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Priapism Pathophysiology: Clues to Prevention

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Priapism Pathophysiology: Clues to Prevention International Journal of Impotence Research (2003) 15, Suppl 5, S80–S85 & 2003 Nature Publishing Group All rights reserved 0955-9930/03 $25.00 www.nature.com/ijir Priapism pathophysiology: clues to prevention AL Burnett1* 1Department of Urology, The James Buchanan Brady Urological Institute, The Johns Hopkins Hospital, Baltimore, Maryland, USA Priapism, in which penile erection persists in the absence of sexual excitation, is an enigmatic yet devastating erectile disorder. Current endeavors to manage the disorder suffer from a poor fundamental knowledge of the etiology and pathogenesis of priapism. These endeavors have remained essentially reactive, which commonly fail to avert its pathological consequences of erectile tissue damage and erectile disability, not to mention its psychological toll. The role of preventative management seems paramount with respect to priapism. As a prerequisite to formulating prevention strategies, gaining understanding of its pathogenic features and likely pathophysiologic mechanisms is viewed to be quite important. This review combined an analysis of clinicopathologic reports as well as a summary of clinical and basic science investigations on the subject to date. These assessments support the basic classification of priapism into low-flow (ischemic) and high-flow (nonischemic) hemodynamic categories, resulting from venous outflow occlusion and unregulated arterial overflow of the penis, respectively. In addition, consistent with the hypothesis that dysregulative physiology of penile erection accounts for some presentations of priapism, several plausible molecular mechanisms influencing the functional state of the erectile tissue are discussed. Current progress in the field suggests prevention possibilities using androgenic suppressive therapy, adrenergic agonist therapies, and effectors of the nitric oxide-dependent erection regulatory pathway in the penis. New ideas for prevention may emerge from targeting molecular mechanisms involved in regulating erectile tissue function. International Journal of Impotence Research (2003) 15, Suppl 5, S80–S85. doi:10.1038/sj.ijir.3901077 Keywords: priapism; etiology; pathogenesis; penis; erection Introduction interventions offered subsequent to the onset of priapism are frequently inadequate emphasizes the role of prevention of the problem. However, while Priapism, defined as prolonged penile erection in the optimal therapy for this disorder may be its the absence of sexual stimulation, probably repre- prevention, the key element in this management sents the greatest challenge in therapeutic manage- practice is having a sound understanding about the ment among erectile disorders. The disorder has an pathogenic basis of the disorder. At this time, obscure etiology and often unpredictably affects scientific ignorance persists in this regard. Such select individuals without a clear pathogenic basis. fundamental questions require resolution: What Furthermore, it may cause significant physical and causes priapism? Who is most susceptible? Are psychological debilitation, commonly rendering there predisposing factors or conditions pertaining complete impotence in a young man who before its to its onset or recurrence? Is there scientific occurrence was sexually intact. Finally, treatments evidence for a pathophysiologic mechanism that offered for the disorder often are administered too can be targeted for preventive treatment? late to redress the problem fully or restore normal To advance prevention objectives, further under- erectile function. standing about the pathophysiology of priapism is Conventional treatments in the field are mostly required. Insights, both now and in the future, will reactive, administered usually after the priapic draw from clinical study as well as from basic episode has already happened. The knowledge that science investigation in this field. Clinical study relates to epidemiologic approaches as well as to observations from procedures used to treat the *Correspondence: AL Burnett, MD, The Johns Hopkins disorder. Basic science investigation relates to Hospital, 600 North Wolfe Street, Marburg 407, Baltimore, unraveling the molecular determinants of the dis- MD 21287-2411, USA. order, akin to the type of progress made recently in E-mail: [email protected] the field of erectile dysfunction. In this essay, we Priapism prevention AL Burnett S81 discuss the pathophysiology of priapism, with Table 2 Conditions associated with high-flow priapism emphasis on these subject areas. The essay con- Traumatic arteriocavernous fistula cludes with the postulate that priapism results from Vasoactive drugs derangements in the complex, integrative control Penile revascularization surgery system involved in normal penile erection, from Neurologic conditions which new preventive strategies can be considered. hematologic dyscrasias, which are also associated Abnormal penile blood flow with tumor infiltration and obstruction from hema- togenous spread.8,9 An additional concept for priapism resulting from Frank Hinman Sr1 can be credited with providing an disturbed blood flow is high-flow, nonischemic early, comprehensive study of the pathophysiology priapism, in which arterial overflow is considered of priapism. He understood the effects of and gave to be pathogenic.12,13 Trauma seems to be the primary relevance to ‘mechanical’ disturbances primary basis for this entity, either commonly from involving the penile circulation, which he asso- blunt trauma to the perineum or genitalia14–16 or ciated with ‘thrombosis of the veins of the corpora’. from vascular laceration such as that resulting from He identified the relationship to priapism of such needle passage with intracavernosal pharmacother- clinical conditions as pelvic abscess formation, apy17 (see Table 2). Following trauma, the penile penile tumorous growths, perineal or genital injury, vasculature is structurally damaged, which permits and hematologic dyscrasias. His description pro- uncontrolled blood entry and filling within the vided the foundation for the concept of low-flow, corpora cavernosa. Commonly, a fistula forms ischemic priapism, in which a veno-occlusive between arterial inflow vessels and the venous and pathology is believed to be a major cause of sinusoidal outflow circulation of the penis. Penile priapism. arterial revascularization surgery for arteriogenic Distinctive veno-occlusive pathologies include impotence provides another setting for the compli- (see Table 1): sickle cell disease, which is associated cation of high-flow priapism.18,19 with sickled erythrocytes producing a sludge ef- fect;2,3 parenteral hyperalimentation particularly combined with fat emulsion, which is associated Abnormal erection neuroregulation with increased intravascular viscosity, stimulated blood coagulability, or the development of fat A ‘neural’ variant of priapism was initially sup- embolism;4,5 hemodialysis, which is associated with ported by Hinman Sr, who recognized that a increased intravascular viscosity as a consequence substantial number of patients presenting with of hemoconcentration and hypovolemia following priapism exhibit neurologic disease.1 He suggested treatment;6 intracavernosal heparin administration, that this form of priapism affected ‘erectile centers’ which is associated with increased blood coagul- of the nervous system and included infections such ability paradoxically on the basis of its stimulating as syphilis, brain tumors, epilepsy, intoxication, and platelet aggregation;7 local primary or metastatic brain and spinal cord injury as causative factors.1 neoplastic processes, which are associated with Several mechanisms have been proposed to explain direct tumor infiltration and obstruction;8–11 and how these neurologic diseases cause priapism, mostly in line with concepts related to the neuror- egulatory basis for penile erections. One explanation Table 1 Conditions associated with low-flow priapism pertains to abnormal activation of neural reflexo- Sickle cell disease and other hemoglobinopathies genic mechanisms involved in erection following Vasoactive drugs genital stimulation.20–24 Another explanation relates Neoplastic disease (local or metastatic) to disturbances in central neurotransmission that Penis 25 Urethra mediates penile erection. Knowledge of the tradi- Prostate tional autonomic sympathetic nervous system that Bladder mediates detumescence and penile flaccidity has Kidney supported the general belief that pathogenic failure Gastrointestinal tract of this system could readily predispose to the Hematologic dyscrasias 26,27 Leukemia development of priapism. Polycythemia Traumatic injury Hyperlipidic parenteral nutrition Priapism variants Hemodialysis Heparin treatment Fabry’s disease Neurologic conditions Priapism variants are worth examining briefly to acknowledge that they do not readily fit the contexts International Journal of Impotence Research Priapism prevention AL Burnett S82 of the classically described hemodynamic disorders. blunting sensory input conveyed in the dorsal nerve In addition, as unique priapism presentations, their of the penis of reflexive erectile pathways;61 oral consideration may reveal pathogenic aspects about and intracorporal alpha-adrenergic agonists, the disorder. Idiopathic priapism, which according which exert contractile effects on erectile tissue, to some investigators constitutes as much as half of thus indicating the likely pathogenic role of uncon- all registered cases,28–30 has long been recognized as trolled non-adrenergic
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