This document discusses maternal mortality and various causes of death during or after pregnancy. It covers direct causes like preeclampsia, amniotic fluid embolism, and postpartum hemorrhage. Indirect causes discussed include sudden cardiac death, venous thromboembolism, and infections. The document provides details on evaluating different conditions pathological findings. It stresses the importance of a thorough autopsy including samples, cultures, and examination of key organs to determine the cause of maternal death.

1. Recent Advances in Histopathology - 23
Sebastian Lucas

2.  MMR: 11.4/1,00,000 (UK), 120 death a year
 India : 178 per 1,00,000
 Possible cause of death is very wide
 Evaluation of causation is complex
 Medical, social and legal consequences are
profound, prolonged and expensive

3.  Death at anytime during pregnancy, delivery
and up to 42 days postdelivery
 Deaths after 42days from delivery are
included only if they result from a problem
that arose before that caesura
 PPCM
 Prolonged survival in intensive care

4.  Direct
 Pre-eclampsia, AFE, genital tract trauma and
sepsis, PPH
 Indirect
 Sudden cardiac death, DOA, CHD,VTE, AIDS,
SLE, SUDEP, APLA,Tumors
 Coincidental
 Homicide, road collision, drug toxicity, Cancers

5.  Cause of death
 Standard protocol
 Information and samples
 Placenta

7.  Classic form – sudden cardioresp collapse
 Clinical triad
 Hypotension / cardiac arrest
 Pulmonary vasospam
 Coagulopathy with severe bleeding
 High mortality ; treatment is supportive

8.  Amniotic fluid, amniotic and fetal squamous
cells and hair embolise to small vessels of the
lungs
 H and E
 AB
 HMWCK
 CD31

10.  Renal glomeruli – fibrin thrombi in capillary
lumen – DIC
 Uterus – mucosal bleed – entry of AF into
uterine veins – via CS incision or mucosal split

12.  Pathogenesis – debated
 Acute anaphylactic response with cardiopulm
shutdown + triggering the clotting cascade
and consumptive coagulopathy
 ? Eg of SIRS – inappropriate release of
endogenous inflammatory mediators, an
abnormal maternal response to fetalAg

13.  Used as defence against claims of clinical
negligence – Fatal peri or PPH
 AFE : inevitably fatal

14.  Pre-eclampsia and eclampsia – 3rd trimester
 Increased BP, oedema and proteinuria
 Predisp : essential HT, renal disease & obesity
 Clonic-tonic seizures in pre-eclampsia
 HELLP Syndrome

15.  Etiopathogenesis – poorly understood
 Generalised vasculopathy
 Mode of acute death
 HT type intracerebral Hm
 Encephalopathy caused by vasogenic edema (
severe generalized version of PRES – due to
endothelial damage)
 Fatal cardiac arrhythmia
 HELLP : intra abdominal Hm

16.  Brain
 Intracerebral Hm without pre-exisiting berry
aneurysm or predisposing factor (60%)
 Diffuse cortical petechial Hm – occipital lobes
 Swelling and diffuse cerebral oedema

17.  Kidney
 Glomerular endotheliosis (unique)
 Endothelial cells are swollen ; glomerular capillaries
appear bloodless
 Glomerulus may also herniate into proximal tubules
 Endothelial cells maybe vacuolated with lipid
 Silver staining : string of beads appearance

19.  Uterus and placenta
 Effects of reduced arterial blood supply on villi + foci
of infarction
 Decidua – atherosis, fibrinoid necrosis of spiral
arterioles
 Liver
 Gross : blotchy focal or confluent Hm necrosis
 Histo : periportal fibrin deposition, Hm and
hepatocyte necrosis ( unique )

20.  General autopsy findings of hypovolemic
shock
 Pallor
 Pituitary infarction
 Hypoxic – ischaemic neuronal necrosis in brain

21.  Uterine atony – commonest cause
 Placenta praevia
 Retained placenta
 Placental abruption – severe coagulopathy
 Creta syndromes
 Accreta (villi attach direct to uterine muscle)
 Increta (invade further into myometrium)
 Percreta ( through myometrium)

23.  Genital tract trauma – large babies / iatrogenic
 ENBLOC removal of genital tract
 Uterine rupture – big baby/ small pelvis/
prolonged labour/ drugs
 Abortion
 Spont ( <24 weeks) : septic or aseptic : genital tract
sepsis/ uterine Hm/ molar preg
 Legal termination of preg
 Criminal : infection/Hm

24.  Several syndromes with diff pathogensis
 Severe cases – end results : bacteraemic
septic sock and multiorgan failure with DIC
 Placental examination – critical +
microbiological culture + HPE
 Maternal blood cultures : aseptic – neck veins
or heart

25. CATEGORY TYPICAL INFECTION
AGENT
PATHOLOGY
1. Unsafe abortion Clostridium spp Genital tract necrotising
sepsis ; septic shock;
MOF
2. Ruptured membranes E coli Infected and inflamed
placenta, cord and
membranes, genital tract
sepsis; MOF
3. Post delivery Group A Streptococcus
pyogenes (GAS)
Genital tract sepsis,
sometimes necrotising
with high bact load; MOF

26. CATEGORY TYPICAL INFECTION
AGENT
PATHOLOGY
4. Community acquired
sepsis
GAS, pneumococcus TSS ; MOF
5. Post partum sepsis
related to birth process
but genital tract not
involved
Gram negative and
positive organisms
Localised sepsis, leading
to MOF

28.  Collapse and die suddenly
 Critical to examine the entire length of pulm
artery
 Pregnancy is a procoagulant state
 Prevents severe Hm when placenta detaches from
decidua
 10X relative risk ofVTE (through out preg to week
after delivery)

29.  Common category
 Aneurysm, dissection and rupture – 3rd trimester
 Etiology :multihit
 Inherent predisposition + progestrone-associated
weakening of the media
 Histo : elastic degeneration, mucin deposits and
attenuated muscle
 Outcome : collapse from shock

30.  Congenital heart lesion with pulmonary HT
 Inheritable cardiomyopathy – HOCM, ARVCM
 Acquired cardiac muscle disease – IHD,
endocardial fibroelastosis, myocarditis
 SADS – sudden unexpected arrhythmic
cardiac syndrome – negative autopsy – long
QT syndrome
 Obesity and sudden cardiac death
 Valvular disease

31.  Heart failure during last month of pregnancy
and upto 5 months post delivery
 Dilated cardiomyopathy
 Nonsp histology
 Oxidative proapoptotic stress on myocytes,
related to prolactin

32.  Pregnancy increases risk ofTTP
 Abnormalities of vWF physiology – platelet
clustering and adhesion to endothelia of the
microvasculature – brain, kidney, heart
 Postpartum confusion, MAHA and renal
failure
 Lab : low platelet but normal CF and fibrin

33.  Preg – relative immunodep state [CMI ]
 Viral infection ( HS , hepatitis , influenza )
 Listeriosis
 Tb

34.  2009-10 pandemic – type A/H1N1
 3rd trimester preg – influenze pneumonitis
and A/c lung injury
 Acquired secondary bacterial pneumonia
 Preg was the pre-eminent risk factor for
death with H1N1 infection

35.  Maternal mortality raises by 10 fold
 Late presentation at around time of delivery
 Death –Tb or opportunistic infections, sepsis
or complications of abortion

36.  Obtain as much as clinical information and lab
data as possible before starting the autopsy
 Take sterile blood culture; later, retain a femoral
venous blood sample
 Pay close attention to pulm artery , heart and
genital tract
 ‘Negative’ autopsy : retain a piece of spleen in
freezer

37.  To establish cause of death – discuss the case
openly with obstetricians, physicians,
anaesthestists and intensivists