100 CHAPTER 3 Bladder outlet obstruction
Management of nocturia and nocturnal polyuria
Nocturia can be particularly resistant to treatment.
First, establish whether the patient is polyuric (>3 L of urine/24 hr) by having the patient complete a frequency–volume chart. If polyuric, this may account for the daytime and nighttime voiding frequency. Establish whether the patient has a solute or water diuresis and the causes thereof (see Box 3.3).
If nonpolyuric (<3 L urine output/24 hr), determine the distribution of urine output over the 24-hour period. If >1/3 of urine output is between the hours of midnight and 8 a.m., then the patient has nocturnal polyuria (NP).
Nonpolyuric nocturia
BPH medical therapy
The impact of A-blockers, 5A-reductase inhibitors, and anticholinergics on nocturia is modest.
TURP
Nocturia persists in 20–40% of men after TURP.
Medtronic InterStim therapy for nocturia
Patients preselected on the basis of a favorable symptomatic response to a test stimulation can experience a reduction in nocturia,1 but not all patients respond to the test stimulation. The treatment is expensive and not yet widely available in all countries.
Treatment for nocturnal polyuria
The evidence base for NP treatments is limited (very few randomized, placebo-controlled trials).2
Fluid restriction
Many patients have reduced their afternoon and evening fluid intake in an attempt to reduce their nighttime diuresis.
Diuretics
Diuretics, taken several hours before bedtime, reduce nocturnal voiding frequency in some patients.3
DDAVP
DDAVP is a synthetic analogue of arginine vasopressin (endogenous ADH), which, if taken at night, can reduce urine flow by its antidiuretic action. It has been suggested that NP may be caused by a lack of endogenous production of ADH in elderly people.
However, adults both with and without NP have no rise in ADH at night (i.e., ADH secretion remains remarkably constant throughout the day in adults with and without NP). Furthermore, the diuresis in adults with NP is a solute diuresis due to a nocturnal natriuresis.4
Thus, lack of ADH secretion at night is not the cause of the diuresis in nocturnal polyuric adults, and thus from a theoretical perspective, there
MANAGEMENT OF NOCTURIA AND NOCTURNAL POLYURIA 101
is no logical basis for using DDAVP in NP.5 There is limited evidence that it reduces nighttime voiding frequency (at least in responder enrichment studies) and increases sleep duration in a proportion of patients with NP.6
Side effects include hyponatremia (Na <130 mmol/L) in 5% of patients. Measure serum Na 3 days after starting DDAVP and stop its use if hyponatremia develops.
Nocturia and sleep apnea
Obstructive sleep apnea (OSA) is highly prevalent in those over 65 years of age. It is often manifested by snoring. There is a strong association between OSA symptoms and nocturia.7
Large negative intrathoracic pressure swings may trigger a cardiac-medi- ated natriuresis and hence cause NP.
Box 3.3 Investigation of the polyruic patient (urine output of >3 L/24 hr)
Urine osmolality?
•>250mosm/kg = solute diuresis
•<250mosm/kg = water diuresis
Solute diuresis
•Poorly controlled diabetes mellitus; saline loading (e.g., postoperative diuresis); diuresis following relief of high-pressure chronic retention
Water diuresis
•Primary polydipsia; diabetes insipidus (nephrogenic—e.g., lithium therapy, central—ADH deficiency)
1 Spinelli M (2003). New sacral neuromodulation lead for percutaneous implantation using local anesthesia: description and first experience. J Urol 170:1905–1907.
2 Kujubu DA, Aboseif SR (2008). An overview of nocturia and the syndrome of nocturnal polyuria in the elderly. Nat Clin Pract Nephrol 4(8):426–435.
3 Reynard JM, Cannon A, Yang Q, Abrams P (1998). A novel therapy for nocturnal polyuria: a double-blind randomized trial of frusemide against placebo. Br J Urol 81:215–218.
4 Matthiesen TB, Rittig S, Norgaard JP, Pedersen EB, Djurhuus JD (1996). Nocturnal polyuria and natriuresis in male patients with nocturia and lower urinary tract symptoms. J Urol 81:215–218.
5 McKeigue P, Reynard J (2000). Relation of nocturnal polyuria of the elderly to essential hypertension. Lancet 355:486–488.
6 Mattiasson A (2002). Efficacy of desmopressin in the treatment of nocturia: a double-blind place- bo-controlled study in men. Br J Urol 89:855–862.
7 Umlauf M (1999). Nocturia and sleep apnea symptoms in older patients: clinical interview. Sleep 22:S127.
102 CHAPTER 3 Bladder outlet obstruction
High-pressure chronic retention (HPCR)
HPCR is maintenance of voiding, with a bladder volume of >800 mL and an intravesical pressure above 30 cmH2O, accompanied by hydronephrosis.1,2 Over time, this leads to renal failure. When the patient is suddenly unable to pass urine, acute-on-chronic high-pressure retention of urine has occurred.
A man with high-pressure retention who continues to void spontaneously may be unaware that there is anything wrong. He will often have no sensation of incomplete emptying and his bladder may be insensitive to the gross distension. Often the first presenting symptom is that of bedwetting. This is such an unpleasant and disruptive symptom that it will cause most people to visit their doctor.
Visual inspection of the patient’s abdomen may show marked distension due to a grossly enlarged bladder. The diagnosis of chronic retention can be confirmed by palpation of the enlarged, tense bladder, which is dull to percussion.
Acute treatment
Catheterization relieves the pressure on the kidneys and allows normalization of renal function. A large volume of urine is drained from the bladder (often on the order of 1–2 L, and sometimes much greater).
The serum creatinine is elevated and an ultrasound will show hydronephrosis with a grossly distended bladder if the scan is done before relief of retention.
Anticipate a profound diuresis following drainage of the bladder. This is due to the following:
•Excretion of salt and water that has accumulated during the period of renal failure
•Loss of the corticomedullary concentration gradient, due to continued perfusion of the kidneys with diminished flow of urine through the nephron (this washes out the concentration gradient between the cortex and medulla)
•An osmotic diuresis caused by elevated serum urea concentration
A small percentage of patients have a postural drop in blood pressure. It is wise to admit patients with HPCR for a short period of observation, until the diuresis has settled.
A few patients will require intravenous fluid replacement if they experience a symptomatic fall in blood pressure when standing.
Definitive treatment
Treatment is with TURP or a long-term catheter. In those unable to void who have been catheterized, a trial without catheter is clearly not appropriate in cases where there is back-pressure on the kidneys.
Very rarely, a patient who wants to avoid a TURP and does not want an indwelling catheter will be able to empty their bladder by intermittent self-catheterization, but such cases are exceptional.
1 Mitchell JP (1984). Management of chronic urinary retention. BMJ 289:515–516.
2 Abrams P, Dunn M, George N (1978). Urodynamic findings in chronic retention of urine and their relevance to results of surgery. BMJ 2:1258–1260.
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