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Patients with spinal-cord injury (SCI) may have or develop the same diseases, including a variety of metabolic disorders, as their still-ambulatory counterparts. The complications or sequelae of these conditions may compound or aggravate those related to the SCI itself. Impotence is a common complication of many metabolic disturbances, especially diabetes mellitus, and since diabetes is quite a prevalent disease, sexual dysfunction related to it may be a serious problem for SCI patients. This article will address the impact of diabetes mellitus, liver disease, and several miscellaneous metabolic disorders on sexual function.

Renal functional insufficiency often develops in patients with chronic spinal-cord injury (SCI), is associated with substantial morbidity, and frequently progresses to end-stage renal disease (ESRD). As renal function deteriorates, virtually all organ systems are adversely affected. Over the past ten years, there has been increasing interest in the abnormalities of sexual and reproductive function that occur in patients with ESRD (20a). The main focus of this chapter will be the impact of advanced renal failure on sexual function. Even though chronic dialysis has become more widely available, including an expanded capability for patients with SCI and renal failure, there have been no systematic observations of sexual function in patients with both SCI and advanced renal failure. Although our comments are based on observations in able-bodied patients with ESRD, there is no prima facie reason why these cannot be extended to the SCI patient with renal failure.

We evaluated neutrophil adhesive function in patients undergoing chronic hemodialysis using either prostacyclin or heparin as antithrombotic agents. Patients underwent successive hemodialyses with prostacyclin (4 ng/kg/min) and heparin. There were no significant differences noted in neutrophil adhesive function during either dialysis: transient neutropenia developed in each case; impaired neutrophil adhesiveness to plastic developed during both dialyses; neutrophil aggregation was diminished when compared to predialysis responses during both dialyses. Furthermore, the number of circulating Fc-receptor-bearing neutrophils fell significantly during both prostacyclin and heparin hemodialysis. Our study demonstrates that substitution of prostacyclin for heparin in doses that do not cause hypotension, does not prevent neutropenia or alter the diminished neutrophil adhesiveness that occurs during heparin hemodialysis.

We studied prostacyclin as a substitute for heparin in 12 patients who underwent maintenance hemodialysis. All subjects underwent initial hemodialysis with prostacyclin as the sole anticoagulant; 10 of the 12 were restudied during heparin hemodialysis. Few adverse reactions occurred during prostacyclin hemodialysis in the 10 patients in whom dialysis was performed against a bicarbonate-containing dialysate; however, significant hypotension developed in two subjects when an acetate bath was used. Platelet aggregation progressively decreased during prostacyclin hemodialysis (p less than 0.02), but not during heparin hemodialysis, and returned toward control values after hemodialysis. Platelet thromboxane release decreased during both prostacyclin and heparin hemodialysis. Intradialytic percent decrements in serum urea nitrogen and creatinine were greater during prostacyclin than heparin administration (42 +/- 2.9 percent versus 36 +/- 2.6 percent [p less than 0.05] and 33 +/- 2.6 percent versus 29 +/- 2.1 percent [0.05 less than p less than 0.1], respectively). The plasma concentrations of 6-keto-prostaglandin-F1 alpha, a prostacyclin metabolite, reached peak levels by 120 minutes of hemodialysis and declined biexponentially toward predialysis concentrations during 120 minutes after hemodialysis, thereby providing an index of cumulative prostacyclin dosage. We conclude that prostacyclin is not only a safe alternative to heparin anticoagulation during hemodialysis, but that prostacyclin might also increase the efficiency of hemodialysis.