Penile cavernous vein leakage, also known as impaired closure of the cavernous veins of the penis, is a common cause of impotence. The ability of the penis to have a hard erection is due to the ability to maintain a high level of intracavernous pressure in the penile cavernous body of the penis. For example, when the human penis is erect, the normal intracavernous pressure should be maintained at 80-100 mm Hg. With an internal pressure lower than this level, the hardness of the penis erection decreases and impotence occurs. During coitus, there are 2 changes in the blood vessels of the penis: blood flow from the arteries increases rapidly, while at the same time blood flow from the veins decreases gradually. The result is that the cavernous body of the penis fills up with blood, the intracavernous pressure rises, and the penis gets an erection; on the contrary, there is a lack of erection in the penis. (Below is a diagram of the cavernous blood vessels.) Venous leakage can occur for both primary and secondary reasons. Primary venous leakage is caused by abnormalities in the development of the veins themselves and the corpus cavernosum, such as congenital anomalies of corpus cavernosum development, weak tunica albuginea, and so on. Secondary venous leakage, on the other hand, is venous leakage caused by insufficient arterial blood supply. The closure of the veins of the corpus cavernosum is passive when the penis is erect, and the increase in arterial blood supply during erection leads to a rise in pressure in the sinusoidal space of the corpus cavernosum, and the vein back is compressed by the distended tunica albuginea and closes. If the arterial blood supply is insufficient, the pressure within the sinusoidal space is insufficient to compress the vein, and the vein closes poorly. Thus insufficient arterial blood supply can also cause venous leakage. （To summarize our previous clinical data, the vast majority of patients with venous leakage impotence also have insufficient arterial blood supply. Therefore, ligation of veins for venous leakage is often unsatisfactory. Because vein ligation only reduces venous return, the arterial blood supply to the penis during erection is not increased at the same time. This leads to insufficient pressure in the cavernous sinus during erection, and erection hardness will naturally be insufficient. The solution to this problem is to further increase the blood flow into the cavernous body of the penis at the same time that venous ligation reduces venous blood return. To accomplish this, arteries from other sites can be transposed and anastomosed to the dorsal penile vein, or artery. Currently, the majority of international cases are usually anastomosed with the inferior abdominal wall artery and the dorsal penile vein, i.e., arterializing the vein. From our clinical cases, the combined arterial transposition or grafting procedure, which arterializes the cavernous veins, can significantly increase the blood flow into the cavernous body during erection. The surgical result is superior to ligation of the dorsal penile vein alone. A schematic of the submental artery is shown above. After separation, it is transposed through a subcutaneous tunnel to the dorsal penile vein, which is anastomosed to the dorsal vein. This way less blood flows out of the penis through the dorsal vein during erection. In addition, the blood flow from the inferior celiac artery also flows through the dorsal penile vein into the cavernous body of the penis, increasing the blood flow to the penis during an erection, and thus increasing the hardness of the erection. (The diagram below shows the anastomosis between the inferior celiac artery and the dorsal vein.)