Clinical overview
Urinary retention is the inability to empty the bladder adequately, and it presents in two clinically distinct forms. Acute urinary retention (AUR) is the sudden, usually painful inability to pass urine despite a full, palpable and percussable bladder, relieved dramatically by catheter drainage (a typical drained volume is 500–1000 mL or more). Chronic urinary retention (CUR) is a gradual, frequently painless failure to empty, defined by a persistently elevated post-void residual (PVR), sometimes with overflow incontinence, and — when storage pressures are high — a genuine and under-appreciated threat to the upper urinary tracts.
The crucial point for the gynaecologist is that, unlike in men, retention in women is not explained by prostatic obstruction, so it must never be dismissed as "just retention". There is almost always a specific, findable cause, and several of those causes are emergencies or sentinel events. A young woman in painless retention may have cauda equina syndrome; a peripartum woman may have an over-distended, at-risk bladder; an older woman may have a pelvic malignancy, severe prolapse, or silent high-pressure chronic retention damaging her kidneys. To "appraise" the patient — the verb in this objective — means to take retention as a presentation to be explained, not a diagnosis in itself: confirm it objectively, decompress safely, and then hunt the cause systematically. This chapter covers the physiology of normal micturition, the pathophysiology and full differential of retention in women, and a structured, safe approach to assessment and management. It links closely to Genital prolapse, Urinary incontinence, and the puerperal context of Normal puerperium.
Core knowledge
Normal micturition — the neural control of storage and voiding
Figure C1.1 — Normal micturition as a storage–voiding switch (sympathetic storage via the hypogastric nerve vs parasympathetic voiding via the pelvic nerve), and the three ways it fails to empty: weak detrusor, outlet obstruction, and dyssynergia.
Continence and voiding depend on a coordinated switch between two phases, controlled by autonomic and somatic nerves and integrated in the brainstem and cortex:
- Storage phase (sympathetic-dominant). As the bladder fills at low pressure (detrusor compliance), afferents signal volume via the pelvic and hypogastric nerves. The hypogastric nerve (T10–L2) releases noradrenaline: β3-adrenoceptors relax the detrusor (accommodating filling) while α1-adrenoceptors contract the bladder neck/internal sphincter. The somatic pudendal nerve (Onuf's nucleus, S2–S4) keeps the external striated sphincter contracted — the guarding reflex — and a pontine storage (L) centre with cortical control maintains socially appropriate continence.
- Voiding phase (parasympathetic-dominant). When voiding is sanctioned, the pontine micturition centre (Barrington's nucleus) coordinates the act: the pelvic nerve (S2–S4) releases acetylcholine onto M3 muscarinic receptors → a sustained detrusor contraction, with simultaneous, coordinated relaxation of the urethral sphincter and pelvic floor. Effective voiding therefore requires three things together — a detrusor that contracts, an outlet that opens, and coordination between them.
Retention results when any element fails: a detrusor that cannot contract (atonic/hypocontractile, "failure to empty due to the bladder"), an outlet that will not open ("failure to empty due to the outlet" — mechanical or functional obstruction), or a loss of coordination between them (detrusor–sphincter dyssynergia in neurological disease).