Sleep apnoea as a cause of daytime and nocturnal enuresis

A 60-year-old man developed urinary stress incontinence and enuresis after a prostatectomy. The patient leaked urine with straining and complained of urine loss during sleep. Naps were associated with immediate enuresis requiring five protective undergarments daily. Incontinent episodes averaged three times a day and nocturia twice per night. His wife reported that he fell asleep quickly with snoring, gasping, and irregular respiration. The patient denied any nasal obstruction, sleep paralysis, or cataplexy. Over 5 years his weight had increased 4·5 kg. His history included hyperthyroidism, diverticulosis, slipped lumbar disc, and dietcontrolled diabetes mellitus. He was on no medication, denied smoking, but consumed alcohol as he had done before surgery. Examination revealed a healthy white man weighing 130·6 kg with a height of 1·88 m. His blood pressure was 146/80 mm Hg with a heart rate of 80 per min. Nose and throat examinations were clear and neurological examination was normal. Extremities revealed no clubbing, oedema, or cyanosis. Urinalysis was normal. Videourodynamics demonstrated stress incontinence with a low abdominal leak point pressure of 97 cm water indicating sphincter deficiency. An involuntary bladder contraction occurred at 322 mL, without evidence of residual urine, outlet obstruction, or sensory loss. Three transurethral collagen injections corrected the stress incontinence. However, enuresis persisted despite imipramine 50 mg three times a day or intanasal desmopressin 20 mg in the evening. Prompted voiding or reduced fluid consumption did not influence incontinence. Because of a history suspicious of sleep apnoea, sleep polysomnography was performed with conventional methods. His sleep study documented 4·8 apnoeas and 42·7 hypopnoeas which correlated with 32 episodes of desaturation per hour of sleep, and upper-airway obstruction. The average lowest saturation was 87·5% and the mean saturation 90·9%. Nasal continuous positive airway pressure (CPAP) at 11 cm water eliminated apnoeas and hypopnoeas and increased mean oxyhaemoglobin saturation to 95·8%. Following institution of home nasal CPAP, enuresis was abolished and undergarments were no longer required. This report represents another case of incontinence temporally linked to sleep apnoea. In both cases correction of sleep apnoea abolished enuresis. Although incontinence following radical prostatectomy can occur, urinary loss with sleep is rare. Sphincter deficiency is the usual cause of postprostatectomy incontinence and in our case, was corrected by the collagen injections. Yet the enuresis persisted indicating an additional cause for incontinence. Enuresis occurs in 0·6 to 1% of adults. Enuresis in childhood has been identified as a risk factor for incontinence. Enuresis has been attributed to a developmental delay in central autonomics or a decrease in nocturnal vasopressin release. During rapid-eye movement sleep serotonin-containing raphe neurons in the brainstem, which inhibit bladder activity, decrease firing. Patients with disorders affecting central autonomics can exhibit apnoea and incontinence. Low oxyhaemoglobin saturation could also have activated autonomic neurons, thereby triggering an involuntary detrusor contraction and enuresis. Indeed, enuresis has been reported in a high percentage of sickle-cell patients with hypoxia. The correction of apnoea and desaturation episodes in this patient suggests that the enuresis is directly triggered by sleep apnoea. Apnoea can evoke release of atrial natriuretic factor as a consequence of hypoxia or low intrapleural pressure. Increased atrial natriuretic factor may explain nocturia as a symptom of sleep apnoea. However, incontinence and enuresis occurring within moments of the patient falling asleep during the daytime is inconsistent with a volume-induced aetiology. Moreover, desmopressin failed to correct enuresis. The appearance of enuresis following surgery is curious. Possibly, subsequent weight gain worsened unsuspected apnoea. Alternatively, surgery could trigger detrusor instability. The onset of enuresis or nocturia in an adult with a history suspicious for apnoea should prompt sleep evaluation. Nasal CPAP may correct both incontinence and apnoea. A decrease in central inhibition during sleep may promote an opportunity for nocturia or enuresis.