Objective: to examine the extent to which color-coded duplex sonography permits complete clarification of vessel-dependent erectile dysfunction (ED).

Material and Methods: A total of 215 patients with ED were examined All patients underwent pharmacocolor-coded duplex sonography (PHCCDS; 20 μg of prostaglan-din El, PGE1, intracavernosally) as well as pharmacocavernosometry and -graphy (PHCM and PHCG; 20 μg of PGEl intracavernosally). the penile vessels were visualized, i.e. the dorsal arteries, the cavernosal arteries, and the anastomoses between them, as well as the venous pathways. Peak flow and end-diastolic flow in all arteries and, when present, anastomoses were determined after stimulation. Induction flow to achieve maximal tumescence/rigidity as well as maintenance flow were determined during PHCM. Finally, for the morphological visualization of the cavernous body and possible venous insufficiencies, a radiography in 2 planes was produced with infusion of a water-soluble contrast medium.

Results: in 145 patients with a grade 0-III tumescence after stimulation with 20 μg of PGEI, PHCCDS revealed an end-diastolic flow of >5 cm/s, with a peak flow velocity >25 cm/s in the 2 cavernosal and 2 dorsal arteries. the deep dorsal vein of the penis was visualized in 110 of these 145 patients with a blood flow >5 cm/s, and in 35 cases with a blood flow <5 cm/s. Venous drainage to the corpus spongiosum was visualized in 80 patients with a blood flow >10 cm/s. All patients had a pathologically increased induction (normal value <100 ml/min) and maintenance venous flow (normal value <10 ml/min) in the PHCM as well as venous drainage in the PHCG. Sixty patients with a tumescence grade of IV-V (rigidity) had a peak flow velocity clearly >25 cm/s, an end-diastolic flow <5 cm/s in the 2 cavernosal and 2 dorsal arteries in the PHCCDS, as well as induction values <100 ml/min and maintenance flow values <10 ml/min in the PHCM, without visible insufficient efferent venous pathways on the PHCG. in 29 patients (13.5%) hemodynamically active anastomoses perforating the tunica albuginea could be detected. Ten patients with a tumescence grade of III had a peak flow velocity <25 cm/s and an end-diastolic flow <5 cm/s without venous leakage in PHCM and PHCG.

Conclusion: PHCCDS allows for the assessment of arterial flow disorder as well as of venous leakage in ED. PHCM and PHCG should only be carried out in patients in whom surgical or radiological interventional procedures at the efferent venous pathways are planned.