To explore the problem of initial manifestations of the diabetic neurogenic bladder, diabetic patients with and without neuropathy and nondiabetic controls, all without symptoms or signs referable to the urinary tract, were studied urologically. The nondiabetic controls and the diabetics without neuropathy were normal. In striking contrast, 83 per cent of diabetic patients with neuropathy had clear, objective evidences of neurogenic bladder involvement as manifested by abnormal cystometrograms, and grossly enlarged bladders. However, the absence of residual urine was the rule. The typical case had no pyuria or bacteriuria, a negative bladder urine culture, no azotemia, pyelonephritis, sepsis or significant albuminuria. This differs sharply from the advanced diabetic neurogenic bladder with paralysis where there is a marked residual urine with secondary infection, pyuria, bacteriuria, positive urine cultures, pyelonephritis, sepsis, azotemia and conspicuous albuminuria. The disparity is determined by the factor of residual urine which is the measure of decompensation.It is suggested that the progressive decompensation of the incipient asymptomatic diabetic bladder is a cause of the increased frequency of renal infection in the diabetic. DIABETES 16:331-35, May, 1967. Neurogenic vesical dysfunction with paralysis has been clearly delineated as a neuropathic manifestation of diabetes. 1 The atonicity of the distended bladder, the residual urine, and the inevitability of secondary infection leading to pyelonephritis, sepsis and azotemia have been well documented. 2 However, the mode of onset and the progressive developmental course of this condition from incipient asymptomatic stages are unknown. Such knowledge may help to anticipate and prevent the deleterious effects of the fully developed paralytic bladder. An explanation for the increase in renal infection in the diabetic could be forthcoming.There is a paucity of information in the literature concerning the existence of a "preparalytic" bladder. Two reports do indicate that unsuspected bladder involvement may occur in the diabetic. Larcan et al. 3 did cystomanometric studies on a group of thirty-two unselected diabetics, none of whom had urinary manifestations. They found that twenty-two of this group had increased capacity, atony, or diminished sensitivity of the bladder. The residual urine in these cases varied from 25 to 250 cc. Although they assumed this to be a neuropathic manifestation, no correlation was made with diabetic neuropathy. Fagerberg 4 performed urologic investigations on seventy-five diabetic patients, none of whom had symptoms suggesting involvement of the genitourinary tract. These patients were unselected except that no males over forty-five were included because of the possibility of coexisting prostatic hypertrophy. Slightly over half were found either to have sphincter disturbances or increased bladder capacity or both. He observed that neuropathy and angiopathy were more common amongst subjects with atony of the bladder.
MATERIAL AND...
