Monday, April 9, 2012

Pathophysiology of pelvic floor disorders (part1)

Pathophysiology of pelvic floor disorders (part1)


Pathophysiology and mechanisms underlying female urinary incontinence

Etiology and types of female stress urinary incontinence

A-   Genuine stress incontinence with urethral hypermobility (type I and II)

B-   Intrinsic sphincter deficiency (ISD) (type III)

      C- Coexistence of ISD with type II stress incontinence

Detrusor instability

Definition and classification of pelvic organ prolapse

Pathophysiology of pelvic organ prolapse and relaxation

Etiologies of pelvic organ prolapse
A-  Anterior vaginal wall prolapse (Descent)
B-   Posterior vaginal wall prolapse and perineal descent
C-   Vaginal apex prolapse and enterocele

Effects of pelvic floor dysfunction

Other risk factors in the development of pelvic organ prolapse, urinary incontinence and voiding dysfunction

Trauma from childbirth has a major effect on the development of POP and UI, but the exact cause is unknown (Smith et al, 1989). These pelvic changes occur in most women after their first baby (Allen et al, 1990)There are remarkable advances in knowledge of patient histology, biochemistry and neurophysiology that control BN and urethral support and function. It now believes that multiple physiologic factors make up female continence mechanism. Defects in any of these factors can contribute to presence and severity of SUI in women (Walters and Newton, 1999). One third of healthy nulliparous women had experienced UI at one time or another (Nygaard et al, 1994).

Pathophysiology and mechanisms underlying female urinary incontinence

  Urinary Incontinence
(UI): The involuntary loss of urine resulting from pathologic, anatomic, or physiologic factors.

  Stress urinary incontinence (SUI): small losses of urine during an increase of intra-abdominal pressure produced from activities such as coughing, sneezing, laughing or exercising, also known as outlet incompetence.

  Urge incontinence: urine loss due to abnormal detrusor muscle contractions and is sometimes associated with some degrees of urinary retention, characterized by an abrupt and strong desire to void; a major component of “overactive bladder” syndrome.

  Overflow incontinence: urine loss due to over-distension of the bladder, symptoms vary and may include urgency; frequent urination, constant dribbling, and both urge and stress incontinence.

  Total incontinence: continuous loss of urine with minimal activity, usually seen in women with severe SUI.

  Functional incontinence: urine loss due to acute or chronic impairment of both physical & cognitive function.

  Mixed incontinence: symptoms of both stress and urge incontinence (University of Texas at Austin, 2002).

The distribution of UI is evenly divided among GSI, detrusor instability and mixed incontinence. Patients with GSI are more likely to have pelvic floor prolapse and symptoms of pure SUI (Klingele et al, 2002). Overactive bladders is diagnosed by the clinical symptoms of frequency, urgency and urge incontinence, either singly or combined, in the absence of local pathological features explaining these symptoms (Abrams and Wein, 1998).

Using PU, pathophysiology of SUI revealed that urethra did not “drop” of the pelvis all of sudden, but rather rotated gradually from a resting position to a position where funneling of BN developed or worsened and incontinence could be seen. Urethra did not rotate as a single unite, but rather, the anterior and posterior walls of proximal urethral segment rotated away from pubis differently. As rotational descent commenced, proximal urethra traveled as one unit. However, a point was reached at which anterior wall movement diminished while posterior wall movement did not. Continued rotation of posterior wall of urethra in continuity with vagina then gave appearance that the posterior wall was being sheared away from anterior wall (Mostwin et al, 1995) (Figure 1).
Figure 1 Effect of pubourethral complex on arrest of rotational descent of the urethra. A, Urethra closed at rest. B, Rotation produces a shearing effect at the proximal urethra separating the anterior and posterior walls. The anterior portion appears to be stopped in its motion by the sub pubic suspensory complex, while the posterior wall continues to travel along with the vaginal wall (Quoted from Mostwin et al, 1995).

Opening and closure of the proximal urethra and BN are regulated by a battery of surrounding structures, the most important being the pubourethral-vesical ligaments, the suburethral vaginal wall “the hammock”; the pubococcygeus muscles, the levator plate and the CT which like glue connects these structures to each other. Inappropriate function in one of these structures can, to some extent, be compensated for by an improved function in another hereby maintaining continence. However, a significantly deteriorated function in the support of urethra will result in pronounced SUI. What is said so far must not exclude the importance of recognizing the role of the internal urethral structures to maintain continence, in particular the quality of urethral muscles, CT and vascularization. In some specific cases of mixed incontinence it can be speculated whether the urge symptom can be caused by an anatomical dysfunction causing the proximal urethra and the BN to remain involuntary open or to open promptly at even minor pressure provocation. If so distension of the BN and proximal urethra may activate stretch receptors located here which will induce uninhibited detrusor contractions (Ulmsten, 1997).

       Figure 2 indicates how childbirth may damage CT of vagina and it's supporting ligaments to cause both uterovaginal prolapse and urinary dysfunction. Vaginal laxity in all three zones (anterior, middle and posterior zones) may prevent peripheral control mechanism from supporting urine column, so that stretch receptors at bladder base, fires off prematurely, "bladder instability or over active bladder" resulting in more frequent micturition (frequency)  and smaller volumes (low bladder capacity ) (Petros and Ulmsten, 1993).
Figure 2 Damage to vagina at childbirth.  The circles represent the fetal head overstretching the CT of vagina and its supporting ligaments as it descends through the birth canal.  1: hammock and pubo-urethral ligament (PUL) laxity.  2: cystocele and arcus tendineus fasciae pelvis (ATFP) laxity.  3: uterosacral/cardinal (USL) ligament laxity (uterine prolapse and enterocele).  4: rectocele (Quoted from Petros and Ulmsten, 1993).
I- Etiologies and types of female SUI
The etiology of SUI is more complex than the simple theories that evoke anatomic or neurologic injury during childbirth. These injuries unmask a susceptibility to SUI, which is defined genetically (tissue strength, mechanical and anatomic relationships) and behaviorally (nutrition, smoking, and exercise) (Walters and Newton, 1999). The prevalence of UI is 28% and 3.5% having daily (persistent) leakage (Samuelsson et al, 2000).

A-Genuine stress incontinence with urethral hypermobility (type I and II)
          Descent and mobility of BN and proximal urethra with stress are generally regarded as an important etiologic component of urethral sphincter incompetence. Basic anatomic defect appears to be loss of integrity of vaginal musculo-fascial attachments that support BN and urethra in a retropubic position. Hypermobility and descent of these structures with increased intra abdominal pressure lead to impaired pressure transmission to urethra, ineffective compression caused by an unstable suburethral layer (Hammock hypotheses) and possibly an inefficient periurethral skeletal muscle response to stress (DeLancey, 1994) (figure 3).
Figure 3 Hammock hypotheses for stress continence and incontinence: A, abdominal pressure (arrows) forces urethra against stable supportive layer (black) and compresses urethra closed. B, Unstable supportive layer (shaded) is ineffective in providing resistant backstop against which urethra can be compressed. C, despite low, extra abdominal position of urethra and presence of cystourethrocele, supportive layer is firm and provides adequate backstop against which urethra may be compressed closed (Quoted from DeLancey, 1994).  
B-Intrinsic sphincter deficiency (type III)
When the urethra no longer functions as a sphincter and cannot maintain a watertight seal even at rest, the condition is called intrinsic sphincter deficiency (ISD). The BN and urethra can be hyper mobile or fixed. The causes of ISD are not completely known but are probably related to neuromuscular changes and damage as with aging and vaginal delivery or trauma as with prior BN surgery. The muscles involved in urethral closure can be very lax, or the urethral wall can be rigid and scarred. Either mechanism can lead to failure of urethral coaptation and explains the radiologic finding of an open BN at rest (Blaivas and Olsson, 1988). Vaginal delivery can cause extensive perineal nerve damage to the striated urethral sphincter, chronically increased pressure on the pelvic floor from severe asthma, chronic cough, obesity, constipation and previous anti-incontinence procedures that include anterior vaginal wall dissection are causes of intrinsic urethral sphincter deficiency (Benson and McClellan, 1993).

C- Coexistence of ISD with type II SUI
The etiology of SUI comprises hypermobility of the BN and proximal urethra (types I/II) and ISD (type III) (Blaivas and Olsson, 1988).

II- Detrusor instability (DI)
Unstable bladder is one that contracts involuntarily or can be made to contract involuntarily. International Continence Society (ICS) accepted two terms for use in describing an over active detrusor.  The first, unstable bladder or detrusor instability (is a condition in which the bladder is objectively shown to contract either spontaneously or with provocation during the filling phase of a cystometry in a neurologically intact female patient while she is attempting to inhibit micturition). The second, detrusor hyperreflexia is defined as detrusor over activity caused by disturbances of the nervous control mechanisms. Because out flow obstruction is very rare in women and the majority of women with detrusor over activity are neurologically intact, DI is felt to be an idiopathic condition (Karram, 1999 I).

Urinary tract infection and DI versus GSI
Patients who had significant bacteruria, which were treated and retested, DI was abolished in sex of nine, but GSI also resolved in 10 of 20 (Bhatia and Bergman, 1986)



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