Continence and Prolapse: What Happens When the Floor Gives Way
Continence is the quietest achievement of the human body. Nobody praises it, nobody notices it, and it is holding — every second, awake and asleep, through a cough, a laugh, a flight of stairs and a heavy suitcase — against a column of pressure that rises and falls all day long. It is not one muscle and it is not willpower. It is a layered system of smooth muscle, skeletal muscle, fascia, nerve and reflex, and each layer can be named, examined and repaired. Millions of people live with urinary leakage, faecal leakage, or the strange heavy dragging feeling of something descending, and they often assume it is simply what age does. It is not. Almost every one of these problems is a failure of a specific anatomical structure, in a specific place, with a specific name — and that is exactly why anatomy, not resignation, is the beginning of the treatment.
She is fifty-one, and she has stopped going to the aerobics class she loved for nine years. She did not stop because of her knees. She stopped because three months ago, mid-jump, she leaked — a small amount, through a thin pair of leggings, in a room full of people — and she has not been back since. She now knows exactly which movements do it: the cough at the end of a cold, lifting her grandson from the floor, the sneeze she cannot suppress. She wears a pad every day "just in case", and she has quietly started drinking less water before leaving the house. She has told nobody, not her sister and not her doctor, because she believes this is simply what happens after three deliveries and fifty years. When she finally does mention it, at the end of an appointment about something else, hand on the door, the examination takes four minutes and finds exactly what the history predicted: a urethra that no longer has a firm surface underneath it to be pressed against when the abdomen squeezes. Nothing is diseased. A hammock has come loose.
Four locks on one door: urinary continence
Continence is not a sphincter. It is four mechanisms working at once, and each of them is anatomy you can name. The FIRST mechanism is the INTERNAL URETHRAL SPHINCTER: a collar of smooth muscle at the bladder neck, continuous with the detrusor and the trigone, under SYMPATHETIC control from L1–L2 through the hypogastric nerves and therefore entirely involuntary. It holds tonically closed all day without your knowledge, and it relaxes only when the parasympathetic outflow of micturition takes over. Its most important anatomical fact is that it is UNEQUAL between the sexes: in the male it is a well-formed, genuinely competent sphincter — and it doubles as the genital sphincter that closes the bladder neck during ejaculation to prevent retrograde flow. In the female it is poorly developed, little more than a functional thickening. The SECOND mechanism is the EXTERNAL URETHRAL SPHINCTER (rhabdosphincter): skeletal muscle encircling the urethra as it passes through the deep perineal pouch, supplied by the PUDENDAL nerve from S2–S4 and therefore VOLUNTARY — the muscle you use to stop the stream mid-flow. Because the female internal sphincter is weak, the external sphincter is the principal mechanism in the woman, a fact that explains a great deal of what follows. The details of the tube itself — the female urethra of about 4 cm against the male's 20 cm with its prostatic, membranous and spongy parts — are set out in the urethra.
The third mechanism is not a muscle around the urethra at all. It is the surface underneath it. This is the SUBURETHRAL SUPPORT, and it is the single most important idea in female continence: DeLancey's HAMMOCK HYPOTHESIS. The urethra does not float in the pelvis; it lies on a supportive layer formed by the anterior vaginal wall and its endopelvic (pubocervical) fascia, and that layer is anchored laterally on each side to the ARCUS TENDINEUS FASCIAE PELVIS — the white line of condensed fascia running from the pubic bone to the ischial spine — and to the medial aspect of the LEVATOR ANI. When intra-abdominal pressure rises in a cough, the pressure is transmitted to the urethra from above; the urethra is then COMPRESSED against this firm backing layer and flattens shut. Continence in that instant depends less on the strength of any sphincter than on the FIRMNESS OF THE BACKBOARD. If the hammock is intact, a cough closes the urethra. If its lateral attachments have avulsed or stretched, the same cough simply pushes the urethra downwards and backwards into a soft, mobile space — and it opens instead of closing. The FOURTH mechanism completes the system: a REFLEX PRE-CONTRACTION of the pelvic floor and external sphincter that fires a fraction of a second BEFORE a cough or a lift, tightening the floor in anticipation. It is a learned, trainable, feed-forward reflex, and teaching a patient to perform it deliberately — "the knack" — can abolish leakage before a single muscle has grown stronger. The muscular floor that carries all of this is described in the pelvic floor.
Lay a garden hose on a paving slab, then stand on it: the hose flattens instantly and the water stops, because the sole of your foot presses it against something that does not give. Now lay the same hose on a loose trampoline and stand on it with exactly the same force. The hose simply descends with the fabric, the pressure is never concentrated across its wall, and the water keeps running. The hose has not changed. The foot has not changed. Only the surface underneath has. That is the whole of stress incontinence in one image: the urethra is the hose, the cough is the foot, and the anterior vaginal wall with its lateral fascial attachments is the difference between a slab and a trampoline.
Three kinds of leakage, three different mechanisms
STRESS urinary incontinence is leakage on effort — coughing, sneezing, laughing, lifting, jumping — with no urge whatsoever before it. It is a failure of the support system: loss of the suburethral hammock (URETHRAL HYPERMOBILITY), or weakness of the sphincters themselves (INTRINSIC SPHINCTER DEFICIENCY), and frequently both together. The volume is usually small, the timing is exactly synchronous with the rise in pressure, and it never happens lying still in bed. URGENCY incontinence is a completely different disease that happens to share a symptom. Here the bladder itself misbehaves: the DETRUSOR contracts involuntarily during filling, generating a sudden desperate need to void that arrives without warning and cannot be deferred, followed by leakage of a large volume. Nothing is wrong with the sphincters or the fascia — the pressure is being generated on the wrong side of them. The clinical portrait is different too: frequency, nocturia, urgency triggered by the sound of running water or the key in the front door, and leakage on the way to the toilet rather than at the moment of a cough. That mechanism, and the antimuscarinic and beta-3 agonist drugs aimed at it, belong to the overactive bladder. MIXED incontinence — both together — is extremely common, and it is the reason the history must be taken carefully rather than assumed. OVERFLOW incontinence is the third pattern and the most dangerous to miss: a chronically distended, poorly emptying bladder, from outflow obstruction (most classically prostatic) or from a hypocontractile detrusor in diabetic or neurological disease, dribbling continuously once its capacity is exceeded. The patient describes constant small leakage, hesitancy and a poor stream, and the bladder is palpable. Treating this as if it were urgency — with a drug that relaxes the detrusor further — can precipitate complete retention.
Faecal continence: a harder problem, solved in layers
Holding solid, liquid and gas — and telling them apart without looking — is a more delicate task than holding urine, and it is solved by six mechanisms in descending order of importance. FIRST and greatest is the resting tone of the INTERNAL ANAL SPHINCTER — the thickened continuation of the circular smooth muscle of the rectum, involuntary, sympathetically maintained, and responsible for roughly 70–85% of resting anal pressure. It is the mechanism that holds you at three in the morning while you sleep, and it is the reason continence does not require consciousness. SECOND is the ANORECTAL ANGLE, an approximately 80–100° kink maintained by the PUBORECTALIS sling of the levator ani, which loops from the pubic bones around behind the anorectal junction and pulls it forwards. The angle acts as a flap valve: rising abdominal pressure presses the anterior rectal wall down onto the top of the anal canal and closes it, so that the very force which should expel stool is used to hold it. THIRD is the squeeze pressure of the EXTERNAL ANAL SPHINCTER — skeletal muscle, PUDENDAL (S2–S4), voluntary, and capable of doubling anal pressure for perhaps a minute of maximal effort. It is not a resting mechanism; it is the emergency brake that buys you the time to reach a toilet. FOURTH are the ANAL CUSHIONS, the vascular submucosal pads at the 3, 7 and 11 o'clock positions, which fill and complete the seal against gas and liquid the way a rubber gasket completes a valve — and whose enlargement is what haemorrhoids actually are. FIFTH is RECTAL COMPLIANCE: the rectum's ability to relax and accommodate an arriving bolus without a rise in pressure, lost in radiation proctitis and inflammatory disease, which is why those patients have urgency out of all proportion to their sphincters. SIXTH is the sensory system. The RECTOANAL INHIBITORY REFLEX makes rectal distension relax the internal sphincter, allowing a small quantity of contents to descend to the exquisitely sensitive mucosa BELOW the pectinate line; there the somatic pudendal innervation identifies it as solid, liquid or gas — the SAMPLING REFLEX — and the external sphincter is contracted or relaxed accordingly. That is how a person passes flatus in company with confidence, and the anatomy that makes it possible, above all the great divide of the pectinate line, is laid out in the anal canal.
Each of those six can fail, and each failure has a signature. OBSTETRIC ANAL SPHINCTER INJURY (OASI) is the commonest cause of faecal incontinence in women worldwide: a third- or fourth-degree perineal tear that divides the external sphincter, the internal sphincter, or both, sometimes recognised and repaired at delivery and sometimes occult, declaring itself as urgency and soiling twenty years later when age has taken the reserve away. PUDENDAL NEUROPATHY is the quieter mechanism: the nerve is stretched during a long second stage, or chronically by years of straining at stool with perineal descent, and the muscles it supplies weaken and thin without ever having been cut — the anatomy of that vulnerable, tethered nerve at the ischial spine is in the pudendal nerve. Loss of the anorectal angle from puborectalis weakness produces leakage with no sphincter defect at all. Excision of the anal cushions in over-enthusiastic haemorrhoid surgery removes the fine seal and leaves a patient continent for solid but not for gas or liquid. And RECTAL PROLAPSE — full-thickness intussusception of the rectal wall through the anus — chronically dilates the sphincter complex and abolishes the angle at once, which is why the majority of these patients are incontinent before the prolapse is ever repaired.
- URINARY continence has four mechanisms: (1) the internal urethral sphincter — smooth muscle at the bladder neck, sympathetic L1–L2, well developed in the male, poor in the female; (2) the external urethral sphincter — skeletal, pudendal S2–S4, voluntary, and the MAIN mechanism in the female; (3) the suburethral hammock; (4) reflex pre-contraction before a cough.
- DeLancey's HAMMOCK HYPOTHESIS: the anterior vaginal wall and endopelvic fascia, anchored laterally to the ARCUS TENDINEUS FASCIAE PELVIS and the levator ani, form a firm backing against which rising abdominal pressure COMPRESSES the urethra shut. Lose the backing and the same cough opens the urethra instead of closing it.
- STRESS incontinence = leakage on effort from lost support (urethral hypermobility) and/or sphincter deficiency. URGENCY incontinence = involuntary detrusor contraction — a different organ, a different mechanism. OVERFLOW = chronic retention with dribbling, and it must not be treated as urgency.
- FAECAL continence, in order of importance: internal anal sphincter resting tone (70–85% of resting pressure, involuntary); the anorectal angle held by the PUBORECTALIS sling (a flap valve closed by the very pressure that would expel); external anal sphincter squeeze (pudendal, voluntary, an emergency brake); the anal cushions completing the seal; rectal compliance; and the sensory reflexes.
- The RECTOANAL INHIBITORY REFLEX relaxes the internal sphincter on rectal distension, letting contents reach the sensitive mucosa BELOW the pectinate line, where the SAMPLING REFLEX distinguishes flatus from liquid from solid — somatic pudendal sensation doing work no muscle could do.
- Faecal continence fails through obstetric sphincter injury (OASI, third/fourth-degree tear — the commonest cause worldwide), pudendal neuropathy from stretch or chronic straining, loss of the anorectal angle, excision of the anal cushions, and rectal prolapse dilating the sphincter complex.
DeLancey's three levels: the map that names every prolapse
The vagina is suspended, attached and fused — three different mechanisms at three different heights, and each produces its own named failure. LEVEL I is APICAL SUSPENSION. The upper vagina and cervix hang from the pelvic sidewall and sacrum by the CARDINAL (transverse cervical) ligaments, carrying the uterine vessels, and the UTEROSACRAL ligaments running backwards to the sacrum. These are the true suspensory apparatus, and their failure lets the top of the vagina descend: UTERINE PROLAPSE, or — after hysterectomy has removed the cervix that anchored them — VAGINAL VAULT PROLAPSE, and ENTEROCELE, in which peritoneum and small bowel from the pouch of Douglas herniate down between vagina and rectum. LEVEL II is LATERAL ATTACHMENT. Along the middle third, the vaginal walls are held out sideways like a hammock by the pubocervical fascia in front and the rectovaginal (Denonvilliers') fascia behind, each attaching laterally to the ARCUS TENDINEUS FASCIAE PELVIS and the fascia over the levator ani. Failure here does not lower the vagina, it lets its WALLS bulge: anteriorly a CYSTOCELE, the bladder pressing into the anterior vaginal wall, and posteriorly a RECTOCELE, the rectum pressing into the posterior wall. LEVEL III is DISTAL FUSION. In the lowest portion there is no ligament at all: the vagina is fused directly to its neighbours — anteriorly to the urethra, posteriorly to the PERINEAL BODY, and laterally to the levator ani and the urogenital diaphragm. Failure here produces URETHROCELE, PERINEAL DESCENT and a gaping introitus. The framework is worth learning because it converts a confusing bulge into a precise question with a precise answer: which level has failed, and therefore which operation restores it.
Name the prolapses precisely, because the names ARE the anatomy. CYSTOCELE: bladder bulging into the anterior vaginal wall. URETHROCELE: the urethra descending with it — the two together are a cystourethrocele. UTERINE PROLAPSE: descent of the cervix and uterus down the vaginal canal, and when the whole uterus lies outside the introitus with the vagina inverted around it, PROCIDENTIA. VAGINAL VAULT PROLAPSE: descent of the blind top of the vagina after hysterectomy. ENTEROCELE: a true hernia of peritoneum and small bowel, usually through the apex. RECTOCELE: rectum bulging into the posterior vaginal wall. Staging is by the POP-Q system, and its central idea is beautifully simple: the HYMEN is the fixed reference point, at zero. Defined points on the vaginal walls and apex are measured in centimetres above the hymen (negative) or below it (positive) during maximal straining. Stage 0 is no descent; stage I, the leading point stays more than 1 cm above the hymen; stage II, it lies within 1 cm either side of it; stage III, it is more than 1 cm below but not fully out; stage IV is complete eversion. Importantly, symptoms track the hymen too — most women are unaware of prolapse that stays above it, and become aware almost exactly when the leading edge reaches it.
Prolapse and stress incontinence are not two diseases that happen to keep company. They are two symptoms of ONE anatomical event — the loss of level II lateral support along the anterior vaginal wall. That is why the woman with a cystocele so often leaks, and why anyone who understands the hammock is unsurprised. It also explains a trap that catches clinicians every year: a LARGE anterior prolapse can KINK the urethra and mask the leakage, so a woman whose only complaint is a bulge becomes newly, distressingly incontinent the day after her prolapse is repaired. This is occult or latent stress incontinence, and it is looked for deliberately before surgery by reducing the prolapse with a pessary or a speculum and then asking the patient to cough. And it explains the happiest fact in this whole subject: because both problems arise from the same failed support, the same pelvic floor muscle training improves both at once.
Why floors fail: the risk factors, read anatomically
VAGINAL DELIVERY is the dominant risk factor, and it damages the floor in three distinct ways at once: mechanical AVULSION of the puborectalis from its pubic insertion (demonstrable on imaging in a substantial minority of first vaginal births, and essentially irreversible); STRETCH INJURY to the pudendal nerve and the nerve to levator ani as the presenting part descends; and direct tearing of the fascia and of the perineal body. The forces involved, and why instrumental delivery, a prolonged second stage and a large baby multiply them, are described in the anatomy of childbirth. AGE AND OESTROGEN LOSS act on the connective tissue itself — after the menopause collagen content and quality decline in fascia and ligament, and the urethral mucosa and its vascular cushion thin, so support and urethral coaptation both deteriorate. CHRONICALLY RAISED INTRA-ABDOMINAL PRESSURE is the slow, relentless factor and the one most often modifiable: obesity, a chronic cough, chronic constipation with habitual straining, and repetitive heavy lifting at work all deliver years of load to a hammock designed for intermittent stress. CONSTIPATION deserves particular respect, because straining both raises pressure and stretches the pudendal nerve, and it is the reason that treating the bowel is a genuine treatment for the pelvic floor. Finally, CONNECTIVE TISSUE DISORDERS — Ehlers-Danlos and Marfan syndromes — produce prolapse in young, nulliparous women and are the clearest possible proof that the problem is fundamentally one of collagen, not of effort. Race, family history and previous pelvic surgery, particularly hysterectomy, complete the list.
The FIRST is sixty-two and describes "a dragging feeling, worse by the evening, better when I lie down", and says that when she washes she can feel something at the introitus that was not there a year ago. That posture-dependence and that heaviness are almost pathognomonic of prolapse; examination in the left lateral position with a Sims speculum while she strains defines which wall is descending. The SECOND is forty-eight with a posterior wall bulge and a complaint she is embarrassed to make: she can feel that stool is present, she strains without result, and she has learned that if she presses backwards on the perineum or inserts a finger into the vagina to reduce the bulge, evacuation follows immediately. That is OBSTRUCTED DEFECATION from a rectocele — the pocket fills and the bolus is diverted forwards into it rather than down the anal canal — and the need for DIGITAL SUPPORT is so specific a symptom that it is worth asking about directly, because patients rarely volunteer it. The THIRD is a man of sixty-eight, three months after radical prostatectomy, leaking on standing up and on the stairs. His prostate, prostatic urethra and bladder neck — the entire internal sphincter mechanism — were removed with the specimen. He now depends ENTIRELY on his external urethral sphincter, which is exactly why pelvic floor training in men after prostatectomy is not an optional extra but the whole of the remaining anatomy.
Putting the floor back: repair, read as anatomy
Every operation in this field is an attempt to restore one named attachment, and knowing which one tells you why it is done that way. PELVIC FLOOR MUSCLE TRAINING is first-line for both stress incontinence and mild prolapse, and it works — but only if the right muscle contracts. The correct action is an inward lift and squeeze around the urethra, vagina and anus, exactly as though stopping wind and urine, engaging PUBORECTALIS and the levator plate. What patients do instead is squeeze the GLUTEALS and ADDUCTORS and hold their breath, which raises intra-abdominal pressure and pushes the floor DOWN — the precise opposite of the intended movement. This is why supervised training with digital or biofeedback confirmation outperforms a printed leaflet by a wide margin, and why the pre-contraction "knack" is taught alongside it. A PESSARY is a silicone device that sits in the vagina and mechanically restores level I and II support from within; it is not a lesser option but the treatment of choice for many women, particularly those unfit for surgery or not yet finished childbearing. Surgically: SACROSPINOUS LIGAMENT FIXATION suspends the vaginal apex to the sacrospinous ligament through a vaginal approach — a level I repair, and one whose risk is entirely anatomical, since the pudendal nerve and vessels hook around the ischial spine at the ligament's lateral end, so sutures are placed two finger-breadths medial to it. SACROCOLPOPEXY fixes the vault to the anterior longitudinal ligament over the sacral promontory with a mesh, abdominally or laparoscopically, and remains the most durable apical repair. ANTERIOR and POSTERIOR REPAIR (colporrhaphy) plicates the stretched fascia of level II. And PERINEAL BODY reconstruction restores level III.
For stress incontinence specifically, the MID-URETHRAL SLING is the operation that grew directly out of the hammock hypothesis, and its most instructive feature is its position. The sling is deliberately placed loosely beneath the MID-urethra, not at the bladder neck, because the mid-urethra is where the pubourethral ligaments and the natural backing layer act; the tape does not lift or obstruct, it simply RECREATES THE FIRM SURFACE against which a cough compresses the urethra. It sits tension-free at rest, which is why a correctly placed sling does not impair voiding. Colposuspension and autologous fascial slings restore the same support by other routes, and urethral bulking agents work on the fourth mechanism, improving mucosal coaptation in intrinsic sphincter deficiency. The pharmacological options for the same problem are collected in stress incontinence, nocturia and enuresis. For urgency that has failed drugs, SACRAL NEUROMODULATION places an electrode through the S3 foramen to modulate the very afferents that drive the detrusor. And for faecal incontinence with a demonstrated defect, overlapping SPHINCTEROPLASTY repairs the torn external anal sphincter, while sacral neuromodulation has become the mainstay where the sphincter is intact but weak. Notice the pattern running through every one of these: none of them invents a new mechanism. Each one restores a named anatomical structure to the place it occupied before.
- LEVEL I (apical suspension by the CARDINAL and UTEROSACRAL ligaments) fails → uterine prolapse, or after hysterectomy vaginal VAULT prolapse and ENTEROCELE.
- LEVEL II (lateral attachment of the vaginal walls to the ARCUS TENDINEUS FASCIAE PELVIS and levator ani) fails → CYSTOCELE anteriorly, RECTOCELE posteriorly. LEVEL III (distal fusion to the perineal body, urethra and levator) fails → URETHROCELE and perineal descent.
- POP-Q stages prolapse against the HYMEN as the zero reference: above it is negative, below it positive, measured at maximal strain — and symptoms typically begin when the leading edge reaches the hymen.
- Risk factors are anatomical: vaginal delivery (levator/puborectalis AVULSION, pudendal stretch, fascial and perineal body tearing), age and oestrogen loss (collagen quality), chronically raised intra-abdominal pressure (obesity, chronic cough, constipation and straining, heavy lifting), and connective tissue disorders.
- Pelvic floor training must engage PUBORECTALIS — an inward lift, not a squeeze of the gluteals or adductors and never with a held breath, which raises abdominal pressure and pushes the floor down. Add the pre-contraction "knack" before a cough.
- Repairs restore named attachments: pessary (mechanical level I–II), sacrospinous fixation and sacrocolpopexy (level I), anterior/posterior colporrhaphy (level II), perineal body reconstruction (level III), the MID-urethral sling (recreating the suburethral backing — placed at the mid-urethra, tension-free), sacral neuromodulation (S3) and overlapping sphincteroplasty.
- Treating stress and urgency incontinence as one condition. Stress leakage is a failure of SUPPORT and sphincter closure and is treated with pelvic floor training, a pessary or a sling; urgency leakage is an involuntary DETRUSOR contraction treated with bladder retraining, antimuscarinics or beta-3 agonists. Give an antimuscarinic to a man with overflow from outflow obstruction and you may precipitate acute retention.
- Believing that continence depends on how strong the sphincter is. In the female the internal sphincter is poorly developed, and the decisive factor in a cough is whether there is a firm suburethral layer to compress the urethra against. A patient can have a normal sphincter and leak with every sneeze because the hammock has detached laterally.
- Repairing a large anterior prolapse without first testing for OCCULT stress incontinence. The bulge may be kinking the urethra and hiding the leak; reduce the prolapse with a pessary or speculum and ask the patient to cough before operating, or she may wake up continent of her bulge and newly incontinent of urine.
A 54-year-old woman leaks a small volume of urine every time she coughs, sneezes or lifts her grandchild, with no preceding urge and never at night. Examination shows descent of the anterior vaginal wall on straining, and she has a well-preserved voluntary squeeze. Which anatomical failure best explains her leakage?
- Urinary continence rests on four mechanisms: the internal urethral sphincter (smooth muscle, bladder neck, sympathetic L1–L2, strong in the male and weak in the female), the external urethral sphincter (skeletal, pudendal S2–S4, the main mechanism in the female), DeLancey's suburethral HAMMOCK of anterior vaginal wall and endopelvic fascia anchored to the arcus tendineus and levator ani, and a reflex pre-contraction before a cough.
- Stress incontinence is failure of that support (± sphincter deficiency) — leakage on coughing, sneezing and lifting; urgency incontinence is detrusor overactivity, an entirely different mechanism; overflow incontinence is dribbling from chronic retention and must never be treated as urgency.
- Faecal continence, in order: internal anal sphincter resting tone (70–85%), the anorectal angle held by puborectalis, external sphincter squeeze, the anal cushions, rectal compliance, and the sampling and rectoanal inhibitory reflexes — failing through obstetric sphincter injury, pudendal neuropathy and rectal prolapse.
- DeLancey's three levels name every prolapse — level I apical (cardinal and uterosacral → uterine, vault, enterocele), level II lateral (arcus tendineus → cystocele, rectocele), level III distal (perineal body and urethra → urethrocele, perineal descent) — staged by POP-Q against the hymen; repairs restore the failed level, and pelvic floor training engaging puborectalis helps prolapse and stress incontinence at once because they are one anatomical problem.
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- Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy — Pelvis and Perineum: support of the pelvic viscera, urinary and faecal continence, prolapse.
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- DeLancey JOL. Anatomic aspects of vaginal eversion after hysterectomy (the three levels of vaginal support). American Journal of Obstetrics and Gynecology.
- Bump RC, et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction (POP-Q). American Journal of Obstetrics and Gynecology.
- Last RJ. Last's Anatomy: Regional and Applied — The pelvic floor, perineal body and anal canal; TeachMeAnatomy — The Pelvic Floor; Pelvic Organ Prolapse.
