It is postulated that intraoperative injury to the cavernosal nerves results in hemodynamic and histologic changes within the penis, which manifest clinically as ED. We hypothesize that non-neuronal cause, such as vascular insults due to intraoperative tissue handling, may also have a minor but definite role in penile ischemia and consequent postoperative sexual dysfunction. Between May 2008 and July 2008, 64 patients were enrolled in the study (group 1). Following sterilization, the Odissey Tissue Oximeter probe was placed on the shaft of the penis, 2 cm from its base. The patient underwent continuous penile tissue saturation monitoring. Surgical dissection was altered whenever the oxygen saturation alarm went off until it was restored to 85%. In addition, 192 patients, matched for age, preoperative prostate-specific antigen, clinical stage, baseline sexual function, Charlson comorbidity index and nerve-sparing status operated between October 2007 and July 2008, formed the control group (group 2). These patients did not have any intraoperative tissue oxygenation monitoring. Opening of the endopelvic fascia and steps of nerve sparing were associated with significant drops in oxygen levels, especially if done using torque. Drop in oxygen levels were also noted whenever excessive traction was applied on the Foley catheter, seminal vesicles or prostate during apical dissection. We deliberately modified our surgical steps to make surgery more traction free. A significantly higher percentage of group 1 patients with bilateral nerve sparing had no ED compared with group 2 patients at 6 weeks (24.5% vs 10.4%; P=0.014) and 52 weeks (83.7% vs 68%; P=0.029). Overall, 93.9% of patients in study group had Sexual Health Inventory for Men (SHIM) score of 17 (mild to no ED) at 1 year compared with 78.4% of patients in the control group. We demonstrated that avoidance of ischemic stress, aided by intraoperative penile oxygenation monitoring, may help surgeons improve their technique and thus functional outcomes in patients.