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Idiopathic high-flow priapism due to bilateral internal pudendal artery shunting A healthy 45-year-old man presented to the emergency department with a 4-week history of persistent partial erection following a single dose of sildenafil. He denied pain or antecedent trauma. Three months earlier, he had required cavernosal aspiration and intracavernosal metaraminol injection for an episode of priapism following intracavernosal alprostadil injection. Examination revealed a subtotal erection that could be detumesced with manual pressure. There was no evidence of ischaemia. Paired arterial and cavernosal blood gas analysis was consistent with high-flow priapism (Table 1). Computed tomography angiogram revealed prominent draining veins in the root of the penis but no evidence of arteriovenous fistula. A diagnosis of idiopathic highflow priapism was made and conservative management with manual pressure resulted in complete resolution. The patient re-presented 2 weeks later with a spontaneous painful erection of 3 days duration. He refused aspiration under local anaesthesia and was taken to theatre. Venous blood was aspirated from the corpora cavernosa and, given clinical suspicion of ischaemic priapism, a corporoglanular shunt was performed. This failed to achieve detumescence and the patient proceeded to angiography. Bilateral hypertrophic internal pudendal (IPA) and common penile arteries were identified angiographically with early arterial filling of the corpora cavernosa bilaterally. The dorsal penile artery was predominantly supplied from the right IPA (Fig. 1). No arteriovenous fistula or aneurysm was found. Subsequently, a superselective coil embolization of the right common penile artery was performed with endovascular coils. The control angiogram demonstrated significantly reduced flow into the corpora cavernosa (Fig. 2). Immediate partial detumescence was observed in the angiography suite. The left IPA was not embolized and showed persistent filling of the corpus cavernosum from the deep cavernosal arteries (Fig. 3). The patient achieved complete detumescence over the following 48 h. At 6 months follow-up, he has no further episodes of priapism and continues to take intermittent tadalafil. Priapism involves a persistent erection that is not associated with sexual stimulation.1 Two categories of priapism are described: lowflow (ischaemic) and high-flow (arterial, non-ischaemic) priapism.

Low-flow priapism arises from deficient venous outflow from the penis and represents a urological emergency. Without prompt drainage, ischaemic damage and fibrosis can ensue with subsequent longterm erectile dysfunction.1 High-flow priapism is a much rarer entity comprising less than 5% of all priapism episodes.1 It involves excessive arterial inflow, usually from an arteriocavernous fistula following perineal trauma. High-flow priapism is often painless and is confirmed by cavernosal blood gas analysis similar to arterial blood. Management of high-flow priapism is less urgent as ischaemia rarely develops.1 Hence, a conservative approach can be adopted in most patients. If this fails, angiography with selective embolization of the underlying lesion is regarded by many to be the gold standard.2,3 Surgical ligation is an alternative reserved for cases where embolization fails.1 There are very few cases of non-traumatic high-flow priapism reported in the literature.4 Previous authors have reported cases of high-flow priapism following shunting procedures for ischaemic priapism; however, these typically have an angiographic lesion at the

Table 1 Matched radial and cavernosal blood gas analysis revealed similar values, suggesting a high-flow (non-ischaemic) priapism Parameter

Radial arterial sample

Cavernosal sample

pH PO2 PCO2

7.41 69 mmHg 42 mmHg

7.41 61 mmHg 42 mmHg

© 2014 Royal Australasian College of Surgeons

Fig. 1. Pelvic arterial angiogram. Hypertrophy of both internal pudendal and common penile arteries with bilateral blush of the corpus cavernosum (arrows). Dorsal penile artery predominantly fills from the right side.

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Fig. 2. Delayed phase arterial angiogram of the right internal iliac artery. Significantly reduced flow into the corpus cavernosum and dorsal penile artery after superselective placement of three coils (arrow) within the right common penile artery.

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site of the surgical shunt.3 In our case, the exact cause of conversion from low-flow to high-flow priapism is unclear. It may have been secondary to the drainage procedures performed previously or trauma from self-administered intracavernosal injections. Given that blood gas analysis confirmed high-flow priapism prior to creation of a surgical corporoglanular shunt, it is unlikely to represent a surgical complication. Other authors have theorized that ischaemic necrosis of the penile vasculature during prolonged ischaemic priapism may convert it to the high-flow variety, which would explain the hypertrophy of common penile arteries and early arterial cavernosal blush/ shunting in this case.3–5 To our knowledge, non-traumatic bilateral shunting of arterial blood from the internal pudendal arteries to the corpora cavernosa seen on angiography has not previously been reported in the literature. Bilateral internal pudendal artery embolization has been advocated for traumatic high-flow priapism where either bilateral fistulas or no lesions are identified on angiography.2,3,6 However, in the described case, unilateral embolization was sufficient to achieve complete detumescence. Unilateral embolization theoretically reduces the risk of secondary erectile dysfunction compared with bilateral embolization.4 In case of incomplete detumescence, a second-stage contralateral embolization procedure remains an option. Idiopathic high-flow priapism is a rare clinical entity. In this reported case, unilateral superselective embolization of the common penile artery was sufficient to achieve complete detumescence and a return to baseline erectile function.

References 1. Broderick GA, Kadioglu A, Bivalacqua TJ, Ghanem H, Nehra A, Shamloul R. Priapism: pathogenesis, epidemiology, and management. J. Sex. Med. 2010; 7: 476–500. 2. Ankem MK, Gazi MA, Ferlise VJ, Hartanto VH, Doshi NM, Diamond SM. High-flow priapism: a novel way of lateralizing the lesion in radiologically inapparent cases. Urology 2001; 57: 800. 3. Bertolotto M, Ciampalini S, Martingano P, Mucelli FP. High-flow priapism complicating ischemic priapism following iatrogenic laceration of the dorsal artery during a Winter procedure. J. Clin. Ultrasound 2009; 37: 61–4. 4. Cohen GS, Braunstein L, Ball DS, Roberto PJ, Reich J, Hanno P. Selective arterial embolization of idiopathic priapism. Cardiovasc. Intervent. Radiol. 1996; 19: 47–9. 5. Pryor J, Akkus E, Alter G et al. Priapism. J. Sex. Med. 2004; 1: 116–20. 6. Lee YC, Shen JT, Shih MC, Chen CC, Chou YH, Huang CH. Bilateral superselective arterial microcoil embolization in post-traumatic high-flow priapism: a case report. Kaohsiung J. Med. Sci. 2003; 19: 79–83.

Fig. 3. Angiographically moderate filling of the corpus cavernosum from the left common penile artery via deep cavernosal arteries (arrows). Previously deployed coils within the right common penile artery (arrowhead).

Nicholas Davies,* MBBS Fadi Nuwayhid,* MD, FRACS Jens J. Froelich,† MD, PhD *Urology Department and †Medical Imaging, Royal Hobart Hospital, Hobart, Tasmania, Australia doi: 10.1111/ans.12802

© 2014 Royal Australasian College of Surgeons

Idiopathic high-flow priapism due to bilateral internal pudendal artery shunting.

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