This action might not be possible to undo. Are you sure you want to continue?
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.
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
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue listening from where you left off, or restart the preview.