RECENT ADVANCES IN HISTOPATH - 23

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