Liver and GIT disorders in pregnancy
‫ بتول عبد الواحد هاشم‬0‫د‬
Physiological changes in pregnancy:
Pregnancy causes decreased lower esophageal pressure,
Decreased gastric peristalsis and delayed gastric emptying,
Gastrointestinal motility is reduced,
Increased small bowel and large bowel transit times.
There is 20- 40% fall in serum albumin concentration, partly due to dilution resulting from
the increase in total blood volume,
Total serum protein concentration also decreases
Alkaline phosphatase concentration more than doubles due to production by the placenta,
which increases with gestation.
Level of alanine transaminases(ALT), serum glutamic pyruvic transaminase(SGPT),
aspartamine transaminase(AST), and serum glutamic-oxaloacetic transaminase(SGOT) fall,
and there is a fall in the upper limit of the normal ranges for both enzymes.
Nausea, vomiting, and hyperemesis
Nausea and vomiting are common symptoms in early pregnancy, affecting over 50% of
pregnant women.
The onset is at around 5-6 weeks' gestation.
Hyperemesis occur if the woman is unable to maintain adequate hydration and nutrition,
either because of severity or duration of symptoms, it's less common in incidence, and can
be dangerous if inadequately or inappropriately treated.
It's associated with marked weight loss, muscle wasting, ketonuria, dehydration and
electrolytes disturbance, including hypokalemia, and a metabolic hypochloremic alkalosis.
Ptyalism-inability to swallow saliva- is common,
Complications of hyperemesis gravidarum include:
Fetal growth restriction, maternal hyponatremia leading to central pontine myelinolysis,
and thiamine deficiency leading to Wernick's encephalopathy.
Markers of severity
Weight loss>10%
Abnormal thyroid function tests ( raised freeT4 and suppressed TSH),
Abnormal liver function tests with raised transaminases.
Management:
Other possible causes of nausea and vomiting should be excluded.
UTI
Thyrotoxicosis
Cholestasis
Ultrasound is needed to exclude H. mole and multiple pregnancy (both of which increase the
risk of hyperemesis gravidarum)
Treatment is to ensure adequate rehydration. This should be with normal saline with added
potassium chloride sufficient to correct tachycardia, hypotension and ketonuria, and to
return electrolyte level to normal.
Dextrose- containing fluids are to be avoided, high concentration of dextrose in particular
may precipitate Wernicke's encephalopathy, this is prevented by routine administration of
oral or intravenous thiamine.
Antiemetics may be liberally and safely used in pregnancy.
Trial of corticosteroids may be considered in severe cases unresponsive to conventional
treatment.
Gastroesophageal reflux:
2/3 of women experience heartburn in pregnancy, commonly in the 3rd TMS
Management
Postural changes such as sleeping in semi recombent position, especially in late pregnancy
Avoid food or fluid intake immediately before retiring
Antiacids are safe, liquid preparations are more effective
Metoclopramide, sucralfate, and histamine2-receptor blocker are safe in pregnancy
Omeprazo a proton pump inhibitor appear to be safe from limited data.
Peptic ulcer:
Is rare in pregnancy due to prostaglandins induced by pregnancy which have a protective
effect on gastric mucosa, gastrointestinal endoscopy is safe in pregnancy.
Management
Helicobacter pylori has causal role but eradication therapy is usually deferred until after
delivery, misoprostol protects the gastric mucosa but is contraindicated during pregnancy.
Inflammatory bowel disease(IBD)
Both Crohn's and ulcerative colitis tend to present in young adulthood.
Ulcerative colitis is more common in women and is more commonly encountered during
pregnancy.
The course of IBD is not usually affected by pregnancy
The risk of flare in pregnancy is reduced if colitis is quiescent at the time of conception
Most exacerbations occur early in pregnancy and cause abdominal pain, diarrhea and
passage of rectal mucus and blood
Women with Crohn's disease may experience postpartum flare.
Pregnancy outcome is usually good in women with IBD
Active disease at time of conception is associated with an increased risk of miscarriage,
active disease late in pregnancy increase rate of prematurity
Prior surgery for IBD does not preclude successful pregnancy.
management
encourage pregnancy during periods of disease remission
oral or rectal sulfasalazine, mesalazine and other 5- aminosalicylic acid may be safely used
throughout pregnancy and breastfeeding, 5 mg folic acid supplement should be used
preconceptually and in pregnancy to reduce the incidence of neural tube defects,
cardiovascular defects, oral clefts and folate deficiency.
Oral or rectal corticosteroids for acute treatment or maintenance and are safe in pregnancy.
Azathioprine may be needed to maintain remission and this should be continued in
pregnancy.
Be aware of the possible surgical complications of IBD (intestinal obstruction, haemorrhage,
perforation or toxic megacolon)
Cesarian section is indicated in presence of severe perianal Crohns disease with deformed,
inelastic or scarred rectum.
Acute and chronic viral hepatitis
The course of most viral hepatitis is not altered by pregnancy. Pregnant women may
contract acute hepatitis in the same way and with the same clinical features as non pregnant
women.
Hepatitis A
Presentation and diagnosis
In adults clinical manifestations can vary from mild non specific to fulminant hepatic failure
Raised serum alanine transaminase indicate acute hepatic injury
Serology show presence of antihepatitis A IgM
Management
Supportive, complete recovery is the usual outcome
Human serum immunoglobuline protects against hepatitis A, protection is short lived and
injections need to be repeated every 3-6 mo. Vaccine give up to 10 years protection.
The safety of hepatitis A vaccine in pregnancy has not been determined, although the
theoretical risk to the fetus of inactivated vaccine is low, there are no long term fetal
consequences of fetal hepatitis infection.
Hepatitis B
A blood born, double-stranded DNA virus, has three major structural antigens:
(HBsAg), (HBcAg), (HBeAg)
non specific hematological tests commonly show lecopenia, may show anemia,
thrombocytopenia
diagnosis
by the presence of HBsAg, the presence of HBeAg shows the disease is active with viral
shedding into the blood stream, antibodies to e begin to appear in the serum at the time
Hbe Ag is disappearing , the presence of the e antigen indicates a period of high patient
infectivity, and the presence of e antibodies indicates low infectivity.complete resolution of
disease is indicated by presence of surface Abs, and disappearance of HBsAg.
Management:
Antepartum :
All women are routinely offered testing forHB antibodies at their antenatal booking visit
It test positive the infectivity should be ascertained by serology
Testing for other sexually transmitted disease HIV
Intrapartum:
Fetal scalp electrodes and fetal blood samling should be avoided
The use of forcepse rather than ventouse is preferred for instrumental delivery
Postpartum:
Neonates infected at birth have > 90% chance of becoming chronic carriers of hepatitis B
virus, with associated risk of subsequent cirrhosis and hepatocellular carcinoma
Management plan should thus include administration of passive immunoglobulin in the
1st24hr after birth to the newborns of mother with high infectivity.
And administration of the active hepatitis B vaccine to neonates whos mothers have low
infectivity.
Obstetric cholestasis:
Is a liver disease specific to pregnancy, characterized by pruritus mainly on palms and the
soles, and abnormal liver function
It's more common in women from south America, Indian subcontinents, and Finland.
Aetiology is unknown, but relates to genetic predisposition(1/3 of patients have positive
family history) to the cholestatic effect of estrogen
It usually presents in the 3rd trimester at around 30-32 wks of pregnancy
diagnosis (is by exclusion)
hepatic transaminases(ALT,AST) are only mildly elevated, raised bile acid, liver US, serology
for viral hepatitis,Ebstien –Bar virus, CMV and liver autoantibodies.
differential diagnosis
extrahepatic obstruction with gallstone
viral hepatitis
primary billiary cirrhosis(PBC)
chronic active hepatitis(CAH)
complications
postpartum haemorrhage(vit K deficiency –fat malabsorption-)
premature labour
meconium stained liquor
fetal distress
intrauterine fetal death
management
counseling the mother regarding the risks
regular monitoring of liver function tests and clotting times
delivery should be induced at 37-38 wks
vit K 10 mg orally daily once the condition is diagnosed
fetal surveillance with CTG and US
symptoms control with antihistamines and emollients
ursodeoxycholic acid(UDCA) lead to rapid reduction in pruritus and liver function but not the
fetal risk.
There is no long term detrimental effect on maternal health, but symptoms might recur with
combined oral contraceptives so they should be avoided
Recurrence in subsequent pregnancy is >90%.
Acute fatty liver of pregnancy:
A pregnancy-specific liver disease, usually presents in the 3rd TMS with abdominal pain,
nausea, vomiting, anorexia and sometimes jaundice.markedly deranged liver function, renal
impairment,markedly elevated uric acid, raised WBCs, hypoglycemia,and coagulopathy.
Perinatal and maternal mortality and morbidity are increased.
Management
Intensive care unit and multidisciplinary team, delivery should be expedited after correction
of hypoglycemia and coagulopathy( with 50%dextrose, FFP, and IM vitK), management after
delivery is conservative.