Fig. 11.1
Muscles and ligament of the pelvic floor. 1 uterosacral ligament, 2 levator plate, 3 longitudinal muscle of anus, 4 perineal body, 5 rectovaginal fascia, 6 muscle of perineal membrane, 7 anterior portion of pubococcygeus muscle, 8 ligament and fascia of pubourethral ligament
Fig. 11.2
Role of vaginal connective tissue in bladder and anorectal dysfunction
These help in understanding of concomitancy of the symptoms manifesting primarily from one compartment but may be originating from a structural lacunae in other compartments. It may appear clinically that defecation disorders are caused by posterior compartment dysfunction, but at times a prolapse in other two compartments may cause pudendal stretch neuropathy resulting in anal sphincter dysfunction. Similarly a predominantly defecatory dysfunction with disproportionate straining may be associated with rectocele leading to genital laxity resulting in sexual dysfunction. Sexual dysfunction in males may also be a manifestation of pelvic floor dysfunction. Denonvillier’s fascia is intimately attached to the anterior mesorectal fat but loosely attached to the seminal vesicles. In defecatory dysfunction with disproportionate straining with accompanying internal prolapse, intussusceptions, or rectocele, the deep parasympathetic nerves lying between the rectum and prostate, seminal vesicle complex, may undergo stretch neuropathy leading to sexual dysfunction. Any of these can lead to disalignment of bladder outlet dynamics causing urinary symptoms. Hence, it is clinically important to evaluate all the three compartment-based symptoms, whenever faced with a predominant symptoms from any one compartment. The pelvic dynamics and tri-compartmental association of various manifestations are unique as the pelvic nerves traveling to sacral segments are more important for conveying sensations. This is due to higher density of neurons traveling towards sacral segments. Sensory traffic is conveyed by small C fibers and larger A fibers, both being unmyelinated and more vulnerable to stretch insult.
The major known causes for pelvic floor disorders include obesity, pregnancy, menopause, childbirth, and chronic straining at stools and urination. Some patients have congenital weakness of connective tissue and fascia.
11.3 Clinical Features
The plethora of manifestations of pelvic floor dysfunction defies any comprehension of the symptomatology (Haylen et al. 2010). For ease of clinical evaluation and planning of treatment, the symptoms may be classified as below.
11.3.1 Urinary Continence
This may be stress, postural, urge, nocturnal, or coital incontinence. These symptoms may occur alone or in combination.
11.3.2 Bladder Storage/Sensation Symptoms
This may present as increased daytime frequency, nocturia, urgency, overactive bladder syndrome, increased bladder sensation, reduced bladder sensation, or absent bladder sensation
11.3.3 Voiding/Micturition Symptoms
Patient may present with hesitancy, low stream, intermittency, straining, spraying/splitting of stream, sense of incomplete evacuation, need to immediately re-void, position-dependent micturition, dysuria, or retention.
11.3.4 Pelvic Organ Prolapse Symptoms
These include vaginal bulge, pelvic drag/pressure/bulge, bleeding/discharge/infection unrelated to menstruation, need for splinting/digitations, or low backache (or period-like sensation).
11.3.5 Sexual Dysfunction Symptoms
Dyspareunia, superficial/introital dyspareunia, deep dyspareunia, obstructed penetration, vaginal symptoms, or vague symptoms during coitus can occur.
11.3.6 Anorectal Dysfunction Symptoms
These include incontinence (involuntary flatus or fecal escape), rectal urgency, diminished rectal sensation, rectal prolapse, perianal dyshygeine/irritation, and symptoms of obstructed defecation syndrome (ODS).
11.3.7 Pelvic Pain Syndrome/Pudendal Neuralgia (Nantes Criteria)
Pain in the anatomical region of pudendal innervations that is worse on sitting is the classical symptom. However, there is no waking at night with pain and no sensory deficit on examination. Symptoms are relieved with pudendal block. Recurrence with demonstrated pelvic floor dysfunction may occur.
11.3.8 Erectile Tissue Denervation (S2–S4) Symptoms
These patients may present with sexual arousal disorder, female orgasonic disorder, devascularization-led pelvic floor dyssynergy, and erectile dysfunction in males
11.4 Evaluation for Pelvic Floor Dysfunction
A patient with pelvic floor dysfunction should undergo the standard clinical history and examination in addition to symptom-specific evaluation. Since pelvic floor dysfunction involves all three compartments of the pelvic floor, thorough history and clinical examination of the three compartments are necessary. For a pelvic floor colorectal surgeon, special emphasis needs to be given to symptoms of pelvic organ prolapse and those of anorectal dysfunction apart from complete urodynamic assessment.
11.4.1 Examination for Pelvic Organ Prolapse
Examination for pelvic prolapse should be done with an empty bladder and in a position that the patient reports as best for demonstration of prolapse, i.e., left lateral, supine, standing, or lithotomy. The hymen is the index point for prolapse staging (Figs. 11.3 and 11.4).
Fig. 11.3
Stages of pelvic organ prolapse (Front view)
Fig. 11.4
Stages of pelvic organ prolapse (Lateral view)
Stage 0: No demonstrable prolapse
Stage I: Prolapse ends more than 1 cm above the hymen level
Stage II: Prolapse reaches within 1 cm or beyond the hymen level
Stage III: Prolapse reaches more than 1 cm beyond the hymen level
Stage IV: Complete eversion of total length of the lower genital tract
With stage IV, pelvic prolapse can further be defined as uterine/cervical prolapse, vaginal vault/cult scar prolapse, anterior vaginal wall/bladder prolapse, or posterior vaginal wall/rectal prolapse.
11.4.2 Evaluation for Anorectal Dysfunction
Achieving of perfect continence with perfect evacuation is the aim of any treatment protocol. Hence, due diligence is needed to clinically evaluate these two aspects of anorectal function (Agarwal et al. 2011).
11.4.3 Evaluation for Anorectal Incontinence
Several scoring systems have been described. We have found Wexner scoring system to be easy for patient compliance (Table 11.1).
Table 11.1
The Wexner score
Frequency | |||||
|---|---|---|---|---|---|
Type of incontinence | Never | Rarely | Sometimes | Usually | Always |
Solid | 0 | 1 | 2 | 3 | 4 |
Liquid | 0 | 1 | 2 | 3 | 4 |
Gas | 0 | 1 | 2 | 3 | 4 |
Wears pad | 0 | 1 | 2 | 3 | 4 |
Lifestyle alteration | 0 | 1 | 2 | 3 | 4 |
11.4.4 Evaluation for Functional Defecation Syndromes
Obstructed defecation syndrome (ODS) is a functional disorder leading to defecatory dysfunction leading to sense of outlet obstruction in the absence of any pathological findings. Constipation is a very common presentation to a practicing surgeon. Any constipation that defies the existing understanding merits consideration for evaluation for ODS. The constipation can be of primary or secondary variety.
Three pathophysiological subtypes of primary constipation have been described:
1.
Constipation predominant irritable bowel syndrome (C-IBS)
2.
Slow-transit constipation
3.
Dyssynergic defecation
Before proceeding to evaluate primary constipation, a thorough history and examination must be undertaken for all the known causes of secondary constipation.
11.4.4.1 Approach to Rule Out Secondary Constipation
Secondary constipation may be due to several factors in isolation or combination. These may be lifestyle and diet-related factors, medical drug intake-related factors, behavioral or psychiatric factors, metabolic or endocrinal disturbances, or neurological or other structural pathologies. A problem-specific history and physical examination should be performed in such patients (level of evidence IV: grade of recommendation B). These should proceed as shown in Table 11.2. The drug intake history should include various drugs as shown in Table 11.3.
Table 11.2
Etiology of acquired constipation
Lifestyle-related causes | Infectious etiology | Anatomic abnormalities | Functional abnormalities | Physiological and other abnormalities |
|---|---|---|---|---|
Diet Pace of life Medications Weight loss/anorexia/laxative abuse | Trypanosomiasis | Neoplasms Strictures Adhesions Volvulus Rectal prolapse – full thickness, internal Rectocele | Non-relaxing puborectalis Slow-transit colonic constipation Megacolon/megarectum Descending perineum | Diabetes mellitus Hypothyroidism Hypopituitarism Porphyria CNS trauma Parkinson’s disease Brain and CNS tumors |
Table 11.3
Medical causes and medicines leading to constipation
Amiodarone | Carboplatin |
|---|---|
Antacids (e.g., aluminum) | Cholestyramine |
Anticholinergics | Erythropoietin |
Anticonvulsants | Filgrastim [granulocyte colony-stimulating factor (G-CSR)] |
Antidepressants | Iron |
Calcium channel blockers | Lovastatin |
Diuretics | Mesalamine |
Ganglionic blockers | Narcotics/opiates |
Antiparkinsonians | Pravachol |
Bismuth | Sandostatin |
Bromocriptine | Valproic acid |
Bulk laxatives with inadequate hydration | Vincristine |
Abnormal colonic transit study will show large amounts of stool and retention of more than five radiopaque markers mostly in the right colon in a subject with constipation.
11.4.4.2 Ruling Out Constipation Predominant Irritable Bowel Syndrome (C-IBS)
Irritable bowel syndrome can present as Constipation predominant, diarrhoea predominant or alternating diarrhoea with constipation. Irritable bowel syndrome needs to be excluded as per Rome II criteria. Rome II criteria define irritable bowel syndrome as symptoms in the absence of any identifiable structural or metabolic disturbances to explain the symptoms. These symptoms include abdominal discomfort/pain of more than 12 weeks duration consecutively or nonconsecutively in the last 1 year along with any two of the following three features:
1.
Symptoms are relieved by defecation/passage of flatus.
2.
Onset of symptoms is associated with a change of stool frequency.
3.
Onset of symptoms is associated with change in stool form in the absence of laxative usage.
11.4.4.3 Ruling Out Dyssynergic Defecation
In normal defecation there is increase in intrarectal pressure (IRP) with simultaneous fall in intra-anal pressure. This recto-anal pressure synergy leads to a propulsive recto-anal pressure gradient (RAG). The pressure is estimated by rectal manometry.
There are four types of dyssynergic defecation as given in Table 11.4.
Table 11.4
Types of dyssynergic defecation
Type | IRP | IAP | RAG |
|---|---|---|---|
I | Rise (+IRP) | Rise (+IAP) | 0 |
II | No rise (=IRP) | Rise (+IAP) | –ve |
III | Rise (+IRP) | No fall or <20 % fall | 0 or –ve |
IV | No rise (=IRP) | Fall | 0 or –ve |
Normal | Rise (+IRP) | Fall (−IRP) | +ve |
11.4.4.4 Rule Out Slow-Transit Constipation
Slow-transit constipation needs specialized investigation. It can be suspected on clinical history by absence of normal bowel urge that is experienced either getting up in the morning or having a meal. If it is suspected, further evaluation should be done. Assessment of the speed at which stool moves through the colon provides objective measurement of colonic transit. Colon transit time can be measured by three methods:
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1.
Radiopaque marker test: A single capsule with 24 plastic markers is given for the patient to ingest followed by a plain abdominal radiograph on day 6 (120 h later). Retention of at least 20 % markers or more than six markers after 120 h is indicative of slow-transit constipation, as shown in Fig. 11.5.
Fig. 11.5
Abnormal colonic transit study with large amount of stool and retention of more than five radiopaque markers mostly in the right colon in a subject with constipation.
2.
Radioisotope scintigraphy provides noninvasive quantitative evaluation of total and region colonic transit. The isotope used is Indium III or 99Tc and is ingested as a capsule that dissolves in the terminal ileum. Gamma images are obtained at specific time intervals to give an objective transit data.
3.
Wireless motility capsule (WMC) provides a noninvasive method of measuring gastric, small bowel, and colonic transit times. In addition to transit time, it provides the pH changes and intraluminal pressure changes as it courses through the gut. It is very sensitive and specific modality but is not available commercially as of yet. A typical tracing obtained from WMC is shown in Fig. 11.6.
