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Compendium April 2005 (Vol 27, No 4)

Update on Equine Therapeutics: Priapism in Horses

by Frederik Pauwels, DVM, Jim Schumacher, DVM, MS, DAVCS, Dickson D. Varner, DVM, MS, DACT

    Priapism (i.e., persistent erection without sexual excitement) occurs when the erect penis fails to detumesce.1 Although priapism is uncommon in horses, it is an economically important disease because unresolved priapism leads to impotence. The condition occurs in both stallions and geldings,2,3 but geldings are less commonly affected.4

    Cause

    Major etiologic factors in the development of priapism in humans include perineal trauma, hematologic diseases that cause vascular sludging (e.g., leukemia, sickle cell anemia), and use of antihypertensive and antidepressant drugs.1 The condition in horses usually occurs subsequent to administration of a phenothiazine-derivative tranquilizer, usually acetylpromazine2,3 (Figure 1). Less commonly reported causes of the condition in horses include general anesthesia,5,6 neoplasia of the pelvic canal,4 and nematodiasis of the spinal cord.7

    Priapism occurs when arterial inflow or venous outflow becomes disturbed, resulting in failure of an erect penis to detumesce.1 In humans, priapism is classified as high flow (i.e., arterial) when increased arterial blood flow overrides compensatory venous drainage or as low flow (i.e., venoocclusive) when the neural mediation of detumescence is altered or primary vascular or hematologic alterations occur.8 High-flow priapism is usually painless, produces rigid to semirigid engorgement of the entire penis, and almost always results from blunt or penetrating trauma to the perineum or penis. Color-flow Doppler ultrasonography may confirm high-flow priapism by demonstrating an arterial-cavernosal shunt. Gas analysis of blood aspirated from the corpus cavernosum penis may help differentiate low-flow from high-flow priapism.9 Low-flow priapism is characterized by a pH less than 7.25, partial pressure of oxygen less than 30 mm Hg, and partial pressure of carbon dioxide greater than 60 mm Hg. High-flow priapism in humans is rare compared with low-flow priapism and has not been documented in animals.10,11

    Administering phenothiazine-derivative tranquilizers, the most common cause of priapism in horses, may cause failure of detumescence by blocking a-adrenergic impulses that bring about detumescence. Regardless of its cause, the low-flow form of priapism is characterized by stasis of blood within the corpus cavernosum penis.1 Vascular stasis causes the partial pressure of carbon dioxide in the stagnant blood to increase, resulting in aggregation (i.e., sickling) of erythrocytes (Figure 2). The sickled erythrocytes can occlude the venous outflow of the corpus cavernosum penis, resulting in trabecular edema. The edematous trabeculae eventually become fibrotic, decreasing the cavernosal tissue's capacity for expansion necessary for normal erection. Arterial supply to the cavernous tissue remains patent during early stages of priapism, but it too eventually becomes occluded. Priapism in horses may result in injury to the pudendal nerves, apparently from tension on the nerves or compression of the nerves against the ischium, causing penile paralysis.4 If unresolved, priapism in horses results in loss of erectile function of the corpus cavernosum penis and decreased sensitivity of the penis.

    Clinical Signs

    The penis of a horse with priapism may appear to be protruded rather than erect, but turgidity of the corpus cavernosum penis can be detected during palpation. The corpus spongiosum penis remains uninvolved in the erection. During ultrasonographic examination of a horse chronically affected by priapism, the corpus cavernosum penis appears densely echogenic4,12 and the horse may not respond when a normally painful stimulus is applied to the distal portion of the penis (Figure 3).

    Treatment

    Horses with priapism have been treated by massaging the penis, applying an emollient dressing to the penis, and elevating the penis with slings.13 These treatments are important in preventing edema and further injury to the penile and preputial integument, but they do not resolve the condition.

    When priapism is the result of a-adrenergic blockade, such as that caused by administering acetylpromazine, an affected horse can sometimes be treated successfully by cholinergic blockade using an acetylcholine antagonist—benztropine mesylate.3,6 This drug is more likely to be successful in treating horses with priapism when treatment is initiated soon after the onset of the condition. An average-sized horse should receive 8 mg slow IV. Administering other drugs such as terbutaline, which also has anticholinergic action, may be beneficial in treating affected horses.14 This b2-agonist has been used successfully in humans at a dose of 5 mg PO or IV. Other b2-agonists such as clenbuterol (Ventipulmin syrup, Boehringer Ingelheim, St. Joseph, MO) could have a similar effect. Horses with chronic obstructive pulmonary disease are sometimes treated by administering clenbuterol at a dose of 0.8 to 3.2 mg/kg PO. A similar dose might be effective in treating horses with priapism.15

    Humans with low-flow priapism resulting from idiopathic, neurologic, or pharmacologic causes are usually treated by corporeal aspiration and injection of phenyl­ephrine or adrenaline into the corpus cavernosum penis.16 a-Adrenergic agents injected into the corpus cavernosum penis of humans in the early stages of priapism may promote contractility of cavernous and arterial smooth muscle to bring about penile detumescence.16 Injecting 10 mg of 1% phenylephrine, an a-adrenergic agent, directly into the erect corpus cavernosum penis is often effective in resolving priapism in horses. The response to intracavernosal injection is generally quite prompt and dramatic. When administered to horses in the acute stage, one treatment may permanently resolve priapism. For protracted cases, the treatment is generally effective but short-lived (i.e., 4 to 6 hours), and other corrective measures must also be instituted.

    A horse that does not respond to medical therapy within a few hours of the onset of priapism should be treated by irrigating stagnant blood from the corpus cavernosum penis with heparinized, physiologic saline solution. The corpus cavernosum penis can be irrigated with the horse standing, but the procedure is most easily accomplished with the horse anesthetized and dorsally recumbent. Physiologic saline solution containing 10 U heparin/ml should be introduced under pressure through a 12- or 14-gauge needle inserted into the erect corpus cavernosum penis just proximal to the glans penis. The physiologic saline solution along with the stagnant blood should exit 10 to 15 cm distal to the ischium through a similar-sized needle inserted into the corpus cavernosum penis or through a stab incision in the corpus cavernosum penis. The corpus cavernosum penis should be irrigated until fresh hemorrhage appears in the efflux (Figure 4). Injecting 2 to 10 mg of 1% phenylephrine into the corpus cavernosum penis at the end of the lavage may be beneficial. An incision in the tunica albuginea of the corpus cavernosum penis should be sutured when irrigation has been completed. Failure of arterial blood to appear at the exit portal after stagnant blood has been evacuated may indicate that the arteriolar supply to the corpus cavernosum penis has been permanently damaged and impotence is likely.

    The point at which pathologic changes to the cavernosal tissue become irreversible after the onset of priapism has not been determined for horses; therefore, guidelines have not been established to indicate when irrigation of the corpus cavernosum penis should be initiated. Because prolonged erection may damage the pudendal nerves, we believe that the corpus cavernosum penis should be irrigated within a few hours after priapism has been recognized (if treatment by cholinergic blockade or a-adrenergic stimulation fails).

    Erection recurs following irrigation if venous outflow remains occluded as long as arteriolar inflow remains patent. If erection persists after irrigation of the corpus cavernosum penis, trapped blood within the corpus cavernosum penis can be shunted through the corpus spongiosum penis. The corpus spongiosum penis offers a convenient exit for blood trapped in the corpus cavernosum penis because the former is not involved in priapism.1,17

    To create the shunt, the horse should be anesthetized and dorsally recumbent.17 The horse's penis and perineal region should be prepared for aseptic surgery and a stallion catheter inserted into the urethra. A 15-cm incision should be made on the perineal raphe about 5 cm caudal to the base of the scrotum to expose the shaft of the penis. The bulbospongiosus muscle, which covers the ventral aspect of the corpus spongiosum penis, should be identified and the right or left edge of the bulbospongiosus muscle elevated from the edge of the urethral groove to expose 4 to 5 cm of the underlying tunica albuginea of the corpus spongiosum penis, which surrounds the catheterized urethra (Figure 5). A 3-cm, longitudinal incision should be made through the tunica albuginea of the corpus cavernosum penis adjacent to the exposed corpus spongiosum penis, and stagnant blood should be evacuated from the cavernous spaces of the corpus cavernosum penis through this incision using irrigation as already described.

    The axial edge of the incision through the tunica albuginea of the corpus cavernosum penis should be sutured to the tunica albuginea of the corpus spongiosum penis with 2-0 absorbable suture using a simple continuous suture pattern. A matching 3-cm, longitudinal incision into the corpus spongiosum penis should be created adjacent to this suture line, taking care to avoid penetrating the catheterized urethra. Bright-red hemorrhage should flow from the incised corpus spongiosum penis, and at this point in the procedure, suction is usually required to maintain visibility. To complete the shunt, the abaxial edge of the incision in the corpus cavernosum penis should be sutured to the axial edge of the incision in the corpus spongiosum penis with 2-0 absorbable suture using a simple continuous suture pattern (Figure 5 and Figure 6). The bulbospongiosus muscle should be sutured to its origin on the tunica albuginea of the corpus cavernosum penis at the edge of the urethral groove, and the subcutaneous tissue and skin should be apposed. Horses do not appear to be uncomfortable after the surgery, and swelling should be minimal.

    Complications of the cavernosal shunt in humans include urethrocavernous or urethrocutaneous fistula, penile gangrene, infection, painful corpus spongiosum penis during erection, and impotence.1,18 Males receiving a vascular shunt to treat priapism may become impotent from failure to achieve or maintain pressure in the corpus cavernosum penis required for intromission, and this failure may be due to damaged corporeal tissue or the shunt itself.17 The shunt may close as normal blood outflow in the corpus cavernosum penis resumes, but closure is not always essential for return to potency. Bulls have become impotent after developing a trauma-induced shunt between the corpus cavernosum penis and corpus spongiosum penis,19 but a shunt created surgically between the corpus cavernosum penis and the corpus spongiosum penis of normal stallions does not interfere with subsequent erection and ejaculation, even if the shunt does not close.17 Failure of a stallion af­fected by priapism to develop a normal erection or to ejaculate after creation of a shunt between the corpus cavernosum penis and the corpus spongiosum penis is most likely due to trabecular damage caused by persistent erection rather than by the shunt. Geldings that develop priapism can be treated with partial phallectomy if medical therapy and lavage are unsuccessful in resolving the condition.5 Horses are unlikely to experience greater than normal hemorrhage from the penile stump after phallectomy.

    Erectile function in humans with damaged cavernous tissue caused by priapism has been enhanced by injecting a vasoactive drug, such as phenoxybenzamine or phentolamine, into the cavernous tissue.1 Doses of these drugs for injection into the corpus cavernosum penis of horses have not been described. Administering a vasoactive drug into the cavernous tissue may also be useful for enhancing erectile function in horses with damaged erectile tissue. The copulatory ability of a stallion with damaged cavernosal tissue and decreased penile sensitivity resulting from prolonged priapism may also be enhanced by lowering a horse's ejaculatory threshold by administering a tricyclic antidepressant, such as imi­p­ramine hydrochloride (3 mg/kg PO), before breeding.20 Testosterone-impregnated cream applied topically to the glans penis may also improve penile sensitivity.

    Acknowledgment

    The authors thank Debbie Haines for illustrating Figure 5 .

    1. Pohl J, Polt B, Kleinhans G: Priapism: A three phase concept of management according to aetiology and progress. Br J Urol 58:113, 1986.

    2. Lucke JN, Sansom J: Penile erection in the horse after acepromazine. Vet Rec 105(1):21-22, 1979.

    3. Sharrock AG: Reversal of drug-induced priapism in a gelding by medication (benztropine). Aust Vet J 58(1):39-40, 1982.

    4. Blanchard TL, Schumacher J, Edwards JF, et al: Priapism in a stallion with generalized malignant melanoma. JAVMA 198(6):1043-1044, 1991.

    5. Van Harreveld PD, Gaughan EM: Partial phallectomy to treat priapism in a horse. Aust Vet J 77(3):167-169, 1999.

    6. Wilson DV, Nickels FA, Williams MA: Pharmacologic treatment of priapism in two horses. JAVMA 199(9):1183-1184, 1991.

    7. Oyamada T, Miyajima K, Kimura Y, et al: Priapism possibly caused by spinal nematodiasis in a stallion. J Equine Sci 8(4):101-107, 1997.

    8. Rochat MC: Priapism: A review. Theriogenology 56(5):713-722, 2001.

    9. Stock KW, Jacob AL, Kummer M, et al: High-flow priapism in a child: Treatment with superselective embolization. Am J Roentgen 166:290-292, 1996.

    10. Lue TF, Hellstrom WJ, McAninch JW, Tanagho EA: Priapism: A refined approach to diagnosis and treatment. J Urol 136(1):104-108, 1986.

    11. Harmon WJ, Nehra A: Priapism: Diagnosis and management. Mayo Clin Proc 72(4):350-355, 1997.

    12. Love CC, McDonnell SM, Kenney RM: Manually assisted ejaculation in a stallion with erectile dysfunction subsequent to paraphimosis. JAVMA 200:1357-1359, 1992.

    13. Pearson H, Weaver BM: Priapism after sedation, neuroleptanalgesia and anaesthesia in the horse. Equine Vet J 10(2):85-90, 1978.

    14. Shantha TR, Finnerty DP, Rodriguez AP: Treatment of persistent penile erection and priapism using terbutaline. J Urol 141:1427-1429, 1989.

    15. Erichsen DF, Aviad AD, Schultz RH, Kennedy TJ: Clinical efficacy and safety of clenbuterol HCl when administered to effect in horses with chronic obstructive pulmonary disease (COPD). Equine Vet J 26(4):331-336, 1994.

    16. van Driel MF, Hesselink JW: Priapism in the stallion and in man. Tijdschr Diergeneeskd 128(8):255, 2003.

    17. Schumacher J, Varner DD, Crabill MR, Blanchard TL: The effect of a surgically created shunt between the corpus cavernosum penis and corpus spongiosum penis of stallions on erectile and ejaculatory function. Vet Surg 28(1):21-24, 1999.

    18. Cosgrove MD, La Rocque MA: Shunt surgery for priapism. Urology 4:1, 1974.

    19. Walker DF: Surgery of the penis, in Walker DF, Vaughan JT (eds): Bovine and Equine Urogenital Surgery. Philadelphia, Lea & Febiger, 1980, p 10.

    20. McDonnell SM: Oral imipramine and intravenous xylazine for pharmacologically-induced excopula ejaculation in stallions. Anim Reprod Sci 68(3-4):153-159, 2001.

    References »

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