Stress Incontinence, Nocturia and Enuresis: The Other Bladder Problems

First, name the type — because the drug follows the mechanism

Urge and stress incontinence fail at opposite ends of the same plumbing. Continence depends on two things being in balance: a bladder that stays relaxed while it fills, and a urethral outlet that stays firmly shut until you choose to open it. Urge incontinence — the overactive bladder covered in the sibling chapters — is a storage problem: the detrusor muscle contracts when it shouldn't, which is why an antimuscarinic (or a β3-agonist like mirabegron) helps. Stress incontinence is the opposite failure, an outlet problem: the sphincter and pelvic floor are too weak to hold back a sudden rise in abdominal pressure, so urine escapes on coughing, sneezing or exertion. Overflow incontinence is a third thing entirely — a bladder that cannot empty (from obstruction or a weak, atonic detrusor) fills until it dribbles over the top. And functional incontinence is a normal urinary tract defeated by something outside it: immobility, confusion, or simply not reaching the toilet in time. Four mechanisms, four managements. Get the type wrong and the pharmacology cannot work.

Stress incontinence: first-line is not a drug

This is the one most likely to catch students out: the first-line treatment for stress urinary incontinence is conservative, not pharmacological. Supervised pelvic-floor muscle training — a proper programme of at least three months — genuinely strengthens the sphincteric support and is the mainstay, alongside weight loss and treating anything that raises abdominal pressure (chronic cough, constipation). If conservative measures and surgery are exhausted or unsuitable, there is exactly one drug worth knowing: duloxetine. It is a second-line option, offered when physiotherapy has failed and a woman wants to avoid or defer surgery — never the opening move.

Duloxetine works on the nerve to the sphincter, not on the bladder. Duloxetine is a serotonin–noradrenaline reuptake inhibitor (SNRI) — the very same class used as an antidepressant and for neuropathic pain, which is why it also appears in the Central Nervous System section. Its effect here is on a specific spinal reflex. In Onuf's nucleus, in the sacral cord, the motor neurones that drive the external (striated) urethral sphincter are switched on by serotonin and noradrenaline. By blocking reuptake of both, duloxetine raises their concentration at this synapse, increases pudendal-nerve tone to the external sphincter, and produces a stronger, more sustained sphincter contraction during bladder filling. The outlet grips harder, so less leaks on exertion. It is a modest effect — it reduces the frequency and severity of leaks rather than curing them — and its usefulness is limited in practice by tolerability.

The limiting adverse effect is nausea, common enough at the start that gradual titration is the norm and many patients stop before they get a fair trial. The rest are the class effects of any SNRI: dry mouth, constipation, insomnia or somnolence, dizziness, sweating, and — the safety points that matter — a small rise in blood pressure, the risk of serotonin toxicity if combined with other serotonergic drugs, and a withdrawal syndrome if stopped abruptly rather than tapered. The suicidality warning that attends all antidepressants applies. For the whole story of SNRI mechanism, monitoring and interactions, the Central Nervous System section is the home chapter; here you only need to remember why an antidepressant molecule ends up tightening a urinary sphincter.

One more agent belongs in the stress-incontinence conversation, though it treats the terrain rather than the sphincter: topical (vaginal) oestrogen. In postmenopausal women, oestrogen deficiency thins and weakens the urethral and vaginal tissues — the genitourinary syndrome of menopause — and a low-dose vaginal oestrogen cream, pessary or ring can improve urogenital atrophy and its urinary symptoms, including some stress and urge complaints. Crucially it is local, not systemic HRT: minimal absorption, so it is not the same risk conversation as the systemic oestrogen covered in the Menopause chapter. It is an adjunct for atrophic tissue, not a cure for a mechanically incompetent sphincter.

Nocturia: the drug that concentrates the night's urine

Waking to pass urine is not one disease — find the cause before you reach for a drug. Nocturia — waking one or more times at night to void — is easy to dismiss, but in older people it is a major cause of broken sleep, daytime exhaustion and, dangerously, falls and fractures on the way to the bathroom. The first move is never a prescription; it is to work out why. Some patients simply drink or take diuretics too late in the day, or have a small-capacity bladder from an overactive detrusor. But a large group have true nocturnal polyuria — they make a disproportionate share of the day's urine overnight. Causes to hunt for include heart failure and peripheral oedema that redistributes fluid when the patient lies down, chronic kidney disease, poorly controlled diabetes, and obstructive sleep apnoea. A simple corrective step is to review the drug chart and move an evening diuretic to earlier in the day. Only when reversible causes are addressed does a specific drug come into play.

That drug is desmopressin — a synthetic analogue of vasopressin (antidiuretic hormone, ADH). Native ADH is released by the posterior pituitary and acts on V2 receptors in the renal collecting ducts, inserting aquaporin water channels so that water is reabsorbed and urine is concentrated. Desmopressin is engineered from the natural hormone to keep the antidiuretic (V2) action while dropping the vasopressor (V1) effect on blood vessels, and to last longer. Given at night, it tells the kidney to concentrate urine and make less of it for a few hours, so the patient sleeps through instead of waking to a full bladder. It doesn't treat the bladder at all — it reduces how much urine the kidney produces overnight. This is the same molecule the Endocrine section uses to treat cranial diabetes insipidus, where ADH is deficient; here it is borrowed to blunt night-time urine production. It also has roles in bleeding disorders (releasing von Willebrand factor), which the Haematology section covers.

Bedwetting in children: the alarm before the drug

Nocturnal enuresis — bedwetting — is common and usually benign in young children, and the great majority need reassurance and time, not a prescription. Behavioural and conservative measures come first: sensible fluid timing (more in the day, little in the evening), avoiding caffeinated drinks, regular toileting before bed, and rewarding effort rather than dry nights. Where active treatment is warranted in a child old enough to engage with it, first-line is the enuresis alarm — a moisture sensor that wakes the child at the first drops, training the brain over several weeks to rouse to a full bladder or hold on. It has the best long-term cure rate because it teaches a skill rather than masking the problem, though it takes commitment from the whole family.

Desmopressin buys quick, temporary dryness — for the sleepover, the school trip. The pharmacological option in children is the same desmopressin, and it suits a different need: rapid, short-term control. Where an alarm is impractical or a child needs to be reliably dry for a specific occasion — a sleepover, a school trip, a camp — desmopressin at bedtime concentrates the overnight urine and can give quick results. But it tends to work only while it is taken; wetting often returns when it stops, which is why the alarm remains first-line for a lasting cure. The same hyponatraemia caution applies, translated for children into one firm instruction: no large drinks in the evening, and none for an hour before and eight hours after the dose. A child who takes desmopressin and then drinks a lot at night is the classic setup for water intoxication.

And a historical footnote worth carrying for exams: imipramine, a tricyclic antidepressant, was once used for childhood bedwetting and does reduce wet nights (through a mix of anticholinergic bladder effects, altered sleep architecture and some antidiuretic action). It has fallen almost entirely out of use, and the reason is safety, not efficacy: tricyclics are dangerously cardiotoxic in overdose — a real hazard for a drug kept in a home with children — causing arrhythmias and hypotension through sodium-channel blockade. Where a household already worries about accidental ingestion, prescribing a cardiotoxic tricyclic for a benign, self-limiting condition is hard to justify. The full tricyclic story — mechanism, the QRS-widening overdose, and its bicarbonate treatment — lives in the Central Nervous System section.

Don't forget the two remaining types — because their drugs are different again. Overflow incontinence, from a bladder that cannot empty, is treated by relieving the cause rather than by any continence drug. If the problem is bladder-outlet obstruction — most often benign prostatic enlargement — the answer is an α-blocker (tamsulosin) to relax the smooth muscle of the prostate and bladder neck, and a 5α-reductase inhibitor (finasteride) to shrink the gland, exactly as the Benign prostatic hyperplasia chapter details. If instead the detrusor is weak and atonic, drugs help little and intermittent catheterisation is often the mainstay. Functional incontinence is a reminder that not every leak is urological: a mobile, continent bladder can still be defeated by immobility, dementia or an inaccessible toilet, and the management is practical and environmental, not pharmacological. Chasing it with a drug simply adds side effects to a problem that a commode or a walking frame would solve.