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This chapter addresses urologic conditions that are either initially or eventually associated with an emergency procedure or may need to be performed in the absence of a urologic surgeon.
Testicular torsion is a scrotal emergency that can be challenging to diagnose under the best clinical circumstances. Although surgical exploration is the only definitive diagnostic and therapeutic procedure, many urologists prefer an initial diagnostic imaging study prior to surgical exploration, provided imaging can be obtained expediently while simultaneously preparing for operative intervention. This chapter addresses bedside maneuvers for this entity, including manual testicular detorsion.
Emergency penile conditions include paraphimosis and priapism. This chapter addresses bedside paraphimosis reduction techniques, as well as penile aspiration-irrigation-injection for relief of ischemic priapism. In addition, relief of phimosis complicated by the inability to void by means of a dorsal slit of the penile foreskin will be detailed for completeness ( ).
Access to and the subsequent evaluation of the bladder and urine are clinically important to all emergency practitioners. Various approaches to urine sampling and bladder drainage, including the techniques and complications of male and female urethral catheterization in various clinical situations and emergency suprapubic bladder access, are addressed.
Finally, a discussion of radiographic imaging of the genitourinary (GU) system is provided, with an emphasis on assessing lower urinary tract injury. Although the timing of GU radiologic examinations within the workup of the critically ill, multitrauma patient must be individualized, general guidelines for successful imaging are provided.
Although acute scrotal pain comprises less than 1% of overall emergency department (ED) visits, this presentation may provoke great anxiety for the patient or caretaker, given its highly sensitive nature. One of the most challenging aspects of scrotal complaints is that a wide variety of clinical conditions may present in a similar fashion: a male patient complaining of an acute, painful, swollen, and tender hemiscrotum. Although the differential is extensive, testicular torsion is the principle fertility threat that needs to be ruled out. Definitive management of testicular torsion involves surgical exploration and orchiopexy. Manual detorsion, with or without spermatic cord anesthesia, can be attempted while simultaneously preparing for operative intervention.
Indications: testicular torsion.
Contraindications: alternative cause of acute scrotal pain.
Complications: worsening ischemia, increased pain.
Equipment:
for spermatic cord anesthesia: 1% lidocaine (10 mL for an adult, or age-/weight-appropriate local anesthetic dosing for child), 27-gauge (or similar) needle for anesthetic infiltration.
for manual detorsion: bedside sonography may be helpful in assessing for pre- and postprocedure intratesticular blood flow.
Initiate urologic consultation and simultaneous preparation for surgical intervention.
Administer spermatic cord anesthesia (optional).
Administer systemic analgesia or light sedation (optional).
Keep the patient comfortable in a reclining or supine position.
Stand beside the stretcher (right side if right-hand dominant, or vice versa).
Rotate the testicle from medial to lateral (two thirds of torsion occurs lateral to medial).
Rotate 180 degrees initially; it may ultimately require two to three rotations to alleviate pain.
If mechanically difficult or there is increased pain, detorse in the opposite direction.
The end point is relief of pain or return of intratesticular blood flow on sonogram.
Consult urology department for definitive surgical scrotal exploration.
An acute scrotum is defined as an acute, painful swelling of the scrotum or its contents, accompanied by local signs or general symptoms. Although the list of diagnostic possibilities for a patient with an undifferentiated acute scrotum is extensive, early identification and skillful management of testicular torsion is critical as it may threaten testicular viability and future fertility if not managed expediently. Acute epididymitis is commonly the cause of acute scrotal pain in adolescents and adults. Testicular (or epididymal) appendage torsion is another frequent cause of acute scrotal pain in prepubertal boys.
Differentiating testicular torsion from alternative conditions takes precedence over a definitive diagnosis. The presence of an intact cremasteric reflex and testicular sonography are frequently utilized, yet imperfect, diagnostic tools in assessing for testicular torsion.
A congenital anomaly of fixation of the testis, termed the bell-clapper deformity , is associated with the development of testicular torsion. This occurs when the intrascrotal portion of the spermatic cord lacks firm posterior adhesion to the scrotal wall and remains surrounded by the tunica vaginalis ( Fig. 55.1 A ). As a result of the abnormal attachment, the testis may be suspended horizontally. These anatomic features predispose the affected testis to rotation.
Testicular salvage rates decrease with time from the onset of ischemia. A meta-analysis of 1140 patients in 22 series demonstrated a greater than 90% salvage rate with surgery within 6 hours of pain onset. Testicular atrophy may lead to subfertility. Furthermore, testicular loss may lead to contralateral testicular dysfunction through immune-mediated or other mechanisms.
The testis may torse, detorse, and retorse, so clinicians should be cautious about assigning an exact time as the time of onset and deferring urologic consultation based on an erroneous assumption that the testis is not salvageable. The gold standard for determining testicular viability is intraoperative visualization of the affected testis, which dictates early urologic involvement. Although all clinicians recognize the need for expedient surgery in the setting of known torsion, not all consultants will agree on surgical exploration without some adjunctive testing.
When utilized in the appropriate clinical setting, ultrasound remains the most useful diagnostic modality in the evaluation of GU complaints ( Fig. 55.2 ). A patient with compelling historical and examination findings of testicular torsion does not require any preoperative diagnostic tests. Color flow Doppler ultrasonography (CDUS) may be very helpful in all other cases. The classic sonographic finding suggestive of testicular torsion is diminished intratesticular blood flow. In addition, examination of the spermatic cord with high resolution gray-scale ultrasonography may reveal “coiling” or “kinking” of the cord at the site of torsion. Sonography is used not only to exclude testicular torsion, but also to search for alternative causes of acute scrotal pain. In epididymitis, perfusion may be normal (or increased) due to the effects of inflammatory mediators on local vascular beds, although this is a nonspecific finding. An infarcted appendage may be visualized on ultrasound as well. It has been suggested that emergency physicians may be able to accurately assess for intratesticular blood flow in patients presenting with acute scrotal pain using bedside sonography.
Color flow Doppler ultrasound has long been regarded as the diagnostic modality of choice in assessing for testicular torsion. However, false-negative ultrasound results have been reported. Many of these studies are case reports or case series, limited by small numbers and retrospective design. Two larger series reported documented intratesticular blood flow with CDUS in 6 of 23 (26%) and 50 of 208 cases (24%), respectively, of confirmed testicular torsion. Doppler ultrasound may reveal seemingly adequate intratesticular blood flow in partial torsion, which can be very misleading to the practitioner.
Radionuclide scintigraphy and CDUS show similar sensitivity, as well as false-negative rates, for the diagnosis of testicular torsion. However, given the widespread availability and expertise with ultrasound technology, combined with the risks of isotope radiation exposure, radionuclide procedures have fallen out of favor. The use of magnetic resonance imaging has been explored, but limitations include speed of imaging and availability.
Intravaginal testicular torsion is a congenital bilateral abnormality. The ischemic testis must be detorsed and pexed with nonabsorbable (e.g., nylon, polypropylene, or Prolene [Ethicon Inc.]), rather than absorbable (e.g., chromic, polyglactin, or Vicryl [Ethicon Inc.]), suture. The torsed testis that is pexed with absorbable suture remains at risk for subsequent postoperative torsion. Given the bilateral nature of the congenital abnormality, orchiopexy of the nonischemic contralateral testis is necessary.
Once the diagnosis of testicular torsion is suspected, immediately place a call to notify a urologist of the suspected diagnosis, the perceived need for surgical exploration, and the fact that you will be attempting testicular detorsion while awaiting patient transport to the operating room. At some point before the patient leaves the ED, meticulous charting to document time, suspected diagnosis, notification of the urologist, and any manipulation of the affected testis must be done. All efforts are then focused on attempting testicular detorsion.
Testicular torsion may be relieved by manual detorsion. A study of 162 cases of testicular torsion revealed that anticipated lateral to medial rotation occurred in 67% of cases, with medial to lateral rotation in the remaining 33%. This challenges the standard dogma of medial to lateral rotation, or “opening the book,” as the standard method for detorsion. There may be a cranial-caudal component to torsion as well. The end point of manual detorsion is relief of pain, or the return of intratesticular blood flow as seen on ultrasound imaging. Although manual detorsion may allow for reperfusion of the testis, a lesser degree of residual torsion may remain. Given that infarction can occur with as little as 180 degrees of torsion, immediate surgical exploration after what is thought to be a successful manual detorsion is still advocated. The bottom line is that specialty consultation and plans for possible immediate surgical exploration need to occur regardless of outcome of the detorsion procedure. Detorsion, however, may convert an emergency procedure to an urgent one.
Presence of an alternative cause of acute scrotal pain is a relative contraindication to the detorsion procedure. However, precise diagnosis may be impossible prior to definitive surgical exploration. A nonanomalous, appropriately fixated testicle should not be adversely affected by an initial trial (e.g., 180 degrees) of manual detorsion if circumstances are highly suspect for spermatic cord torsion.
Manual detorsion is performed in the following manner. Advise the patient that the procedure will be uncomfortable and painful and offer systemic analgesia or light sedation if appropriate. The rationale for not using spermatic cord anesthesia with attempted detorsion is that the anesthesia takes away an important subjective end point: relief of the patient's pain after manipulation of the testis. However, many authors do advocate spermatic cord anesthesia before detorsion, and if anesthesia of the spermatic cord is elected, it can be done in the following manner.
Local anesthesia of the spermatic cord using 1% plain lidocaine is usually done at the external inguinal ring (see Fig. 55.1 B ). First prepare the skin with an antiseptic solution. The cord can usually be grasped between the thumb and the index finger, and 10 mL of 1% plain lidocaine (for an adult) can be directly injected into the cord. If the cord is swollen, as is often the case in testicular torsion, or if the testicle is lying very high in the hemiscrotum as a result of spermatic cord torsion (so as to preclude grasping), the cord may be palpated at the pubic tubercle as it passes over the pubis and the lidocaine injected at this landmark. Lee and colleagues were able to perform manual detorsion with local spermatic cord anesthesia in 11 of 16 adult cases of torsion; Kresling and associates had success in 15 of 16 patients.
The goal of manual detorsion is to reestablish or increase blood flow to a previously ischemic testis. This should be done in conjunction with preparation of the operating suite. It should never delay operative intervention.
Before initiating detorsion, ensure that the patient is as comfortable as possible in a reclining or supine position. Lithotomy position gives the examiner the most access to the patient's genitalia and prevents the patient from retreating during the procedure. If light analgesia and/or sedation are selected, implement them at this time.
Manual detorsion begins with the clinician standing comfortably at the side of the bed or stretcher, preferably on the patient's right side if the clinician is right-handed, or vice versa. Detorsion is begun just as one would open a book (i.e., an initial 180 degree detorsion of the patient's right testis is done in a counterclockwise fashion) (see Fig. 55.1 C and D ). The patient's left testis is detorsed 180 degrees in a clockwise fashion. Pain relief is an objective end point. If one rotation relieves some but not all the pain, continue with another rotation. The degree of torsion may range from 180 to 1080 degrees with medians of 360 to 540 degrees. Therefore many patients require two or three rotations to alleviate pain. If the initial detorsion is mechanically difficult (which it will be if one is detorsing in the wrong direction) or makes the pain worse, detorse the testis in the opposite direction and observe the result. Approximately one third of testicular torsions occur in the lateral, or unexpected, direction. The objective success of any testicular manipulation can be substantiated by an increase in Doppler signal and the patient's relief of pain.
With successful detorsion, the testicle returns to its normal anatomic position. Resolution of induration and swelling of the spermatic cord, testis, and epididymis will depend on the degree and duration of ischemia. Thus, the more severe the torsion and the longer it has been present, the longer it will take for the edema and induration to resolve. With significant ischemia, the entire epididymis often becomes enlarged like a link sausage (uncommon in epididymitis except in severe cases or those that are initially misdiagnosed or seen late in their clinical course), and the testis becomes quite firm, simulating a testicular tumor. In some authors' experience, these reversible changes usually resolve over 3 to 4 hours.
Provide systemic analgesics as needed for discomfort. Importantly, even though manual detorsion will save an ischemic testicle, it should not be substituted for definitive scrotal exploration.
In a portion of cases, the testis will torse in the opposite direction (medial to lateral) or have multiple twists. This may become apparent as the clinician assesses the results of the detorsion procedure by palpation, relief of edema, and return or increase of the Doppler signal.
Spermatic cord torsion may be relieved by manual detorsion. In two thirds of cases, this is accomplished by medial to lateral rotation of the affected testicle. However, in the remaining one third of cases, lateral to medial rotation is necessary to untwist the spermatic cord. In all cases, manual detorsion, even when successful, only serves as a temporizing bridge to definitive surgical management.
Priapism is defined as prolonged erection of the penis, generally lasting over 4 hours, in the absence of sexual desire or stimulation ( Fig. 55.3 ). This medical condition was named after Priapus, an ancient Greek god of fertility and horticulture who was endowed with oversized genitalia.
Priapism can be divided into two main categories. Ischemic priapism, also known as low-flow priapism, is the most commonly seen variant and is due to painful venous engorgement of the corpora cavernosa and requires emergency treatment. Nonischemic (high-flow) priapism is quite rare and is often painless. It is caused by increased arterial inflow to the penis as a result of traumatic arteriocavernosal fistulas and does not require urgent treatment.
Ischemic priapism can be thought of as a compartment syndrome of the penis. The corpora cavernosa becomes engorged with stagnant, oxygen-depleted venous blood due to either an intraluminal obstruction of venous blood flow or an inability of the penile muscle tissue to adequately contract and augment venous outflow.
Indications: failure of an initial trial of subcutaneous or oral terbutaline (optional).
Contraindications: high-flow (nonischemic) priapism, stuttering priapism.
Complications: hematoma formation, infection, systemic absorption, and subsequent effects of α-adrenergic agents; permanent impotence may result from priapism regardless of promptness of therapeutic interventions.
Equipment: see later.
Administer parenteral opioid analgesic or light sedation.
Give a trial of 0.25 to 0.5 mg subcutaneous terbutaline (repeat in 15 minutes), or 5 mg terbutaline by mouth (optional).
Give an intracorporal injection of α-adrenergic agents and, if necessary, repeat every 20 minutes for a total of three doses (minimally invasive approach).
If unsuccessful, aspirate 20 to 30 mL of corporal blood.
If detumescence is not achieved, irrigate with saline or a dilute α-adrenergic agonist solution (aspirate-irrigate-aspirate cycle, as needed).
A visible change from venous (dark red) to arterial (bright red) blood is a marker of success.
For persistent erections, consult urology for possible shunt placement (cavernosum-spongiosum shunt).
If the procedure is successful, loosely wrap the penis in an elastic bandage.
A 3-day course of an oral α-adrenergic agent is reasonable at the time of discharge.
Arrange for urgent urology follow-up and administer strict return precautions.
Priapism is manifested by a persistent, usually painful, penile erection, unrelated to sexual stimulation and not relieved by ejaculation.
Over one third of patients with severe priapism may suffer permanent erectile dysfunction despite treatment, with obvious functional and emotional sequelae.
Priapism is characterized clinically by a soft glans penis and spongy urethra in the presence of two erect penile bodies (corpora cavernosa) ( Fig. 55.4 ). Two important concepts are worthy of mention. First, there is communication of blood flow between the corpora cavernosa, therefore in most cases the operator needs to access only one of the corpora. Secondly, introduction of vasoactive or other agents into the corpora is akin to an intravenous injection, so systemic effects may be precipitated, particularly after partial or full detumescence is achieved.
The pathophysiology of priapism is complex. The pharmacologic basis for treatment is based on manipulating blood flow via the α- and β-adrenergic receptors. Priapism is believed to result from increased arterial inflow of blood into the corpora cavernosa secondary to dilatation of the cavernosal arteries. Relaxation of the cavernosal tissue occurs and secondary compression of the emissary veins leads to engorgement of both corpora cavernosa during an erection. When the cavernosal pressure approaches the arterial pressure, blood flow is markedly reduced. Ischemic or low-flow priapism results after several hours of continuous painful erection, leading to intracavernosal acidosis and sludging of blood, with subsequent thrombosis of the cavernosal arteries, fibrosis of the corporal tissue, and irreversible impotence.
High-flow priapism is less common than low-flow priapism and usually results from traumatic production of arteriocavernosal fistulas. It is not associated with intracavernosal ischemia or acidosis and is therefore painless and may be treated electively rather than emergently.
In the past, priapism was most often encountered as a complication of a number of medical (e.g., hematologic, neoplastic, and drug-related) conditions ( Table 55.1 ). Today, many cases are iatrogenic, resulting from the current practice of using vasoactive substances (e.g., papaverine and phentolamine) and other newer erectile dysfunction medications to induce penile erections in impotent men. Sickle cell disease continues to be a leading cause of priapism. Sickle cell patients may experience such a high rate of recurrence that home self-injection of vasoactive drugs into the penis has been advocated. Cocaine use is one etiology that is likely underreported. A drug screen may unravel some discrepancies between clinical findings and history. As an end result, vasoactive drugs promote engorgement of the corpora cavernosa and reduction in venous outflow, which may result in low-flow or ischemic priapism. Several phosphodiesterase inhibitors and prostaglandin E1 are the drug treatments for impotence approved by the U.S. Food and Drug Administration (FDA). These medications act by increasing penile blood flow and enhancing smooth muscle relaxation. The incidence of priapism with these medications is quite low, particularly with the phosphodiesterase inhibitors. Penile rigidity due to a nondeflating penile prosthesis (pseudopriapism) or malignant replacement of the corpora in patients with bladder or prostate cancer should not be confused with true priapism.
CATEGORY | EXAMPLES |
---|---|
Medications | |
Impotence agents | Intracavernosal therapies (prostaglandin E1, papaverine, phentolamine) |
Oral agents (sildenafil) | |
Anticoagulants | Heparin, warfarin |
Antihypertensives | Hydralazine, prazosin, doxazosin |
Antidepressants | Trazodone, fluoxetine, sertraline, citalopram |
Antipsychotics | Phenothiazines, atypical antipsychotics |
Hormones | Gonadotropin-releasing hormones, testosterone |
Illicit substances | Cocaine, marijuana, alcohol |
Miscellaneous | Hydroxyzine, metoclopramide, omeprazole, total parenteral nutrition, general anesthetics |
Hematologic/Oncologic Disorders | |
Sickle cell disease | |
Hematologic malignancies | Leukemia, myeloma |
Other malignancies | Prostate, bladder, metastatic cancer |
Central Nervous System | |
Brain | Cerebrovascular accident |
Brain stem | Medulla injury |
Spinal cord | Spinal stenosis, spinal cord injury, lumbar disk herniation |
Others | |
Genitourinary trauma | Straddle injury |
Infections | Malaria, rabies |
Toxins | Black widow, scorpion, carbon monoxide |
Metabolic | Amyloidosis, gout, hypertriglyceridemia |
Idiopathic |
The emergency clinician should attempt to identify reversible causes for low-flow priapism and, often in conjunction with a urologic surgeon, initiate specific corrective therapy as soon as possible. Low-flow priapism in children and young adults may be due to sickle cell disease and such cases may respond to noninvasive standard anti-sickling measures. However, the role of transfusion therapy in patients with priapism due to sickle cell anemia is uncertain.
Regardless of the etiology, this distressing condition is first treated with adequate analgesia, often consisting of parenteral opioids, with or without benzodiazepines.
A urologic surgeon typically manages acute priapism. However, emergency treatment for ischemic priapism will frequently need to be initiated while awaiting specialty consultation. The classic teaching is that the initial treatment, oral (or subcutaneous) terbutaline, is the same regardless of the inciting etiology, although its utility and efficacy are debated. It is thought that terbutaline, a β2-adrenergic agonist, increases venous outflow from the engorged corpora by way of relaxation of venous sinusoidal smooth muscle. Terbutaline is of unproved benefit; however, given its limited propensity for adverse effects, a trial is reasonable in select circumstances while awaiting specialty consultation.
If terbutaline fails to work rapidly, the next step is penile blood aspiration, saline irrigation of the corpora cavernosum, and intracorporal instillation of an α-adrenergic receptor agonist such as dilute phenylephrine or epinephrine.
A subtype of ischemic priapism is known as stuttering priapism. This entity is typically observed in patients with sickle cell disease. Patients experience recurrent episodes of priapism that often last less than 3 hours and often do not require emergency treatment unless symptoms become markedly prolonged. High-flow (nonischemic) priapism is treated surgically (elective repair).
A suggested algorithm for the initial treatment of acute nonischemic priapism in the emergency setting is presented in Box 55.1 . Options for treatment include:
Minimally invasive technique (direct intracorporal injection of α-adrenergic agent, without aspiration or irrigation).
Aspiration of corporal blood
may be performed with or without saline irrigation.
following aspiration, may be followed by injection of α-adrenergic agent.
alternatively, corpora can be irrigated with a dilute α-adrenergic agent–containing solution.
Proceed with treatment of acute priapism in the following order until detumescence is achieved:
Parenteral narcotic analgesia/sedation.
Terbutaline, 0.25 to 0.5 mg subcutaneously (may be repeated in 15 minutes), or terbutaline, 5 mg orally (one dose only).
Intracorporal injection of adrenergic agents. May repeat every 20 minutes for a total of three doses.
If unsuccessful, perform corporal aspiration of 30 to 60 mL of blood, followed by observation. If detumescence is not achieved, irrigate (inject and remove 10- to 20-mL aliquots) with a diluted α-agonist solution (e.g., phenylephrine, 10 mg in 500 mL of normal saline, or 1 mg epinephrine in 1 L of normal saline). Multiple irrigations may be required. The initial aspiration removes venous blood (dark red), and return of arterial blood (bright red) may serve as a marker of success.
For persistent erections, consult urology for possible corpus cavernosum-spongiosum shunt placement.
If treatment is successful in the emergency department, discharge is possible. A 3-day course of an oral α-adrenergic agent such as pseudoephedrine to promote continued vasoconstriction is recommended. The value of this intervention is unproven, however.
For patients with recurrent priapism secondary to sickle cell disease, consider intramuscular injections of leuprolide (Lupron) (consult a hematologist for recommended doses).
Relief of priapism by simple injection of vasoactive solutions into the corpus cavernosum has been reported. Intercavernous injection therapy for the management of priapism is simple to perform, less traumatic, and less invasive than aspiration and irrigation. This minimally invasive procedure may be attempted as an initial approach. This same procedure may be used as a self-injection technique for home treatment of recurrent priapism. With this technique, a 25- to 27-gauge needle is used to inject vasoactive substances into the corpus at the proximal end of the penis (2–4 cm distal to the shaft origin), with the goal of pharmacologically reversing priapism ( Fig. 55.5 A ). Often, this can be accomplished without anesthesia. One option is to draw up 0.5 mg (0.5 mL) of phenylephrine and add 0.5 mL of saline diluent for a final volume of 1 mL ( Table 55.2 ). Puncture the corpus with the needle at the 10 o'clock or 2 o'clock position at the base of the penis (with 12 o'clock being the dorsal vein of the penis), aspirate blood to confirm position, and inject the solution. If detumescence is not achieved in 20 to 30 minutes, give a repeat injection, up to a total of three injections. In one small study, successful detumescence was achieved in eight of nine patients by simple intracorporal injection of phenylephrine with this regimen, with three or fewer injections required. Alternatively, 0.1 mg of epinephrine (0.1 mL of 1 : 1000) diluted with 0.9 mL of saline may be used (1 mL total volume). Regardless of medication used, only one side needs to be injected, but two or three injections might be necessary. Wait at least 20 minutes after each injection before additional interventions. Note that this is essentially an intravenous injection and systemic effects may occur. As such, proceed with caution in patients with cardiovascular disease. Success has also been noted by injecting the corpus cavernosum with 1 mL of the local anesthetic lidocaine (2%) with epinephrine (1 : 100,000) into each side, or 2 mL into one side.
AGENT | DOSE | VOLUME |
---|---|---|
Phenylephrine a | 0.2–0.5 mg | Dilute with saline; final volume, 1 mL a |
Epinephrine (1 : 1000) | 0.1 mg (0.1 mL) | Dilute with 0.9 mL saline; final volume, 1 mL |
Lidocaine (2%) with epinephrine (1 : 100,000) (local anesthetic solution) | 40 mg lidocaine 0.02 mg epinephrine (2 mL) |
1 mL injected into each side of the corpus cavernosum; final volume, 2 mL b |
a Single side injected with the entire amount. See text for preparation of the phenylephrine injection solution.
b Total amount divided into two doses. Inject each side with half the total volume (1 mL) or inject the total volume (2 mL) into one side.
Box 55.2 lists the equipment needed for aspiration and irrigation of the corpus cavernosum. This procedure entails drainage of blood from the erect penis, irrigation with saline if necessary (e.g., inadequate return of blood with lack of detumescence), and finally the instillation of a vasoactive medication. Alternatively, irrigation with aliquots of a dilute vasoactive solution may be effective (aspirate-infuse-aspirate cycle as needed).
27-gauge needle (for penile block)
1-mL syringe (for local anesthetic)
1% lidocaine without epinephrine (for penile block)
Sterile drapes
Gauze sponges
Chlorhexidine preparation solution
19-gauge butterfly needles (for aspiration)
Two 10-mL to 30-mL syringes (for aspiration)
Sterile basin for aspirated blood
Blood gas syringe with cap
Irrigation fluid (one of the following vasoactive agents a
a Systemic absorption of vasoactive agents may occur and result in adverse cardiovascular effects.
is diluted with 500 mL of normal saline and 20 to 30 mL is administered in small aliquots; 5000 units of heparin added to the solution is optional):
Phenylephrine, 10 mg/500 mL of saline
Norepinephrine, 1 mg/500 mL of saline
Epinephrine, 0.5 mg/500 mL of saline
Place the patient in the supine position. Parenteral analgesia and sedation are suggested. Local anesthesia at the puncture site is recommended. An injection of 1% plain lidocaine placed at the base of the penis for a dorsal penile nerve block or placement of a circumferential penile block can be performed, but are usually not necessary (see Fig. 55.5 B ). Prepare and drape the penis in sterile fashion. Grasp the shaft of the penis with your nondominant thumb and index finger. Palpate the engorged corpus cavernosum laterally (2 and 10 o'clock positions) and insert a 21- to 19-gauge butterfly needle into the corpus cavernosum.
Alternatively, a 20-gauge intravenous catheter may be used, but the butterfly needle is preferred. A dialysis access butterfly needle may also be used ( Fig. 55.6 ). If palpation fails to demonstrate the corpus, blindly inserting the needle at either 10 o'clock or 2 o'clock will usually gain access to this large vascular structure. Because there is communication of blood flow between both sides, the operator needs access to only one of the corpora. Either side may be punctured. The site of needle placement is typically anywhere from the base to the proximal shaft, 2 to 4 cm distal from the shaft origin. The glans should not be used as a puncture site.
The needle is advanced at a 45-degree angle, using constant suction. Blood is usually readily aspirated; once it is obtained do not advance the needle further. Next, stabilize the needle. Avoid deep penetration to minimize the risk of injury to the cavernosal artery during this procedure.
Aspirate an initial 20 to 30 mL of corporal blood while milking the corpus with the nondominant hand. Do not apply excessive suction because this often halts the aspiration. A common error is to use too much suction with a 60-mL syringe. Using a 10-mL syringe, and changing it if it fills with blood, is preferable. Use of a butterfly reduces the danger of dislodging the needle when changing syringes.
Continue aspiration until the original egress of dark blood ceases and bright red arterial blood returns or when complete detumescence is obtained and persists. Because multiple anastomoses exist between the two corpora cavernosa, bilateral aspiration is not required. If there is inadequate return of blood with a lack of detumescence, consider irrigating with 20 to 30 mL of saline.
If detumescence is achieved after initial aspiration with or without saline irrigation, no further treatment may be required. If this is successful, some clinicians advise instilling an aliquot of vasoactive substance. Phenylephrine is recommended as the agent of choice as it may minimize the risk of cardiovascular side effects more commonly seen with other sympathomimetic agents. Inject 0.1 to 0.5 mg of phenylephrine (in 1 mL of normal saline). It is important to note that the recommended concentration for instillation is similar to that recommended for the minimally invasive technique detailed earlier. Lower concentrations in smaller volumes should be used for patients with cardiovascular risk factors or for children. If irrigation is performed with a dilute vasoactive substance as delineated hereafter, additional medication instillation is not suggested.
If detumescence is not achieved following aspiration (with or without saline irrigation), irrigation with a dilute vasoactive substance is another option. A number of dilute irrigation solutions have been suggested, but none have been proven to be superior. Some suggest 20 to 30 mL of a phenylephrine/normal saline solution (10 mg of phenylephrine in 500 mL of normal saline) as the exchange for 20 to 30 mL of aspirated corporal blood. Some clinicians add 2500 to 5000 units of heparin to the solution, but the use of heparin is of unproven value. Alternatively, 1 mg of epinephrine can be added to 1 L of saline, with irrigation performed using 20- to 30-mL aliquots. It is important to note that corporal irrigation is performed with a much less concentrated solution (phenylephrine, 20 µg/mL) as compared with that used for the minimally invasive technique or vasoactive instillation of 1 mL aliquots following detumescence detailed earlier (phenylephrine, 500 µg/mL).
Note that the corpus cavernosum has ready access to systemic circulation, and injecting a drug into it is essentially the same as an intravenous injection. When detumescence occurs, the unmetabolized drug enters the systemic circulation; therefore vasoactive drug dosages should be monitored carefully.
Observe the patient in the ED for recurrence. Although the ideal observation period is unknown, 2 hours has been suggested. Fig. 55.5 B , step 4 demonstrates the entire penis loosely wrapped with elastic (ACE, 3M) bandage to prevent hematoma formation at the injection site(s). Strict return precautions must be provided for priapism recurrence, and urgent urology follow-up should be ensured. A short course of an oral α-adrenergic agent, such as pseudoephedrine for 3 days, is often recommended. However, the value of this intervention is of questionable value and unproven benefit.
Although hematoma formation or infection can occur with properly performed aspiration, these complications are infrequent. Injected or instilled vasoactive agents can be absorbed systemically, with the potential for toxic effects. Therefore the intracavernosal use of vasoactive agents is relatively contraindicated in patients with conditions sensitive to these agents (e.g., severe hypertension, dysrhythmias, monoamine oxidase inhibitor use, etc.). Blood pressure and cardiac rhythm should be monitored throughout the procedure if the patient is at risk. Failure to aspirate blood is a potential complication, usually because of a misplaced needle, applying excessive suction, or if blood has clotted. Because impotence is a well-recognized complication of priapism regardless of the cause or the promptness of therapeutic intervention, the patient should be advised regarding this potential long-term consequence.
Because prolonged priapism increases the risk of subsequent erectile dysfunction, an aggressive management strategy is advised. After 4 hours of persistent priapism, there is heightened release of inflammatory cytokines in the acidotic and hypoxic corpora cavernosa. Inflammation may include smooth muscle changes including cell death and fibrosis, which may cause permanent erectile dysfunction. Recurrence is not uncommon, and some patients require multiple procedures on a recurring basis. Surgical shunting procedures by the urology team might be required if these other measures are met without success.
Paraphimosis is the inability to completely reduce the penile foreskin distally, back to its natural position overlying the glans penis. This condition occurs exclusively in uncircumcised males and is a urologic emergency.
Paraphimosis may occur at any age, but often occurs in the extremes of life ( Fig. 55.7 ). The condition can be quite subtle and may be either unrecognized or misdiagnosed as an allergic reaction, penile trauma, infection, or edema resulting from systemic volume overload (e.g., congestive heart failure, nephrotic syndrome) ( Fig. 55.8 ).
Iatrogenic paraphimosis may occur following urinary catheterization or medical examination if the foreskin is not returned to its native location overlying the glans. Poor hygiene or balanoposthitis are also associated with development of paraphimosis. Inflammation can result in contracture of the distal foreskin. Later when the foreskin is retracted proximally over the compressible glans, the contracted foreskin forms a constrictive band and gets stuck in the retracted position.
Indications: emergency reduction of paraphimotic foreskin.
Contraindications: none.
Complications: skin tears or lacerations; failure of the reduction procedure necessitates surgical intervention (dorsal slit or definitive circumcision).
Equipment: for simple manual reduction, all that is needed is a topical anesthetic lubricant. Adjunctive equipment for alternative reduction techniques and maneuvers as described in this chapter are optional.
Apply a topical anesthetic lubricant to the distal penis (foreskin and glans).
Administer a systemic analgesic (optional).
Compress the foreskin and glans with a snugly grasped hand.
Use the thumbs to invert the glans penis proximally through the phimotic ring.
Use the index and long fingers to reduce the phimotic ring distally.
If unsuccessful, try alternate maneuvers to reduce edema before reattempting manual reduction.
Consider an optional trial of glans adjuncts: administer an ice pack or a compressive bandage to reduce glans edema.
Consider an optional trial of foreskin adjuncts: administer micropuncture wounds, use sugar, or use hyaluronidase to reduce foreskin edema.
If unsuccessful, reduce the paraphimosis surgically by dorsal slit or definitive circumcision.
Arrange urgent urology follow-up following reduction.
Paraphimosis is a urologic emergency that must be treated promptly to prevent glans necrosis. Paraphimosis can be managed in the ED without the need for emergency specialty consultation, but if possible, urology involvement will be needed for postprocedure management. There are many reported methods of successful paraphimosis reduction ( ). The most commonly employed initial maneuver involves manual compression of the distal penis to decrease edema, followed by reduction of the glans penis back through the proximal constricting band of foreskin (phimotic ring).
The penis consists of the paired corpora cavernosa, or erectile bodies, which lie dorsal to the corpus spongiosum (see Fig. 55.4 ). The corpus spongiosum surrounds the penile urethra. The corpora cavernosa and the corpus spongiosum are wrapped by a thin connective tissue layer, the tunica albuginea. The glans is the distal portion (head) of the penis. The foreskin, or prepuce, in uncircumcised males lies over the glans and can be retracted proximally to expose the glans. The coronal sulcus distinguishes the glans penis from the penile shaft (see Figs. 55.7 B and 55.8 B ).
Patients will present with a red, painful, and swollen glans penis associated with an edematous, proximally retracted foreskin that forms a circumferential constricting band. The penile shaft proximal to the constricting band is typically soft. The entrapped foreskin forms a constricting band on the penile shaft. Compression inhibits venous drainage of the glans and results in a cycle of progressive glans edema. The normal anatomy and identification of the foreskin may be obfuscated by edema, and the condition can be asymmetric and rather bizarre appearing ( Fig. 55.9 , step 1 ). Glans edema may become so severe that arterial flow is compromised, which can result in necrosis and gangrene of the glans penis.
Emergency reduction is indicated whenever a paraphimosis exists.
There are no contraindications.
The current standard for reducing paraphimosis is manual reduction. This can be accomplished by using a nonirritating topical anesthetic lubricant applied to the inner surface of the foreskin (not to the shaft of the penis) and the glans to reduce friction and decrease the discomfort of the procedure. A penile block may be performed if necessary (see Fig. 55.9 , steps 2 and 3 ). If there is significant discomfort or patient apprehension, systemic analgesia or procedural sedation may be useful adjuncts. For young children, general anesthesia may be necessary.
Compress the foreskin and glans with a snugly grasped hand for several minutes to reduce as much edema fluid as possible (see Fig. 55.9 , steps 4-6 ). Use the thumb to push the glans through the foreskin that has been encircled by the entire palm (see Fig. 55.9 , step 7 ). Alternatively, place the index and long fingers of both hands in apposition just proximal to the phimotic ring. Align both thumbs on the urethral meatus. Apply constant force with the thumbs to try and invert the glans penis proximally while using the index and long fingers to reduce the phimotic ring distally over the glans penis and into its normal anatomic position (see Fig. 55.9 , step 8 ). Successful reduction results in the appearance of an uncircumcised penis with a phimotic foreskin (see Fig. 55.9 , steps 9 and 10 ). The key to success in both these maneuvers is the application of slow, steady pressure.
Several alternative methods for reducing the edema have been described in the literature. These methods can be used before attempting manual reduction, or if simple manual reduction fails.
Babcock clamps (noncrushing tissue clamps) can be used to reduce the paraphimotic foreskin ( Fig. 55.10 A ). Apply six to eight Babcock clamps spaced evenly around the foreskin, straddling the phimotic ring (one edge just proximal and the other edge just distal to the phimotic ring). Grasp all clamps and apply simultaneous distal traction to pull the phimotic ring over the glans. After reduction, remove the clamps. It is important to inspect the foreskin for injuries.
Other techniques focus on reduction of glans or foreskin edema (or both), followed by reduction of the paraphimosis. Diminished glans edema facilitates foreskin reduction to its natural position. One suggested maneuver is to apply an ice pack. In the “iced-glove” method, use cold compression to reduce foreskin swelling and induce vasoconstriction in the glans penis (see Fig. 55.10 B ). Half fill a large glove with crushed ice and water, and tie the cuff end securely. Invaginate the thumb of the glove and then draw it over the lubricated paraphimotic penis. Hold the thumb of the glove securely in place over the glans for 5 to 10 minutes. The combination of cooling and compression usually decreases the edema sufficiently to permit manual reduction of the foreskin. Wrapping the penis in a compressive bandage is another alternative. A 2-inch compressive bandage (such as an ACE [3M] bandage or similar) can be wound snugly around the penis from the glans to the base, and removed in 5 to 7 minutes.
Alternatively, techniques focusing on reduction of foreskin edema have been advocated ( Box 55.3 ). The Dundee technique involves creating multiple micropunctures of the edematous foreskin and then expressing edema fluid. Hyaluronidase has been reported to result in rapid reduction of prepuce edema that facilitates manual reduction of the foreskin. This enzyme, when injected into the swollen retracted foreskin, causes hydrolysis of hyaluronic acid that, in turn, increases tissue permeability so the edema in the foreskin is diffused out into the surrounding penile tissue. There have even been advocates of a noninvasive way to reduce the foreskin edema via the application of granulated sugar to the penis. Sugar forms an osmotic gradient that draws out edema fluid, but this may take several hours. Publications on these alternative procedures are generally observational in design with very small numbers. To date, there have not been any large studies of comparative effectiveness; as such it is difficult to recommend any one method as superior.
Dundee micropuncture technique : Make approximately 20 puncture holes in the edematous foreskin tissue with a 26-gauge (or similar) needle and express the fluid.
Hyaluronidase technique : Inject 1 mL of hyaluronidase (150 U/mL) by tuberculin syringe into one or two sites in the edematous foreskin to reduce edema fluid immediately.
Sugar technique : Granulated sugar has been studied, but a better alternative for patients in the emergency department is to soak a swab in 50 mL of 50% dextrose solution and leave it wrapped around the paraphimotic foreskin for 1 hour.
Iced-glove technique: see Fig. 55.10 B .
If the previous methods are unsuccessful, it may be necessary to incise the constricting phimotic tissue to permit reduction of the foreskin over the glans by dorsal slit procedure. In adults, this can generally be carried out under penile-block anesthesia, but procedural sedation or general anesthesia may be necessary for young children.
Observe the patient to ensure adequate local hemostasis, ability to void spontaneously, and recovery from analgesia or sedation, if utilized. Replacing the foreskin to its native position following examination, catheter placement, sexual activity, or any other manipulation is essential to preventing recurrent episodes. Patients should be referred to a urologist for evaluation of possible surgical options, including circumcision.
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