INTRODUCTION

Injury or illness to an expectant mother can affect the developing brain in the
fetus during pregnancy. Heredity are continually examining the role of
heredity and genetics in the development of seizure disorders. It might help to
keep a diary and keep track of events, this may help show a pattern which
may pinpoint an avoidable cause.
➢Infections illnesses.
➢Fever.
➢Fatigue.
➢Low blood sugar due to poor diet.
➢Stress or anxiety.
➢Insomnia.
➢Alcoholism and drug abuse.
➢Uncommon medicines, anti–depressants, anti–psychotic medication.

DEFINITION.
Epilepsy can be defined as a group of disorders characterized by abnormal
electrical activity in the brain leading to altered behavior which may manifest
as a change in a person’s consciousness, movement, or actions. These
physical changes are called epileptic seizures.Epilepsy is therefore sometimes
called a seizure disorder.
CAUSES OF EPILEPSY

Head injury: People who sustain a head injury as a result of an automobile

accident, sports injury, fall, or act of violence may develop epilepsy.

Birth trauma: Infants who suffer a lack of oxygen during birth may develop
resulting damage to the brain’s electrical system.

Poisoning: Lead poisoning has been associated with the development of

epilepsy.

Infection: Infections that can affect the brain like meningitis, viral encephalitis,
mumps, measles, and diphtheria can result in epilepsy

CLINICAL MANIFESTATIONS

➢Blunt trauma

➢Miscarriage

➢Premature rupture of membranes

➢Placental abruption.

➢The indicates that antiepileptic drug(AED) used to treat epilepsy are the major
cause of foetal defects like clept lip and palate ,cardiac defects and neural
tube defects.
EFFECTS OF EPILEPSY ON PREGNANCY
Incidence of fetal malformations,IUGR, oligohydramnios and still births is
increased.Birth defects are increased by two fold.This could be related to the
severity of the disease with its genetic predilection and also due to the
hazards of anticonvulsants used.All the drugs are implicated,maximum with
phenytoin and least with carbamazepine.The malformations include-cleftlip
and/or plate,mental retardation,cardiac abnormalities,limb defects and
hypoplasia of the terminal phalanges.Sodium valproate is associated with
neural tube defects.There is chance of neonatal haemorrhage and is related to
anticonvulsant induced vitamin k dependent coagulopathy.

MANAGEMENT :
The dose of the drug should be kept as low as possible and to be monitored
regularly from the serum level. The commonly used drugs are:

• Phenobarbitone 60-180 mg daily in 2-3 divided doses.

• Phenytoin 150-300 mg daily in two divided doses.
• Carbamazepine 0.8-1.2mg daily in divided doses.
• The fits are controlled by intravenous diazepam 10-20 mg.
• Folic acid 1 mg must be continued throughout pregnancy.
• And beginning 36 weeks many physician prescribe vitamin K 10mg
supplementation because AED therapy can lead to vitamin K –deficient
hemorrhage of the newborn.termination of pregnancy may have to be
considered in consultation with a neurologist.
• There is no contraindication for breast feeding.The infant may be
drowsy.Readjustment of the anticonvulsant dosage is necessary and to
bring down the dose to the pre-pregnant level by 4-6 weeks
postpartum.Steroidal contraceptives are better to be avoided due to
hepatic microsomal enzyme induction.

HEPATIC NECROSIS
 Acute viral hepatitis is the most common cause of jaundice in pregnancy. The
course of acute hepatitis is unaffected by pregnancy, except in patients with
hepatitis E and disseminated herpes simplex infections, in which maternal and
fetal mortality rates are significantly increased. Chronic hepatitis B or C
infections may be transmitted to neonates; however, hepatitis B virus
transmission is effectively prevented with perinatal hepatitis B vaccination and
prophylaxis with hepatitis B immune globulin. Cholelithiasis occurs of
pregnancies; complications can safely be treated with surgery. Women with
chronic liver disease or cirrhosis exhibit a higher risk of fetal loss during
pregnancy. Preeclampsia is associated with HELLP syndrome, acute fatty liver
of pregnancy, and hepatic infarction and rupture. These rare diseases result in
increased maternal and fetal mortality. Treatment involves prompt delivery,
whereupon the liver disease quickly reverses. Therapy with penicillamine,
trientine, prednisone or azathioprine can be safely continued during
pregnancy.

PREGNANCY AND HEPATITIS

ACUTE VIRAL HEPATITIS

Viral hepatitis is the most common cause of jaundice in pregnancy.The course
of most viral hepatitis infections (e.g., hepatitis A, B, C and D) is unaltered by
pregnancy. However, a more severe course of viral hepatitis in pregnancy has
been noted in patients with hepatitis E and disseminated herpes simplex virus
(HSV) infections.

• Hepatitis E is a waterborne virus spread through fecal-oral transmission.

Infection occurs most commonly in developing countries after flooding.
Pregnant women with hepatitis E infection exhibit markedly increased fatality
rates
• Disseminated HSV infection is associated
with prodromal systemic illness, vesicular skin rash and leukopenia. Maternal
and fetal mortality rates reach without treatment. Acyclovir (Zovirax)
effectively treats early disseminated HSV infection.
HEPATITIS D
It is seen in patients infected with HBV either as a co-infection .Perinatal
transmission is known.Neonatal immunoprophylaxis for HBV is almost
effective against HDV.
HEPATITIS B VIRUS

Pregnant women who are hepatitis B surface antigen (HBsAg)-positive deliver

annually. Universal screening of pregnant women for HBsAg is now performed
to reduce perinatal transmission of hepatitis B virus. It is transmitted by
 parenteral route, sexual contact,vertical transmission and also through breast
milk..The risk of hepatitis B virus transmission to the fetus is proportional to
maternal hepatitis B virus DNA, as reflected in hepatitis B antigen (HBeAg)
and antibody (HBeAb) status.The risk of hepatitis B virus vertical transmission
in mothers with negative HBeAg and positive HBeAb and those with positive
HBeAg. The risk of chronic hepatitis B virus infection in a neonate who does
not receive immunoprophylaxis and vaccination for hepatitis B virus.

• Infants of HBsAg-positive mothers should receive hepatitis B immune globulin

immunoprophylaxis at birth and hepatitis B vaccine at one week, one month
and six months after birth. This regimen reduces the incidence of hepatitis B
virus vertical transmission to zero to 3 percent.
• In cases of acute hepatitis B virus infection complicating pregnancy, the
prevalence of neonatal infection depends on the time during gestation that
maternal infection occurs.Neonatal hepatitis B virus infection is rare if
maternal infection takes place in the first trimester. The infection occurs of
neonates of women infected in the second trimester, of those infected in the
third trimester and in virtually all of those infected in the immediate
postpartum period. Neonates of mothers experiencing acute hepatitis B virus
infection should receive immunoprophylaxis and vaccination.

HEPATITIS C VIRUS
Chronic hepatitis C virus infection is rising most rapidly among persons 20 to
45 years of age. Therefore, an increasing number of patients with hepatitis C
virus infection are requesting information about vertical transmission of the
virus during pregnancy.

• Patients with risk factors for hepatitis C virus infection, such as intravenous
drug use or other parenteral exposures, should undergo screening for
hepatitis C virus infection before pregnancy with second- or third-generation
hepatitis C virus antibody assays to confirm exposure to the virus. Women
with documented hepatitis C virus infection who are contemplating pregnancy
should be encouraged to undergo human immunodeficiency virus (HIV) testing
and repeated quantitative hepatitis C virus RNA measurements to determine
their probable risk of hepatitis C virus vertical transmission.
• Vertical transmission of the virus occur in two of three infants of mothers with
acute hepatitis C virus infection, suggesting a higher risk of vertical
transmission than occurs in patients with chronic infection, secondary to the
high levels of hepatitis C virus RNA that occur in acute infection. Interferon
therapy should not be administered during pregnancy because of its possible
adverse effects on the fetus.
 HEPATITIS D:
It is seen in patients infected with HBV either co- infection.Perinatal
transmission is known.Neonatal immunoprophylaxis for HBV is almost
effective against HDV.

CHOLELITHIASIS IN PREGNANcy Pregnancy-induced changes in bile

composition predispose these patients to cholelithiasis. The bile salt pool
decreases in the second trimester, and biliary cholesterol levels may increase,
resulting in lithogenic bile .In addition, gallbladder emptying slows in the
second trimester, increasing the risk of cholelithiasis.

SIGN & SYMPTOMS

➢ Fullness abdominal distension,

➢ Vague pain in the right upper quadrant of the abdomen .
➢ The distress may follow a meal rich in fried foods.

DIAGNOSIS

➢ Leukocytosis and mild to moderate elevations of transaminase and bilirubin

levels.
➢ The alkaline phosphatase level progressively increases during normal
pregnancy and is unhelpful in distinguishing hepatobiliary disease.
➢ A liver ultrasound examination is most helpful in determining the presence of
cholelithiasis.

MANAGEMENT

➢ Surgical treatment (i.e., laparoscopic cholecystectomy) of biliary colic can be

safely accomplished in the first or second trimester. As the uterus enlarges,
surgery becomes more difficult and should be avoided during the third
trimester.
➢ Surgical emergencies were attributable to biliary tract disease.
Choledocholithiasis accounts for patients with jaundice in pregnancy. Of
patients presenting with pancreatitis during pregnancy, have
choledocholithiasis. Gallstone pancreatitis is associated with maternal
mortality rate and fetal mortality rate. One group of investigatorsreported
safely performing endoscopic retrograde cholangiopancreatography and
endoscopic retrograde sphincterotomy without complications in five pregnant
women (in the second and third trimesters) with choledocholithiasis using
 minimal fluoroscopy and lead aprons to shield the abdomen. All of the women
delivered healthy babies at term.

PREGNANCY-SPECIFIC LIVER DISEASE

INTRAHEPATIC CHOLESTASIS OF PREGNANCY

Intrahepatic cholestasis of pregnancy occurs of pregnancies. It typically arises
in the third trimester of pregnancy, although it has been reported as early as
13 weeks' gestation..Pruritus alone occurs of patients; pruritus and jaundice
develop of patients. . Intrahepatic cholestasis complicates of pregnancies but
disease is rare in black patients

DIAGNOSIS

Bilirubin level less than 5 mg per dL (85.5 µmol per L), minimal or no elevation
in transaminase, cholesterol and triglyceride levels, and infrequent, mild to
moderate steatorrhea. Liver histopathology reveals centrilobular bile stasis.
Intrahepatic cholestasis of pregnancy is associated incidence of prematurity, a
incidence of fetal distress and an increased perinatal mortality rate

MANAGEMENT

• Multiple medications have been tried as treatments for cholestasis of

pregnancy. Parenteral vitamin K (phytonadione; AquaMephyton)
supplementation is advocated in patients with prolonged cholestasis
(secondary to malabsorption of this fat-soluble vitamin). Ursodeoxycholic acid
(Actigall), given at dosages of 15 mg per kg per day, has been the most
successful therapy for cholestasis of pregnancy, as it ameliorates both the
pruritus and liver function abnormalities and is well-tolerated by both mother
and fetus. Ursodeoxycholic acid has been proved safe in trials of cholestatic
liver disease in infants, children and adults. However, in pregnant patients
with cholestatic liver disease, the pruritus can be severely disabling, and
ursodeoxycholic acid therapy provides safe and effective relief.
• Cholestyramine (Questran) binds bile acids and may improve pruritus;
however, it may exacerbate steatorrhea and does not alter liver function or
fetal prognosis. Phenobarbital has not been shown to improve pruritus or alter
liver tests and may cause neonatal respiratory depression.
• Patients exhibiting cholestasis of pregnancy should receive close fetal
surveillance at delivery.Symptoms of cholestasis usually resolve within two
days of delivery. Elevated serum bilirubin and alkaline phosphatase levels
return to normal four to six weeks after delivery3
 PREECLAMPSIA

Hepatic dysfunction with preeclampsia associated with other findings in the

HELLP syndrome. The haemolysis (H), elevated liver enzymes (EL) and low
platelets (LP) syndrome is a severe form of preeclampsia that threatens the
patient and her fetus. Pre-eclampsia associated with microthrombi,
thrombocytopaenia, coagulopathy and a poor prognosis. It may appear from
mid-second trimester until several days postpartum.

SIGN & SYMPTOMS

Right upper quadrant pain

Malaise.
Weight gain or edema;
Nausea or emesis.

DIAGNOSIS

• Notable hepatic abnormalities in the HELLP syndrome include hemolysis (with

elevated bilirubin levels and lactate dehydrogenase levels greater than 600 IU
per L), moderately elevated transaminase levels (AST and ALT levels of 200 to
700 IU per L) and a platelet count less than 100,000 per mL (100 × 109 per L).
No correlation has been noted between extent of hypertension, liver function
test abnormalities or liver biopsy findings.

MANAGEMENT

• The most effective treatment for HELLP syndrome is prompt delivery

Postpartum corticosteroids have proved efficacious in improving maternal
platelet counts, ALT levels and blood pressure. Caesarean section is the most
common mode of delivery.Therapies that have not proved efficacious include
plasmapheresisantithrombotic agents and immunosuppression

ACUTE FATTY LIVER OF PREGNANCY

Acute fatty liver of pregnancy is a rare but dangerous disorder .It is most
frequently complicates the third trimester and is commonly associated with
preeclampsia.

DEFINITION

Acute fatty liver of pregnancy may be defined as acute liver failure with
reduced hepatic metabolic

capacity in the absence of other causes.

CLINICAL FEATURES:
➢Anorexia,
➢Nausea, emesis,
➢Abdominal pain,
➢Jaundice,
➢Headache and
➢Central nervous system disturbances.

DIAGNOSIS

Raised transaminases:Typically 3 -10 times the upper limit to

normal,transaminase levels above 1000 iµ/L may occur with hepatic ischemia.
Hyperbilirubinemia
Hypoglycaemia
Hyperuricemia
Prolonged prothrombin time.

MANAGEMENT

• All vital signs should be measured and recorded clearly on a 24 hour.

• Glucose assessments should be made atleast every 2 hours and
hypoglycaemia treated with large doses of high concentration intravenous
glucose.PTT should be measures every 6 hours along with LFTs, RFT and
electrolytes and full blood count.
• Some children of mothers with acute fatty liver of pregnancy have been noted
to express homozygous deficiency of long-chain 3-hydroxyacyl-CoA
dehydrogenase, resulting in severe metabolic and neurologic consequences to
the infants.Their mothers were found to exhibit a heterozygous deficiency of
long-chain 3-hydroxyacyl-CoA dehydrogenase, contributing to acute fatty liver
of pregnancy.The treatment of acute fatty liver of pregnancy is expeditious
delivery and intensive care. Patients usually improve promptly following
delivery and, in the absence of long-chain 3-hydroxyacyl-CoA dehydrogenase
deficiency, the prognosis in pregnancies following acute fatty liver of
pregnancy is good.

HEPATIC RUPTURE AND INFARCTION

Hepatic rupture and infarction, extremely rare complications of preeclamptic
liver disease, usually occur in the third trimester.Older multigravida mothers
with preeclampsia (75 to 85 percent) are at higher risk. Less commonly,
hepatic rupture complicates growth of hepatic adenomata or other masses
during pregnancy. Hepatic rupture most commonly involves the right lobe.It is
believed to be a continuum of preeclampsia, in which areas of coalescing
hemorrhage result in thinning of the capsule and intraperitoneal hemorrhage.
SIGN AND SYMPTOMS

• Patients with hepatic rupture typically present in shock, with preceding right
upper quadrant pain,
• Hypertension,
• Elevated transaminase levels (greater than 1,000 IU per L) and coagulopathy.

DIAGNOSIS

Hepatic infarction is best detected by using computed tomographic scans or

magnetic resonance imaging.Patients typically present with fever and marked
elevations in transaminase levels.

TREATMENT

Therapy for hepatic rupture has included transfusion of blood products and
intravenous fluids, surgical evacuation and arterial embolization. These
therapies have met with only moderate success; a 59 to 70 percent maternal
mortality rate and a 75 percent perinatal mortality rate have been noted in
hepatic rupture.
COMPLICATION
Hepatic rupture include hepatic abscess formation and pleural effusions.

CHRONIC LIVER DISEASE

An increased risk of fetal loss has been noted in pregnant patients with
chronic liver disease. Therapy with penicillamine (Cuprimine), trientine
(Syprine), prednisone or azathioprine (Imuran) can be safely continued during
pregnancy in patients with Wilson's disease or autoimmune hepatitis.In
patients with primary biliary cirrhosis, ursodeoxycholic acid therapy can be
safely continued. In patients with chronic hepatitis B or C infection, interferon
therapy should be discontinued during pregnancy, as its effects on the fetus
are

• A marked reduction in fertility has been noted in cirrhotic patients.Cholestasis

may worsen during pregnancy in patients with primary biliary cirrhosis. Infants
of patients with marked hyperbilirubinemia during pregnancy may require
exchange transfusion at birth.
SUBMITTED TO: MRS SUNDARAM

HOD OBG NURSING DEPARTMENT

P.I.O.N

SUBMITTED BY: MS DIMSEY.R.MARAK

MSC NURSING 1ST YEAR

P.I.O.N