Lucasdiac death that is non-ischaemic (atheroma) and non-valvular(with the exception of mitral valve mucoid degeneration)in causation. The classification is divided in<strong>to</strong>those where the death is explained on gross and his<strong>to</strong>logicalcriteria and those where it remains unexplained at ourcurrent state of knowledge. PPCM, ARVCM, myocarditis,left ventricular hypertrophy and fibrosis, and hypertensiveheart disease are ‘explained’; unexplained cardiac death inepilepsy, alcohol abuse, obesity and diabetes are ‘unexplained’.Under the SADS label come those unexplained caseswith a morphologically normal heart by gross examinationand his<strong>to</strong>logy. A proportion can be demonstrated by electrographicexamination of relatives (and sometimes of thewoman before death) <strong>to</strong> have a conduction defect, a channelopathy,e.g. long QT syndrome. In this triennium, no<strong>deaths</strong> were ascribed <strong>to</strong> a specific arrhythmia, but thatprobably reflects the imperfect evaluation of them.SADS, cardiac hypertrophy andobesity in pregnancyThis is the area of cardiac death evaluated least well his<strong>to</strong>rically.In Chapters 10 and 17, the sections on unascertainedcauses of death indicate that some of these might be SADSif better clinicopathological information had been forthcoming.Further, in Chapter 9, the cases described as beingthe result of ‘other causes, hypertrophy and fibrosis’ areprobably SADS cases, of which there are up <strong>to</strong> six. In thesecases, the au<strong>to</strong>psy was not comprehensive enough <strong>to</strong> enablethe assessors <strong>to</strong> allocate the case <strong>to</strong> a particular cardiac category.Four of the women had a BMI ‡30.Here we group <strong>to</strong>gether the women who died of suddenunexpected cardiac death who were not hypertensive duringpregnancy (or who were well treated) and did not have oneof the ‘explained’ cardiac pathologies. It includes those whowere obese and those with otherwise unexplained left ventricularhypertrophy. The reason for this grouping is <strong>to</strong> highlight:• the likelihood that pregnancy presents this scenario morefrequently than is seen in the general population due <strong>to</strong>the physiological stresses of pregnancy and delivery bringingout an underlying potential cardiac arrhythmia• the crucial need for more comprehensive data collectionand better categorisation <strong>to</strong> improve knowledge of theepidemiology of SADS.It is established that obesity and cardiac hypertrophy areassociated in the absence of concurrent hypertension, andthat obesity and cardiac hypertrophy are both risk fac<strong>to</strong>rsfor arrhythmia and sudden cardiac death. Recently, thenotion of ‘obesity cardiomyopathy’ is gaining ground, 2 andit applies particularly <strong>to</strong> those with a central versus aperipheral pattern of obesity. Such women have largehearts, and in the ten women with SADS, the median heartweight was 390 g (range 270–585 g). Of the heart <strong>to</strong> bodyweight ratios, seven of the ten were >0.42% of bodyweight, compared with the normal mean of 0.40% (range0.38–0.42). 3In future, pathologists <strong>reviewing</strong> such cases must documen<strong>to</strong>ptimally the morphology of the body (height,weight, BMI, pattern of obesity) as well as that of the heartso that closer analysis can be undertaken. The heart morphologyrequired is listed in Best Practice points (above).The published European guidelines on examination of theheart provide the necessary information. 4The fact that pregnancy <strong>make</strong>s the obesity–heart issuecomplicated, because of the greatly altered vascular physiologyand the introduction of novel pathologies such as preeclampsia,is shown by the following case study.An obese woman, previously normotensive, was admittedduring her third trimester with a blood pressure of 170/108 mmHg and proteinuria. Despite antihypertensive treatment,her blood pressure rose further, and she developedflash pulmonary oedema with breathlessness, followed bycardiac arrest. A peri-mortem caesarean section resulted ina live birth. At au<strong>to</strong>psy, her heart weighed 585 g, with leftventricular hypertrophy of 2.5 cm lateral wall thickness.His<strong>to</strong>pathology showed cardiac myofibre hypertrophy andmild interstitial fibrosis; the renal glomeruli had the endotheliosislesion of pre-eclampsia. The conclusion on causationwas a combination of obesity-related heart hypertrophyplus pre-eclampsia.Ultimately, these <strong>deaths</strong> are individually unpredictable,and obesity needs <strong>to</strong> be addressed as a public health issueif the fatalities are not <strong>to</strong> rise further in the next report. jReferences1 Silwa K, Fett J, Elkayam U. Peripartum cardiomyopathy. Lancet<strong>2006</strong>;368:687–93.2 Duflou J, Virmani R, Rabin I, Burke A, Farb A, Smialek J. Suddendeath as a result of heart disease in morbid obesity. Am Heart J1995;130:306–13.3 Smith HL. The relation of the weight of the heart <strong>to</strong> the weight ofthe body and of the weight of the heart <strong>to</strong> age. Am Heart J1928;4:79–93.4 Basso C, Burke M, Fornes P, Gallagher PJ, de Gouveia RH, SheppardM, et al. Guidelines for au<strong>to</strong>psy investigation of sudden cardiac death.Virchows Arch <strong>2008</strong>;452:11–8.118 ª <strong>2011</strong> Centre for Maternal and Child Enquiries (CMACE), BJOG 118 (Suppl. 1), 1–203
Chapter 10: Other Indirect <strong>deaths</strong>Chapter 10: Other Indirect <strong>deaths</strong>M de Swiet 1 , C Williamson 2 , G Lewis 3 (on behalf of the Centre for Maternal and Child Enquiries)1 Emeritus Professor of Obstetric Medicine, Imperial College London, London, UK; 2 Institute of Reproductive Developmental Biology,Imperial College London, London, UK; 3 National Perinatal Epidemiology Unit (NPEU), University of Oxford, Oxford, UKCorrespondence: Professor Michael de Swiet, Flat 15, Wren View, 75 Hornsey Lane, London N6 5LH, UK. Email: m.deswiet@imperial.ac.ukKeywords risk, Confidential Enquiry, <strong>maternal</strong>, mortality.Other Indirect <strong>deaths</strong>: specific recommendations• All women who are planning pregnancies that are likely <strong>to</strong> be complicated by potentially serious medical conditionsshould have pre-pregnancy counselling.• Women whose pregnancies are complicated by potentially serious medical conditions should be referred <strong>to</strong> appropriatespecialist centres of expertise where both care for their medical condition and their obstetric care can be optimised.• Lack of consultant involvement remains a problem in the care of women with serious medical problems. Maternityunits should consider developing pro<strong>to</strong>cols <strong>to</strong> specify which medical conditions mandate consultant review.• Health workers who are caring for women in pregnancy with conditions with which they are unfamiliar should consultexperts. If necessary this consultation can be by telephone and most experts are only <strong>to</strong>o pleased <strong>to</strong> help.• Medical conditions that may be the cause of symp<strong>to</strong>ms that are more commonly seen by obstetricians should not beignored, e.g. seizures can be caused by epilepsy as well as eclampsia.• Multiple admissions or attendances for emergency care demand further investigation and are often an indication forreferral <strong>to</strong> specialists in other disciplines.• Undiagnosed pain requiring opiates demands immediate consultant involvement and investigation.• The need remains for physicians who do not work directly with pregnant women <strong>to</strong> know more about the interactionbetween the conditions that they are treating and pregnancy.• Appropriate and professional interpretation services must be made available <strong>to</strong> women who do not speak English.Other Indirect <strong>deaths</strong>: learning pointsMost women with epilepsy require an increased lamotriginedose in pregnancy <strong>to</strong> maintain good seizure control.Clinicians should adjust their managementpro<strong>to</strong>cols accordingly.Women with epilepsy or undiagnosed syncope are stillunaware of the very rare but real risk of drowning whilebathing unattended. A shower is preferable and thebathroom door should remain unlocked.There should be no hesitation in arranging a chest X-ray for women with significant chest symp<strong>to</strong>ms. Similarly,magnetic resonance imaging and computed<strong>to</strong>mography of the brain can be used <strong>to</strong> exclude cerebralpathology.Clinicians should be aware that haemoglobin SC diseasecan cause sickle cell crisis and is as dangerous as haemoglobinSS disease.Women should be given advice about sexual intercoursein the postnatal period as fatal air embolism has beenreported as a result of this. The medical assessors <strong>to</strong> thisEnquiry recommend abstinence for 6 weeks, or gentleintercourse and avoidance of positions where excess aircould be forced in<strong>to</strong> the vagina.IntroductionIndirect <strong>maternal</strong> <strong>deaths</strong> are defined as <strong>deaths</strong> resultingfrom previously existing disease or diseases that developduring pregnancy and which do not have direct obstetricª <strong>2011</strong> Centre for Maternal and Child Enquiries (CMACE), BJOG 118 (Suppl. 1), 1–203 119
- Page 1:
Volume 118, Supplement 1, March 201
- Page 4 and 5:
AcknowledgementsSaving Mothers’ L
- Page 6 and 7:
AcknowledgementsAcknowledgementsCMA
- Page 8 and 9:
Forewordbeen written jointly by a m
- Page 10 and 11:
‘Top ten’ recommendationsServic
- Page 12 and 13:
‘Top ten’ recommendationscommun
- Page 14 and 15:
‘Top ten’ recommendationsof suc
- Page 16 and 17:
‘Top ten’ recommendationsMarch
- Page 18 and 19:
Oates et al.Back to basicsM Oates 1
- Page 20 and 21:
Oates et al.BreathlessnessBreathles
- Page 22 and 23:
Oates et al.appropriate pathway of
- Page 24 and 25:
LewisIntroduction: Aims, objectives
- Page 26 and 27:
LewisAn important limitation of ran
- Page 28 and 29:
Lewismaternal and public health-pol
- Page 30 and 31:
Lewisresult in a live birth at any
- Page 32 and 33:
LewisChapter 1: The women who died
- Page 34 and 35:
Lewiswho would not have been identi
- Page 36 and 37:
Lewis1098Rate per 100 000 materniti
- Page 38 and 39:
LewisTable 1.4. Numbers and rates o
- Page 40 and 41:
Lewis2.50Rate per 100 000 materniti
- Page 42 and 43:
LewisTable 1.9. Number of maternal
- Page 44 and 45:
LewisTable 1.12. Numbers and percen
- Page 46 and 47:
LewisThere were cases where a major
- Page 48 and 49:
LewisBox 1.5. Classifications of Bo
- Page 50 and 51:
LewisTable 1.20. Number and estimat
- Page 52 and 53:
LewisNew countries of the European
- Page 54 and 55:
LewisTable 1.23. Direct and Indirec
- Page 56 and 57:
LewisTable 1.26. Characteristics* o
- Page 58 and 59:
Lewis4 Lewis G (ed). The Confidenti
- Page 60 and 61:
DrifeTable 2.1. Direct deaths from
- Page 62 and 63:
Drifewomen who died in 2006-08 had
- Page 64 and 65:
Drifedelivery she became breathless
- Page 66 and 67:
DrifePathological overviewFourteen
- Page 68 and 69:
NeilsonChapter 3: Pre-eclampsia and
- Page 70 and 71: Neilsontrue, and what might be the
- Page 72 and 73: NeilsonConclusionThe number of deat
- Page 74 and 75: NormanBackgroundIn the UK, major ob
- Page 76 and 77: Normanwhich there was catastrophic
- Page 78 and 79: Normanrecommendations made in succe
- Page 80 and 81: DawsonBox 5.1. The UK amniotic flui
- Page 82 and 83: Dawsontry despite an extensive sear
- Page 84 and 85: O’HerlihyTable 6.1. Numbers of Di
- Page 86 and 87: O’Herlihytoxic shock syndrome aft
- Page 88 and 89: HarperGroup A b-haemolytic streptoc
- Page 90 and 91: Harperthe 6-week postnatal period,
- Page 92 and 93: Harpera major intrapartum haemorrha
- Page 94 and 95: HarperBox 7.1. Signs and symptoms o
- Page 96 and 97: Harperwoman was given several litre
- Page 98 and 99: Harper2 Lamagni TL, Efstratiou A, D
- Page 100 and 101: LucasTable A7.1 Proposed new catego
- Page 102 and 103: Lucasthe same infection scenario as
- Page 104 and 105: McClure, CooperChapter 8: Anaesthes
- Page 106 and 107: McClure, Cooperaddress, but protoco
- Page 108 and 109: McClure, CooperPostpartum haemorrha
- Page 110 and 111: McClure, CooperWorkloadA number of
- Page 112 and 113: Nelson-PiercyTable 9.1. Indirect ma
- Page 114 and 115: Nelson-Piercynary arteries. In view
- Page 116 and 117: Nelson-Piercynormal left ventricle
- Page 118 and 119: LucasAnnex 9.1. Pathological overvi
- Page 122 and 123: de Swiet et al.causes but are aggra
- Page 124 and 125: de Swiet et al.died of SUDEP before
- Page 126 and 127: de Swiet et al.for 6 weeks after de
- Page 128 and 129: de Swiet et al.mised. The obstetric
- Page 130 and 131: de Swiet et al.CancerPregnancy does
- Page 132 and 133: de Swiet et al.a thorough autopsy w
- Page 134 and 135: Oates, CantwellChapter 11: Deaths f
- Page 136 and 137: Oates, CantwellTable 11.1. Timing o
- Page 138 and 139: Oates, CantwellTable 11.5. Maternal
- Page 140 and 141: Oates, CantwellChild protection iss
- Page 142 and 143: Oates, CantwellAll women who are su
- Page 144 and 145: Oates, Cantwell4 Kendel RE, Chalmer
- Page 146 and 147: Lewismaternal mortality rates or ra
- Page 148 and 149: Annex 12.1. Domestic abuseAnnex 12.
- Page 150 and 151: Annex 12.1. Domestic abuseshe could
- Page 152 and 153: Garrod et al.supportive but challen
- Page 154 and 155: Garrod et al.• Culture and system
- Page 156 and 157: Garrod et al.the second stage and s
- Page 158 and 159: Garrod et al.through the still heal
- Page 160 and 161: ShakespeareChapter 14: General prac
- Page 162 and 163: Shakespeareemergency caesarean sect
- Page 164 and 165: ShakespeareCardiac diseaseDeaths fr
- Page 166 and 167: Shakespearereduce the risks to the
- Page 168 and 169: ShakespeareManaging a maternal deat
- Page 170 and 171:
Hulbertin the ED was of a high qual
- Page 172 and 173:
HulbertPre-eclampsia/eclampsia: lea
- Page 174 and 175:
HulbertTransfersWhen the obstetric
- Page 176 and 177:
Clutton-Brocksimply the case that s
- Page 178 and 179:
Clutton-BrockDiagnosis of sepsisTak
- Page 180 and 181:
Clutton-Brockpulseless electrical a
- Page 182 and 183:
Clutton-BrockImprovement Scotland (
- Page 184 and 185:
Lucas, Millward-Sadler95 mmHg. This
- Page 186 and 187:
Lucas, Millward-Sadleran agreed mai
- Page 188 and 189:
Annex 17.1. The main clinico-tholog
- Page 190 and 191:
MillerAppendix 1: The method of Enq
- Page 192 and 193:
MillerDatanotificationNotificationR
- Page 194 and 195:
Knight• investigating different m
- Page 196 and 197:
Knightbaseline incidence against wh
- Page 198 and 199:
LennoxAppendix 2B: Summary of Scott
- Page 200 and 201:
LennoxEvidence of effective managem
- Page 202 and 203:
Appendix 3: Contributors to the Mat
- Page 204 and 205:
Appendix 3: Contributors to the Mat