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Obstetrics > liver disease in obstetrics > Flashcards

liver disease in obstetrics Flashcards

1
Q

How do LFTs change in a normal pregnancy

What is the effect on liver metabolism

A

Reduction: in serum protein, AST ALT(normal 30 in T3)
Increased: fibrinogen, ALP, carrier molecules eg caeruloplasmin(carries Cu) transferrin, thyroid binding globulin, corticosteroid binding globulin.
Liver metabolism increases

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2
Q

ALP
What is it?
What if it is over 1000

A

Alkaline phosphatase is a group of enzymes that catalyzes the hydrolysis of phosphate esters in a basic environment to aid transport across cell membranes.
Probably placental but can do isoenzymes to exclude a bone (pagets, mets, #) or liver source

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3
Q

Causes of viral hepatitis

A

Hep A B C D E

CMV EBV HSV

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4
Q

Hepatitis A
Transmission
Progress + rate of chronic infection
Vertical transmission +management of neonate

A

Hep A is transmitted by the faecal oral route
It is acute, self limiting and does not result in chronic infection. Maternal fetal transmission is rare
If at or around delivery - baby should be given immunoglobulin at birth

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5
Q

Hep B screening and prevention (generally and in pregnancy)

What is the incubation time

A

Screen on booking bloods for HBsAg

Immunization in national scheme at Infanrix- hexa 6/52 3/12 5/12
Health care workers immunized + blood and bodily fluid precautions
Immunisation of children, house hold contacts and sexual partners of Hep B +

Treat Hep B in pregnancy to reduce the risk of vertical transmission

Incubation 1-6 months

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6
Q

Infanrix hexa - given when? what is in it?

A

Diptheria, tetanus, pertussis, polio, hep B, haemophilis influenzae B 6/52 3/12 5/12

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7
Q

Hep B - what are the risks of vertical transmission
what are the risk factors
When does it occur
what procedures increase the risk

A

Invasive procedures increase the risk (CVS amnio)
Recommend NIPT, if needs, then amnio better - avoid transplacental amnio
Increased in abruption, PTL Threatened miscarriage
Risks increased if HBV viral load high + HBsAg
+ HBsAg 70-90%
-ve HBsAg 10-40%
5% transmission AN 95% Intrapartum

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8
Q

If a woman has a positive screening on her booking bloods what other Ix need to be requested

A 
HbeAg (hep B e antigen) 
Anti HBe 
HBV viral load
LFTs liver USS 
Prothrombin time
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9
Q

What is the risk of disease progression of Hep B in pregnancy

A

1% woman have AN hepatic flares

25% PN hepatic flares - need close monitoring

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10
Q

When do we treat mums withHep B in pregnancy and with what

How effective is it

A

AN Tx at 30-32 weeks with tenofovir 300 mg daily until 6/52 PP if HBV viral load is over 200000 IU/ml
Reduces neonatal infection 18% to 5%
Ensure referral to gastro enter for monitoring
(lamivudine - resistance)

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11
Q

Intrapartum management of Hep B in pregnancy

A

Np FSE or FBS LSCS for normal indications

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12
Q

How do we treat newborns to reduce the risk of hep B transmission

A

Wash the baby before IM immunisations
If HBsAg + mother then for Immunoglobulin at birth and first immunisation within 12 hours of del
then to have Infanrix hexa 6/52 3/12 5/12
For testing at 5/12 (can be weakly positive due to immunoglobulin given at birth - if so immunize at 6/12 + 7/12 and retest at 8/12
Treating babies as above 85-95% protective

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13
Q

Can hep B + mums breastfeed

A

if vaccinated and had IG then yes - HBV is present in the breast milk but if treated then protective
Take car with cracked and bleeding nipples

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14
Q

How common is hep B in NZ

How is it transmitted

A

1-2 % of the population
50% of cases are vertical transmission
Otherwise blood/ bodiy fluid exposure,

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15
Q

Progress of hep B (not in pregnancy )
chronic transmission
mortality

A

Chronic carriers have a 25 % chance of dying from hep B
neonates have a 90% risk of becoming chronic carriers
adults with acute hep B 5 % conversion

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16
Q

Out of pregnancy - who gets treatment and rates of success?

A

Out of pregnancy interferon sustains remission in 30% HBeAg + and 15% HBeAg -ve
Oral antivirals are lifelong therapy and achieve suppression in most people

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17
Q

Obstetric outcomes associated with hep B

A

No increase in BW PTB Delivery perinatal mortality

But if cirrhosis then associated with IUGR PTB IUD INteruterine infection

18
Q

Rate of hepatitis C in fertile woman

A

1%

19
Q

Should we and when should we test for Hep C

A

RANZCOG considers that all pregnant
women should be screened for Hepatitis C so that risk stratification can be performed and measures taken to both reduce perinatal transmission and minimise occupational exposure
Ideally pre preg so treatment can occur

20
Q

Hep C positive - what other tests should be done and why

A

PCR for HCV Viral load as this affects the risk of vertical transmission
LFTS including PTB
HIV as coinfection increases the rate of vertical transmission

21
Q

What increases the risk of HCV vertical transmission

What is the rate of vertical transmission

A

VT around 5% (20% if coinfected with HIV)

FBS FSE
HIV coinfection 
High viral load 
PROM 
LSCS not recommended as a means of reducing transmission
22
Q

How do you manage neonates born to hep C + mums

A

bath the baby before IM injections (VITK)
No imunogloblin no vaccine
All infants of HCV positive mothers should be screened following delivery to determine whether they have been infected. Care should be taken to ensure the
appropriate interval has passed for the neonate to become PCR+/- antibody positive. - 2 samples 3 months apart or +ve after 18 months

23
Q

Can Hep C infected mums breastfeed

A

HCV infection is not a contraindication to breastfeeding except in the presence of cracked or bleeding nipples. In this instance, expression and discarding of the
milk is advised whilst waiting for healing of the cracked nipple

24
Q

Treatment of hep C around pregnancy
what is the guidance ?
What is the cure rates

A

Pre preg screening to treat any + HCV woman
cure up to 95%
Treatment for HCV eg ribavirin not recommended
during pregnancy or breast feeding. In particular ribavirin is teratogenic (Category X).
For all women and male partners receiving Ribaviran, reliable contraception must be used during treatment and for 6 months after completion of treatment.
combo ribaviran and interferon

25
Q

Risk of hep C
Mortality
What are the rates of chronic infection
What is the risk of pregnancy on hep C

A

5% of chronically infected Hepatitis C patients will die of their disease, due to liver failure or hepatocellular
carcinoma
80% develop chronic infection - 20% of those get cirrhosis
Pregnancy does not cause deterioration in hep C
No change to obstetric outcomes
Increase in obstetric cholestasis

26
Q

how is hep C transmitted

A

Blood products (15%)
IVDU (50-90% IVDU are hep C +ve)
Sexual transmission unusual <5%

27
Q

what is hepatitis E

Transmission

A

Hep E is transmitted via the faecal oral route
from contaminated water
mild self limiting illness usually but mortality rate (5%) associated with pregnant woman - hepatic encephalopathy and liver failure (20%)

28
Q

Obstetric cholestasis

epidemiology

A

0.5 - 1% pregnancy higher in Indian and Pakistani woman

29
Q

Obstetric cholestasis
Clinical presentation
Sx, Ix, progress
pathogenesis

A

Sx - puritis limbs and trunk, particulrly palms and soles, 80% after 30 weeks, insomnia, malaise, no rash, Abnormal LFTs, dark urine, anorexia, malabsorption, steatorrhoea,
(if hep C +ve often onset earlier - mean 29 weeks vs 34 weeks)
Rapid PN recovery within 48 hours
LFTs can take 4-6 weeks to recover
LFTs: moderate increase in transaminases, Raised ALP, 20% cases raised GGT, mild elevation in bilirubin, increase bile acids,
Puritis may preceed abnormal LFTs,

30
Q

Obstetric cholestasis
genetics
pathogenesis

A

Increase in circulating oestrogens
- affect sulphation of bile acids,
- affect bile acid acid transports within the hepatocytes,
- decrease in hepatocyte membrane fluiditiy
This occurs by a defect in methylation of the membrane phospholipids and a modification in the cholesterol to phospholipid ratio

35% +ve FH
autosomal dominant sex linked inheritance

31
Q

If a woman has +ve tests for obstetric cholestasis what other Ix need to be performed

A

Liver USS - GS
Viral serology - Hep B,C, A E EBV and CMV
Liver autoantibodies - anti smooth muscle antibody, chronic active hepatitis (CAH) anti mitochondrial antibodies, primary biliary cirrhosis

32
Q

Obstetric cholestasis
Risks to mum

Risks to baby

A

Mum:
Vit K deficiency - PPH
Baby: Intrapartum FD 22%, Mec 25-50%, PTB 25%, Fetal IC Haemorrhage + IUD 1.5% (2.5X increase)
IUD does not correlate with Sx or LFTs. perhaps with bile acids - bile acids are vasocontrictors and may affect placental perfusion, bile acids may cause arrhythmia.
Bile acids are in high concentraion in fetal blood + amniotic fluid
Falling perinatal mortality due to intervention
now 0-2% when del pre 38 weeks

33
Q

How to monitor + manage maternal and fetal wellbeing with obstetric cholestasis

A 
No correlation with dopplers / CTGs  
LFTs and Bile acids weekly 
PT pre delivery 
del 37-38 weeks (no increase in LSCS)
Neonatal Vit K
close labour monitoring
34
Q

Treatment for obstetric cholestasis + why / how we use them

A

Prolonged PT then vit K 10 mg orally daily (water soluable form)
UDCA - endogenous hydrophilic bile acid reducing the proportion of hydrophobic, hepatotoxic acids
1000-1500mg daily in 2-3 divided doses improves Sx and BA
For Sx chlorpheniramine 4mg tds or promethazine 25 mg nocte
dexamethasone is not recommended - suppresses oestrogen production in the placenta
rifampicin - anecdotal data only
cholestyramine - chelation - worsens VitK def

35
Q

recurrence obstetric cholestasis

A

90 % recurrence
Avoid OCP with oestrogen - POP has risk too so if used then should monitor LFTs
HRT is ok as replacing physiological levels

36
Q

Acute fatty liver of pregnancy

epidemiology and mortality

A

rare 1/10000
Primip
Male fetus 3:1, multiple pregnancy 20% of cases
2% maternal mortality and 10 % fetal mortality

37
Q

Acute fatty liver of pregnancy

clinical presentation

A 
After 30 weeks - ofter 35+
Gradual onset N and V - severe V 60% pain 60% 
often mild PET 
Jaundice and ascites within 2 weeks 
Abn LFTs 
Coagulopathy90%  (+/-normal platelets) 
AKI
Lactic acidosis 
develop fulminant liver failure and encephalopathy 
Hypoglycaemia  70% hyperuricaemia 90%
Features diabetes insipitus

Imaging - hepatic steatosis

38
Q

Genetic predisposition to HELLP + AFLP

A

woman - heterozygous for long chain 3-hydroxy- acyl-coenzyme A dehydrogenase LCHAD - disorder of mitochondrial fatty acid oxidation
Baby may be homozygous for BFatty acid oxidation disorders

39
Q

how does a liver biopsy differ between HELLP and AFLP

A

HELLP - hepatic cell necrosis and subcapsular haemorrhage

AFLP - microvesicular fatty infiltrates no increased inflammation

40
Q

Management AFLP

A 
Deliver
Coagulopathy - FFP and VIt K (10mg IV) 
Hypoglycaemia 10 or 50% glucose
Antibiotics as often associated with sepsis 
DI - desmopressin

Severity: PT, Gluose, pH, lactate, encephalopathy

Obstetrics (41 decks)

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