Preterm Labour, Preterm Rupture Of Membrane PDF

Preterm labourAnd Preterm Rupture Of Membrane Dr Alaa yousif mahmood obstetric and gynecology department MRCOG (LONDON)/DOG/M.B.ch.B  Objectives: At the end of this lecture you should be able to 1-Define preterm labour 2- know the ris...

Preterm labourAnd Preterm Rupture Of Membrane Dr Alaa yousif mahmood obstetric and gynecology department MRCOG (LONDON)/DOG/M.B.ch.B  Objectives: At the end of this lecture you should be able to 1-Define preterm labour 2- know the risk of preterm labour 3.-categorize risk factor for preterm labour 4.-predict preterm labour 5.-Design plane for prevention of preterm labour 6- Create plane for management of preterm labour 7- Define the premature rupture of membranes 8-Identify risks factors of premature rupture of membranes 9.-Understand the current intervention to treat premature rupture of membranes 10-Discuss the care for women experienced preterm rupture of membranes  Case senario Mrs. Thikra is a 17 year old primigravida; she is a secondary school student her LMP was at the 7thJune 2022, she is pregnant with twin pregnancy, has low BMI, non-smoker and is not known to have chronic disease What is her EDD? What is the gestational age GA at 15th of Nov.2022? She developed spontaneous premature pre-labour rupture of fetal amniotic membrane(PPROM), for which she was put on conservative treatment, her ultrasound reports all show marked oligohydraminios, at the 20 th of Dec. 2022. She developed spontaneous preterm labour, lastly she gave birth through caesarean section for presumed fetal compromise in labour to viable twins both are male neonates. What is the gestational age at delivery? At this gestational age, how much the neonates do should reach of their eventual birth weight. Hassan the 1st twin was 965 grams, Hussein the 2nd twin was 824 grams, however according to standard growth centile chart the predicted birth weight for their GA was 1.1 kg.  Are they appropriate or small for gestational age (SGA)?  What do you think the factors that were responsible for such type of growth?  Shortly after birth Hassan suffered from respiratory difficulty for which the baby needed assisted ventilation  What do you think the cause behind this respiratory problem? Is Hassan chance to develop this respiratory problem higher or lower than neonate of same GA, with uncomplicated preterm labour? Why?  What is other lung developmental problem that might occur in preterm babies born to mothers with prolonged history of PPROM and long standing oligohydraminios at early gestational age?  Why?  As the birth happened in winter are the neonates at increased risk of hypothermia?  hours after birth, Fasting blood sugar record for both twins was 45, 37 mg /dl this was treated by hypertonic glucose infusion, how do you explain this new event?  A 37 year-old woman primigravida with a pregnancy from In vitro fertilization (IVF) and normal antenatal progress presented to antenatal day unit (ANDU) at 26 weeks of gestation with a history suggestive of ruptured membranes.  Outline your immediate management Assuming rupture of membrane is confirmed, describe your subsequent management.  Definition Preterm labour (PTL) is the onset of labour before 37 weeks’ gestation And after 24 weeks of pregnancy Affect 5-10 of all pregnancy It account 75% of perinatal mortality  Cervical weakness Cervical weakness is classically associated with painless premature cervical dilatation and is suggested by a history of painless second trimester pregnancy loss. There is almost certainly an overlap between cervical weakness and other factors such as ascending infection, as during pregnancy, the cervix not only acts as a physical obstacle, keeping the pregnancy in the uterus, but also as a barrier to ascending infection through the synthesis of a thick mucus plug in the cervical canal that has bactericidal properties. Several studies have demonstrated a strong relationship between cervical length and the risk for PTD, and a previous history of cervical surgery is a common risk factor for cervical weakness.  Infection Infection of the fetal membranes, chorioamnionitis, is a major cause of preterm birth particularly in deliveries before 32 weeks with intact membrane In most cases, infection ascends from the vagina, although the route of infection may be transplacental or introduced during invasive procedures. Cervical weakness, resulting in early shortening, as described earlier, can predispose to ascending bacterial infection 33% of all pregnancies delivered after PPROM are complicated by infection Chorioamnionitis not only drives PTL, but it is also associated with fetal brain damage, since intrauterine infection drives a fetal inflammatory response, involving a proinflammatory cytokinaemia and, a vasculitis of the umbilical cord and/or the vessels of the chorionic plate. The release of inflammatory cytokines during maternal infection is harmful to the developing brain of the unborn infant, causing periventricular white matter damage also known as periventricular leukomalacia I, increased amniotic fluid IL-6 levels are associated with intraventricular haemorrhage (IVH) and PVL and high levels of cytokines have been found in brains of infants who die with evidence of PVL  Multiple pregnancy Multiple pregnancy and uterine distension Overall, 56% of multiple births deliver before 37 weeks and 10–15% before 32 weeks. Consequently, although multiple pregnancies only make up 2% of the pregnant population, they contribute disproportionately to PTDs and, consequently, Neonatal Intensive Care Unit (NICU) admissions. The risk of PTD rises with fetal number, with triplets delivering on average at 32 weeks and quadruplets delivering at 28 weeks. Multiple pregnancies have an increased risk of pre-eclampsia, FGR and other medical complications of pregnancy Twins have a six to seven fold increased risk of cerebral palsy and this rises to 100-fold if one twin dies antenatally  Polyhydramnios Polyhydramnios, the presence of too much amniotic fluid, also increases the risk of PTL and PPROM, PTD occurring in between 7 and 25% of fetuses depending on the degree. Severe polyhydramnios can be managed with amnio-drainage, but this may itself precipitate PTL and/or PPROM. Alternatively, indomethacin, a non-steroidal anti- inflammatory drug (NSAID), may be used as it reduces fetal urine production, but flow through the ductus arteriosus has to be closely monitored as the inhibition of PGE production by indomethacin may result in premature closure.  Uterine müllerian anomalies Congenital müllerian anomalies are often unrecognized but are estimated to occur in up to 4% of women of reproductive age. They occur as a consequence of abnormal embryologic fusion and canalization of the müllerian ducts and result in an abnormally formed uterine cavity, which can range from an arcuate uterus, which results in minimal fundal cavity indentation, to complete failure of fusion resulting in uterine didelphys. They are associated with adverse pregnancy outcome in up to 25% of women, including first and second trimester miscarriage, PPROM, preterm birth, FGR, breech presentation and caesarean section  Hemorrhage Antepartum haemorrhage and placental abruption may lead to spontaneous PTL. The presence of a subchorionic haematoma in early pregnancy increases the risk of later PPROM, either through an effect of thrombin on membrane strength or through the occurrence of infection in the haematoma. Acute bleeding leads to the release thrombin that directly stimulates myometrial contractions. Placental abruption complicates 1% of all pregnancies and the maternal or fetal effects depend primarily on its severity and the gestational age when it occurs. Risk factors include: pre-eclampsia and hypertension, previous abruption, trauma, smoking, cocaine use, multiple pregnancy, polyhydramnios, thrombophilias, advanced maternal age and PPROM. When an abruption involves 50% or more of the placenta it is frequently associated with fetal death.  Stress Stress There is growing evidence that either maternal or fetal stress may be associated with PTL. A link between maternal stress and PTL is suggested by its increased prevalence among unmarried and poor mothers, as well as in stressful sociodemographic conditions (such as loss of employment, housing or partner). Prematurity is also more common among women reporting increased stress or anxiety. The biochemical pathway through which maternal and fetal stress promotes PTL is uncertain, but may involve a premature increase in circulating corticotrophin-releasing hormone (CRH).  Management of preterm labour Up to 70% of women who present with threatened PTL to the labour ward will not deliver during the current admission, and up to 50% will not deliver until term. Deciding who is and who is not in PTL has been helped by testing the cervicovaginal fluid levels of fetal fibronectin (fFN), a glycoprotein found in cervicovaginal fluid, amniotic fluid, placental tissue and in the interface between the chorion and decidua. It acts like ‘glue’ at the maternal–fetal interface and its presence in cervicovaginal fluid between 22 and 36 weeks’ gestation has been shown to be a predictor of PTD. Negative fFN testing has a very high negative predictive value, enabling most women with threatened PTL and a negative fFN test to be sent home. Those with a positive fFN test can be admitted for tocolysis and steroids for fetal lung maturation.  Medical treatment for PTL Progesterone Studies support the use of progesterone supplementation to reduce preterm birth in patients at high risk for recurrent preterm delivery. Tocolytics are used to delay delivery long enough for corticosteroid administration to improve neonatal lung function and, if necessary, for in utero transfer to a NICU. Calcium channel blockers They exert their effect by binding to L-type channels, reducing intracellular levels of calcium and blocking the transmembrane influx of calcium ions into muscle cells. Comparing nifedipine with other tocolytics (including beta-sympathomimetics, NSAIDs, magnesium sulphate and Oxytocin receptor antagonists [OTR-A]), no significant reductions were shown in the primary outcome measures of birth within 48 hours of treatment or in perinatal mortality. adverse drug reactions, discontinuation due to side-effects, neonatal RDS, necrotizing enterocolitis, intraventricular haemorrhage and neonatal jaundice were least for OTR-A, intermediate for nifedipine and greatest for beta-sympathomimetics.  Magnesium sulphate Magnesium sulphate Magnesium decreases the frequency of depolarization of smooth muscle by modulating calcium uptake, binding and distribution in smooth muscle cells and results in inhibition of uterine contractions. The American College of Obstetricians and Gynecologists (ACOG) supports the use of magnesium sulphate for neuroprotection stating that “magnesium sulphate reduces the risk of cerebral palsy in surviving infants”. Non-steroidal anti-inflammatory drugs The first NSAID to be widely used in the management of PTL was indomethacin. It is a reversible, non-specific competitive cyclooxygenase (COX) inhibitor. Iindomethacin has been shown to effectively delay delivery for 48 hours, 7–10 days and beyond 37 weeks, so reducing the incidence of low birthweight , they do have several adverse fetal effects. PG synthesis is responsible for the maintenance of a patent ductus arteriosus and inhibition can lead to its premature closure. This can occur as early as the late second trimester, with the incidence increasing dramatically from 32 weeks. This may lead to persistent pulmonary hypertension in the fetal circulation of the neonate. The effect is completely reversible with early identification and discontinuation of treatment. In addition, indomethacin use has been associated with an increased risk of necrotizing enterocolitis and neonatal renal dysfunction. The latter probably occurs because inhibition of fetal PG synthesis reduces renal perfusion and fetal urine output, resulting in reversible (after discontinuation of the drug) oligohydramnios.  Oxytocin receptor antagonists Oxytocin receptor antagonists OTRs play an important role in the onset and progression of labour. The OTR-A atosiban is a competitive antagonist of oxytocin and vasopressin, binding to both the OTRs and the vasopressin V1a receptors within the myometrium. Administration of atosiban results in a dose-dependent inhibition of uterine contractility and oxytocin-mediated PG release. In pregnant women atosiban is 46–48% plasma protein bound and only a small amount appears to cross the placenta into the fetal circulation. It has a similar efficacy as beta sympathomimetics, but is much better tolerated. Compared to placebo, more atosiban-treated patients remained undelivered at 24 hours, 48 hours and 7 days.  Beta-sympathomimetics Beta-agonists Beta-sympathomimetics Beta-agonists (ritodrine, salbutamol and terbutaline) are predominantly β2 adreno-receptor agonists), which mediate myometrial relaxation by stimulating cyclic adenyl monophospate (AMP) production. They are effective in delaying delivery, but do not improve neonatal outcome or ultimate PTD rates. They have significant maternal side-effects, which means that they are rarely used in the context of threatened PTL The most serious side-effect is pulmonary oedema, with an estimated incidence of 1:350–1:400 treated patients. Maternal deaths from acute cardiopulmonary compromise are described, with greater risks if beta-agonists are given in large fluid volumes, in multiple pregnancies and in women with cardiac disease.  Corticosteroid therapy Corticosteroid therapy The administration of corticosteroids has the greatest influence on preterm neonatal outcome. Although the use of recombinant surfactant in neonates has also had a major impact on the incidence and consequences of RDS, antenatal corticosteroids are still associated with significant reduction in neonatal mortality principally through reduced rates of RDS and IVH Their mechanism of action is complex; they affect not only fetal lung maturation, but also fetal growth, organ system maturation, fetal brain development, immune function and the fetal hypothalamic–pituitary– adrenocortical axis. Currently, betamethasone or dexamethasone are recommended; both are able to cross the placenta in their active form and have comparable properties, but some dexamethasone preparations contain a sulphite preservative that has been linked with neurotoxicity and should be avoided.  Antibiotics Antibiotics Despite a clear link between bacterial infection and preterm birth, the results of antibiotic treatment as an attempt to prevent PTL have been disappointing. The ORACLE trials focused on the use of antibiotics in PPROM These trials demonstrated that, in singleton pregnancies with PPROM, erythromycin improved neonatal outcomes, but that antibiotic treatment in women with intact membranes had no benefit.  Management of PPROM PPROM occurs in approximately 2% of all pregnancies and accounts for up to one-third of preterm deliveries. Fifty percent of women deliver within 1 week and 75% within 2 weeks of PPROM. Although postnatal survival following PPROM is directly related to birthweight and gestational age at delivery, in pregnancies complicated by PPROM prior to 23 weeks, pulmonary hypoplasia may develop leading to an increased risk of neonatal death, even if delivery occurs at later gestational ages. Pulmonary hypoplasia following PPROM occurs in approximately 50% of women with PPROM at 19 weeks, falling to about 10% at 25 weeks. The presence of amniotic fluid greater than 2 cm on ultrasound is associated with a lower incidence of pulmonary hypoplasia  Diagnoses Of PPROMs PPROM is diagnosed through clinical history and the demonstration of a pool of liquor in the vagina on speculum examination. Nitrazine test—a sterile cotton-tipped swab should be used to collect fluid from the posterior fornix and apply it to Nitrazine paper. In the presence of amniotic fluid, the Nitrazine paper turns blue, demonstrating an alkaline pH (7.0–7.25). The “fern” test (4) U/S fetal size and amniotic fluid index (5) Amniocentesis. to determine fetal lung maturity and the presence of infection ???? Laboratory Studies complete blood count with differential. genital tract swab  Complications o Of PPROMs maternal (1) Infection : endometritis (2) Placental abruption (3) Preterm delivery Fetal (1) Preterm Baby and their Complications : (RDS / Fetal and Neurologic dysfunction Intracranial hemorrhage) (2) Pulmonary hypoplasia and fetal compression syndrome (3) Prolapse or compression of umbilical cord (4) Abruptio placenta  Management of Of PPROMs Management balances the risk of prematurity (if delivery is encouraged) versus the risk of maternal and fetal infection (if delivery is delayed). In general, conservative management is followed in PPROM before 34 weeks’ gestation unless there is evidence of chorioamnionitis and immediate induction of labour is advised in women after 37 weeks’ gestation.  Conservative management Conservative management includes intensive clinical surveillance for signs of chorioamnionitis including regular recording of maternal temperature, heart rate, cardiotocography and maternal biochemistry, with a rising white cell count or a rising C- reactive protein indicating development of chorioamnionitis. Lower genital tract swabs are routinely taken, but cultures do not correlate well with the risk of chorioamnionitis. In the majority of cases of PPROM there is time for administration of corticosteroids and in utero transfer before the onset of PTL. Tocolysis is contraindicated due to the increased risk of maternal and fetal infection in patients with PPROM.  Prediction of preterm delivery Past obstetric history Having had a previous PTD increases the risk of PTL in a subsequent pregnancy four times in comparison to a woman who had a previous delivery at term Ultrasound measurement of cervical length Cervical length measured by transvaginal ultrasound has been shown to be more accurate than transabdominal ultrasound or digital examination. There is a direct relationship between cervical length and the risk of PTD Cervical length surveillance with serial measurement of cervical length throughout the second and early third trimester is now used to monitor women at high risk of PTD The combination of cervical length and obstetric history can predict 80.6% of extremely early spontaneous PTD (10% screen- positive rate).  Prevention of preterm delivery Prevention of preterm delivery In those found to be at high risk of PTD, two interventions are currently available, progesterone and cervical cerclage. Progesterone Progesterone has been known to be important in maintaining pregnancy for more than 80 years and is thought to promote uterine quiescence and inhibit the production of proinflammatory cytokines and PGs within the uterus. In women with a previous preterm birth, there is some evidence that intramuscular hydroxyprogesterone caproate is effective in reducing the risk of recurrence. Hydroxyprogesterone caproate is licenced in the USA for preterm birth prevention in women with a previous preterm birth.  Prevention of preterm delivery Cervical cerclage Tranvaginal cervical cerclage may be placed in three different circumstances: following multiple midtrimester losses or preterm deliveries (history indicated cerclage); when the cervix shortens (usually less than 25 mm) in women with a history of cervical surgery or previous preterm birth (ultrasound indicated cerclage); or when the cervix is dilating in the absence of contractions (rescue cerclage). The exact mechanism by which cerclage helps to prevent or delay PTL is not entirely understood. It is likely, however, that cerclage provides structural support to a weakened cervix, and enhances the cervical immunological barrier by improving retention of the mucous plug and preventing ascending infection by maintaining cervical length.