 \200 This page intentionally left blank \200 DIC and coagulation defects 88 \200 DIC in pregnancy is always secondary to stimulation of coagulation by pro- coagulant substa nce release in the maternal circulation. Known triggers are: retention of a dead fetus (of greater than 20 weeks \200\231 gestation which has been dead for >3 weeks); pre-eclampsia; placental abruption; endotoxic shock; am- niotic \202 uid embolism; placenta accreta; hyd atidiform mole; prolonged shock from any cause; acute fatty liver of pregnancy (p26). Patho genesis: Thrombo- plastins are released into the circulation, \201 brin and platelets are consumed as intravascular clotting occurs. Tests: Kaolin \200\223cephalin clotting time \200\200 ( \200\201 factors II, V, VII), \201 brinogen \200\201, \201 brin degradatio n products \200\200. In situations where DIC is a possibility send blood for crossmatch, p latelets, partial thromboplastin time or accelerated whole blood clotting time, prothrombin time, \201 brinogen estimation, and \201 brin degradation products. Preliminary result s should be available in 30min. Management: Presentation may be as heavy bleeding and shock , and the \201 rst measures must be the correction of shock. \200 Give O2 at 15 L/min vi a a tight \201 tting mask with reservoir. Set up at least 1, preferably 2, wide-gauge IVI s, take bloods as above, and give blood fast (group-compatible blood \200\224available in 5 \200\22310min or O Rh \200\223ve blood if desperate). Stored blood is de \201 cient in cl otting factors. Give fresh frozen plasma to normalize the kao- lin \200\223cephalin clottin g time and the prothrombin time. Platelets are indicated with prolonged bleeding and low pl atelet count. Calcium is sometimes needed to counteract citrate in stored blood (eg 10mL of 10% calcium gluconate IVI, eg after 6U of blood). Seek expert help from a hematologist. Th e condition is usually self-limiting if the stimulus can be removed. In the case of intraut erine death and abruption (p56) removal of the uterine contents is the way to cor- rect the stimulus, and this should be done as promptly as possible. Mortality: <1% if placental abr uption; 50 \200\22380% if infection/shock. Autoimmune thrombocytopenic purpura (AiTP) Incid ence 1 \200\2232 : 10,000 pregnancies. IgG antibodies cause thrombocytopenia (associated wi th in- creased bone marrow megakaryocytes) in the mother and, being able to cross the place nta, they cause thrombocytopenia in 10% of fetuses. Exclude sys- temic lupus erythematosus in the mother (thrombocytopenia may be an early presentation; do DNA binding, OHCM p540). Consider maternal HIV. If maternal platelets fall below 20 \211\210 109/L or 50 \211\210 109/L near delivery, give steroids. Rarely, splenectomy is necessary during pregnancy (idea lly in the second trimester). Immunoglobulin IgG 0.4g/kg IV for 5 days is sometimes used ne ar expected date of delivery, inducing maternal and fetal remission for up to 3 weeks, but it is extremely expensive. Aim for non-traumatic delivery for both mother and baby. Neonata l platelet count may fall further in the \201 rst days of life, then gradually rise to no rmal over 4 \200\22316 weeks. Treatment is not needed unless sur- gery is contemplated. Mat ernal mortality due to AiTP is now negligible, but fetal mortality remains (due to intracra nial bleeding). Take cord blood at deliv- ery. If platelets <20 \211\210 109/L give baby I gG 1g/kg IVI at birth. If platelets low at birth observe baby for 2 \200\2235 days as furth er falls likely. Causes of thrombocytopenia in pregnancy s c i r t e t s b O 1 Spurious (try citrated bottle). 2 Pregnancy-associated thrombocytopenia (benign gestation al thrombocy- topenia) \200\224mild and self-limiting (platelets stay above 100 \211\210 109/L). 3 Autoimmune thrombocytopenia. 4 Pre-eclampsia (platelets may fall early, preceding clottin g abnormality). 5 DIC (above) and haemolytic uraemic syndrome (p176)/thrombotic throm- bocy topenic purpura (2 ends of a microangiopathic spectrum, OHCM p332). 6 Folate de \201 ciency. 7 Congenital (May \200\223Heggin anomaly, hereditary macrothrombo cytopenia). 8 Marrow disease; hypersplenism. 89 Amniotic \202 uid embolism This condition, with a mortality of up to 61% (20% in 2006 \200\2238 UK), presents with sudden dyspnoea and hypotension heralded in 20%, by seizures. 50% also develop DIC, and of those who survive the initial collapse 70% go on to develop pu lmonary oedema (acute respiratory distress syndrome, ARDS, OHCM p178). There may be premoni tory symptoms such as breathlessness, chest pain, feel- ing cold, light-headedness, restles sness, distress, panic, paraesthesiae in \201 n- gers, nausea and vomiting. 183 These may be from immediately before until up to 4h before collapse. An anaphylactic type of respons e occurs to (possibly abnormal) amniotic \202 uid in the maternal circulation. Presentati on is often at the end of the \201 rst stage of labor or shortly after delivery but can c omplicate amniocentesis, or termination of pregnancy, abruption, trauma, cesarean section, and has even occurred up to 48h postpartum. Medical induction does appear to double risk, a lthough absolute excess risk is low. 184 Management \200 The \201 rst priority is to pre vent death from respiratory failure. Give mask oxygen and call an anesthetist urgently. End otracheal intubation and ventila- tion may be necessary. Set up IVI in case DIC should supe rvene. Cardiovascular collapse is due to left ventricular failure. DIC and hemorrhage then usually fol- low. Treatment is essentially supportive \200\224important steps are detailed below. Diagnosis may be diffi cult: exclude other causes of obstetric shock (p55). s c i r t e t s b O \200 Cardiopulmonary resuscitation if indicated. \200 Give highest available O2 concentra tion. If unconscious, ventilate and use 100% inspired O2. \200 Monitor for fetal distress. \200 If hypotensive, give \202 uids rapidly IVI to inc rease preload. If still hypotensive consider inotropes: dobutamine (a better inotrope than dopamine), eg in a dose range of 2.5 \200\22310 g/kg/min IVI may help. \200 Pulmonary artery catheterization (Swan \200\223Ganz catheter if available) helps guide haemodynamic management. \200 After initial hypotension is corrected, give only maintenance requirements of \202 uid to avoid pulmonary oedema from acute respiratory distress syndrome. Transfer to intensi ve care unit as soon as possible. \200 Treat DIC with fresh whole blood or packed cells and fresh frozen plasma. Use of hepa rin is controversial; there are insuffi cient data to warrant routine heparinization. \200 If the mother dies it is recommended to deliver the baby abdominally. Peri- mortem ce sarean within 5 minutes can aid resuscitation of the mother. Most mortality occurs in the \201 rst hour. Mortality rates reported: 26.4 \200\22361%. ( In 2006 \200\2238 there were and 13 deaths in England and Wales.) Report suspected cases to National Amniotic Fluid Embolism Register (at UKOSS).1 Should the woman die, perform autop sy as soon as possible. Speci \201 cally request that the lungs be examined for the presen ce of amniotic squames or lanugo hair (his- tology and immunochemistry to con \201 rm the diagnosis). In future complement measurement or serological or lung tissue tests for fetal antigen sialyl Tn may be the tests of choice. 1 UKOSS The National Perinatal Unit, Old Road Campus, Old Road, Headington, Oxford, OX37LF, e-mail www.npeu.ox.ac.uk Birth injuries 90 \200 \200\207Give all babies with signs of trauma vitamin K 1mg IM at birth (unless already giv en as part of routine measures). To the baby \200\224Molding: This is a natural phenomenon, not an injury. The skull bones can override each other (p42) to reduce the diameter of the head. Molding is assessed by degree of overlap of the overriding at the sutures. If moldin g is absent, skull bones are felt separately. With slight molding, the bones just touch, th en they override but can be reduced; \201 nally they over- ride so much that they cannot be reduced. Excessive molding during labor indicates cephalo \200\223pelvic disproportion, and can result in intracranial damage. Cephalhaematoma: This is a subperiostial swelling on the fetal head, and its boundaries are therefore limited by the individual bone margins (c ommonest over parietal bones). It is \202 uctuant. Spontaneous absorption occurs but may take weeks and may cause or contribute to jaundice. Caput succedaneum: This is an oedematou s swelling of the scalp, super \201 cial to the cranial periosteum (which does not, theref ore, limit its extent) and is the result of venous congestion and exuded serum caused by pr essure against the cervix and lower segment during labor. The presenting part of the head t herefore has the swelling over it. It gradually disappears in the \201 rst days af- ter b irth. When ventouse extraction is used in labor a particularly large caput (called a chigno n) is formed under the ventouse cup. Erb \200\231s palsy: See \201 g 1, p77. This may res ult from a diffi cult assisted delivery, eg shoulder dystocia (so \200\200 \211\210 10 in UK diabetic pregnancies). \200\2259 The baby \200\231s arm is \202 accid and the hand i s in the \200\230porter \200\231s tip \200\231 posture (p764). Exclude a fractured clavicl e and arrange physiotherapy. If it has not resolved by 6 months, the out- look is poor. Sub aponeurotic haematoma: Blood lies between the aponeurosis and the periosteum. As haematoma is not con \201 ned to the boundaries of one bone, collections of blood may be large enoug h to result in anemia or jaundice. They are associated with vacuum extractions. Skull fract ures: These are associated with diffi cult forceps extractions. They are commonest over par ietal or frontal bones. If depressed fractures are as- sociated with CNS signs, ask a neuro surgeon if the bone should be elevated. Intracranial injuries: Intracranial hemorrhage is e specially associated with diffi cult or fast labor, instrumental labor, and breech delivery . Premature babies are especially vulnerable. Normally a degree of motility of intracranial contents is buff ered by cerebrospinal \202 uid. Excessive molding and sudden changes in pressure reduce this eff ect and are associated with trauma. In all cases of intracranial hemorrhage check babies \200\231 platelets. If low, check moth- er \200\231s blood for plat elet alloantibodies (PLA1 system). Subsequent babies are at equal risk. IV maternal immunog lobulin treatment is being evaluated. s c i r t e t s b O Anoxia may cause intraventricular hemorrhage (p108). Asphyxia causes intracerebral hemorrha ge (often petechial) and may result in cerebral palsy. Extradural, subdural, and subarachno id hemorrhages can all occur. Babies aff ected may have convulsions, apnoea, cyanosis, abno rmal pallor, low heart rate, alterations in muscle tone, restlessness, somnolence, or abnor mal move- ments. Treatment is supportive and expectant. See p108 & p110. 91 Birth injuries to the mother: anal sphincter injury Obstetric anal sphincter injury (OASI) is common, and is not totally prevent- able by episiotomy (p93). Of the 1% who suff er anal sphincter injury with vaginal delivery 30% have problems with \202 atus incontinence, 8 % problems with liquid stool incontinence, and 4% with solid stool (though usually less tha n once a week). Fecal incontinence is a source of misery, and requires expert attention. Risk of mechanical injury is greatest after the \201 rst vaginal delivery. Trau- matic st retching of the pudendal nerves occurs in >30% of primips, but is mostly asymptomatic, or m ildly/transiently so. These patients are at \200\200 risk in subsequent deliveries (cumula tive pudendal nerve injury is well recog- nized). Other risk factors: \200 Baby >4kg \200 Persistent occipito-posterior position \200 Induced labor \200 Epidural \200 2n d stage >1h \200 Midline episiotomy \200 Forceps. s c i r t e t s b O If rectal incontinence occurs, and especially if there is a recto \200\223vaginal \201 st u- la, get expert surgical help. 186 If symptomatic or abnormal anorectal manom- etry or ab normality on endoanal ultrasound after previous repair, consider elective cesarean for subs equent delivery, as 17 \200\22324% develop worsening fae- cal symptoms after subsequent vag inal delivery. 187 Elective cesarean may not protect against symptoms caused by pudendal ne rve neuropathy. 188 Vesicovaginal \201 stula This abnormal opening between bladder and va gina leading to urinary incon- tinence, a common sequel to obstructed labor is thought to a ff ect 3 million women worldwide, 189 now almost exclusively in developing countries. Obstructed labor is particularly a problem for malnourished girls who be- come pregnant bef ore full pelvic maturation. In obstructed labor the pelvic head progressively compresses th e soft tissues of vagina, bladder, and rectum against the pelvis causing ischaemic damage t o these tissues and fetal as- phyxiation. 2 days after the fetus dies it becomes macerated, softens, and can be vaginally expelled. A few days later the mother passes sloughed ischae mic tissue leaving a \201 stula between bladder, urethra, and vagina or rectum and vagina (or both). Damaged tissues adjacent to the sloughed tissue heal poorly, often with \201 brosis. Vagina and rectum may later stenose; chronic pyelone- phritis and renal failure can ensue. Incontinent women are often shunned by family, divorced by their husbands, and stig matized (especially in cultures where the affl iction is believed to be punishment by God). Treatment is with continuous urinary drainage for 3 months if presenting with vesicovaginal \201 stula early (<3 months postpartum) or surgery if later. Operation is most successfu l for 1st operation and small defects (<2cm) with successful closure rates of up to 85% (bu t 16 \200\22332% of these women remain incontinent). Good obstetric management of obstructed labor prevents \201 stulas. Early treatment can a llow healing without recourse to surgery. Sadly it is those parts of the world where there is poor access to obstetric facilities where women develop \201 stulas and where the chan ce of having subsequent repair is also limited. Read.1 1 Living with obstetric \201 stula (A patient \200\231s Journey) F Aliyu 2011 BMJ 342 136 0 Episiotomy and tears 92 \200\207Examine gently. Unless marked bleeding, allow the mother some bonding time with ba by before examination and repair. \200 106 Perineal tears These are classi \201 ed by the degree of damage caused. Risk fac- tors for development are discussed on p91. Labial tears Common; these heal quickly and suturing is rarely helpful. First degree tears These tears are super \201 cial and do not damage muscle. Suture unless skin edges well apposed to aid healing. \200 106 Second degree tears These lacerations involve perineal muscle. Repair i s similar to that of episiotomy (see below). Third degree tears Damage involves the anal sp hincter muscle. Classi \201 cation: 3a External anal sphincter (circular \201 bres) thic kness <50% torn; 3b External anal sphincter thickness >50% torn; 3c Both external and inter nal anal sphincters (longitudinal \201 bres) torn. If rectal mucosa also involved it is a fourth degree tear. See p91. Repair by an experienced surgeon, under epidural or GA in the ater with intra-operative antibiotic cover. Rectal mucosa is repaired \201 rst using abso rbable suture from above the tear \200\231s apex to the mucocutaneous junction. Muscle is i nterposed. Vaginal mucosa is then sutured. Internal anal sphincter is repaired with inter- rupted sutures. Overlap and repair severed ends of the external anal sphincter. Finally rep air skin. Give antibiotic prophylaxis with 3rd and 4th degree tears. Give high- \201 bre d iet and lactulose for 10 days to avoid constipation. Arrange pelvic \202 oor exercise phy siotherapy for 6 \200\22312 weeks. Arrange consultant ob- stetrician follow-up at 6 \200 \22312 weeks; if pain or incontinence refer to specialist gynecologist or colorectal surgeo n for endoanal ultrasound or manometry. \200\225187 Episiotomy This is performed to enlarg e the outlet, eg to hasten birth of a dis- tressed baby, for instrumental or breech deliver y, to protect a premature head, and to try to prevent 3 tears (but anal tears are not red uced by more episi- otomies in normal deliveries). Rates: 8% Holland, 12% England, 50% USA. s c i r t e t s b O The tissues which are incised are vaginal epithelium, perineal skin, bulbocav- ernous muscl e, super \201 cial, and deep transverse perineal muscles. With large episiotomies, the ext ernal anal sphincter or levator ani may be partially cut, and ischiorectal fat exposed. Tec hnique: Hold the perineal skin away from the presenting part of the fetus (2 \201 ngers i n vagina). In \201 ltrate area to be cut with local anesthetic, eg 1% lidocaine (=lignocai ne). Still keeping the \201 ngers in the introitus, cut medio- laterally towards the isch ial tuberosity, starting midline (6 o \200\231clock), so avoiding the Bartholin \200\231s g lands. Repair: (See \201 g 1) NB: use resorbable suture \200\224eg polyglactin 910. In li thotomy, and using good illumination, repair the vaginal mucosa \201 rst. Start above the apex using continuous non-locked stitches 1cm apart, 1cm from wound edges. Tie off at muco cutaneous junction of fourchette. Then repair muscles with continuous non-locked technique \200 106 to obliterate any dead spaces. Finally close the skin with subcuticular stitch. P erform rectal examination afterwards to check sutures have not penetrated the rectal mucosa . Problems with episiotomy: Bleeding (so may increase chance of spread of HIV from mother t o baby); infection and breakdown; haematoma formation. For comfort some suggest ice packs, salt baths, hair dryer to dry perineum. 60% of women suff er perineal damage (episiotomy or tear) with spontaneous vaginal delivery; rectal diclofenac can provide eff ective analgesi a. Super \201 cial dyspareunia: see p310. If labia minora are involved in the skin bridge, the in- troitus is left too small. If the deep layers are inadequately sutured, the introi - tus becomes rather rounded exposing the bladder to coital thrusts. 93 1 2 Swab the vulva towards the perineum. In \201ltrate with 1% lidocaine ( \200\203arrows). Place tampon with attached tape in upper vagina. Insert 1st suture above apex of vaginal cu t (not too deep as underlying rectal mucosa nearby). s c i r t e t s b O 3 4 Bring together vaginal edges with continuous stitches placed 1 cm apart. Knot at introitus under the skin. Appose divided levator ani muscles. Close perineal skin (subcuticular continuous stitch is shown here). 5 When stitching is \201nished, remove tampon and examine vagina (to check for retained swa bs). Do a PR to check that apical sutures have not penetrated rectum. Fig 1. Repairing an episiotomy. The puerperium 94 \200 The puerperium is the 6 weeks after delivery. The uterus involutes, from 1kg weight at deli very to 100g. Felt at the umbilicus after delivery, it is a pelvic organ at 10 days. Afterp ains are felt (especially while suckling) as it contracts. The cervix becomes \201 rm ove r 3 days. The internal os closes by 3 days, the external os by 3 weeks. Lochia (endometrial slough, red cells, and white cells) is passed per vaginam. It is red (lochia rubra) for th e 1st 3 days, then becomes yellow (lochia serosa) then white over the next 10 days (lochia alba), until 6 weeks. The breasts produce milky discharge and colostrum during the last tri mester. Milk replaces colostrum 3 days after birth. Breasts are swollen, red, and tender wi th physiological engorgement at 3 to 4 days. The \201 rst days Is thromboprophylaxis need ed? (p16) If Rh \200\223ve, give anti-D, within 72h, p9. Check T , BP, breasts, legs, loch ia, fundal height if heavy PV loss. Teach pelvic \202 oor exercises. Persistent red lochi a, failure of uterine involu- tion, or PPH (p84) suggest retained products. Sustained hyper tension may need drugs (OHCM p134). \200\207Check rubella immunity. Vaccinate if non-immun e (simultaneously but diff erent limb from anti-D, or wait 3 months). \200 190 Check Hb on postnatal day 1 or \211 day 7: postpartum physiological haemodilution occurs from days 2 \200\2236. Discuss contraception (see BOX OPPOSITE). Puerperal pyrexia is T >38 C in the \201 rst 14 days after delivery or miscarriage. Examine fully (chest, breasts, legs, loc hia, and bimanual vaginal examination). Culture MSU, high vaginal swabs, blood, and sputum. 90% of infections will be urinary or of the genital tract. Super \201 cial perineal infec tions occur around the second day. Endometritis gives lower abdominal pain, off ensive loch ia, and a tender uterus (on bimanual vaginal exam). Endometritis needs urgent IV an- tibiot ics (below) and uterine curettage. For breast infection give \202 ucloxacil- lin 250mg/6h PO early for \211 10 days, to prevent abscesses. Suckling or breast expression should con tinue to prevent milk stagnation. Even if the cause of pyrexia is unknown, it is wise to tr eat with amoxicillin 500mg/8h PO/IV + met- ronidazole 400mg/8h PO. NB: puerperal infection can be prevented by cleansing the birth canal at every vaginal examination with 0.25% chlor hexidine. Super \201 cial thrombophlebitis This presents as a painful tender (usually var- icose) vein. Give NSAID, eg ibuprofen 400mg/8h PO pc. Bandage and elevate the leg. Recover y is usual within 4 days. Deep vein thrombosis: See p32. Puerperal psychosis (1 : 500 birth s): \200\207See p408. This is distinguished from the mild depression that often follows bi rth by a high suicidal drive, severe de- pression (p336), mania, and more rarely schizophre nic symptoms (p358) with delusions that the child is malformed. If an acute organic reactio n (p350) is present, suspect puerperal infection. Presentation is by day 7 postpartum in 50 %, by 3 months in 90%. Onset is usually sudden and deterioration rapid. Refer to heath trus t \200\231s community psychiatric team for pregnancy. Admission to specialist mother and ba by unit may be needed. See p408 for a fuller discus- sion of postnatal depression. 10% of m others develop postnatal depression; in \205\223 - of these depression is severe. The 6- week postnatal examination gives a chance to: \200 See how mother and baby relate. \200 Do BP & weight. \200 Do FBC if anemic postnatally. \200 Arrange a cervical smear due. \200 Check contraceptive plans are enacted (see OPPOSITE). \200 Ask about depression, b ackache, incontinence. Ask: \200\234Have you resumed intercourse? \200\235(CEMACE recommen ds abstinence or \200\230gentle intercourse \200\231 for \201 rst 6 weeks postpartum to prevent fatal air embolism). 191 Sexual problems are common, and prolonged: 50% report tha t intercourse is less satisfactory than pre-pregnancy, with major loss of libido, and dyspa reunia the chief com- plaints. Vaginal examination to check healing is not usually needed. s c i r t e t s b O 95 Contraception after a baby Lactational amenorrhoea (LAM) 192 This is Nature \200\231s contr aception. Breast- feeding delays return of ovulation (suckling disrupts frequency and ampli - tude of gonadotrophin surges so that although there is gonadotrophin rise in response to falling placental sex steroids after delivery, ovulation does not occur). Women who are ful ly breastfeeding day and night (ie breast milk is baby \200\231s sole nutrient), and are le ss than 6 months postpartum, and amenor- rhoeic can expect this method to be 98% eff ective . Average 1st menstruation in a breastfeeding mother is at 28.4 weeks (range 15 \200\22348) . Contraceptive ef- \201 cacy of LAM is decreased after 6 months, if periods return, if b reastfeeding frequency reduces, night feeding stops, there is separation from the baby (eg return to work), if the baby receives supplements, or if mother or baby be- come ill or str essed. In the UK although 69% of mothers initiate breastfeeding only 21% still feed at 6 mo nths. Aim for additional contraception once de- creased effi cacy is anticipated. Progester one only Pill (PoP, p302) These may be started any time post-par- tum but if started after day 21 additional precautions are needed for 2 days. They do not aff ect breast milk produc tion. Low doses (<1%) of hormone are secreted in the milk but have not been shown to aff ec t babies. Combined Pills Start at 3 weeks if not breastfeeding. They aff ect early milk pro duction and are not recommended if breastfeeding until 6 months (but can be used from 6 wee ks if other methods unacceptable). Levels of hormone in breast milk are similar to that of ovulatory cycles. Emergency contraception Use of progesterone method (p299) is suitable for all. It is not needed before 21 days postpartum. Depot injections These are not recommende d until 6 weeks in those breast- feeding (theoretical risk of sex steroid to baby \200\231s immature nervous system and liver). Medroxyprogesterone acetate 150mg given deep IM 12-wee kly can start 5 days postpartum if bottle feeding, or norethisterone enanthate 200mg into g luteus maximus 8-weekly (licensed for short-term use only, but can be given immediately pos tpartum when medroxyprogesterone use can cause heavy bleeding). Progesterone implants Inser tion is not recommended until 6 weeks in those who are breastfeeding. 0.2% of daily dose of etonogestrel is excreted in breast milk. Implant at 21 \200\22328 days in those bottle fee ding. Intrauterine contraceptive devices (IUCD) These should be inserted with- in the \201 rst 48h postpartum or delayed until 4 weeks. This is to minimize risk of uterine perfo ration at insertion. Levonorgestrel-releasing intrauterine de- vices are also inserted at 4 weeks. Diaphragms and cervical caps The woman needs to be \201 tted at 6 weeks as diff e rent sizes may be required from previously. Alternative contraception is needed from day 21 until the new ones are con \201 dently handled. Sterilization Unless sterilization highly advisable at cesarean section (eg repeated sections, family complete), it is best to wait an appropriate interval as immediate postpartum tubal ligation has possible increased failu re rate and is more likely to be regretted. s c i r t e t s b O \201\201Ideas, beliefs, art, work : none are worth sacri \201 cing life for; the one thin g Maternal mortality 96 worth sacri \201 cing life for is life itself. All mothers sacri \201 ce themselves to so me degree: some pay a higher price: we dedicate this page to them. \200 \200 Worldwide perspective In North Europe a woman \200\231s lifetime risk of dying in pregnancy or childbirth is 1 : 30,000; in the world \200\231s poorest parts it is 1 : 6. 193 Maternal mortality is de \201 ned in the UK as the death of a mother while preg- nant or w ithin 42 days of the pregnancy ending, from any cause related to or aggravated by the pregn ancy or its management, but not from accidental or incidental causes (called coincidental d eaths). Deaths are subdivided into those from \200\230direct causes \200\231 \200\224those in which the cause of death is directly at- tributable to pregnancy (eg abortion, eclampsi a, hemorrhage) \200\224and indirect deaths \200\224those resulting from previous existing d isease or disease developed during pregnancy, and which were not due to direct obstetric ca uses but were aggravated by pregnancy (eg heart disease). Late deaths are those occurring b etween 42 days and 1 year after termination, miscarriage, or delivery that are due to direc t or indirect maternal causes. History Since 1952 there have been 3-yearly con \201 dentia l enquiries into mater- nal deaths. Prior to 1979, many deaths were considered to have had \200\230avoidable factors \200\231 (denoting departures from acceptable standards of care by individu- als, including patients) but since 1979 the wider term of \200\230substandard care \200\231 has been used to cover failures in clinical care and other factors, such as shortage of resources and back-up facilities. Reports allow analysis, re \202 ection, and rec- ommended actions so each death should improve future care. s c i r t e t s b O Maternal mortality has reduced since reports started, (deaths per 100,000 maternities (live birth, or stillbirth \211 24wks gestation) were 67.1 in 1955 \200\2237, 33.3 in 1964 \200\2236 & 11.39 in 2006 \200\2238 of which direct deaths were 4.67/100,000). 194 Mat mort 2011 Internationally, \201 gures are given from death certi \201 cation (rather than proac- t ive case seeking as in the UK), and expressed per 100,000 live births. This would give a 20 06 \200\2238 \201 gure of 6.69. Rates rise with maternal age (especially \211 40yrs). Mu ltiple pregnancy \200\200 risk \211\2103.9. Risk of dying in pregnancy, childbirth, or fr om abortion is 1 : 65 in developing countries (1 : 9000 in the UK). Note: pregnancy is very protective as all-cause mortality in 15 \200\22345-yr-old women is 58.4 : 100,000/ year (i e rates of death 4 \211\210 lower in pregnancy and 1 year after). In 2006 \200\2238, 261 UK deaths were recorded excluding 33 late direct and 24 late indirec t deaths. 107 were direct obstetric deaths; 154 were indirect and 50 were coincidental (in no way related to pregnancy, eg car accident). Death was increased in non-whites ( \211\210 3.5 if black, \211\210 1.5 if Asian), if partner unem- ployed ( \211\2106). 26% of those dying were poor attenders, or had not booked by 18 weeks \200\231 gestation (in 2010, 87% o f pregnant women had booked by 13 weeks); 19% of those dying were obese or morbidly obese, and 16.6% were substance abusers. In 2006 \200\2238 genital sepsis was the chief cause of direct death in the UK (24.2% of di rect, excluding late deaths), and cardiac disease the commonest cause overall. Other direct (excluding late) causes: pre-eclampsia (17.7%); thromboembolism (16.8%); amniotic \202 u id embolism (12.1%); early pregnancy (10.2%, mainly ectopic pregnancy at 5.6%); hemorrhage (9.25%); anaesthet- ic deaths (6.5%); fatty liver (2.8%). Deaths from suicide were as rare as from amniotic \202 uid embolism. 59% of women dying had undergone cesarean section (and 21 babies born at the 38 peri/postmortem cesareans were live born, 9 dying neonatally). The maternal mortality rate was lower than in the previous triennium for direct deaths (4.6 7 vs 6.24 : 100,000), and again there were more indirect than direct deaths. Care was consi dered substandard in 70% of cases of direct and 55% cases of indirect death in 2006 \200 \2238. \200\230Substandardness \200\231 includes pregnant women who refuse medical advice, lack of knowledge skills to recognize severity of illness, and lack of consultant support and of patient assessment. 97 Perinatal mortality This is the number of stillbirths and deaths in the 1st week of life (e arly neonatal deaths)/1000 births. Stillbirths only include those fetuses of >24 weeks \200 \231 gestation; if a fetus of <24 weeks \200\231 gestation is born showing signs of life, a nd then dies, this is counted as a perinatal death in the UK (if dying within the 1st 7 day s). Neonatal deaths are those infants dying up to and including the 28th day after birth. O ther countries use diff erent criteria \200\224including stillbirths from 20 weeks and neon atal deaths up to 28 days after birth, so it is not al- ways easy to compare statistics. \200 Perinatal mortality is aff ected by many factors. Rates are high for small (61% of deaths a re in babies <2500g) and preterm babies (70% of deaths oc- cur in the 5% who are preterm). See p50 & p128. Regional variation in the UK is quite marked. There is a social class varia tion with rates being less for so- cial classes 1 and 2 than for classes 4 and 5. Teenage m others have higher rates than mothers aged 20 \200\22329. From 35yrs rates rise until they are 1.5-fold higher than the low-risk group (25 \200\22335yrs) by age >40. Second babies ha ve the lowest mortality rates. Mortality rates are doubled for fourth and \201 fth childr en, trebled by sixth and seventh (this eff ect is not independent of social class as more l ower social class women have many children). Rates are low- er for singleton births than fo r multiple ( \200\200 \211\21010 for triplets vs singletons). 195 Time to conception also h as an in \202 uence with mortality rates being 3 times more if it has taken a long time to conceive compared with short time (in Denmark). 196 Perinatal mortality in UK* (* \201 gu res exclude Scotland) is twice as high in off spring of mothers of black ethnicity; 1.5 tim es commoner if of Asian ethnicity. 197 s c i r t e t s b O Perinatal mortality rates in the UK have fallen over the years from 62.5 : 1000 in 1930 \200\2235 to 7.6 : 1000 in 2009 for UK*. Declining mortality re \202 ects improvement in s tandards of living, improved maternal health, and declining parity, as well as improvements in medical care. The main causes of stillbirth were congeni- tal abnormalities (9%), antep artum/intrapartum hemorrhage (11%), placen- tal conditions (12%) in 2009. The cause in 28% of stillbirths was unexplained. The main causes of neonatal death were prematurity (48%) an d malformation (22%). Examples of how changed medical care may reduce mortality \200 Worl dwide, treatment of syphilis, antitetanus vaccination (of mother during pregnancy), and cle an delivery (especially cord techniques) have the greatest in \202 uence in reducing perin atal mortality. Antenatal detection and termination of malformed fetuses. \200 Reduction of mid-cavity pr ocedures and vaginal breech delivery. \200 Detection of placenta praevia antenatally. \200 Prevention of rhesus incompatibility. \200 Preventing progression of preterm labor. \200 Better control of diabetes mellitus in aff ected mothers. \200 Antenatal monitori ng of \200\230at risk \200\231 pregnancies. \201\201While we must try to reduce morbidity and mortality still further, this must not blind us to other problems that remain, such as the \200\230over-medi- calization \200\231 of birth; the problem of reconciling maternal wishes to be in charge of her own d elivery with the immediate needs of the baby; and the problem of explaining risks and bene \201 ts in terms that both parents understand, so that they can join in the decision-makin g process. who are you, little i (5 or 6 years old) peering from some high window 98 2 Pediatrics e e cummings Cardiovascular: History & examination 100 \200\2232 \200 Is this child seriously ill? 103 Common infant sy mptoms 104 \200 The ill and feverish child 106 Infective endocarditis 166 Rheumatic fever 166 Gastrointestinal: Diarrhea 168 Malnutrition 168 Abdominal pain & distension 170 Coeliac disease 171 Some acute surgical pr oblems 172 Neonatology \200 Resus. and ITU 107 \200\2238 Ventilatory support for neonates 110 \200 T he ill neonate 112 Examining the neonate 114 Jaundice 115 Rhesus haemolytic disease 116 Res piratory distress syndrome 118 BPD; pulmonary hypoplasia 119 Necrotizing enterocolitis 120 Meconium aspiration 120 The bleeding neonate 120 Minor neonatal problems 121 Enteral & pare nteral feeding 122 Breastfeeding & bottle feeding 124 \200\2237 Preterm and light babies 12 8 Genitourinary: Urinary tract infection 174 Renal disease 176 \200\2239 Growth, Endocrine & Metabolic: Growth and failure to thrive 180 Short stature 180 Ethnospec i \201 c growth charts 181 Endocrine & metabolic disease 182 Phenylketonuria 183 Precociou s puberty 184 Diabetes and \200 ketoacidosis 186 \200\2239 Poisoning: general points 190 S alicylate and \200 paracetamol 192 Malformations GI 130 Genitourinary (incl. Wilms \200\231 and am- Hematology & Immunology: biguous genitalia) 132 \200\2235 Congenital heart disease 136 Murmurs and heart sounds 137 Head & neck and cleft palate 138 \200\2239 Neural tube defects 140 Acute lymphoblastic leukemia 194 Anemia 196 Purpura 197 Primary antibody de \201 ciency 19 8 Neurological: Some viral infections \200 Rising intracranial pressure 200 Migraine 201 \200 Encephalitis 202 \200 Meningitis 202 \200\2235 Epilepsy & febrile convulsions 206 \200\2239 Behavioral problems 210 \200 \22313 Delay in walking and talking 214 Handicap 216 Measles, rubella, mumps 142 Erythrovirus infection 142 Hand, foot and mouth 143 Roseola and other rashes 143 Chickenpox (varicella) 144 Childhood hiv infection 145 Injury & disease p revention Non-accidental injury 146 Sudden infant death 148 Screening & development 150 Imm unization 151 Genetic disease & prevention 152 Genetic counseling 154 Preventing heart dise ase, diabetes Reference intervals/ \202 uids/nutrition Developmental tests 218 \200\22319 Hematology and chemistry 220 Dentition 221; and growth 2 22 \200\2235 Dubowitz system 228 \200\22332 Body surface area 233 Nutrition tables for prem s 234 Fluid regimens 234 etc, starting in childhood 156 Diseases by system \200\224Respiratory: APLS advanced pediatric life support \200 Intraosseus transfusion 236 \200 Adrenaline in anaphylaxis 237 \200 Cardiorespirato ry arrest 239 Respiratory infections; upper lower (including pertussis) 158 \200\22360 Cystic \201 brosis 162 \200 Asthma 164 Other relevant pages: Orthopedics (Chapter 11); Infectious disease (OHCM p372 \200\223447); perinatal infection p36; child psychiatry p389; play therapy p377; squint p422; retinoblas toma p421; pain p718; syndromes: p638 \200\22355. We thank Professor Robert Tasker, our Spe cialist Reader, and Dr Shahzad Arain, our Junior Reader, for their contribution to this cha pter. rowing up can seem like joining the points on a growth chart, with the chief desiderata bei ng that we should not cross the dotted cen- tiles of our pre-determined course, set out in utero, and ending in adulthood or death (these states being synonymous in the mind of the a v- erage alienated 15-yr-old). Examples of points on growth chart might our metaphysical we are individu- be realizing that we lead sepa- als, next that our parents lives to rate Nex t may and carers. that there come a view s h a p i n g is a divinity give way our lives; th is may that this to a more subtle view care much divinity has ceased to a n o t h e r , abo ut us, one way or with each and that we are alone other minds other, those tantalizing we m ust learn that, in order to survive, to read. At last, standing on our own two feet, suppor ted and constrained by the dotted lines of our allowed variability, we realize that our har d-won independence may be an illusion (interdependence not independence is the human rule). Even our own unitary ego may come to look fragile compared with the system of interacting, con \202 icting processes which perpetually dissolve and reform in strange or familiar pa tterns of personal identity. 99 A d o l e s cent pregnancy Street crime e a nd solvent D r u g abuse r a c y Adolescent e r u g a n d solvent Adolescent t i o n a b u s e Prostitution Prostitution s e u T r u ancy s c e n t pregnanc S t reet crime Truancy c y Illit nan c y A ce d n Vio o itution l e P Ad olescent scent pregna s rostitutio c e Viole nt Drug and solvent olescent pre preg n n solv ent ancy n Street n cy Truanc abuse Truanc Viole Prostitution Prostitutio Drug and Adolesce nt pregnancy Illitera itution Vio Drug and y c V i o l e y n a c n u r T S y t i r a l u s n i tr e r Illitera c y Prostitutio n Adolescent T e t u c n a