Hyperemesis Gravidarum
• It is the name given to severe nausea and vomiting that will cause weight loss, dehydration, acidosis due to fasting ketosis, alkalosis and hypokalemia due to HCl loss in pregnancy. It is thought that the formation of this clinical picture is caused by rapidly increasing chorionic gonadotropin or estrogen or both. It is less common in obese patients.
• Prerenal acute renal failure, Mallory Weiss tears, esophageal rupture, pneumothorax and pneumomediastinum have been reported in very severe cases. In many cases, it causes nutritional disorders and especially
Deficiency of both vitamins causes serious complications. Cases developing Wernicke's encephalopathy due to thiamine deficiency have been reported (E 11J. Cases of coagulopathy and epistaxis have also been reported due to vitamin K deficiency. K
Vitamin deficiency can cause embryopathy.
• Effective and safe first-line treatment in these cases is vitamin B6 + doxylamine. If this treatment fails, intravenous crystalloids should be added. Antiemetics (promethazine, chlorpromazine, prochlorperazine, metoclopramide) can also be used safely. There is no evidence to suggest that glucocorticoids are beneficial in hyperemesis gravidarum.
From Inflammatory Bowel Disease (Ulcerative Colitis, Crohn's Disease)
• Pregnancy does not increase the possibility of exacerbation of inflammatory bowel disease, but if there is an exacerbation, it is quite severe. Complications of preterm birth, low birth weight, IUGR and cesarean delivery are 1.5-2 times more common; however, there is no increase in perinatal mortality despite these complications.
Intestinal Obstruction
• Its incidence does not increase in pregnant women and the cause of more than 50% of the cases is adhesions due to previous pelvic surgeries (including cesarean section). Maternal mortality (6%) and fetal mortality (26%) rates are quite high in these cases due to the late diagnosis of the picture.
Appendicitis
• Suspicion of appendicitis is one of the leading reasons for performing laparotomy during pregnancy. However, it is difficult to diagnose appendicitis in case of pregnancy, and therefore, delay in cases causes more rupture of appendicitis and more generalized peritonitis in pregnant women.
Intrahepatic Cholestasis
• The exact cause of obstetric cholestasis is unknown; however, whatever the reason is, bile acids cannot be completely cleared and increase in plasma. Bilirubin and alkaline phosphatase levels are also elevated. In most of the patients, the complaint of itching starts in the following weeks of pregnancy. Jaundice can be seen in 10% of cases.
• Measurement of fasting serum bile acid level is used in the diagnosis (normal level
< 10µmol/L). Elevated AST and ALT levels may also accompany.
• The cause of itching is increased bile acids. Antihistamines are sufficient for this. Cholestyramine is also effective in 50-70% of cases; however, since it reduces the absorption of the fat-soluble vitamin, the already decreased vitamin K may be further reduced with this drug and bleeding may occur (it may lead to fetal coagulopathy and intracranial hemorrhage). Ursodeoxycholic acid relieves itching immediately and also lowers serum transaminases.
• 38-39. week of birth should be considered.
Acute Fatty Liver
• It is the most common cause of acute liver failure during pregnancy. The main causes are fulminant viral hepatitis, drug toxicity and acute fatty liver disease of pregnancy.
• In acute fatty liver, the picture almost always becomes evident in the later stages of pregnancy (usually the third trimester). The disease is more common in nulliparous and pregnant women with male fetuses. 15% of cases occur in multiple pregnancies.
• The picture is very similar to preeclampsia. It presents with fatigue, anorexia, nausea, vomiting, polyuria/polydipsia, epigastric pain, and progressive jaundice. Persistent vomiting is the major finding in most patients. Hypoglycemia, leukocytosis, increase in urea and creatinine levels, increase in transaminases, ascites, encephalopathy and coagulopathy (PT and aPTT prolong, fibrin degradation products and D-Dimer increase) can be added to the picture. Fetal mortality is 10%-1S.
• Emergency delivery should be planned for treatment. Liver functions improve rapidly with birth and the picture improves.
The most useful laboratory test in distinguishing HELLP Syndrome from acute fatty liver of pregnancy is blood glucose measurement (N-17).
Viral Hepatitis
• Hepatitis A: The clinic of hepatitis A is not exacerbated during pregnancy. Hepatitis A virus is not teratogenic and there is no transplecental transmission to the fetus.
• Hepatitis B: The clinic of hepatitis B is not exacerbated during pregnancy. Transplacental transmission of the virus is very rare and the main transmission occurs during breastfeeding.
• Hepatitis C: The clinic of hepatitis C during pregnancy is not exacerbated and does not cause perinatal complications. However, the most important thing is that hepatitis C can be transmitted vertically to the fetus (3-6%). Prenatal screening for hepatitis C is not recommended, as there is currently no method to prevent the transmission of hepatitis C to the fetus.
• Hepatitis E: Hepatitis E progresses more severely during pregnancy . The disease can be transmitted to the fetus transplacental at a high rate.
Cholelithiasis and Cholecystitis
• In pregnancy i. After the third trimester, the volume of the gallbladder is fasting and following a meal.
doubles after contraction. Incomplete emptying of the gallbladder leads to the accumulation of cholesterol crystals and the formation of cholesterol stones. Acute cholecystitis in pregnancy occurs due to these gallstones and surgical treatment may be required.
pancreatitis
• While acute pancreatitis develops as a result of 45% gallstones and 35% alcohol use in non-pregnant women; gallstones in pregnancy are almost always the only cause . The accompanying hypocalcemia, hypovolemia, hypoxia and acidosis in the cases cause high fetal loss. The risk of fetal mortality and preeclampsia increases in acute pancreatitis.