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Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
Cervical ripening and labour induction
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Cervical ripening and labour induction

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  • 1. Dr. N. SRAVANTHI Dr. RENUKA
  • 2.  Induction of labor – Implies stimulation of contractions before the spontaneous onset of labor, with or without membranes. Augmentation refers to stimulation of spontaneous that are considered to be inadequate because of failed cervical dilatation and fetal descent
  • 3. Evaluation before induction of labour MATERNAL FETAL1. Confirm indication for induction 1. Confirm gestational age2. Review contraindications to labor 2. Assess need to document fetal and/or vaginal delivery lung maturity status3. Perform clinical pelvimetry to 3. Estimate fetal weight (either by assess pelvic shape and adequacy clinical or ultrasound of bony pelvis examination) 4. Determine fetal presentation and4. Assess cervical condition (assign lie Bishop score) 5. Confirm fetal well-being5. Review risks, benefits and alternatives of induction of labor with patient
  • 4. WHO RECOMMENDATIONS FOR INDUCTION OF LABOUR Induction of labour should be performed only when there is a clear medical indication for it and the expected benefits outweigh its potential harms. In applying the recommendations, consideration must be given to the actual condition, wishes and preferences of each woman, with emphasis being placed on cervical status, the specific method of induction of labour and associated conditions such as parity and rupture of membranes.
  • 5.  Induction of labour should be performed with caution since the procedure carries the risk of uterine hyperstimulation and rupture and fetal distress. Wherever induction of labour is carried out, facilities should be available for assessing maternal and fetal well-being
  • 6.  Women receiving oxytocin, misoprostol or other prostaglandins should never be left unattended Failed induction of labour does not necessarily indicate caesarean section Wherever possible, induction of labour should be carried out in facilities where cesarean section can be performed
  • 7. Indications Indicated when benefits to mother or fetus outweighs those of continuing the pregnancy
  • 8. ACCEPTED ABSOLUTE INDICATIONS Hypertensive disorders  Fetal compromise  Pre-eclampsia/eclampsia  Fetal growth restriction Maternal medical conditions  Isoimmunization  Diabetes mellitus  Non-reassuring antepartum  Renal disease fetal testing  Chronic pulmonary disease  Oligohydramnios Pre- labor rupture of membranes • Fetal demise Chorioamnionitis  Prolonged pregnancy(>42weeks)
  • 9. RELATIVE INDICATIONS Hypertensive disorders  Fetal anomalies requiring  Chronic hypertension specialized neonatal care Maternal medical condition  Logistic factors  Systemic lupus erythematosus  Risk of rapid labor  Gestational diabetes  Distance from hospital  Hypercoagulable disorders  Psychosocial indications  Cholestasis of pregnancy  Advanced cervical dilatation Polyhydramnios  Previous still birth  Post term pregnancy(>41weeks)
  • 10. CONTRAINDICATIONS ABSOLUTE  RELATIVE  Prior classic uterine incision or  Cervical carcinoma transfundal uterine surgery  Funic presentation  Active genital herpes infection  Malpresentation (breech)  Placenta or vasa previa  Umbilical cord prolapse  Transverse or oblique fetal lie  Absolute cephalopelvic disproportion (as in women with pelvic deformities)
  • 11. RELATIVE INDICATIONS Hypertensive disorders  Fetal anomalies requiring  Chronic hypertension specialized neonatal care Maternal medical condition  Logistic factors  Systemic lupus erythematosus  Risk of rapid labor  Gestational diabetes  Distance from hospital  Hypercoagulable disorders  Psychosocial indications  Cholestasis of pregnancy  Advanced cervical dilatation Polyhydramnios  Previous still birth  Post term pregnancy(>41weeks)
  • 12. CONTRAINDICATIONS ABSOLUTE  RELATIVE  Prior classic uterine incision or  Cervical carcinoma transfundal uterine surgery  Funic presentation  Active genital herpes infection  Malpresentation (breech)  Placenta or vasa previa  Umbilical cord prolapse  Transverse or oblique fetal lie  Absolute cephalopelvic disproportion (as in women with pelvic deformities)
  • 13. Risks CESAREAN DELIVERY  especially increased in nulliparas  two- to threefold risks  rates are inversely related with favorability of the cervix at induction, that is, the Bishop score. CHORIOAMNIONITIS UTERINE ATONY  Postpartum atony and hemorrhage are more common in women undergoing induction or augmentation  Intractable atony was the indication for a third of all cesarean hysterectomies
  • 14.  Cervical ripening : A prelude to the onset of labour whereby the cervix becomes soft and compliant.  This allows its shape to change from being long and closed, to being thinned out (effaced) and starting to open (dilate).  It either occurs naturally or as a result of physical or pharmacological interventions NICE 2008
  • 15. Smooth muscle Cellular Fibroblast Collagen I (70%)Cervix Collagen III (30%) Elastin Extra cellular Proteoglycans Decorin
  • 16. MECHANISM INVOLVED IN CERVICAL RIPENING Cervix is a complex and heterogeneous organ, that undergoes extensive changes throughout gestation and parturition. Chronic process, which begins within the first trimester of pregnancy and progressively proceeds until term Softens, dilates and effaces the cervix This remodeling process is extremely complex and involves  properly timed biochemical cascades,  interaction between cellular and extra cellular components, and  infiltration by inflammatory cells.
  • 17. Hyperplasia of cellular components in early gestation physiologic cell death, in advanced pregnancyUp gradation of -Invasion by neutrophils and macrophages Decorin -Nitric oxide – regulates MMPs and releases PGs. COLLAGEN REMODELLING
  • 18. Enzymatic degradationIncreased CERVICAL Hormonal decorin RIPENING influences Increased Hyaluronic acid
  • 19. Extra-cellular changesDispersion and Disorganization of Collagen Collagenases, Proteases and Elastases (produced by fibroblast and PMN) MMP 1 and 8 – source: stromal cells and neutrophils Proteoglycans e.g. Decorin Inflammatory cells--- increase in degradative enzymes Hyaluronic acid (GAG)- increase water content
  • 20. Remodeling of cervix Degradative Inhibitors enzymes-Collagenases, MMP 1 & - Tissue inhibitors of8, elastases MMPs, alpha 2 macroglobulin-Source – stromal cells,neutrophils andmacrophages-Activity enhanced bycytokines like IL-1B, IL-8
  • 21. AFFECTING ELEMENTS CYTOKINES – e.g. interleukin-1β enhance the activity of collagenases and interleukin 8, Platelet activating factor, monocyte chemotactic factor-1 HORMONAL INFLUENCES – Estrogens increases collagenases Progesterones inhibit collagenases, hyaluronic acid & IL-8 NITRIC OXIDE stimulates leukocytes infiltration induce prostaglandin secretion
  • 22. PREINDUCTION CERVICAL RIPENING The condition of the cervix influences the success of inducing labor. A cervical examination is essential before labor induction is initiated. In 1964, Bishop developed a scoring system to evaluate multiparous women for elective induction at term. The scoring system is based on properties of the cervix that may be assessed clinically at the time of pelvic examination such as dilatation, effacement, consistency, and position as well as the station of the fetal presenting part
  • 23. “Bishop Scoring System” Used for Assessment of Inducibility DILATATION EFFACEMENT STATION CERVICAL CERVICALSCORE POSITION (cm) (%) (–3 to +2) CONSISTENCY 0 CLOSED 0 - 30 -3 FIRM POSTERIOR 1 1-2 40 - 50 -2 MEDIUM MID POSITION 2 3-4 60 - 70 -1 SOFT ANTERIOR 3 >/= 5 >/=80 +1, +2 - -
  • 24.  Bishop score is now widely used to predict the success of labor induction. The higher the Bishop score, the more “ripe” or “favorable” the cervix is for labor induction. A low Bishop score, usually considered less than or equal to 6, is “unripened” or “unfavorable” and will benefit from cervical ripening
  • 25. Other predictors Maternal factors Height, FetalParity Age Fetal factors weight, BMI fibronectin Insulin like growth Factor Fetal weight binding >3.5kg. protein Gestational age fFN in cervical secretions: Not more predictive than Bishop’s score
  • 26. Other scoring systems Field’s system Burnett modification of bishops score Weighted Bishop’s score by Friedman Pelvic score by Lange However, despite this none of the modifications have shown improved predictability.
  • 27. ULTRASOUND IMAGING Adv. Over digital examination: more objective and assesses the entire length of the cervix. Both bishop’s score and TVUS predicted successful induction. Bishop’s score predicted delivery within 24 hrs. and TVUS within 48 hrs. Cervical length related to latent phase of labor, funneling related to both latent and active phase of labor. (Am. J of Obs. Gynecol. 1994;171.) Some other studies have not found any USG parameter predictive, and consider bishop’s score to be superior.
  • 28. METHODS OF CERVICAL RIPENING Unfortunately, women too frequently have an indication for induction but with an unfavorable cervix. As favorability or Bishop score decreases, there is an increasingly unsuccessful induction rate. Methods used for cervical ripening include pharmacological preparations and various forms of mechanical cervical distension.
  • 29. Non pharmacologic means of cervical ripening1. Herbal supplements: evening primrose oil, blue and black cohosh, raspberry leaves.2. Breast stimulation: causes oxytocin release. Adv–non invasive, inexpensive, simple Disadv. – causes FHR abnormalities.3. Castor oil, hot baths, enemas4. Miscellaneous - acupuncture , sexual intercourse
  • 30. 4. (HYGROSCOPIC DILATORS):  Natural osmotic dilators –  Laminaria japonicum  Laminaria digitata  Isapgol  Synthetic osmotic dilators  Lamicel  Dilapan  They absorb endocervical and local tissue fluids, causing the device to expand within the endocervix and provide mechanical pressure.  cause mechanical dilation and release of prostaglandins.  Swell up to 4 – 5 times.  Most rapidly in first 4-6 hours but continue to swell up to 24 hours later.
  • 31. ADVANTAGES DISADVANTAGES  Skill needed for proper placement in Cheap internal os. Outpatient placement  Delay in obtaining maximum effect. Easy for placement  Patient discomfort. No need for fetal monitoring  Inability of tents to be molded without Rapid improvement of compromising mechanical integrity. cervical status  Lack of manufacturer specifications for natural dilators.  Potential for incomplete sterility. ETO gas does not eradicate spores in the interstices of the sea weed stem
  • 32. 5. Membrane stripping:  Release of endogenous PGs. and mechanical dilation.  results in < labor inductions < post dated pregnancies > spontaneous onset of labor - inexpensive, safe, efficacious in promoting labor over several days
  • 33. 6. Balloon devices : Single / Double balloon First described in 1967 Safe Cheap ADVANTAGES: The combination of balloon catheter plus oxytocin is recommended as an alternative method when prostaglandins (including misoprostol) are not available or are contraindicated (previous caesarean) May be useful for outpatient ripening. Can be inserted in presence or absence of membranes. Associated with favorable Bishop scores and no additional side effects.
  • 34. Single Balloon Devices A fluid filled balloon is inserted inside the cervix. A Foley catheter (26 Fr) or specifically designed balloon devices can be used Mechanism of action: The mechanism by which Foley s catheter improves the cervical state is by its mechanical action. It strips the fetal membranes from the lower uterine segment, causing rupture of lysosomes , release of phospholipase A and formation of prostaglandins.
  • 35. Technique of Balloon Placement1. After sterilization and draping, the catheter is introduced into the endocervix either by direct visualization or blindly by sliding it over fingers through the endocervix into the potential space between the amniotic membrane & the lower uterine segment.2. The balloon is inflated with 30 to 50 mL of normal saline and is retracted so that it rests on the internal os.3. Constant pressure may be applied over the catheter. e.g. a bag filled with 1 L of fluid may be attached to the catheter end / An intermittent pressure may also be exerted on the catheter end 2 -4 times per hour.
  • 36. 4. Catheter is removed at the time of rupture of membranes or may be expelled spontaneously which indicate a cervical dilatation of 3 - 4 Centimeters.
  • 37. PHARMACOLOGICAL TECHNIQUES Prostaglandins  PGE2 : Dinoprostone  PGE1 : Misoprostol Oxytocin Others  Estrogen  Relaxin  Hyaluronic acid  Progesterone receptor antagonist
  • 38. PROSTAGLANDINS  The chemical precursor is arachidonic acid  PGs are endogenous compounds found in the myometrium, deciduas, and fetal membranes during pregnancy.  Cervical production of PGE2, PGI2, PGF increases at term. Modulate fibroblast activity - Increase hyaluronic acid production Acting as chemotactic agents, Inflammatory cells further release degradative enzymes, causing cervical ripening.
  • 39.  Prostaglandins administration results in dissolution of collagen bundles and an increase in sub mucosal water content of the cervix.  These changes in cervical connective tissue at term are similar to those observed in early labor. Unlike oxytocin, response to prostaglandins does not change throughout gestation.
  • 40. Preparations PGE2 : Dinoprostone PGE1 : Misoprostol Vaginal gel : Prepidil, CerviprimeTM  MisoprostTM Removable tampon : CervidilTM  CytotecTM Vaginal pessary : Prostin E2TM
  • 41. Prostaglandin E2: (Dinoprostone) Increase in elastase, glycosaminoglycan, dermatan sulfate, and hyaluronic acid levels in the cervix. A relaxation of cervical smooth muscle facilitates dilation.Alter the extracellular ground substance of the cervix Increase in intracellular calcium levels,increases the activity of collagenase in ~ contraction of myometrial muscle the cervix. Cervical Ripening
  • 42.  PROSTAGLANDIN E2 (DINOPROSTONE):  CERVIPRIME GEL - is commonly used for cervical ripening .  is available in a 2.5-mL syringe for an intracervical application of 0.5 mg of dinoprostone.  With the woman supine, the tip of a pre-filled syringe is placed intracervically, and the gel is deposited just below the internal cervical os.  After application she remains reclined for at least 30 minutes. Doses may be repeated every 6 hours, with a maximum of three doses recommended in 24 hours.
  • 43. Prepidil Intracervical placement
  • 44.  Dinoprostone should only be administered at hospital. Continuous Uterine activity & FHR monitoring. If optimal response is not achieved by 6 hours, another dose can be administered. The maximum allowed dose is 3 doses be administered per 24 hours. Oxytocin should not be initiated until 6 to12 hours after the last dose because of the potential for uterine hyperstimulation with concurrent oxytocin and prostaglandin administration.
  • 45. Cervidil placed in posterior vaginal fornix
  • 46.  Vaginal insert containing 10 mg of dinoprostone in a timed-release formulation. The vaginal insert administers the medication at 0.3 mg/h and may be left in place for up to 12 hours. ADVANTAGE: the insert may be removed with the onset of active labor, rupture of membranes, or with the development of uterine hyperstimulation.
  • 47. Vaginal pessary : Prostin E2TM
  • 48. COCHRANE REVIEW Vaginal Prostaglandin E2 versus placebo/no treatment (37 trials, 6511 women) vaginal No Rx / risk 95% PGE2 Placebo ratio confidence (RR) interval (CI)risk of the cervix remaining unchanged/ 5 trials, 467 women 21.6% 40.3%, 0.46 0.35 to 0.62unfavourable after12 to 24 hoursreduction in failure to achieve vaginal delivery 2 trials, 384 women 18.1% 98.9%, 0.19 0.14 to 0.25within 24 hoursuse of oxytocin augmentation 12 trials, 1321 women 35.1% 43.8% 0.83 0.73 to 0.94Uterine hyperstimulation with FHR changes 14 trials, 1259 women 4.4% 0.49%, 4.14 1.93 to 8.90Hyperstimulation without FHR changes 13 trials, 3636 Women 1.4% 0.4% 2.48 1.17 to 5.26
  • 49. COCHRANE REVIEWVehicle comparisons PGE2 gel is as efficacious as PGE2 tablets. PGE2 gel does reduce the need for oxytocin augmentation, Gel was associated with less uterine hyperstimulation. Sustained release pessaries in comparison with gel  have not been shown to significantly reduce caesarean section rates  have not been shown to improve adverse neonatal or maternal outcomes.  There is reduction in the use of oxytocin augmentation and the reduction in instrumental delivery rates.  The frequency of vaginal examinations is reduced when using sustained release pessaries.
  • 50.  INTRACERVICAL PGE2: although this route of administration is effective, it offers no advantages when compared to other methods of administration, namely the vaginal route. Intracervical prostaglandins are effective compared to placebo, but appear inferior when compared to intravaginal prostaglandins.
  • 51. PGE2 can cause Uterine hyperstimulation, Fetal distress and Cesarean section.Uterine hyperstimulation :- More common with intra vaginal application.- 1-5%, similar to low dose oxytocin <=4mu/ml. - Begins within 1 hr - Removal, irrigation of Cervix, vagina : not helpful - Rapidly reversed with terbutaline or removal of insert. - Hence fetal heart rate monitoring is needed for 2 hours following single dose and longer if contractions persist after that.
  • 52.  A retrospective study of case notes (n = 3099) investigated women who underwent induction with PGE2 (vaginal tablet, gel and intracervical gel). Uterine hyperstimulation (defined as contraction frequency being more than five in 10 minutes or contractions exceeding 2 minutes in duration) occurred in 5.8% patients, of which 31.5% were associated with FHR abnormalities. Administration of tocolytic treatment with β2-adrenergic drugs  (hexoprenaline at 0.3 micrograms/minute OR  single dose of terbutaline 250 micrograms intravenously or subcutaneously)  successful in normalising uterine contractions and reversing any FHR abnormality in (98.3%). Improvement usually began within 5 minutes regardless of hyperstimulation patterns. NICE 2008
  • 53. Systemic effect  Nausea  Vomiting  Diarrhea  Caution in  Glaucoma  hepatic and renal disease  Asthma
  • 54. Safety in induction for VBAC Concern is with uterine rupture caused by uterotonic effects. In largest cohort study of 5022 patients willing for VBAC  453 patients received intra vaginal gel  The rates of rupture were, 1.3% with PGE2 and 0.7 without its use.  ~ not statistically significant. Am J of Perinatol. 1997;14:157-160
  • 55. Two studies have expanded on the differences in adverse outcomes between prostaglandin and non-prostaglandin (such as intracervical Foley catheter) based induction regimens. In the NICHD study, prostaglandin induction compared with non-prostaglandin induction incurred a non-significantly higher risk of uterine rupture (140/10,000 versus 89/10,000; P = 0.22).In an analysis of nationally collected data from Scotland, prostaglandin induction compared with non-prostaglandin induction was associated with a statistically significantly higher uterine rupture risk (87/10,000 versus 29/10,000) and a higher risk of perinatal death from uterine rupture(11.2/10,000 versus 4.5/10,000).This compares with 6/10,000 risk of perinatal death in women with an unscarred uterus induced by prostaglandin identified by a Cochrane review.RCOG
  • 56.  Given these risks and the absence of direct robust evidence, it is important not to exceed the safe recommended limit for prostaglandin priming in women with prior caesarean birth. RCOG 2007
  • 57. Use with Premature Rupture of Membranes at term. It has not been shown to decrease neonatal infections when compared with expectant management. It could decrease time to delivery, but this can be achieved equally with optimum oxytocin dosing. More important intervention to decrease maternal infectious morbidity is decreasing number of PV examinations.
  • 58. Misoprostol Dosing  25 mcg  50 mcg Very cheap Easy to store
  • 59. Pharmacokinetics Route of administration: Oral, vaginal and sublingual route for induction. Bioavailability: Extensively absorbed from the GIT Metabolism: De-esterified to prostaglandin F analogs Half life: 20–40 minutes Excretion: Mainly renal 80%, remainder is fecal: 15% maximum plasma conc. with 400µg miso. - 34 mins. after oral , 80 mins. After vaginal - rapid onset and greater peak action with oral miso. - longer action with vaginal miso.
  • 60.  Clinical trials indicate that the safe optimal dose and dosing interval is 25 mcg intravaginally every 4-6 hours. ACOG 1999 A maximum of 6 doses was suggested.
  • 61. VAGINAL MISOPROSTOL (comparison)Vaginal misoprostol versus Trials/ No. of women Outcomes Placebo/ Expectant 5 trials/ Reduced risk of not management 769 participants achieving vaginal birth within 24 hrs of induction Intravenous oxytocin •9 trials/1200 participants •Reduced risk of not achieving vaginal birth •25trials/3074 participants •Fewer cesarean sections •13 trials/1906 participants •Fewer infants with apgars below 7 at 5mins Other prostaglandins - •a reduced risk of vaginal birth not achieved within 24 hours •fewer caesarean sections •increased risk of uterine hyperstimulation with fetal heart rate changes
  • 62.  Compared with higher doses of vaginal misoprostol, lower doses (25 μg, 6- hourly) were associated with a reduced risk of uterine hyperstimulation with fetal heart rate changes (16 trials, 2540 participants, RR 0.51, 95% CI 0.37–0.69). The risk of vaginal birth not being achieved within 24 hours was similar with both higher and lower doses
  • 63. ORAL MISOPROSTOL Oral misoprostol versus Trials/ No. of women Outcomes Placebo/ Expectant •1 trials/96 participants •Reduced risk of not achieving vaginal birth management within 24 hrs of induction •6 trials/629 participants •Reduced cesarean births Intravenous oxytocin •8 trials/1026 participants •Similar w. r, t. the risk of priority outcomesIntracervical prostaglandins •More effective in achieving vaginal birth within 24 hrs Vaginal prostaglandins •Reduction in cesarean rates
  • 64.  Lower doses of oral misoprostol (up to 50 μg) were associated with similar outcomes compared with higher doses (100 μg)
  • 65. Oral misoprostol versus vaginal misoprostol Similar with regard to priority outcomes except Oral misoprostol was associated with a lower risk of Apgar score being less than seven at 5 minutes of life (14 trials, 3270 participants, 94 events, RR 0.65, 95% CI 0.44–0.97).
  • 66.  Vaginal misoprostol versus sublingual/ buccal misoprostol : similar with regard to all the priority outcomes Oral versus sublingual/buccal misoprostol: Data are limited
  • 67. Recommendations1. Oral misoprostol (25 μg, 2-hourly) is recommended for induction of labour. (Moderate-quality evidence. Strong recommendation.)2. Vaginal low-dose misoprostol (25 μg, 6-hourly) is recommended for induction of labour. (Moderate-quality evidence. Weak recommendation.)3. Misoprostol is not recommended for women with previous caesarean section. (Low-quality evidence. Strong recommendation.)
  • 68. Misoprostol vs Dinoprostone The mean time to vaginal delivery was significantly shorter in the misoprostol group (925.8 versus 1577.6 minutes), and the mean duration of the active length of labour was significantly shorter in the misoprostol group (353.7 versus 496.8 minutes) Less likely to require a repeated dose of prostaglandin for cervical priming and oxytocin for augmentation of labour. no difference in the rate of Caesarean section More hyperstimulation during labour in the misoprostol group Aust N Z J Obstet Gynaecol. 2001 May;41(2):145-52
  • 69. Oxytocin for cervical ripening : comparisonIntravenous Oxytocin Trials / Outcome versus No womenExpectant management 25 trials; Intravenous oxytocin reduced the failure to 6660 women achieve vaginal delivery within 24 hours when compared with expectant management (8.4% versus 54%)Vaginal PGE2 27 trials; compared with vaginal PGE2, oxytocin was 4564 women associated with more failures to achieve vaginal delivery within 24 hours (70% versus 21%)Intracervical PGE2 14 trials; Oxytocin was associated with increased 1331 women unsuccessful vaginal deliveries within 24 hours when compared with intracervical PGE2 (50.4% versus 34.6%) Increase in cesarean sections (19% versus 13.7%)
  • 70. CONCLUSIONComparison of oxytocin with either intravaginal or intracervical PGE2 reveals that the prostaglandin agents probably increase the chances of achieving vaginal birth within 24 hours.Oxytocin induction may increase the rate of interventions in labour. NICE 2008
  • 71. Risks CESAREAN DELIVERY  especially increased in nulliparas  two- to threefold risks  rates are inversely related with favorability of the cervix at induction, that is, the Bishop score. CHORIOAMNIONITIS UTERINE ATONY  Postpartum atony and hemorrhage are more common in women undergoing induction or augmentation  Intractable atony was the indication for a third of all cesarean hysterectomies

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