Demystifying Nocturia: Identifying the Cause and Tailoring the Treatment

Paula Laureanno, RN; Pamela Ellsworth, MD, FACS, FAAP


Urol Nurs. 2010;30(5):276-287. 

In This Article

Evaluation of Nocturia

An important first step in the evaluation of nocturia is establishing whether the individual has awakened at night to void or voids because the individual is already awake. Health care providers need to be aware that there may be discrepancies between the actual causes of the patient's awakening and the reason given. In a sleep study performed by Pressman, Figueroa, Kendrick-Mohamed, Greenspon, and Peterson (1996), explanations provided by patients as to the cause of their awakenings rarely matched the "objective" findings from polysomnograms. An accurate history is crucial to determine if there is a treatable underlying medical condition present as listed in Tables 2, 3, and 4. If the patient has risk factors for obstructive sleep apnea, further evaluation with a specialist may be warranted (see Table 5). Eliciting any prior history of urinary complaints, treatments and the patient's medication usage, the pattern of fluid intake is also an important component. The voiding diary is the cornerstone of the evaluation of nocturia. It provides important information regarding patterns of micturition, mean and total voided volume, and maximum voided volume. The physical examination is useful to rule out a possible underlying neurologic condition, a distended bladder secondary to increased post-void residual, and benign or malignant enlargement of the prostate, and to assess for lower extremity edema and venous stasis disease.

In patients with diurnal polyuria, an overnight water deprivation test (WDT) can distinguish between diabetes insipidus and primary polydipsia (Adam, 1997). If the osmolality of the first morning void is greater than 800 mOsm/kg H2O, one can conclude there is both normal secretion of ADH and renal response to ADH. Polyuria with a normal WDT is indicative of primary polydipsia If the WDT is abnormal, then the patient either has deficient production of ADH (central diabetes insipidus) or an inappropriate renal response to ADH (nephrogenic diabetes insipidus). A renal concentrating capacity test (RCCT) can distinguish between central and nephrogenic diabetes insipidus. This is accomplished by administering demopressin (Minirin®, Ferring®, DDAVP®) orally (0.4 mg) or intranasally (40 mcg or 0.4 ml) after restricting water. The bladder is emptied, and a urine sample is collected three to five hours later. A urine osmolality greater than 800 mOsm/kg demonstrates normal renal concentrating ability indicating the patient has central diabetes insipidus. If the RCCT yields low urinary osmolality (< 500 mOsm/kg), polyuria is due to nephrogenic diabetes insipidus (Weiss, Weinberg, & Blaivas, 2008).


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