liver disorder in pregnancy

Liver disorders in pregnancy

Hepatic physiology , anatomy and histology in pregnancy

Physiological changes in LFT:

TSB , transaminases (SGOT,SGPT), PT : unchanged
Protiens : total serum protien decreased in first trimester,
Albumin , globulin , fibrinogen increased until term
:Lipids: cholesterol , TG increased , enzymes e.g alkaline phos. Increased.

Anatomy:

Liver anatomical relation not changed in first and second trimester .in the third trimester liver occupied more posterosuperior position with decreased in liver dullness(palpable liver in pregnant female=diseased liver).

Histology :

Non specific changes , dilation of bile ducts.

Jaundice in pregnancy:

incidence:1/2000
It is divided :
1:disorders specific to pregnancy :
less than 10% of jaundice in preg.it includes :
a:hyperemesis gravidarum
b:PE/eclamptic liver disease
C:intrahepatic cholestasis of pregnancy.
D:acute fatty liver of pregnancy.


2:disorders incidental to pregnancy.
A:viral hepatitis
B:fulminant hepatic failure.
C:cirrhosis.

Hyperemesis gravidarum : jaundice due to HEG now is very rare and it is due to severe malnutrition ,severe protien deficiency .

Pre-eclampsia and eclamptic liver disease :

Liver is the target organ for severe PE and eclampsia ,it is not involve in the primary process of the disease .in severe PE there is diffuse arterial spasm , necrosis , thrombosis of portal venules and hepatic artery radicles .in more advanced cases---liver necrosis and haemorrhage..

c/f :

There is obvious increase in BP + proteinuria with epigastric and right hypochondrial pain (due to focal hepatic bleeding +stretching of liver capsule).more commonly pt. present with no symptoms related to liver but only abnormal LFT.
Commonly pre-eclamptic liver is accompanied with thrombocytopenia , haemolysis forming HEELP SYNDROME
Hepatic failure and encephalopathy are not usual feature of PE liver disease.

IX:
Modest increase in transaminase
TSB (2-4 mg/dl)
Renal u/s
Lipids
s.Creatinine
Maternal risk ; subcapsular haematoma,liver rupture ,coagulopathy.
Fetal risk; IUGR ,fetal distress ,placental abruption
Treatment:termination of pregnancy without delay.VD is the safest option


Intrahepatic cholestasis of preg.(IHC) :
It is a liver disease specific to preg,the aetiology is unknown but related to a genetic prediposition s (1/3 of the patient have +ve family HX) to cholestatic effect of oestrogen. The ostrogen induce stagnation or stasis of bile in the intrahepatic ducts.

c/f :

Idiopathic condition with adverse effect that resolve only after delivery .the symtoms usually start in the third trimester as generalized pruritis Which is the dominant feature (scratch skin changes but no dermatological or skin lesions). started 1-2 WKs prior to the jaundice in otherwise healthy mother .it may recur in the next pregnancy or when she use OCP.

Ix :

TSB INCREASE rarely above 4-5mg/dl
Alk.phos.markedly increase
Marginal increase in SGOT,SGPT
u/S TO exclude extrahepatic causes
Icrease uric acid

Prognosis :

Generally benign condition for the mother and the fetus
Fetal complication :increase PTL (40%),increase intrapartum asphyxia and distress.
Increase meconium stained liquor (40%)due to retention of bile acids.

Treatment :

1 - is induction of labor as soon as lung maturity achieved .
Maternal risk ; increase PPh due to vit.k malabsorption so female need vit .k injection during labor and postparum period.
2 - Pruritis treated with oral antihistamine , cholestyramine , dexamethasone


Management of IHC
PRE-PREGNANCY :
Recur in 75% at the same age or earlier-
Serial u/s for fetal monitoring -
Vit k 10mg/day from 36wks -
Anticipate PTL-
Delivery at 37-38 wks-

Post –natal

-Pruritis subsided 4 days-2wks after delivery
If not resolve after 8wks-----consider liver biopsy
-Avoid oestrogen containing OCP.

ACUTE FATTY LIVER OF PREGNANCY(AFLP) :

It is arare disorder cc by microvesicular stasis on liver histology. it is induced by preg. and returns to normal after delivery. usually appear in the third trimester and may proceed to hepatic failure with high maternal mortality.
Incidence:1/10000 .

There is considerable overlap between AFLP , SEVERE

PE,AND HEELP.(ALL TREATED BY TERMINATION OF PREGNANCY)
Maternal risk is high from hepatic encephalopathy, GIT bleeding , pph ,DIC and sepsis.
Early DX is essential for salvage of the mother and fetus.


C/F :
Vomiting in the third trimester associated with systemic illness(tiredness ,upper abd. pain for few days or wks followed by jaundice. ,with drowsiness Mental state changes , hypoglycemia is frequently present due to liver failure.

IX :

Liver enz. moderatlly increase ,BLOOD FILM(leukoerythroblastic picture).hypoglycemia ,very high serum uric acid
u/s fatty infiltration of the liver
IUFD IS HIGH 85%
TREATMENT:
urgent delivery no role for conservative measures once the DX is suspected after maternal resuscitation , VD is preferable.
Recurence rate 10-20%.

. . .THE END. . .

By :
taher ali taher