Austin. Executive Editor: Heidi Frost. Direct all editorial or subscription-related questions to Pinnacle Publishing, Inc.: 1-800-788-1900 or 770-992-9401 Fax: 770-993-4323 Pinnacle Publishing, Inc. P.O. Box 769389 Roswell, GA 30076-8220 E-mail: [email protected] Web Site: http://www.pinpub.com/emp Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year) by Pinnacle Publishing, Inc., 1000 Holcomb Woods Parkway, Building 200, Suite 280, Roswell, GA 30076-2587. Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of Pinnacle Publishing, Inc. Copyright 2000 Pinnacle Publishing, Inc. All rights reserved. No part of this publication may be reproduced in any format without written consent of Pinnacle Publishing, Inc. Subscription price: $249, U.S. funds. (Call for international shipping prices.) Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer. Emergency Medicine Practice 20 November 2000