s c i r t e t s b O Venous thromboembolism (VTE) in pregnancy 32 \200 \200\207Investigate any unexplained calf or chest symptoms today. Thrombo- embolism is a c hief UK cause of maternal death. VTE risk rises 6-fold in pregnan- cy ( 0.1 \200\2230.2% of pregnancies: 20 \200\22350% occur antenatally \200\224in any trimester). For those at spec ial risk see p16. 50% of those with 1st VTE have thrombophilia (p33), so check for this. Wh ere clinical suspicion is strong but tests negative, start treatment; stop only after repea t negative tests 1 week later. 88 Before starting heparin take blood for: FBC, U&E, LFTs, c oagulation screen. Pulmonary embolism Small emboli may cause unexplained pyrexia, syncope, cough, chest pain, and breathlessness. Pleurisy should be considered due to embolism unless there is high fever or much purulent sputum. Large emboli present as collapse with chest p ain, breathlessness, and cyanosis. There will be a raised JVP, third heart sound, and paras ternal heave. Tests: Do CXR (normal in 50%). Scan legs for venous thrombi (if thrombi seen V/Q and CTPA (below) not needed as treatment indicated). Blood gasses may be helpful (PaO2 \200\201; PaCO2 \200\201). If PE still suspected do V/Q scan, spiral CT, or CT pulmonary angiography (CTPA). Maternal breast radiation is higher with CTPA increasing lifetime breas t cancer risk by 13% but V/Q increases risk of child- hood cancer more, as fetal radiation is higher. Exclude neonatal hypothyroid- ism after CTPA as iodinated contrast medium is use d. Treatment: Massive emboli may require prolonged cardiac massage, thrombo- lysis, percuta neous catheter thrombus fragmentation or pulmonary embol- etomy. Give unfractionated hepari n eg 80U/kg IV stat then 18U/kg/h IVI in 0.9% saline by syringe pump. Omit the stat dose if thrombolysis has been used. Mon- itor APTT at 6h from stat dose and after dose changes, an d /24h. (Target value APTT 1.5 \200\2232.5.) Adjust dose as needed 89 (usual 1000 \200\2232 000U/h). After 3 \200\2237 days IV heparin maintain on longterm heparin (eg 10,000U/12h sc) with careful monitor- ing. Problems: maternal osteopenia (reversible on stopping); thrombo cytopenia; allergic skin rashes; alopecia. Monitor platelets every 2 \200\2233 days from da y 4. s c i r t e t s b O For less massive emboli, low molecular weight heparin (LMWH) eg enoxa- parin (see below) is good treatment. (Warfarin is teratogenic in pregnancy \200\224Conradi \200\223H nermann syndrome, p640 and is used antenatally up to 36 weeks only in those with arti \201 cial he art valves.) SC heparin is continued throughout pregnancy (see below). Treat for at least 6 weeks postpartum and 3 months from embolus. Some choose warfarin instead after 3 days post partum. Deep vein thrombosis (DVT) Suspect if leg pain/discomfort (especially left); swelli ng; oedema; \200\200 T ; \200\200 WCC; lower abdominal pain. Tests: Compression duplex u ltrasound. If iliac vein thrombosis suspected (back pain/entire limb swollen) do MRI or con trast venography. If iliac thrombosis consider use of inferior vena caval \201 lter perin atally. \200\22589 Treatment: Use class 2 compression stockings. Ini- tially elevate the l eg; then mobilize wearing stockings. Give heparin throughout pregnancy eg enoxaparin 1mg/kg /12h SC (based on early pregnancy weight). Check platelets every 2 \200\2234 days (2 \200 \22314 days if on LMWH). Stop injections at onset of labor, 24h before planned delivery. Do not use regional anesthesia until >24h since last dose LMWH. If cesarean section, use drai ns and wound clips or inter- rupted sutures in case of wound haematoma. Restart heparin 3h post-op (or >4h from epidural; do not remove epidural catheter within 12h of LMWH use). Postpartum enoxaparin can be reduced to 1.5mg/kg/24h. If warfarin chosen (after 3rd day) po stpartum, monitor INR meticulously. Treat for at least 6 weeks postpartum and 3 months from thrombosis. Compression stockings should be worn for 2 years (reduces post-thrombotic synd rome incidence from 23% to 11%). \200\22589 Both heparin and warfarin are \201 ne if bre astfeeding. Prophylaxis See p16. 33 Thrombophilia in pregnancy Thrombophilia is a tendency to increased clotting and many under lying causes are now known to contribute. Collectively, the conditions below aff ect at lea st 15% of Western populations, but are found in 50% of those with episodes of venous thromb oembolism. Conditions include: \200 Factor V Leiden mutation* decreases factor V breakdow n by protein C (ac- tivated protein C (APC) resistance). This aff ects 4% of the populatio n and increases thrombotic risk 5 \200\2238.3 times (heterozygotes). Homozygous individu- a ls have 10 \200\22334 times the risk of venous thromboembolism. Protein C de \201 ciency* (aff ects 0.3% of population; increasing thrombotic risk 2 \200\2234.8 times). \200 Protein S de \201 ciency* (aff ects 2% of population; \200 \200 thrombotic risk 3.2 times). \200 Antithrombin III de \201 ciency* (aff ects 0.02% o f population; thrombotic risk is s c i r t e t s b O increased 4.7 \200\22310 times). \200 Acquired thrombophilia. This is lupus anticoagulant cardiolipin antibody*. Women with lupus anticoagulant risk arterial and venous thrombos is; in atypical veins, eg portal or arm. G20210A mutation of the prothrombin gene (1% of the population). Thrombotic risk is increased 3 \200\22310 times for heterozygotes, 26.4 times in homozygotes Homozygosity for the thermolabile variant of methylene tetrahydrofolate reductase (C677T MT HFR), which leads to homocysteinaemia (10% of the population). No association was found bet ween venous thromboembolism and homozygosity for C677T MTHFR mutation, perhaps because plas ma homo- cysteine reduces in pregnancy and folic acid supplements ameliorate hyper- homocys teinaemia. Dys \201 brinogenaemia is rare, and the thrombotic risk variable. Pregnancy is an acquired risk factor for venous thromboembolism; the post- natal period being especially risky. The diffi culty is to know who has throm- bophilia, and what risk this poses to a pregnant wom an. Past thrombosis increases risk, as does family history so thromboprophylaxis is recomme nded for those with history of thromboembolism and known thrombophilia or fam- ily history of thromboembolism (p16) both antenatally and postnatally. Treat- ment is strati \201 ed a ccording to risk. For risks see p16. Women with asymptomatic thrombophilia: Women without p ast thrombo- embolic history but with the higher risk thrombophilias ie antithrombin de \201 - ciency, more than one thrombophilic defect (including homozygous factor V Leiden, ho mozygous G20210A mutation, and compound heterozygotes of factor V Leiden and G20210A mutati ons); and women with other thrombophilias but additional risk factors need expert advice as to whether antenatal thrombo- prophylaxis is required in addition to postnatal use on an i ndividual basis. Women with lower risk thrombophilias but no additional risk factors can ha ve careful surveillance antenatally and 7 days of postnatal low molecular weight heparin. It is not felt that all women should be screened for thrombophilia; although screening is r ecommended for those with a family history of thromboembo- lism and those with past history of idiopathic, or unprovoked thromboembo- lism (ie not estrogen or pregnancy related). Scr eening is also recommended in those with second-trimester pregnancy loss, severe or recurre nt eclampsia, and intrauterine growth restriction. Low molecular weight heparin is recommended for those with thrombo- philia and past history of thromboembolism (see p16). The thrombophilias marked * above, and acquired protein c re sistance are risk factors for develop- ing pre-eclampsia so aspirin 75mg/24h PO is recommen ded from 12 weeks until delivery. 90 Infection: 1 Investigating rash in pregnancy 91 Investigate maculopapular rashes for rubell a and parvovirus B19 (p142) (both these can infect the fetus) and measles. If maternal meas les within 6 days before or after birth, the neonate needs human normal immune globulin 0.6 mL/kg to max 5mL to prevent infection. Maternal chickenpox (p144) in 1st 24h of rash, from 20 weeks \200\231 gestation merits oral aciclovir. Hospitalize her for IV aciclovir if immu nosuppressed, very dense or haemorrhagic lesions, neurological or respiratory symptoms. Mot hers in contact with rashes (15min, same household or room, face to face contact); test for parvovirus B19 (asymptomatic infections aff ect fetus as often as symp- tomatic), and rube lla (unless vaccinated \211\2102 or antibody level \211 10IU/mL \211\2102, or 1 of each) . If she has chickenpox contact and is susceptible (con \201 rmed by ur- gent blood test), varicella zoster immune globulin (VZIG) can be given within 10 days of exposure but still manage her as if infectious 8 \200\22324 days post VZIG: and advise her to see GP if she de velops a rash as protection not always eff ective. Rubella Childhood vaccination prevents r ubella susceptibility. \200\207Asymptomatic reinfection can occur making serology essentia l in all pregnant rubella con- tacts. Routine antenatal screening \201 nds those needing puerperal vaccination (avoid pregnancy for 1 month: vaccine is live). Symptoms (p142) are a bsent in 50%. The fetus is most at risk in the 1st 16 weeks \200\231 gestation. 50 \200\223 60% of fetuses are aff ected if maternal primary infection is in the 1st month of gestation : <5% are aff ected if infection is at 16 weeks. Risk of fetal damage is much lower (<5%) w ith reinfection. Cataract is associated with infection at 8 \200\2239 weeks, deaf- ness at 5 \200\2237 weeks (can occur with 2nd-trimester infection), cardiac lesions at 5 \200\22310 weeks. Other features: purpura, jaundice, hepatosplenomegaly, thrombocyto- penia, cerebral palsy, microcephaly, IQ \200\201, cerebral calci \201 cation, microphthalmia, retinitis, growth disorder. Miscarriage or stillbirth may occur. If suspected in the mother seek expe rt help. Take antibody levels 10 days apart and look for IgM antibody 4 \200\2235 weeks fro m incubation period or date of contact. Cytomegalovirus (CMV) In the uK, cMV causes more co ngenital retardation than rubella. Maternal infection is mild (or \200\200 T , lymphadeno pathy, rash & sore throat). Up to 5 : 1000 live births are infected; 5% develop early multi ple handicaps, and have cytomegalic inclusion disease with nonspeci \201 c signs like rube lla syndrome + microcephaly, hydrops, & choroidoretinitis. Another 5% later develop cerebra l calci \201 cation (IQ \200\201); sensorineural deafness and psycho- motor retardation. \201 : (tricky; ask lab). Paired sera. Are IgM and IgG antibodies found? Amniocentesis at >20wks + shell viral culture can detect fetal trans- mission. Also do throat swab, urine cu lture, and baby \200\231s serum after birth. Re- ducing exposure to toddlers \200\231 urine (the source of much infection) in pregnancy limits spread. NB: reactivation of old CMV may occur in pregnancy; it rarely af- fects the baby. One way to know that +ve serology does n ot re \202 ect old infection is to do serology (or freeze a sample) pre-pregnancy. \201 \227: Hyperimmune globulin may have a role. Toxoplasmosis 40% of fetuses are aff ected if t he mother has the illness (2 \200\2237 : 1000 pregnancies); the earlier in pregnancy the mo re the damage. Symp- toms are like glandular fever. Fever, rash, and eosinophilia also occu r. If symp- tomatic, the CNS prognosis is poor. Diagnose by reference laboratory IgG and Ig M tests. Maternal, \201\227 (Royal College Regimen): Start spiramycin promptly in infected mothers, eg 1.5g/12h PO. In symptomatic non-immune women test every 10 weeks through pregn ancy. If infected consider amniocentesis to see if the fetus is infected. If the fetus is i nfected, give the mother pyrimethamine 50mg/12h as loading doses on day 1, then 1mg/kg/day + sulfadiazine 50mg/ kg/12h + calcium folinate 15mg twice weekly all until delivery. Affect ed babies: (diagnose by serology \200\224>90% asymptomatic). Intracranial calci \201 catio n, hydro- cephalus, choroidoretinitis if severely aff ected. Encephalitis, epilepsy, mental and physical retardation, jaundice, hepatosplenomegaly, thrombocytopenia, and 34 \200 s c i r t e t s b O skin rashes occur. Treat with 4-weekly courses of pyrimethamine, sulfadiazine and calcium f olinate \211\210 6, separated by 4 weeks of spiramycin. Prednisolone is given until signs of CNS in \202 ammation or choroidoretinitis abate. Prevention: Avoid eating raw meat, was h hands if raw meat touched, wear gloves if garden- ing or dealing with cat litter, and avo id sheep during lambing time. HIV See p23. It is a sad fact that for many women in some res ource-poor countries access to retrovirals in pregnancy is still not an option (only 45% in 2008), 92 and the mainstays of prelabour cesarean section and avoidance of breastfeeding, so successful in reducing transmission, are also not an option. It is estimated 430,000 inf ants and children are infected with HIV each year. Intrauterine syphilis Maternal screening occurs (UK screen 55,700 to prevent 1 case. In some parts of London 2 : 1000 women are inf ected); if infection found treat the mother with procaine penicillin 600mg/24h IM daily for 10 days. \205\223 are stillborn. Neonatal signs: rhinitis, snuffl es, rash, hepatospleno megaly, lymphadenopathy, anemia, jaundice, ascites, hydrops, nephrosis, meningitis, kera titis, and nerve deafness. Nasal discharge exam: spirochetes; X-rays: perichondritis; CSF: \200\200 Monocytes and protein with +ve serology. Treatment: Give procaine penicillin 37mg /kg/24h IM for 3 weeks. Listeria Aff ects 6 \200\22315 : 100,000 pregnancies. Maternal symp toms: fever, shiv- ering, myalgia, headache, sore throat, cough, vomiting, diarrhea, vagini tis. Miscarriage (can be recurrent), premature labor, and stillbirth may occur. Infection i s usually via infected food (eg milk, soft cheeses, p t ). \200\207Do blood cultures in any pregnant patient with unexplained fever for \211 48h. Serology, vaginal and rectal swa bs do not help (can be commensal). See OHCM p409. 35 s c i r t e t s b O Perinatal infection usually occurs in 2nd or 3rd trimester. 20% of aff ected fetuses are st illborn. Fetal distress in labor is common. An early postnatal feature is respiratory distr ess from pneumonia. There may be convulsions, hepato-splenomegaly, pustular or petechial ra shes, conjunctivitis, fever, leuco- penia. Meningitis is commoner after perinatal infection . Diagnose by culture of blood, CSF, meconium, and placenta. Infant mortality: 30%. Isolate baby (noso- comial spread can occur). Treat with ampicillin 50mg/kg/6h IV and gentamicin 3 mg/kg/12h IV until 1 week after fever subsides. Monitor levels. Sheep-borne conditions List eriosis, toxoplasmosis, and ovine chlamydia (Chlamydophila abortus) can be contracted from sheep. Ovine chlamydial infection is rare; can cause DIC, septicaemia, and renal failure in pregnant women and miscarriage of the fetus. Diagnose by serology; treat with eryth- romyc in or tetracycline. \200\207Pregnant women should not handle sheep or lambs.1 1 \200\230TORCH \200\231 infections: Toxoplasmosis, Other (eg syphilis, cocksackie, leptos pira, Q fever, Lyme disease, malaria), Rubella, CMV, Herpes (and hepatitis). 1st 4 are acqu ired antenatally (herpes & hepatitis usu- ally perinatally). Other agents: chickenpox p144; HIV, p144 \200\2235. See also erythrovirus (=parvovirus B19, p142). Zoster reactivation in pregnancy is not a risk for the baby. Infection: 2 36 \200 Hepatitis B virus (HBV) All mothers should be screened for HBsAg. Carri- ers have persisten t HBsAg for >6 months. High infectivity is associated with HBeAg so anti-HBe antibodies are negative. Without immunization 95% of babies born to these mothers might develop hepatitis B, and 93% of the ba- bies would be chronic carriers at 6 months. If the mother develops a cute infection in the mid- or third trimester there is high risk of perinatal infec- tion. Her risk of death is 0.5 \200\2233%. Most neonatal infections occur at birth but some (espe cially in the East) are transplacental; hence the seeming failure of vaccination in up to 1 5% of neonates adequately vaccinated. Most infected neonates will develop chronic infection and in infected males lifetime risk of developing hepatocellular cancer is 50%; 20% for \200 . Most will develop cir- rhosis, so immunization is really important. \200\207Give im munoglobulin (200U IM) and vaccinate babies of carriers and infected mothers at birth. See p151. In uncomplicated hepatitis HBV DNA is cleared, anti-core antibodies develop, followed by anti-HBe antibodies with the decline and disappearance of HBeAg and HBsAg at 3 months. Do serology of vaccinated baby at 12 \200\22315 months old. If HBsAg \200\223ve and anti-HB s is present, the child is protected. Hepatitis C See p26. Hepatitis E Risk of maternal mor tality is \200\200 (25% if in 3rd trimester); death is usually postpartum, preceded by ful minant hepatic failure, coma, and massive PPH. 33 \200\22350% of babies become infected. A vaccine is being developed. Herpes simplex (HSV) Neonatal infection can cause blindness, IQ \200\201, epilepsy, jaundice, respiratory distress, DIC, and death (in 30%, even if treat ed). s c i r t e t s b O Prevalence of past (2 ) HSV infection is 25% and recurrence in pregnancy is not usually a problem thanks to maternal antibodies. If a mother develops primary (1st-ever) genital her pes in pregnancy, refer to a genitourinary clinic to screen her (and her partners) for othe r infections and con \201 rm it is primary. If in last trimester give her oral aciclovir o r valaciclovir elective cesarean if 1 infection within 6 weeks of her due date. Type-s peci \201 c HSV diagnosis: PCR. If active primary infection lesions at time of delivery do a caesar, even if membranes have ruptured up to 4h previously. If a mother with primary lesions does deliver vaginally risk of infection to the baby is 41%, so give moth- er (by IVI in labor) and newborn high-dose aciclovir (p200; do PCR at birth). Try to avoid fetal blood sampling, scalp electrodes, and instrumental delivery. Neonatal infection usually appears at 5 \200\22321 days with groupe d vesicles/pustules on a red base, eg at the presenting part or sites of trauma (eg scalp e lectrode) periocular and conjunctival lesions. Non-vesicular rashes also occur. Varicell a zoster If mothers develop chickenpox in last 7 days of pregnancy aim for delivery after 7 days, give babies varicella immune immunoglobulin (VZIG) at birth and monitor for 28 days; and treat with aciclovir if neonate de- velops chickenpox. Babies of non-immune mothers al so need VZIG if contacts in 1st 7 days of life. Earlier in pregnancy, if women with no pers onal history of chickenpox have had signi \201 cant (eg 15 min) chickenpox contact; check blood for varicella antibodies; if none, give VZIG, and manage as still potentially in- fec tious 8 \200\22328 days later and notify doctor if develops rash. Women develop- ing chicke npox in pregnancy should avoid contact with pregnant women, and have oral aciclovir 800mg 5 \211\210daily PO for 7 days if >20wks pregnant if present- ing within 24h of rash. Hospita lize if chest, CNS symptoms, dense/haemorrhag- ic rash or immunocompromized. Fetal varicell a syndrome (FVS) complicates 1% fetuses of mothers infected at 3 \200\22328 weeks of pregn ancy by reactivation in utero. FVS features: skin scarring, eye defects (microphthalmia, ch orioretini- tis, cataracts), neurological abnormalities (microcephaly, cortical atrophy, IQ \200\201, bowel and bladder sphincter disturbances). Refer to fetal medicine specialist f or detailed ultrasound at 16 \200\22320wks, or 5wks post-infection. 93 Chlamydia trachomatis Associations: low birthweight, premature mem- brane rupture, fetal de ath. 30% of infected mothers have aff ected babies. Conjunctivitis develops 5 \200\22314 d ays after birth and may show minimal in \202 amma- tion or purulent discharge. The cornea is not usually involved. Complications: Chlamydia pneumonitis, pharyngitis, or otitis media . Tests: Special swabs are available but may be unreliable. See p285. Treatment: Local clea nsing of eye + erythromycin 12.5mg/kg/6h PO for 3 weeks eliminates lung organisms. Give pa rents/partners erythromycin 94 or azithromycin 1g PO single dose. Gonococcal conjunctivitis Occurs within 4 days of birth, with purulent discharge and lid swelling, corneal hazin g, corneal rupture, and panophthal- mitis. Note, 50% will also have concurrent chlamydial i nfection. Treatment: Infants born to those with known gonorrhea should have cefotaxime 100m g/ kg IM stat, and chloramphenicol 0.5% eye-drops within 1h of birth. For active gonococcal infection give benzylpenicillin 50mg/kg/12h IM and 3-hourly 0.5% chloramphenicol drops for 7 days. Isolate the baby. Ophthalmia neonatorum This is purulent discharge from the eye of a neonate <21 days old. There are many causes: chlamydiae, herpes virus, staphylo cocci, s treptococci, pneumococci, E. coli. Tests: Swab for bacterial and viral culture, microscopy (look for intracellular gonococci), and chlamydia (eg immuno \202 uo- rescence). Treat gon ococcus and chlamydia as above; other infections with neomycin drops or ointment (allows ch lamydia detection \200\224not so with chlo- ramphenicol). Clostridium perfringens: Suspect this in any complication of criminal abor- tion and when intracellular encapsulated Gram +v e rods are seen on genital swabs. It may infect in utero deaths or any other anaerobic site (eg haema- tomas). Signs: Endometritis \200\203septicaemia/gangrene \200\203myoglobinuria \200\203renal failure \200\203death. Treatment: \200 Surgically debride all devitalized t issue. \200 Hyper- baric O2. \200 High-dose IV benzylpenicillin (erythromycin if seriou s penicillin al- lergy). The use of gas gangrene antitoxin is controversial. Seek expert he lp. Preventing neonatal group B strep (GBS) sepsis Give all women IV antibiot- ics at labor \200\231s start or on membrane rupture if: \200 +ve GBS screening swab (vagi- nal or peri neal; do at 35 \200\22337wks \200 Any baby previously infected with GBS \200 Any docume nted GBS bacteriuria (regardless of level of colony-forming units/mL) in this pregnancy \200 Recent swab result unknown and gestation <37wks unless \200\223ve swab in last 5wks \200 Any intrapartum fever \200 If a woman is GBS+ve (swab or bacteriuria), with prelab our rupture of membranes at term, treat with GBS antibiotic prophylaxis and induce labor \200 If culture result unknown and mem- branes are ruptured at term for >18h: GBS prophyla xis (eg penicillin). 15361281 TB All babies born into households with TB, to immigrant mo thers from areas with a high TB prevalence, or who will travel to such areas should have BC G (Bacillus Calmette \200\223Gu rin) vaccination after birth 0.05mL intradermally at delto id \200\231s insertion: 0.03mL if using a multiple puncture gun. Babies not vac- cinated in hospital are unlikely to be vaccinated in the community. 95 Give other vaccinations as usu al, avoiding the BCG vaccinated arm for 3 months. Separate babies from mothers with active or open TB until she has had 2 weeks of \200\224 and is sputum \200\223ve. BCG vaccinate the baby and treat with isoniazid until he or she has a +ve skin reaction. Consider CXR in pregnant women with cough, fever, or weight loss (esp. if recent immigrant). Encourage brea stfeeding. 37 s c i r t e t s b O Abdominal pain in pregnancy 38 \200 \200\207With any pain in pregnancy think, is this onset of labor? If pain is in the sec- o nd half of pregnancy think is this pre-eclampsia? (check BP and urine protein). \200\207Wo men with chest, back or epigastric pain severe enough for opiates need full investigation i ncluding cardiac causes (ECG, CXR, troponin, echocardiogra- phy, CT angiography + CT/MRI ch est scan). Abdominal pain may be from ligament stretching or from symphysis pubis strain. I n early pregnancy remember miscarriage (p260) and ectopics (p262). Abruption The triad of a bdominal pain, uterine rigidity, and vaginal bleeding suggests this. It occurs in between 1 in 80 and 1 in 200 pregnancies. Fetal loss is high if >50% of placenta aff ected. A tender uterus is highly suggestive. Ul- trasound may be diagnostic (but not necessarily so). A li ve viable fetus merits rapid delivery as demise can be sudden. Prepare for DIC, which compl icates 33 \200\22350% of severe cases, and beware PPH, which is also common. See p56. Uteri ne rupture See p80. Uterine \201 broids For torsion and red degeneration, see p277. Uteri ne torsion The uterus rotates axially 30 \200\22340 to the right in 80% of normal pregn ancies. Rarely, it rotates >90 causing acute uterine torsion in mid or late pregnancy wit h abdominal pain, shock, a tense uterus, and urinary retention (catheterization may reveal a displaced urethra in twisted vagina). Fibroids, adnexal masses, or congenital asymmetrica l uterine anomalies are present in 90%. Diagnosis is usually at laparotomy. Delivery is by cesarean section. Ovarian tumors Torsion, rupture, see p282. Pyelonephritis See p28. Append icitis Incidence: 1 : 1000 pregnancies. It is not commoner in pregnancy but mortality is h igher (esp. from 20wks). Perforation is commoner (15 \200\22320%). Fe- tal mortality is 1. 5% for simple appendicitis; 30% if perforation. The appendix migrates upwards, outwards an d posteriorly as pregnancy progresses, so pain is less well localized (often para-umbilical or subcostal \200\224but right lower quadrant still commonest) 96 and tenderness, rebound, and guarding less obvious. Perito- nitis can make the uterus tense and woody-hard. Don \200\231t delay surgery! \200\224lapar- otomy over site of maximal tenderness with patient tilted 30 to the left by an experienced obstetric surgeon (laparoscopy appears to be safe ). 97 Cholecystitis Incidence 1 \200\2236 per 10,000 pregnancies. Pregnancy encourages gall stone formation due to biliary stasis and increased cholesterol in bile. Symptoms are simil ar to the non-pregnant with subcostal pain, nausea, and vomiting. Jaundice is uncommon (5%) . Ultrasound con \201 rms the presence of stones. The main diff erential diagnosis is appe ndicitis, and laparotomy or lapar oscopy is mandatory if this cannot be excluded. Surgery s hould be re- served for complicated non-resolving biliary tract disease during pregnancy as in >90% the acute process resolves with conservative management. For patients requiring su rgery, laparoscopic cholecystectomy can be a safe and eff ective method of treatment, but u terine perforation or injury is a risk. Rectus sheath haematoma Very rarely, bleeding into the rectus sheath and haematoma formation can occur with coughing (or spontaneously) in lat e pregnancy causing swelling and tenderness. Ultrasound is helpful. \201\231 \201\231 : Ab rup- tion. Management: Laparotomy (or perhaps laparoscopy \200\224but not in late pregnancy ) is indicated if the diagnosis is in doubt or if there is shock. 98,99 Pre-eclampsia Abdom inal pain may complicate pre-eclampsia by liver con- gestion. Rarely, in severe pre-eclamps ia the liver ruptures. Pancreatitis in pregnancy is rare, but mortality is high (37% matern al; 5.6% fetal). Diagnose by urinary diastase in 1st trimester when amylase may be low. 100 s c i r t e t s b O This page intentionally left blank Abdominal palpation 40 \200 The uterus occupies the pelvis and cannot be felt per abdomen until 12 weeks \200\231 gest ation. By 16 weeks, its fundus lies half way between the sym- physis pubis and the umbilicu s. By 20 \200\22324 weeks it reaches the umbilicus. In a primip, the fundus is under the ri bs by 36 weeks. At term the uterus lies a bit lower than at 36 weeks, as the head descends into the pelvis. Some midwives prefer to measure the symphysis fundal height (SFH) in cm fr om the symphy- sis pubis (after voiding urine). From 16 weeks the SFH increases 1cm/week. The symphysis fundal height during pregnancy the SFH (cm) \211\210 dates (in weeks) As a r ule of thumb: at 16 \200\22326 weeks the SFH (cm) 2cm \211\210 dates 26 \200\22336 week s 36 weeks to term the SFH (cm) 3cm \211\210 dates SFH is used as a rough guide to \201 nd babies small for gestational age (p52). Suspect t his if the measurement lies >1 \200\2232cm outside these ranges given above. NB: more false positives will occur with the simpler rule of weeks of gestation = cm from pubic symphysis to fundus. 101,102 Other reasons for discrepancy between fundal height and dates: \200 I nac- curate menstrual history \200 Multiple gestation \200 Fibroids \200 Polyhydramni os \200 Adnexal mass \200 Maternal size \200 Hydatidiform mole. s c i r t e t s b O On inspecting the abdomen note any scars from previous operations. Cae- sarean section scar s are usually Pfannenstiel ( \200\230bikini-line \200\231). Laparoscopy scars are just belo w and parallel to the umbilicus or in the left upper quadrant (Palmer \200\231s point). It is common to see a line of pigmentation, the linea nigra, extending in the midline from pub ic hair to umbilicus. This darkens during the \201 rst trimester (the \201 rst 13 weeks ). Palpating the abdomen Measure the SFH and listen to the fetal heart. After 32 weeks palp ate laterally to assess the lie, then bimanually palpate over the lower uterine pole for pr esentation and degree of engagement. Pawlik \200\231s grip (examining the lower pole of the uterus between the thumb and index \201 ngers of the right hand) can also be used for as sessing the degree of engagement. Watch the patient \200\231s face during palpation and sto p if it causes pain. Obesity, polyhydramnios, and tense muscles make it diffi cult to feel the fetus. Mid- wives are skilled at palpation, so ask them if you need help. It is important to determine the number of fetuses (p68), the lie (longitudinal, oblique, o r transverse), the presentation (cephalic or breech, \201 g 2), and the engagement. Ultra sound is useful here. Note the amount of liquor, the appar- ent size of the fetus, and any contractions or fetal movements seen or felt. Auscultation The fetal heart may be heard by Doppler ultrasound from 12 weeks and with a Pinard stethoscope from 24 weeks. Fetal movem ents 103 1st noted by mothers at 18 \200\22320wks, movements \200\200 un- til 32wks then p lateau at average 31/h. Fetuses sleep for 20 \200\22340-min cycles day and night (rarely >9 0mins). Maternal posture aff ects detection (lying> sitting>standing). If mothers feel move ments reduced at 28+ wks, advise ly- ing semi-recumbent for 2h; if <10 movements arrange sa me day CTG (p44), and next available ultrasound if reduction persists or IUGR (p52)/stillbi rth risk. Engagement The level of the head is assessed in 2 ways: engagement, or \201 fth s palpable abdominally. Engagement entails passage of the biggest diameter of the presentin g part through the pelvic inlet. Fifths palpable abdominally states what you can feel, and makes no degree of judgment on degree of en- gagement of the head. In primigravida the head usually enters the pelvis by 37 weeks, otherwise causes must be excluded (eg placenta prae via or fetal ab- normality). In multips the head may not enter the pelvis until onset of la bor. 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.