Self-Administered lntraurethral Chlorpromazine: An Unusual Cause of Priapism STEVEN C. JACKSON, Priapism is a prolonged, painful penile erection unaccompanied by sexual desire and not alleviated by ejaculation. The etiologies of priapism are numemus and diverse. Priapism can be a serious adverse effect of psychotropic medications. The case of a 36-year-old man who demonstrated priapism, 46 hours after inserting a crushed chlorpromazine tablet into the urethral meatus of his penis, is reported. Priapism induced by this mute of drug administration has not been previously described. The pathophysiology and treatment of priapism are reviewed. (Am J Emerg Med 1991;9:171-176. Copyright 0 1991 by W.B. Saunders Company)

Priapism is the sustained, painful penile erection unaccompanied by sexual desire and not alleviated by ejaculation. Ironically named after the Greek god of male procreative power, Priapos, it results in permanent impotence 50% of the time.‘,2 There are numerous and varied causes of priapism. The etiologies include spinal cord trauma, perineal trauma, sickle cell disease, neoplastic diseases, vasculitis, nephrotic syndrome, dialysis, scorpion stings, black widow spider bites, idiopathic, iatrogenic, and pharmacologic agents. 2-4.42-45Psychotropic medication is the most common cause of drug-associated priapism.’ We report a case of priapism induced by inserting a crushed chlorpromazine tablet into the urethral meatus of the penis. Priapism associated with this route of drug administration has not been previously reported. A brief discussion of the mechanism of priapism and its treatment accompanies the report. CASE REPORT A 36-year-old black man presented to the emergency department (ED) with a 48-hour history of a sustained painful erection. The patient’s penis became erect shortly after he placed a crushed 25 mg chlorpromazine tablet into his penile meatus. He intentionally placed the tablet fragments into his penile urethra. believing that it would enhance his sexual endurance and potentiate his orgasm. He initially presented to an outlying ED. 42 hours after the onset of the intractable erection, where he was treated with intravenous hydration and corporeal irrigation without effect. He was then referred to our hospital. Medical history was negative for sickle cell disease, spinal or perineal trauma, malignancies, hematologic disorders. or neurological disease. The patient denied prior psychiatric illness. The patient vehemently denied prior episodes of priapism or attempts at placement of foreign bodies into the penile urethra. He denied any urinary

From the Section of Emergency Medicine and Trauma, Department of Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK. Manuscript received January 9, 1990; revision accepted October 16, 1990. Address reprint requests to Dr Walker, Section of Emergency Medicine and Trauma, University of Oklahoma Health Sciences Center, PO Box 26307, Rm EB 319, Oklahoma City, OK 73126. Key Words: Priapism, chlorpromazine, psychotropic medication. Copyright 0 1991 by W.B. Saunders Company 0735-6757/91/0902-0019$5.00/O

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complaints. Medical history was significant for an ancient history of intravenous drug abuse, but denied recent drug abuse. The patient reports he obtained the chlorpromazine tablet from a “friend.” He denied smoking cigarettes and only rarely drank alcohol. He denied taking any medications regularly or any drug allergies. On physical examination, the patient appeared to be in moderate distress, holding his groin. His vital signs were as follows: blood pressure, I lY70 mm Hg; pulse rate, 72 beats/min; respirations, 20 breaths/min; temperature, 37S”C. The head and neck examination results were normal. The cardiovascular examination results were normal. The abdominal examination results were normal. Genitalia examination showed an uncircumcised erect phallus. The penile shaft was rigid with a moderate hematoma noted on the distal shaft superficial to Buck’s fascia. The glans was flaccid and without lesions or bleeding. The urethral meatus was normal. The testicles and epididymi were nontender and without masses. Rectal examination showed a normal-sized, nontender prostate gland without masses. The remainder of the physical examination was unremarkable. Results of the complete blood count, urinalysis, sickle cell prep, electrolytes, blood urea nitrogen, and serum creatinine were all normal. The patient was administered oxygen by nasal canula at 5 L/min and vigorously hydrated with intravenous normal saline solution. A prompt urologic consultation was obtained and a needle irrigation of the corpus cavernosum was performed by the consultant. The needle irrigation was conducted by placing a 22 gauge butterfly needle into the corporeal body and aspirating 80 mL of dark nonclotting blood. The corpora was then irrigated with a saline and epinephrine solution (I mg of I:1000 epinephrine mixed in I liter of normal saline). This corporeal irrigation resulted in partial detumescence of the penile shaft and complete relief of pain. The patient was then admitted to the urology service. Vigorous intravenous hydration and oxygen were continued until the next day. On the following morning, the penis was still partially (50%) erect and the patient was experiencing only minor discomfort. A corporeal irrigation was repeated resulting in a flaccid pain-free penis. The patient was discharged from the hospital the following day. The patient did not return for his urology clinic appointment and was lost to follow-up.

DISCUSSION Anatomy of Penis The erectile tissue of the penis is made up of three cylindrical bodies, the paired corpora cavernosa, and the corporus spongiosum. The corpus spongiosum surrounds the urethra and distally forms the glans penis.3” The arterial blood supply to the penis is provided by branches off of the paired internal pudendal arteries.4‘6 These penile arteries include the dorsal artery of the penis, deep artery of the penis, bulbar, urethral, helical, and circumflex arteries. Numerous anastomosis exist between the arteries of the penis. Venous drainage of the penis consists of an extensive network of superficial, intermediate, and deep veins as well as with emissary and unnamed communicating veins. The emissary veins are short vessels that connect the cavernous spaces to the intermediate set of veins. The erectile tissue of the two 171

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corpora cavernosa consist of irregular spongelike vascular spaces called sinusoids. These sinusoids contain smooth muscle in their walls as well as the arterioles that supply them. The corpus spongiosum is unassociated with this network of vessels.4-” The penis is innervated by an abundant plexus of somatic and autonomic nerves.4-R The pudendal nerve arising from S, to S, emits sensory branches to the penis. Autonomic innervation includes parasympathetic and sympathetic nerves. Parasympathetic nerve fibers (nervi erigentes) arise from S, to S,, whereas, the sympathetic innervation originates from T,, to L,.4-8 Furthermore, there is a rich adrenergic nerve supply to the corpora. a-Adrenergic receptors outnumber the B-adrenergic receptors 10 to 1.4.5,yThe central nervous system control over sexual function is complex; coordinating multiple sensory inputs including sight. smell, touch, and emotion. Physiology of Erection Penile erection involves the interaction of autonomic, somatic, and psychogenic nerve impulses. Although under neurogenic control, erection is a vascular event.4.6.8 Sympathetic impulses maintain the penis in the flaccid state. Under appropriate psychogenic and reflexogenic stimuli, these adrenergic impulses are inhibited.s,8 Cholinergic nerves and the neurotransmitter, vasoactive intestinal peptide (VIP), have a role in the suppression of adrenergic signals. With the sympathetic impulses inhibited the smooth muscle contained in the arterioles and sinusoids relax.6.12-14 This decrease in resistance allows an influx of blood and subsequent distension of the sinusoids. Penile erection occurs when this blood flow increases to 20 to 50 mL/min.4,6.‘5 Venous outflow is reduced by passive compression of the emissary veins as well as active venous contraction. Once erection has been achieved, maintenance of this tumescent state can be supported with a blood flow of 12 mL/min.4.6,‘5 The tunica albuginea determines the maximum size of the erection. Detumescence involves the reverse process, decreasing the compliance of the arterioles and sinusoids and the reopening of veins. Pathophysiology of Priapism Priapism occurs when blood inflow to the penis exceeds the outflow.2,4 The corpora cavernosa remain distended with blood but not the corporus spongiosum. The reason for the sparing of the spongiosum is because the spongiosum has a separate and more efficient venous drainage than the cavernosa.2,6 The prolonged penile erection occurs from over stimulation or prolonged stimulation of appropriate neurogenic fibers or from vasoocclusion.*.” Accordingly, there is increased arterial inflow and/or impaired venous outflow. Intracavernosal pressures may exceed arterial systolic pressure, causing increased pressures within the confined spaces of the corpora, leading to cellular ischemia, death, and fibrosis. The patient feels pain.2.3 Priapism causes oxygen desaturation of red blood cells. Subsequently, the resultant hypoxia and acidosis cause spasm of the outlet vessels and paralysis of arteriolar and sinusoidal smooth muscle. 2.3 An irreversible state occurs when tissues are no longer responsive to neurogenic signals. This results in thrombosis, cellular ischemia, death, and fi-

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nally, fibrosis.‘.3 The severity and magnitude of the tissue ischemia depends on the severity of the disease. the duration of the priapism, and the individual variation in penile vascular anatomy. Etiologies There are multiple etiologies of priapism. Hematologic diseases include sickle cell disease, leukemia, myeloma, and thalassemia. These cause priapism by sludging of blood and venoobstruction. Sickle cell disease is the most common etiology of priapism in children, affecting 6.4% the boys.” Neurological causes of priapism include central nervous system trauma. tumors, and infarcts. There is a loss of upper motor neuron inhibition of erection.2,3 Pelvic tumors, infections, or trauma are less common etiologies as are vasculitis, amyloidosis. hyperpigmentation, nephrotic syndrome, dialysis. scorpion stings (Buttius quinquesrriatus). and black widow spider bites.‘,‘S,‘y,42-45 Iatrogenic priapism is becoming more common with the advent of intracorporeal injections of vasodilators to treat impotence. Over 60% of priapism is idiopathic.‘.‘.” Drug-induced priapism is a common cause in adults.‘.3.‘s Antipsychotics, antidepressants, and antihypertensives are medications most frequently associated with priapism. Phenothiazines are the most common class of drugs causing priapism.2,2’ Priapism secondary to chlorpromazine is well documented in the literature 2023-26.29 Other phenothiazines associated with priapism include thioridazine (Mellaril, Sandoz Pharmaceutical, East Hanover, NJ), thiothixene (Navane, Roerig, New York, NY). fluphenazine (Prolixin, Princeton Pharmaceutical Products, Princeton. NJ), and mesoridazine (Serentil, Boehringer-lngelheim Pharmaceuticals, Ridgefield. CT).‘“-” Haloperidol is a rarer cause. There has been over 20 reported cases of priapism caused by the antidepressant trazodone.‘“-3’ The antihypertensives causing priapism include prazosin, labetalol, and hydralazine. The pathophysiology of most drug-induced priapism, including chlorpromazine, lies in their a-adrenergic blocking properties. a-Adrenergic blockers such as phentolamine are injected intracorporally to treat impotence.33-37 The incidence of priapism secondary to this form of therapy ranges from 4% to 8.7%.38 Abber et al induced penile erections in dogs by intracorporeal injections of chlorpromazine.‘5 a-Adrenergic agonists such as metaraminol, phenylephrine, norepinephrine, and epinephrine are injected intracorporally to reverse priapism.’ Evaluation and Treatment Priapism is an urologic emergency. The goal of early treatment is to reduce or minimize the incidence of impotence. Treatment should begin as soon as the diagnosis is made. Oxygen should be administered. An intravenous line should be established with isotonic fluid and the patient should be hydrated. Analgesics should be given as necessary. A Foley catheter should be inserted if urinary retention is present. A thorough history and physical examination should be performed. Important components of the history to obtain are (1) past medical and surgical histories, (2) current medications-prescribed and illicit, (3) prior episodes of priapism, (4) time interval from onset of erection until presentation, and (5) precipitating event, ie, trauma, self-manipulation, or

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spontaneous. The physical examination should be thorough, complete, and not just confined to the genitourinary system. Such a detailed examination will show an underlying illness that may have induced priapism. Also, this will identify coexistent medical or surgical problems that may take precedence for treatment.‘.3,” The laboratory evaluation should include a complete blood count, coagulation profile, chemistry panel, urinalysis, blood alcohol, and a drug screen. Sickle cell preparations should also be ordered on all black, Hispanic, and patients of Mediterranean descents. The tests may define an underlying medical etiology for the priapism. Predominantly, these laboratory tests will not prove to be helpful because the most frequent etiology is idiopathic. However, these lab values will be beneficial if a surgical procedure is needed. Again, treatment should begin as soon as the diagnosis is made. Therapy should not be withheld awaiting the results of the tests.2,4 Early consultation with a urologist is important. Sickle cell disease, leukemia, solid neoplasms, and trauma tend to be reversible etiologies of priapism.2,3 Patients with sickle cell disease or trail should receive oxygen, hydration, alkalinization, analgesics, and transfusion, if necessary. Priapism secondary to leukemia often responds to chemotherapy and splenic irradiation. Direct penile irradiation is often effective for priapism secondary to malignant infiltrates. Treatment of the underlying spinal cord injury or direct perineal trauma will aid in the case of priapism secondary to trauma.2,3 If the patient fails to respond to these conservative measures, an invasive approach is usually undertaken. It is known that simple aspiration and irrigation of the corpora cavernosa will accomplish the desired permanent detumescence in approximately half of the patients. Generally, the urologist should be the clinician to perform these more invasive procedures of corporeal aspiration and irrigation. However, in some EDs where priapism is seen frequently, the emergency physicians will initiate aspiration and irrigation if the urologist is going to be delayed (if the urologist agrees).3,” The penis is prepped and draped in a sterile fashion. Using 1% lidocaine without epinephrine the penis is anesthetized locally at the aspiration site or a dorsal penile nerve block is performed. Winter et al recommended entering one of the corpora cavernosa through the dorsal glans using an 18 g needle.* Lue et al prefer using a 19 to 23 g butterfly needle, entering the lateral aspect of each corpora.” Care should be taken to avoid the ventral urethral area or the dorsal neurovascular bundle. Two or three milliliters of blood from the corpora should be aspirated into a heparinized syringe and sent to the laboratory for blood gas analysis. Aspiration of the blood, which initially is dark and viscous, is continued until detumescence occurs and bright red blood is aspirated, or there is difficulty in aspirating any more blood. Next, gently irrigate the corpora cavernosa with 80 to 100 mL of normal saline solution. Aspiration and irrigation can be facilitated by using a three-way stopcock attached to the butterfly tubing and to a 20 mL syringe.39 Blood gas analysis of the corpora cavernosa blood will direct further treatment. The corpora cavernosa blood gas values will aid in identifying a low flow (ischemic) or high flow (nonischemic)

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state.‘*3312 Patients are considered ischemic if the pH < 7.25, PO, < 30 mm Hg, or Pco, > 60 mm Hg. The nonischemic group will have corpora blood gas values more proximate to arterial blood gas values.2,3T’2 For nonischemic priapism, if simple aspiration and irrigation are ineffective, irrigation of the corpora is conducted with an adrenergic agent. Phenylephrine, epinephrine, norepinephrine, and metaraminol are plausible agents. The most preferred solution is diluted epinephrine. Molina et al recommend epinephrine for both its a- and (3-adrenergic properties.40 P-Adrenergic stimulation may dilate penile veins and subsequently improve venous outflow. This solution is made by adding 1 mg of epinephrine to 1 L of normal saline solution. Using the three-way stopcock and 20 mL syringe, irrigate the corpora with up to 200 mL of solution. If irrigation is successful in producing detumescence, the patient should be admitted to the hospital for 24 hours. If the priapism recurs, the patient should have a shunt procedure performed.25’2*40 In ischemic priapism, aspiration, saline irrigation, and epinephrine irrigation are rarely effective.2 Furthermore, the epinephrine may increase the incidence and magnitude of tissue ischemia. For these reasons, epinephrine irrigation is not recommended in the ischemic patient. In this instance, the urologist should perform an emergency shunt procedure. Penile shunts are performed to improve venous outflow from the corpora cavernosa. Corpora pressure monitoring and penile doppler flow studies are used by the urologist to determine the type and extent of shunt procedures. The various shunts include the primary glans-cavernosum shunt, secondary glans-cavernosum shunt, secondary spongiosumcavernosum shunt, secondary saphenous vein shunt, secondary prothesis, and secondary El-Ghorab shunt.2,41 Complications The primary complications or sequelae of priapism are impotence, fibrosis, loss of penile tissue, or infection. Impotence is the best known, as well as the most frequent occurring complication of priapism. The incidence of impotence varies from 18% to 80% with the mean being 50%.2,4 This rate of incidence is influenced by two factors: the underlying etiology for the priapism and the time interval from the onset of tumescence. Generally, the younger a patient is, the better the prognosis for retained potency. Accordingly, older patients have a much lower likelihood of retaining potency. Furthermore, some etiologies of priapism are responsive to medical therapy with subsequent detumescence. However, the majority of cases of priapism will be idiopathic and will not respond to conservative medical therapy. Fibrosis, loss of penile tissue, and infection are all manifestations of penile tissue ischemia.* The extent of fibrosis is related to the amount of tissue ischemia. Erections of 6 hours or less usually exhibit limited ischemia, Erections greater than 6 hours duration are associated with low-flow states and lead to significant tissue ischemia, cellular death, and subsequent fibrosis. Erections greater than 24 hours duration have massive tissue ischemia, cellular death, and extensive tibrosis.4 Patients with prolonged priapism may not respond to aspiration or irrigation because no blood returns through the needle. In these patients, thrombosis or fibrosis is already present. Loss of penile tissue is an end result of this cascade of tissue ischemia and ensuing death. Infection

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is a natural sequel of this ischemic process. The infection may start locally and progress to involve the entire perineum. MEDICAL LEGAL CONSIDERATIONS The treatment and management of priapism is quite litiginous because of the high incidence of resultant impotence, infection, fibrosis, or loss of penile tissue.* It is obvious what effect these complications may have on the sexual activity or libido of an individual. It is important to explain to the patient that it is the disease process and not the treatment that may cause the subsequent complications.’ Prompt recognition and treatment are necessary to reduce the incidence of sequela. Conservative therapy consisting of oxygenation, hydration, and analgesia should be instituted quickly by the emergency physician even before the laboratory tests are back. Care must be taken not to give drugs known to enhance or induce priapism. A urologic consultation should be obtained early. Prior to any procedures, have the patient sign an informed consent form that is witnessed by a family member or friend. It should be emphasized on the consent form that permanent impotence, loss of penile tissue, fibrosis, or infection are known sequela of priapism regardless of whether treatment is rendered.’ SUMMARY Priapism is a urologic emergency. The etiologies of priapism are diverse and numerous. The goal is rapid diagnosis and early treatment in an attempt to avoid the complications of priapism. Impotence occurs in roughly one half of all cases of priapism regardless of the modality of treatment. Accordingly, urologic consultation should be acquired early and obtaining an informed consent form is important. Treatment groups may be divided into ischemic and nonischemic. Treatment options include corpora cavernosa aspiration, saline irrigation, epinephrine irrigation, and shunt operations. Phenothiazines are the most common cause of druginduced priapism. We report a case of priapism due to selfadministered intraurethral chlorpromazine. REFERENCES 1. Stapleton man Mythology.

M: The Illustrated Dictionary of Greek and RoNew York, NY, Peter Bedrick, 1986, p 1982

2. Winter CC, McDowell G: Experience with 105 patients with priapism: Update review of all aspects. J Urol 1988;140:980983 3. O’Brien WM, O’Connor KP, Lyndh JH: Priapism: concepts. Ann Emerg Med 1989;18:131-134 4. Yealy DM, Hogya PT: Priapism. 1988;6:509-520

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6. Newman HF, Northup JD: Mechanism of human erection: An overview. Urology 1981;17:399-407 7. Gray H, Goss CM: Anatomy of the Human PA, Lea and Febiger, 1973, pp 646-648 8. Krane RJ, Siroky MB: Neurophysiology Clin North Am 1981;8:91-101 9. Levin RM, Wein AJ: Alpha

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ceptors in human penile corpus cavernosum. Invest Urol 1980;18:225-226 10. Klinge E, Sjostrand NO: Suppression of the excitatory adrenergic neurotransmission; a possible role of cholinergic nerves in the retractor penis muscle. Acta Physiol Stand 1977;100:368-376 11. Hedlund H, Andersson KE: Effects of some peptides on isolated human penile erectile tissue and cavernous artery. Acta Physiol Stand 1985;124:413-419 12. Lue TF. Hellstrom WJ, McAninch JW, et al: Priapism: A refined approach to diagnosis and treatment. J Urol 1986; 136:104-108 13. Lue TF, Takamura T, Umraiya M, et al: Hemodynamics of canine corpora cavernosa during erection. Urology 1984; 241347-352 14. Lue TF, Takamura T, Schmidt RA, et al: Hemodynamics of erection in the monkev. J Urol 1983:130:1237-1241 15. Pohl J, Pott B, Kieinhas G: Priapism: A three-phased concept of management according to aetiology and prognosis. Br J Urol 1986;58:113-118 16. Juenemann KP, Luo JA, Tanagho EA: Further evidence of venous outflow restriction during erection. Br J Urol 1986; 58:320-324 17. Pryor JP: Priapism. Practitioner 1982;226:1873-1879 18. Tarry WF, Duckett JW, Snyder HM: Urologic complications of sickle cell disease in a pediatric population. J Urol 1987;138:592-594 19. Ekstrom B, Olssom AM: Priapism in patients treated with total parental nutrition, Br J Urol 1987;59:170-171 20. Sagalowski Al: Priapism. Urol Clin North Am 1982;9:255257 21. Gomez EA: Neuroleptic-induced priapis. Tex Med 1985; 81:47-48 22. Fishbain DA: Priapism resulting from fluphenazine hydrochloride reversed by diphenhydramine. Ann Emerg Med 1985; 14:116-118 23. Kogeorgos J, deAlwis C: Priapism and psychotropic medication. Br J Psycho1 1986;149:241-243 24. Griffith SR, Zil JS: Priapism in a patient receiving antipsychotic therapy. Psychosomatics 1984;24:629-631 25. Abber JC. Lue TF, Luo JA, et al: Priapism induced by chlorpromazine and trazodone: Mechanism of action. J Urol 1987;137:1039-1042 26. Balon R, Berchou R, Han H: Priapism associated with thiothixene, chlorpromazine and thioridazine. J Clin Psycho1 1987;48:216 27. Gold DD, Justin0 JD: “Bicycle kickstand” phenomenon: Prolonged erection associated with antipsychotic agents. South Med J 1988;81:792-794 28. Velek M, Stanford GK, Marco L: Priapism associated with concurrent use of thioridazine and metoclopramide. Am J Psychol 1987;144:827-828 29. Dorman BW, Schidt JD: Association of priapism in phenothiazine therapy. J Urol 1976;116:51-53 30. Appel RA, Shield DA, McGuire EJ: Thioridazine induced priapism. Br J Urol 1977;46:160 31. Patt N: More on trazodone and priapism. Am J Psychiatr 1985;142:783-734 32. Scher M, Krieger JN, Juergens S: Trazodone and priapism. Am J Psycho1 1983;140:1362-1363 33. Kursh ED, Bodner DR, Resnick MI, et al: Injection therapy for impotence. Urol Clin North Am 1988;15:625-629 34. Brindley GS: Cavernosal alpha-blockade: A new technique for investigating and treatment erectile impotence. Br J Psycho1 1983;143:332-337 35. Blum MD, Bahnson RR, Porter TN, et al: Effect of local alpha-adrenergic blockade on human penile erection. J Urol 1985;134:479-481 36. Zorginiotti AW, Lefleur RS: Autoinjection of the corpus cavernosum with a vasoactive drug combination for vasculogenie impotence. J Urol 1985;133:39-41 37. Nellans RE, Ellis LR, Kramer-Levian D: Pharmacological

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erection: Diagnosis and treatment applications in 69 patients. J Urol 1987;138:52-54 38. Fouda A, Hassouna M, Beddoe E, et al: Priapism: An avoidable complication of pharmacologically induced erection. J Urol 1989;142:995-997 39. Driscoll CE: Emergency treatment of priapism. Patient Care 1990;24:117-118 40. Molina L, Bejany D, Lynne CM, et al: Diluted epinephrine solution for the treatment of priapism. J Urol 1989;141:11271128

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41. Winter CC: Priapism cured by creating of fistulas between glans penis and corpora cavernosa. J Urol 1978;119:227 42. Lopan DI, Graham AR, Bangut JL, et al: Amyloidosis presenting as priapism. Urology 1980;15:167-170 43. Singhal PC, Lynn RI, Scharschmidt LA: Priapism and dialysis. Am J Nephrol 1986;6:358-361 44. Amitai Y, Mines Y, Aker M, et al: Scorpion sting in children. A review of 51 cases. Clin Pediatr 1985;24:136-140 45. Stiles AD: Priapism following a black widow spider bite. Clin Pediatr 1982;21:174-175