In the name of GOD the beneficent, the merciful
Early and late proctologic complications of delivery prevention and treatment
The earliest evidence of severe perineal injury mummy of Henhenit, 22 yrs old Egyptian woman with rupture of the vagina into the bladder and the lower bowel was found protruding from the anus.
Predisposing factors Childbirth Tissue Damage Nerve Injury Ageing Promoting Factors Obstetrical injury Obesity Menopause Smoking Caucasian race Pelvic Floor Disorder
PF Muscle Stretch during Labour • During 2nd stage the PF muscles stretch x 2-3 of their length • Maximal stretch tolerated by nonpregnant animal muscle tissue = 1.5
Sequelae of Childbirth Perineal problems Perineal pain, perinealhaematoma, perineal wound Infection Bowel problems Anal Fissure, haemorrhoids, constipation Pelvic Organ Prolapse Cystocele, uterine prolapse. Enetrocele , rectocele, rectal mucosal or complete prolapse, descent of PF Incontinence Urinary, fecal (gas, liquid or solid stools) Recto-vaginal Fistula
Pelvic Organ Prolapse Injury to the pelvic floor during childbirth number of vaginal deliveries macrosomicinfant O’Boyle et al: the POPQ stage signifcantlyhigher in the third than in the first trimester Associated co-Risk factors defective collagen race advancing age Hysterectomy chronic raised intra-abdominal pressure
Childbirth and Pelvic Organ Prolapse Women’s Health Initiative: • single childbirth associated with raised odds of: • Uterine prolapse (odds ratio 2.1; 95% CI 1.7–2.7) • Cystocoele (2.2; 1.8–2.7) • Rectocele (1.9; 1.7–2.2) • Every additional delivery increased the risk of worsening prolapse by 10–20% (Hendrix, Am J ObstetGynecol 2002).
ObstructedDefecationSyndrome ObstructedDefecationSyndrome (ODS) isdefinedas the normaldesiretodefecate, butanimpairedabilitytosatisfactory evacuate the rectum
Causes of ODS • Descent (pelvicfloor) • Rectocele • Internalmucosalprolapse • Intususception (recto-rectal/recto-anal) • 5. Complete prolapse • 6. Paradoxpuborectalis • 7. SRU • 8. Puborectalisinsufficiency • 9. Enterocele • 10.Sigmoidocele • 11.Genital Prolapse
Principal pathological Mechanisms Obstructed Defecation • Mechanical Outlet Obstruction • - Dissipation of Force Vectore • rectocele, descent • - Causes Lying inside the Rectum • Intussusception, mucosal or complete prolapse • Functional Outlet Obstruction • Dyssynergia • Impaired Rectal Filling Sensation • megarectum, Hirshprung
Dissipation of Force Vector Rectocele Descent
Mechanical Causes Lying Inside the Rectum Rectal intussusception Mucosal prolapse Complete rectal Prolapse
Anatomical Rectal redundancy Rectocele Rectal prolapse Rectal mucosal prolapse Intussusception Complex Situations Rectocele ± intussusception ± descent ± rectal prolapse ± enterocele ± sigmoidocele ± urogenitalprolapses
Symptoms Straining too much and repeatedly Long standing in toilet Frequent calls to defecate Assisted defecation Incomplete evacuation Fragmeteddefecation Pelvic pressure Rectal discomfort Perinealpain Laxative or enema user Lack of continence Mucorrea Worsen Quality of Life
Treatment Options Non surgical Biofeedback Diet Exercise Behavioural therapy Surgical Abdominal approach (rectopexy ± sigmoidectomy, colpopexy, LAR) Vaginal approach (posterior coloporrhaphy) Perineal/Transanal approach (Altemeir, Delorme, Sleeve mucosal resection, Starr, Transtarr) SNS
Anal sphincter rupture is highly associated with fecal incontinence
85% perineal trauma 69% stitches McCandlishR et al, Br J ObstetGynaecol1998
Fecal Incontinence and Parturition Anal sphincter defects occur at first delivery • Primips: Before 0% After 35% • Multips: Before 40% After 44% Incontinence associated with defect: p=0.0003 • 23% with defects had postpartum incontinence Sultan et al. NEJM 325:1905;1993
Childbirth & Fecal Incontinence 259 consecutive women delivered single unit 31 elective CS no FI Primaparousdelivered vaginally 13% FI AbromowitzDis Colon Rectum 2000 549 prospective fecal urgency vag7.3% vsCS 3.1% Chaliha99 ObstetGyn
Anal Endosonography before and after Delivery in a Primiparous Woman with a Postpartum Defect of the External Anal Sphincter Abdul H. Sultan et al, NEJM, 1993
1. First degree, superficial – skin and subcutaneous tissue – vaginal mucosa – combination of the (multiple superficial lacerations) 2. Second degree, deeper – superficial perineal muscles (B. spongiosus, T. perineal) – perineal body. vaginal birth Suture or not suture unacceptable aesthetics Impaired sexual function Impaired PF muscle strength Incontinence and prolapse less trauma next deliver less pain and infection the wound heals faster
Inadequateanatomy training Identifying 3rd degree tearsDoctors 91% 60%Midwives 84% 61%. Sultan et al. NEJM, 1993
Overlap Endo to end
Repair of third and fourth degree tears End– to – end or overlap repair?
Postoperative management • Antibiotics • Bladder catheterisation • Analgesia • Stool softener • Patient information
Midline episiotomy is highly associated with anal sphincter rupture Sphincter rupture rate • No episiotomy: 0 - 6.4% • Episiotomy: 0 - 23.9% Thacker. Ob Gyn Survey 38:332;1983 Zetterstrom. ObstetGynecol 94:21;1999 Hartmann K et al. JAMA 293(17):2141-8;2005 Fitzgerald for PFDN, ObstetGynecol 109:29;2007
Operative delivery is associated with sphincter rupture Sphincteric Rupture Odds Ratio (p value) Forceps delivery 6.7 (p<0.001) Episiotomy 3.3 (p<0.001) OP position 2.4 (p=0.002) Vacuum delivery 2.3 (p=0.001) Fitzgerald MP for PFDN, ObstetGynecol 109:29;2007
Interventions to Prevent Obstetrical Perineal Trauma Planned Caesarean vs. Planned Vaginal Birth Exercise in Pregnancy Antenatal Pelvic Massage Position during Labor and Birth Epidural vs. Narcotics Pain Relief Early vs. Delayed Pushing Second stage pushing advice Spontaneous vs. Forceps birth Water Birth
Asymptomatic Women Asymptomatic women who have minimal compromise of their anal sphincter function (satisfactory pressure measurements and ultrasound images) should be allowed to have a vaginal delivery. These women should be counselled that they have a 95% chance of not sustaining recurrent OASIS9 or developing de novo anal incontinence following delivery.68 However, the delivery should be conducted by an experienced doctor or midwife.If an episiotomy is considered necessary, e.g. because of a thick inelastic or scarred perineum,amediolateral episiotomy should be performed.There is no evidence that routine episiotomies prevent recurrence of OASIS. The threshold at which these women may be considered for a CS may be lowered if a traumatic delivery is anticipated, e.g. in the presence of one or more additional relative risk factors such as a big baby, shoulder dystocia, prolonged labour, diffi cult instrumental delivery. However,
symptomatic women All symptomatic women are first treated conservatively Conservative management of anal incontinence is described in detail in Chapter 11 and is summarised as follows: • All women are included in the biofeedback programme (Chapter 11). • If muscle contractility is weak or absent, electrical muscle stimulation is commenced. • Women with flatus incontinence are given dietary advice, especially the avoidance of gasproducing foods such as legumes. • Women with faecal incontinence are commenced on a low residue diet and constipating agents such as loperamide can be used.
Women whose symptoms are adequately controlled by conservative measures are offered CS in any subsequent delivery so as to minimise the risk of further compromise to anal sphincter function. Women with faecal incontinence in whom conservative measures have failed should be offered anal sphincter surgery (Chapter 12A), while others may need advanced surgical techniques as described in Chapter 12B. All women who have undergone successful incontinence surgery should be delivered by CS. A management dilemma arises in women who suffer from faecal incontinence but who wish further pregnancies. These women could avoid a CS and undergo a vaginal delivery followed by a secondary sphincter repair at a later date. The only rationale behind this is that most of the damage that occurs during childbirth occurs with the first vaginal delivery68,70 and therefore the risk of further damage during a subsequent vaginal delivery is relatively small. However, there is a potentially unquantified risk of deteriorating pudendal neuropathy.
The Effect of Pregnancy Hormones on Connective Tissue Connective tissue in the area of the urogenital organs is sensitive to hormones. During pregnancy, collagen is depolymerized by placental hormones, and the ratios of the glycosaminoglycans change. (The term ‘proteoglycans’ is used here interchangeably with ‘glycosaminoglycans’.) The vaginal membrane becomes more distensile, allowing dilatation of the birth canal during delivery. There is a concomitant loss of structural strength in the suspensory ligaments. This explains the uterovaginalprolapse so often seen during pregnancy. Laxity in the hammock may remove the elastic closure force, causing urine loss on effort. This condition is described as stress incontinence. Loss of membranous support may cause gravity to stimulate the nerve endings (N) at the bladder base, so causing premature activation of the micturition reflex, expressed as symptoms of ‘bladder instability’. This condition is perceived by the pregnant patient as frequency, urgency and nocturia. Laxity may also cause pelvic pain, due to loss of structural support for the unmyelinated nerve fibres contained in the posterior ligaments. The action of gravity on these nerves causes a ‘dragging’ pain. Removal of the placenta restores connective tissue
Following the advent of endoanal ultrasound (see Chapter 10), Sultan et al.14 demonstrated that 33% of women sustained “occult” OASIS that were not identified at delivery (see Chapter 8 for pathophysiology). Prospective studies11 have identified “occult” injuries ranging between 2015 and 41%. occult or in fact unrecognisedat delivery. It was alarming to find that 87% and 27% of OASIS were not identified by midwives and doctors respectively.
Lal et al.20 showed that significantly more women develop anal incontinence following a second degree tear than with an intact perineum (23% vs 3%, P = 0.01). Benifl a et al.21 identified a 16-fold increase in anal incontinence following a second degree tear (P < 0.05). Both these studies support the findings of Andrews et al. that a large number of OASIS were undiagnosed and wrongly classified as second degree tears.