41 Position \200\223ie which way is the fetus facing? ( \201 gs 1 & 2) Occipitoanterior Back easily felt Limbs not easily felt Shoulder lies 2cm from midline on opposite side from back Back from midline=2 \200\2233cm Occipitolateral Back can be felt Limbs lateral Midline shoulder Occipitoposterior Back not felt Limbs anterior Shoulder 6 \200\2238cm lateral, same side as back >10cm 6 \200\2238cm s c i r t e t s b O Fig 1. Fetal positions. OUP Fig 2. Use \201 gure 1 to help determine the lie, the presentation, and the position from these dissections by William Hunter (1718 \200\22383). William Hunter (1718 \200\2231783). Anatomia uteri humani gravidi tabulis illustrata (The anatomy of the human gravid uterus e xhibited in \201 gures). Pelvis and head 42 \200 The ideal pelvis This has a rounded brim, a shallow cavity, non-prominent ischial spines, a curved sacrum with large sciatic notches and sacrospinous ligaments >3.5cm long. The angle of the brim is 55 to the horizontal, the AP diameter at least 12cm and transverse diamet er at least 13.5cm. The subpubic arch should be rounded and the intertuberous distance at l east 10cm. A clini- cally favorable pelvis is one where the sacral promontory cannot be fel t, the ischial spines are not prominent, the subpubic arch and base of supraspinous ligamen ts both accept 2 \201 ngers, and the intertuberous diameter accepts 4 knuckles when the w oman is examined. The true pelvis Anteriorly there is the symphysis pubis (3.5cm long) and posteriorly the sacrum (12cm long). Zone of inlet: Boundaries: Anteriorly lies the upper bo rder of the pubis, posteriorly the sacral promontory, laterally the ileopectineal line. Tra nsverse diameter 13.5cm; AP diameter 11.5cm. Zone of cavity: This is the most roomy zone. I t is almost round. Transverse diameter 13.5cm; AP diameter 12.5cm. Zone of mid-pelvis: Boun daries: Anteriorly, the apex of the pubic arch; poste- riorly the tip of the sacrum, latera lly the ischial spines (the desirable distance between the spines is >10.5cm). Ovoid in sha pe, it is the narrowest part. Zone of outlet: The pubic arch is the anterior border (desira ble angle >85 ). Laterally lie the sacrotuberous ligaments and ischial tuberosities, poste riorly the coccyx. Head terms The bregma is the anterior fontanelle. The brow lies between the bregma and the root of the nose. The face lies below the root of the nose and supraorbi tal ridges. The occiput lies behind the posterior fontanelle. The vertex is the area betwee n the fontanelles and the parietal eminences. Molding The frontal bones can slip under the parietal bones which can slip under the occipital bone so reducing biparietal diameter. The degree of overlap may be assessed vaginally. s c i r t e t s b O Presentation Flexed vertex Partially de \202 exed vertex De \202 exed vertex Brow Face Relevant diameter presenting Suboccipitobregmatic Suboccipitofrontal Occipitofrontal Mentov ertical Submentobregmatic 9.5cm 10.5cm 11.5cm 13cm 9.5cm Movement of the head in labor (normal vertex presentation) 1 Descent with increased \202 exion as the head enters the cavity. The sagittal suture lies in the transverse diameter of the brim. 2 Internal rotation occurs at the ischial spine level due to the grooved gut- ter of the le vator muscles. Head \202 exion increases. (The head rotates 90 if occipitolateral posit ion, 45 if occipitoanterior, 135 if occipitoposterior.) 3 Disengagement by extension as the head comes out of the vulva. 4 Restitution: as the shou lders are rotated by the levators until the bis- acromial diameter is anteroposterior, the head externally rotates the same amount as before but in opposite direction. 5 Delivery of anterior shoulder by lateral \202 exion of trunk posteriorly. 6 Delivery of posterior shoulder by lateral \202 exion of trunk anteriorly. 7 Delivery of buttocks and legs. 43 Posterior fontanelle 1 4 2 Biparietal diameter 9.5 cm 3 Sagittal suture Anterior fontanelle (bregma) 5 1 Suboccipitobregmatic 9.5 cm \202exed vertex presentation 2 Suboccipitofrontal 10.5 cm partially de \202exed vertex s c i r t e t s b O 3 Occipitofrontal 11.5 cm de \202exted vertex 4 Mentovertical 13 cm brow 5 Submentobregmat ic 9.5 cm face Sacrum I n l e t C a vity Mid pelvis Outlet Coccyx Fig 1. Pelvic diameters vs fetal head. \200\230Life forced her through this gate of suffering \200\231 DH Lawrence, Sons and Love rs. Fetal monitoring 44 In high-risk pregnancy, antepartum cardiotocography and biophysical pro \201 les by ultras ound (p46) are used to monitor fetal activity and responsiveness. The aim is to detect intr auterine hypoxia prenatally. Cardiotocography (CTG): Doppler ultrasound detects fetal heart beats and a tocodynamometer over the uterine fundus records any contractions. A con- tinuo us trace is printed over 30min (eg a paper speed of 1cm/min) with the mother lying semi-re cumbent, or in the left lateral position or half-sitting posi- tion. A normal trace in an a febrile mother at term who is not having drugs has a base rate of 110 \200\223160 beats/min , with a variability of >5 beats/min, and at least 2 accelerations (a common response to mo vement or noise) of an amplitude \211 15 beats/min over a 20-min period. (Fetal heart rate falls by 1 beat/min/week from 28 weeks.) CTG needs to be done every 24h antenatally to id entify the chang- ing fetal heart rate pattern associated with hypoxia (loss of baseline va riability with decelerations). Intrapartum monitoring Death and disability due to complicat ions of labor occur in <1 : 300 labors. Intrapartum fetal heart rate monitoring aims to det ect patterns known to be associated with fetal distress \200\224a diagnosis supported by fe tal hypoxia (acidosis) on blood sampling. Intermittent auscultation (IA) at the end of cont ractions (to listen for decel- erations) with Doppler or Pinard stethoscope is used for low -risk labors. Use every 15min in 1st stage, 5min throughout 2nd stage. If abnormality noted (below) or intrapartum problems occur, start continuous fetal heart rate (FHR) moni- torin g. This has poor predictive value, overdiagnosing fetal distress even if used with fetal bl ood sampling. Its value is uncertain even in high-risk labors, for which it is used through out labor, ideally with a scalp electrode, but it is associ- ated with reduced neonatal sei zures. 104 Where scalp electrode is used it is also possible to monitor the fetal electroca rdiogram: ST waveform analysis is as- sociated with fewer babies with severe metabolic acid osis, less fetal blood sam- pling, less neonatal encephalopathy, and fewer operative vagina l deliveries (but not cesarean sections). 105 Indications: High-risk pregnancy; use of oxyt ocin; abnormality on intermittent auscultation (decelerations noted after a contrac- tion, or rate <110 or >160 beats/min); fresh meconium passed, p72, (consider too if just meconium stained liquor); maternal pyrexia (To >37.5 2h apart, or once To >38); fresh bleeding in l abor; maternal request. \200 106 Disadvantages: Limited maternal mobility and eff ort. Man agement of a poor trace: \200 Lie the mother on her left side and give O2. Stop oxytocin. If there is uterine \200 s c i r t e t s b O hypercontractility give tocolysis with 0.25mg terbutaline SC. Take fetal blood sample. If you do not have this facility, consider rapid deliv- ery if the trace does not improve. Fetal blood sampling: Use to check for hypoxia in presence of pathological FHR trace, but n ot if acute compromise (eg deceleration lasting >3 min). Take with mother in left lateral p osition. Fetal acidosis re \202 ects hypoxia. Scalp blood pH of >7.25 is normal, repeat in <1h if FHR remains pathological. If 7.21 \200\2237.24 it is borderline, repeat within 30mi n if FHR remains pathological, sooner if other abnormality. If <7.2 call consultant obstetr ician. \200 106 Levels <7.2 require immediate delivery unless in second stage when a level as low as 7.15 may be acceptable. CI maternal infection (HIV, hepatitis viruses, and herpe s), fetal suspected clotting disorder, <34 weeks gestation. Fetal pulse oximetry Knowledge of fetal oxygen saturation is not associated with reduction in rate of cesarean section or with improved condition of the newborn.107 Fetal heart rate patterns and their clinical signi \201 cance (Figs 1 & 2) The normal patt ern is described opposite. Accelerations suggest intact sympa- thetic activity and are rare ly associated with hypoxia. Loss of baseline variability Baseline variability of >5 beats/m in shows re- sponse to vagal tone, sympathetic stimuli, and catecholamines in a well-oxy- g enated fetal brainstem. Loss of baseline variability may re \202 ect a preterm fetus who i s asleep, drug eff ects (eg diazepam, morphine, phenothiazine), or hypoxia. Baseline tachyc ardia Heart rate >170 beats/min is associated with maternal fever, or \200 -sympathomimeti c drug use, chorioamnionitis (loss of variation too), and acute/subacute hypoxia. Persisten t rates >200 are associated with fetal cardiac arrhythmia. Baseline bradycardia A heart rat e <110 beats/min is rarely associated with fetal hypoxia (except in placental abruption). I t may re \202 ect \200\200 fetal vagal tone, fetal heart block, or, if spasmodic, cord co mpression. 45 s c i r t e t s b O Fig 1. Rate patterns. Early decelerations coinciding with uterine contractions re \202 ect increased vagal tone as fetal intracranial pressure rises with the contraction. Late de- c elerations, when the nadir of the deceleration develops some 30sec after the peak of the ut erine contraction, re \202 ect fetal hypoxia, the degree and duration re \202 ecting its severity. Variable decelerations, both in degree and relation to uterine contractions, may represent umbilical cord compression around the limbs or presenting part. Fig 2. Fetal heart deceleration patterns. Pathological CTG pattern \200 106 This has 2 or more non-reassuring features (base- line rate 100 \200\223109 or 161 \200\223180 beats/minu te; variability < 5 beats/minute for \211 40 but <90 minutes; typical variable deceleratio ns with >50% contractions, occur- ing over 90 minutes; or a prolonged deceleration of <3 mi nutes) or 1 abnormal feature (rate <100 or >180 beats/minute; variability <5 beats/minute f or \211 90 min- utes; atypical variable decelerations with > 50% contractions, or late dec elera- tions, both over 90 minutes: or a single prolonged deceleration of >3 minutes). Ultrasound 46 \200 In each ultrasound examination, examine placental site and structure, assess liquor volume and fetal structure, and wellbeing (see below). Early in pregnancy If there is bleeding and pain, ultrasound can con \201 rm ectopic or viable intrauterine pregnancy \200\224at 4 we eks + 3 days for regular 28 \200\223day cycle with transvaginal scan. Where there is discre pancy between uterine size and dates, gestation can be estimated, a viable fetus ascertaine d (not missed miscarriage, p260), or twins (and if monochorionic or dichorionic see p68) di agnosed \200\224especially important after the use of fertility drugs or in the presence of hyperemesis gravidarum (also to exclude hydatidiform mole). Estimating gestation Crown \200\223rump length is measured at 6 \200\22312 weeks ( 10mm at 7 weeks; 55mm at 12). From 12 weeks the biparietal diameter can be measured (and femur length from 14 weeks so there are 2 independent estimations with each scan). Biparietal diameter measurements to estimate age are most accurate up to 20 weeks (unreliable from 34 weeks). Knowing- gestational age is vital in managing rhesus disease and in diabetic pregnancy (p24). It also helps if the d ate of the LMP is unknown, or cycles are irregular. Fetal abnormality See fetal nuchal tran slucency, p11; MINIBOX. Many units off er routine scans to \201 nd abnormality at 18 \200 \22320 weeks. With the best ma- chines and sonographers, an increasing range of markers of fetal abnormality are discernible, eg nuchal thickness in Down \200\231s syndrome, but the sign is also +ve in 6% of normal pregnancies. The more such markers, the greater the chanc e of abnormality (see p10 for \200\230soft signs \200\231). It is hard to know how to coun sel women before these discerning scans: full informed consent is time- consuming, and itse lf causes psychopathology (p12). Another problem is that many fetuses with chromosomal abno rmalities suggested by early scans will spontaneously miscarry in subsequent weeks, and one will have overbur- dened the mother needlessly. Fetal echocardiography Off ered to high-ri sk groups (personal or 1st degree relative history of heart disease; associated with \200 \200 nuchal thickness) it is traditionally off ered at specialist centers at 22 \200\22324 weeks. Scanning at 12 \200\22315 weeks at these centers may exclude most major abnormalitie s. 108 Biophysical pro \201 le scoring Ultrasound of the fetus in the womb over a pe- riod of up to 30min aims to assess if the fetus is being aff ected by acute or chronic asphyxia . With acute asphyxia the fetus loses active biophysi- cal variables regulated by central n ervous system out \202 ow (fetal breathing, gross body movement, fetal \202 exor tone, a nd heart rate accelerations with fetal body movement). Reduction in amniotic \202 uid dem onstrated by pockets of \202 uid of less than 1cm depth measured in 2 perpendicular plane s is taken to indicate chronic asphyxia. By use of speci \201 c criteria for these 5 varia bles, a \200\230wellbeing \200\231 score can be reached. Management protocols according to score then help guide the obstetrician as to when intervention should take place. Indications for scan- ning for abnormality \200 Family history of neural tube defect \200 Maternal diabetes \200 Maternal epilepsy \200 Oligohydrammios \200 Multiple pre gnancy s c i r t e t s b O Ultrasound is used as an adjunct to the diagnostic procedures of amniocen- tesis, fetoscopy, cordocentesis, and chorionic villus biopsy. In pregnancies where fetal growth is of concern (p52) growth can be moni- tored by regular scans; the abdominal to skull circumference ratio is of inter- est. Fetal weight can be est imated when planning vaginal delivery of breech presentation (but less accurate for larger fetuses). In later pregnancy, lie and presentation fetus can be determined. If there is APH, placenta praevia can be excluded and the placenta examined for abrup- tion. With secondary PPH, ret ained products of conception may be visualized. 47 Side-eff ects Ultrasound is one of the safest tests ever invented; nevertheless, over the y ears, fears have been expressed about inducing childhood cancers. There is now good evidenc e that this does not occur. There is one randomized trial indicating that repeated ultrasou nd with Doppler is associated with an in- creased risk (1.65) of birthweights below the thi rd centile. Doppler ultrasound and fetal wellbeing Doppler ultrasound is a technique that can be used t o assess circulation on both sides of the placenta. It has not been shown to be of use as a screening tool in routine antenatal care but it has been shown to be of use in high-risk p regnancies. Waveform outlines (velocimetry) have been seen to be abnor- mal in small babies who ultimately died or were severely ill perinatally, and babies known to be small from re al-time ultrasound have been shown not to be at risk if umbilical artery waveforms were nor mal, but if end-diastolic signals are absent the baby is likely to be hypoxic and acidotic. In manage- ment of growth-retarded babies uncomplicated by other obstetric problems survei llance using Doppler velocimetry is more cost-eff ective than use of cardiotocography, and may be suffi cient as the sole extra means of surveil- lance (in addition to ultrasound exa mination of biophysical parameters). Doppler is useful in determining severity of twin \200 \223twin transfusion (p68) in monochorionic twins. 109 \200\207Consider cesarean section i f umbilical artery Doppler velocimetry shows absent or reversed end-diastolic velocities in pregnancies complicated by intrauterine growth restriction and hyperten- sion \200\224to p revent postnatal problems such as cerebral hemorrhage, anae- mia, and hypoglycaemia. These changes correlate with placental intervillous space ischaemia and spasm or occlusion of ter tiary stem arterioles on the fetal side of the circulation. Placental intervillous ischaemi a leads to cen- tralization of fetal circulation so that blood returning from the placenta is shunted to fetal brain, coronary arteries, and adrenals. Intervention stud- ies based on knowledge of abnormal umbilical waveform patterns have re- sulted in babies small-for-gest ational age (SGA) with abnormal waveform patterns being 500g larger than expected when the mothers were given low-dose aspirin rather than placebo from the time of diagnosis. It is also the case that low-dose aspirin delays the onset of hypertension and reduces its severi ty in primiparous mothers whose babies had abnormal umbilical waveforms. However, aspirin h as not been shown to be of bene \201 t in low-risk pregnancies. s c i r t e t s b O \200 Hypertension in pregnancy 48 \200 Pre-eclampsia Terminology: see footnote on p0. This is pregnancy-induced hypertension (PIH) with proteinuria oedema. A multisystem disorder origi- nating in the placenta, the primary defect is failure of trophoblastic invasion of spiral arteries ( \201 g 1, p15) leaving them vasoactive \200\224properly invaded they cannot clamp down in r esponse to vasoconstrictors and this protects placental \202 ow. Increasing BP partially compensates for this. Pre-eclampsia also aff ects hepatic, renal, and coagulation systems. It develops after 20 weeks and usually resolves within 10 days of delivery. Eclampsia (1 in 2000 maternities) is a major cause of maternal death and fetal morbidity/mortality. Pre-ec lampsia may be asymptomatic, so frequent screening is vital. It may recur in a sub- sequent pregnancy. Risk factors: High risk: \200 Chronic hypertension \200 Hypertension in pre vious preg- nancy \200 Chronic kidney disease \200 Diabetes mellitus \200 Autoimmune disease (SLE, antiphospholipid, thrombophilia). Moderate risk: \200 1st pregnancy \200 \211 40y \200 Preg- nancy interval >10y BMI \211 35kg/m2 \200 FH pre-eclampsia \200 Multiple pregnancy. If 1 high-risk or 2 moderate-risk factors take aspirin 75mg/24h PO fro m 12th week of pregnancy until delivery to prevent eclampsia. Fetal: Hydatidiform mole ( \200\200 BP at 20 weeks); multiple pregnancy; placental hydrops (eg rhesus disease). Fetal causes all have increased placental bulk. Effects of pre-eclampsia: Plasma volume \200\201 ; peripheral resistance \200\200; placental ischaemia. If the BP is >180/140mmHg microaneu rysms develop in arteries. DIC may develop. Oedema may develop suddenly (eg weight \200 \200 by 1kg suddenly). Pro- teinuria is a late sign, meaning renal involvement, which may b e detected earlier by doing urate levels (>0.29mmol/L at 28 weeks, >0.34mmol/L at 32 weeks, and >0.39mmol/L at 36 weeks suggest pre-eclampsia). Initially glomerular \201 ltra- tion is normal and only serum urate is \200\200; later urea and creatinine increase. The liver may be involved (contributing to DIC) \200\224and HELLP syndrome (p26) may be present with placental infarcts. Fetal asphyxia, abruption, and small babies (p52 & p47) may also occur . Late effects (mother): Hypertension and renal failure (sometimes); she should be encourag ed to accept screening for hypertension. 110 Preventing eclampsia Antenatal BP checks/urina lysis; use of MgSO4: see be- low. Uterine artery Doppler scans can identify high-risk women in whom low- dose aspirin use results in a signi \201 cant reduction in pre-eclampsia. Sy mptomatic pre-eclampsia may mimic \202 u, with headache, chest or epigas- tric pain, vomi ting, and pulse \200\200 \200\224but also visual disturbance, shaking, hyper- re \202 exi a, and irritability. The mother is now in danger of generalized seizures (eclampsia) and tr eatment must occur. Death may be imminent from stroke (commonest), hepatic, renal, or cardi ac failure. \200\207Prophylactic magnesium sulfate halves risk of eclampsia, and may \200 \201 maternal deaths. (Doses of >50g magnesium sulfate may be toxic to preterm fetal brains .) 111 Management Early phase: Admit if BP rises by >30/20mmHg over booking BP, if BP \211 160/100, if \211 140/90 + proteinuria (1+), or there is growth restriction. In hospital, measure BP 2 \200\2234-hourly, (thigh cuff if arm circumference \211 41cm), 112 weigh dail y, test all urine for protein; regularly monitor \202 uid balance, check U&E, LFT, and pl atelets (beware falls to <110 \211\210 109/L). Do cardiotocography (p44) on admission: rep eat if PV bleed, abdo pain, \200\201fetal movements or deteriorating maternal condition; a nd US scan to check growth, amniotic \202 uid volume and umbilical artery velicometry. In asymptomatic pre-eclampsia, treat if systolic BP \211 160, eg methyldopa 250mg to 1g/8h u nder supervision in hospital, in order to buy time for fetal maturation, and if all other v ariables are satisfactory. If signs worsen deliver the baby (liaise with pediatricians). De livery is the only cure. Give all pre-eclamptic women H2-blockers at onset of labor. Beware BP rise if anesthetic induction needed. s c i r t e t s b O 49 Managing severe pre-eclampsia This applies to those with BP >160/110 with proteinuria or BP \211 140/90 with proteinuria plus one or more of: \200 Seizures \200 Visual disturban ce \200 Papilloedema \200 Clonus (>3 beats) \200 Continuously monitor maternal oxygen saturation, and BP. \200 Use prophylactic magnesium sulfate: 4g (8mL of 50% solution) IVI over Headache or epigastric pain \200 Platelets <100 \211\210 109/L ALT >70U/L Liver tenderness or HELLP (p26) 15min in 100mL 0.9% saline; then maintenance as below. \200 Catheterize: measure urine output (eg use urometer) & T hourly; FBC, U&E, LFTs, cre atinine every 12 \200\22324h. If platelets <100 \211\210 109/L do clotting studies. \200 Monitor fetal heart rate; assess liquor volume and fetal growth by scan; umbilical cord Doppler if possible. Use monitoring in labor. s c i r t e t s b O \200 Delivery is the only cure for these women. When a decision is made to de- liver, cont act on-call consultant, anesthetist, and senior labor ward mid- wife. Deliver appropriately (eg <34 weeks usually by caesar). Give steroids if <34 \200\22336 wks, (p51). At 3rd stage of labor give 5U oxytocin IM/IV slowly. Treatment of hypertension: Beware: automated BP de vices underestimate BP. \200 If BP >160/110mmHg or mean arterial pressure >125mmHg, use la betalol 20mg IV increasing after 10min intervals to 40mg then 80mg until 200mg total is giv en. Aim for BP 150/80 \200\223100mmHg. Alternative is hydralazine 5mg slowly/20min til 20mg given (unless pulse>120bpm ) after 500mL colloid IV. \200 Give prophylactic H2 blockers until normal postnatal care starts. \200 Restrict \202 uids to 80mL/h. Hourly urine output. Renal failure is rare. Main- tain \202 uid rest riction until postpartum diuresis. Fluid restriction is inappro- priate if there is hemorrh age. Treatment of seizures (eclampsia): \200 Treat a \201 rst seizure with 4g magnesium sulfate in 100mL 0.9% saline IVI over 5min + maintenance IVI of 1g/h for 24h. Beware \200\201 respiration. \200 If recurrent seizure give 2g IVI magnesium sulfate over 5 min. \200 Check tendon re \202 exes and respiratory rate every 15min. \200 Stop magnesium sulfate IVI if respirator y rate <14/min or tendon re \202 ex loss, or urine output <20mL/h. Have IV calcium glucona te ready in case of MgSO4 toxicity: 1g (10mL) over 10 min if respiratory depression. \200 Use diazepam once if \201 ts continue (eg 5 \200\22310mg slowly IV). If seizures co n- tinue, ventilate and consider other causes (consider CT scan). Pitfalls in the management o f eclampsia and pre-eclampsia \200 Belief that the disease behaves predictably, and that BP is a good marker. \200 Ignoring mild proteinuria; even if 1+, the patient may be dead within 24h. \200 Believing antihypertensives stop pre-eclampsia (they may stop stroke). T hey don \200\231t. Only delivery cures. Diuretics deplete plasma volume, and are especially contraindicated (except in the rare left ventricular failure or la- ryngeal oedema complic ating pre-eclampsia). Continue antihypertensives postpartum; wean off slowly. Avoid methyld opa (depression). Believing that delivery removes risk. In the UK, 44% of eclamptic \201 ts are postpartum: half of these are >48h postpartum. Continue vigilance until clinically and biochemically n ormal. Avoid discharge <5 postnatal days. \200 Ergometrine should not be used for the 3rd stage (it \200\200 BP and risks stroke). \200 Not replacing signi \201 cant blood loss meticulously. Risks are hypovolaemia or fatal \202 uid overload acute respiratory dis tress syndrome. Have one person (the most experienced) in charge of all the IVIs. Failure to inform anesthetists early and use intensive care facilities. \200 Not asking G P to check for proteinuria at 6 weeks (13% have renal disease or underlying hypertension). Refer to physician if proteinuria still present. Prematurity 50 \200 \200\207This is a leading cause of perinatal mortality and morbidity. Premature infants ar e those born before 37+6 weeks \200\231 gestation. Prevalence: 6% of singletons, 46% of tw in, 79% of triplet or higher-order deliveries. About 1.4% are before 32+0 weeks \200\224whe n neonatal problems are greatest. In 25%, delivery is elective (p62). 10% are due to multip le pregnancy; 25% are due to APH, cervical incompetence, amnionitis, uterine abnormalities, diabetes, pol- yhydramnios, pyelonephritis, or other infections. In 40% the cause is unkno wn, but abnormal genital tract colonization (bacterial vaginosis) with ureaplasma and Mycop lasma hominis is implicated, as either a risk factor or risk marker. If treating 2nd trimes ter vaginosis is necessary, use macrolide or clindamycin, (not metronidazole which is assoc iated with \200\200 premature birth rates). 113 Prophylactic antibiotics in spontaneous pr eterm labor with intact mem- branes increase risk of cerebral palsy,1 and are not recommend ed. 114 Managing preterm rupture of membranes (PROM) Admit; do T MSU, and HVS \200\224usi ng a sterile bivalve speculum. Assess for causes/associations: eg abrup- tion, twins, and p olyhydramnios. If liquor is not obvious its presence is sug- gested if nitrazine sticks (pH -sensitive) turn black (false +ve with infected vaginal discharge, semen, blood, and urine) . Give corticosteroids 115 (see oppo- site page). In 80%, membrane rupture initiates labor. The problem with the 20% who do not go into labor is balancing advantages of remaining in utero (maturity and surfactant \200\200) against the threat of infection (causes 20% of ne o- natal deaths after PROM). Intrauterine infection supervenes after membranes have rupture d in 10% by 48h, 26% by 72h, 40% by >72h. Prophylactic erythro- mycin 250mg/6hPO for 10 day s or until delivery reduces births within 42 hours. If infection develops, do blood culture and give IV antibiotics (eg ampicillin 500mg/6h IV + gentamicin 3 \200\2235mg/kg/8h over \211 3mins IV) and expedite labor (p62). Antibiotics for 24h pre-labor, \200\201 rates of intraventricular hemorrhage and periventricular malacia (below) in the baby. If labor supe rvenes, allow it to progress. If liquor stops draining for >48h (rare) slowly mobilize the mother. Management of preterm labor In 50% contractions cease spontaneously. Treating the c ause (eg pyelonephritis) may make it cease. Give corticosteroids (p51). Attempts to suppres s contractions (tocolysis) are unlikely to succeed if membranes are ruptured or the cervix >4cm dilated. The rationale for toco- lytic drug use was that delay of preterm labor would improve fetal outcome without causing harm to mother or fetus. Trials have shown them to be of almost no clinical bene \201 t, and only nifedipine is associated with improvement of fetal outcome. It is quite reasonable not to use tocolytic drugs; though they may be consid ered desirable in certain circumstances eg to give time for cor- ticosteroids to work, or f or in utero transfer. Use only between 24 \200\22333 weeks. Consider transfer to hospital w ith NICU facilities. Call pediatrician to attend to the baby at birth. See cord-cutting rec ommendations opposite. Tocolytics Absolute CI: chorioamnionitis, fetal death or lethal abno rmality, condition (fetal or maternal) needing immediate delivery. Relative CI: fetal growt h restriction or distress, pre-eclampsia, placenta praevia, abruption, cer- vix >4cm. \200 -sympathomimetics, associated with maternal \202 uid overload and pulmonary oedema are n ot recommended. Atosiban (licensed in Europe) has fewer maternal eff ects, has not been sho wn to bene \201 t the fetus. Nifedipine is as eff ective, and associated with less newborn respiratory distress and admis- sion to intensive care. Regimen: nifedipine 20mg PO then 1 0 \200\22320mg/6 \200\2238h ac- cording to uterine activity (unlicensed use). Use up to 48h . SE: \200\201 BP; headache; \202 ushing; pulse \200\200 (transient); myocardial infarc tion (very rare); CI: heart disease (caution diabetes, multiple pregnancy as pulmonary oede ma risk). 116 s c i r t e t s b O 1 Co-amoxiclav or erythromycin in threatened preterm labor with intact membranes \200\200 risk cerebral palsy: the number needed to harm with erythromycin is 64 and with co-amoxicla v 79. 117,118 Glucocorticoids Dose: Betamethasone 12mg IM with a 2nd dose 12 \200\22324h later (or dexame thasone 6mg/12/h \211\2104 doses). These help fetal surfactant production, lowering mortal ity (by 31%) and com- plications of RDS (p118) by 44%. They also help close patent ductuses and protect against periventricular malacia, a cause of cerebral palsy. \200 Use in all women (but note cautions, below) at risk of iatrogenic or spontane- ous preterm birth betwe en 24+0 and 34+6 weeks. \200\225119 \200 If growth restriction too, use up to 35+6 wee ks. \200 If risk at 23+0 \200\22323+6 weeks use only on senior advice. \200 Use before all elective Cesarean sections up to 38+6 weeks. \200 Consider use at 35 \200\2236 weeks if delivery expedited for pre-eclampsia (NICE). 120 \200 Use with caution if maternal sys temic infection eg TB, maternal sepsis: if overt chorioamnionitis seek senior opinion befor e use. If diabetic, monitor glucose. Bene \201 t occurs within 24h (and lasts for 7 days). Repeat doses (eg every 2wks until 33wks \200\231 gestation or delivery) did more harm than good in the MACS study (babies weighed less, had smaller heads). 121 A further \200\230re scue \200\231 dose is only rec- ommended if the \201 rst course was given before 26 weeks and a new obstetric indication arises. 119 Magnesium sulfate Studies show a neuroprotectiv e eff ect if given antena- tally for babies<34 weeks \200\231 gestation. It is estimated th at 63 women will need treatment to prevent one case of cerebral palsy. Australian draft nat ional clini- cal guidelines recommend a maternal loading dose of 4g IV over 20 \200\22330 m inutes followed by 1g/h maintenance infusion for up to 24h (or birth, if earlier), and use if fetus <30 weeks gestation. 122 Delivery Babies delivered at <28 weeks \200\231 gestatio n should be delivered in a room with temperature of 26 C, wrapped in food grade plastic wr ap or bag without drying after birth and be placed under heat whilst stabilizing (keep wrap ped until temperature checked in NICU). 123 Older babies are wrapped in dry towels. A 3-min delay in cutting the cord, (if premature babies are vigor- ous and not needing active resu scitation), and holding the baby 20cm below the introitus, results in higher haematocrit le vels, and reduces transfusion and oxygen supplement requirements in premature babies, and r educes rates of intraventricular hemorrhage, but increases need for phototherapy. 123 Prema turity, survival, and disability \200\224the \201 gures \200 Cerebral palsy is present in 20% of surviving babies born at 24 \200\22326 weeks \200\231 gestation (compared with 4% at 32 weeks) in a large French study. 124 Viability thresholds for very premature babies h ave reduced by 1 week per decade for the last 40 years. Survival before 22 weeks is very ra re. In 1995, 1% of babies born at 22 \200\22323 weeks survived to leave hospital, 11% at 23 \200\22324; 26% at 24 \200\22325; 44% at 25 \200\22326. Of surviving babies born between 2 3 \200\22324 weeks two- thirds had moderate or severe disability; by 25 to 26 weeks two-thi rds had no or only mild disability. These \201 gures have lead to guidelines for consider ation of treatment at diff erent gestations, eg not resuscitating babies of less than 22 we eks \200\231 completed gestation unless speci \201 cally requested by parents after discus sion with senior pediatrician; but normally admitting babies of >23 weeks \200\231 complete d gestation to neonatal intensive care. 125 The \201 gures for Eng- land, Wales and North ern Ireland were that 58% of babies born at 24 weeks \200\231 gestation survived the neonat al period, increasing to 77% at 25 weeks; (85% at 26 weeks; 92% at 27 and 28 weeks; 96% at 29 weeks; 97% at 33 weeks). 126 51 s c i r t e t s b O Small for gestational age (SGA) 52 \200 \200\207When talking to parents, avoid the term growth retardation as this may imply to th em the inevitability of mental handicap \200\224which is not the case. Distinguish prematur e babies from those who are small-for-gestational age (SGA): they are at risk from diff ere nt problems after birth. Causes of growth restriction (IUGR) Growth restricted neonates are those weighing < the 10th centile for their gestational age (Tables, p129). Maternal facto rs: Multiple pregnancy, malformation, infection, smoking, dia- betes, BP \200\200, Hb \200\201, pre-eclampsia, heart or renal disease, asthma. 10% are to mothers who only ever produce small babies. Asymmetric growth restriction: Where placental insuffi ciency was the cause, head circumference is relatively spared (the baby has been starved). Antenatal diag nosis 50% are undetected before birth, and many babies suspected of IUGR do not have it. Me asuring fundal height progress from the symphysis pubis is recommended by NICE to measure g rowth, (ideally use with centile charts). Oligohydramnios and poor fetal movements are othe r indica- tions of placental insuffi ciency. If growth restriction is suspected, monitor gr owth in utero by serial ultrasounds of head circumference and abdominal circumference. If u mbilical cord Doppler blood \202 ows are normal the outcome of growth restricted pregnanc ies is better (fewer premature births and still- births). Those with abnormal Dopplers may bene \201 t from maternal low-dose aspirin (p47), eg 75mg/24h PO. Biophysical pro \201 le monitoring (p46) and ante- natal cardiotocography (p44) are used to try to detect those ba bies who are becoming hypoxic in utero and who would bene \201 t from delivery to prevent stillbirth. Advise the mother to stop smoking, and to take plenty of rest. Labor and afterc are Growth restricted fetuses are more susceptible to hypoxia, so monitor in labor (p44). I f steroids needed, note later gestation (p51). After birth, temperature regulation may be a problem, so ensure a warm welcome; nurse those <2kg in an incubator. After being relativel y hypoxic in utero the Hb at birth is high, so jaundice is more common. They have little st ored glycogen so are prone to hypoglycaemia. Feed within 2h of birth and measure blood gluc ose before each 3-hourly feed. If hypoglycaemic despite regular feeds, transfer to a specia l care unit. They are more susceptible to infection. Routine induction at 36 weeks does not show bene \201 t over induction if needed. 127 Distinguishing growth restriction from pre maturity Before 34 weeks \200\231 gestation there is no breast bud tissue; from then it dev elops at 1mm diam- eter/week. Ear cartilage develops between 35 and 39 weeks so premature b a- bies \200\231 ears do not spring back when folded. Testes lie in the inguinal canal at 3 5 weeks, in the scrotum from 37. Labia minora are exposed in premature girls. Skin creases on the anterior \205\223 of the foot appear by 35 weeks (on anterior \205\224 by 39, and all over from 39). \200\230Prems \200\231 have red, hairy skin. Vernix is made from 28 wee ks and is maximal at 36 weeks. Prems do not lie with legs \202 exed until 32 weeks. All l imbs are \202 exed from 36 weeks. Eff ects of IUGR in adult life By age 23yrs, milder cog nitive problems have often been overcome 128 \200\224but new problems begin to be manifest: \200 Hypertension \200 Type 2 diabetes mellitus So fetal malnutrition casts a long sha dow. Speci \201 c early de \201 ciencies are im- portant too (eg iodine, iron). s c i r t e t s b O Coronary artery disease \200 Autoimmune thyroid disease. 53 Large for gestational age These are babies above the 90th centile in weight for gestation. Causes: Constitutionally large (usually familial \200\224the largest 10% of the pop- ulatio n); maternal diabetes (p24); hyperinsulinism; Beckwith \200\223Wiedemann syndrome (p638). L abor and aftercare: Large babies risk birth injury (see impacted shoul- der, p72). Large ba bies are prone to immaturity of suckling and swallowing and may need temporary tube feeding . They are prone to hypoglycaemia and hypocalcaemia. Polycythaemia may result in jaundice. They are also prone to left colon syndrome: a self-limiting condition clinically mimicking Hirsch- sprung \200\231s disease (p130) whereby temporary bowel obstruction (possibly also with meconium plug) occurs. Rarely, there is renal vein thrombosis. s c i r t e t s b O Postmaturity (prolonged pregnancy) 54 \200 De \201 nition Prolonged pregnancy is de \201 ned as that exceeding 42 completed weeks of pregnancy (gestation having been assessed by ultrasound at <16 weeks \200\231 gestation). Incidence 5 \200\22310% of pregnancies. Problems \200 Possible placental insuffi ciency \200 Larger fetuses (25% >4000g) \200 Fetal skull more ossi \201 ed so less mouldable \200 Increased meconium passage in labor (25-40%) \200 Increased fetal distress in labor \200 Increased cesarean rates for labors after 41 completed weeks. Management At 38-week visit discuss what is recommended if spontaneous labor does not occur by 41 completed week s, including membrane sweep and induction. Arrange for visit at 41 weeks if not delivered. 1 Membrane sweep. On vaginal examination as much membrane is swept from the lower segment a s possible by a \201 nger inserted through the cervix. It is thought to induce natural pr ostaglandins. This may cause discomfort and a little bleeding but may induce labor \200 \230naturally \200\231. 8 women are mem- brane swept for 1 formal induction avoided. Off er at 40- and 41-week visit in nullips, at 41 weeks in multips. s c i r t e t s b O 2 A policy of induction after 41 completed weeks \200\231 pregnancy does reduce fetal death rate. 129 NICE says to off er induction between 41+0 and 42+O weeks. \200 130 Induction i s with vaginal prostaglandin followed by oxytocin (p62). After induction, monitor the fetus in labor (p44). It is estimated that 500 induc- tions are needed to prevent 1 perinatal de ath.