St. Luke’s College of Medicine-William H. Quasha Memorial
Batch 2012
Lecture trans + Recording
OB Block 4
Hyperemesis Gravidarum
Severe vomiting
Gastrointestinal Disorders in Pregnancy
Gastrointestinal Disorders in Pregnancy
Hyperemesis gravidarum
Peptic ulcer
Constipation
Intestinal obstruction
Appendicitis
Obesity
Intrahepatic cholestasis
Preeclampsia- eclampsia
Viral hepatitis
Cirrhosis
Acetaminophen overdosage
Cholelithiasis/cystitis
Pancreatitis
– weight loss, dehydration, acidosis from starvation, alkalosis (loss of HCl) and hypokalemia
Due to high level of HCG or estrogens
Remind your patient that this is something temporary
Somehow has familial clustering – blame the
HCG; HCG peaks at the 8-10 th week = peak of hyperemesis gravidarum
This will wean off slowly
Vomiting may persist in the 14-16 th wk
Teach the patient to look for the food that are acceptable; sometimes pregnant women don’t like sautéed food, (haha) and odor of husband
Food – ice chips, chichirya, soup, ice cream, champoy – finding the food that will alleviate her
Christine Fernando- Palma MD
November 5, 2009
Peptic Ulcer
Young women: usually involves duodenum rather than stomach
Caused by Helicobacter pylori o Aspirin, NSAIDS use
Peptic Ulcer and Pregnancy o Peptic ulcer 90% remission o Normal pregnancy change
Dec gastric secretion
Dec motility
Inc mucus secretion o So ulcer is not frequently seen in pregnancy, so it’s said that the hyperacidity that is felt by the patient is due to his hyperemesis gravidarum o Antacids: 1 st line treatment o H2 receptor blocker o Proton pump inhibitors: not recommended
Constipation and Pregnancy
Decreased small bowel motility – she still feels
that there’s food in the stomach
Colon has increased muscular relaxation – increased absorption of water and sodium
( feces becomes harder and dehydrated)
Prevented by high fiber diet and bulk forming laxatives
Intestinal Obstruction
60-70% due to adhesions from previous abdominal surgery; 2 nd is volvulus ( intestine from her desire to vomit
She will feel nauseated, the first three months, the ideal weight gain is 2 pounds – so she doesn’t have to force herself to eat ( because some pregnant women feel guilty that they are not eating)
so they push themselves to eat and vomit some more; but during the time that they are vomiting, they just have to rest their bowels, NPO
Advice: small frequent meals
However, if there’s severe dehydration IV crystalloid for hydration and correct electrolyte deficits
Antiemetics: Promethazine, Prochlorperazine,
Chlorpromazine, Metoclopramide IV;
Metoclopramide locally available- apparently, no known ill effect
Heartburn
Retrosternal burning sensation – felt during the
13-35 th wk – because of the increase in the size of the uterus, the acid in the stomach will reflux back
Gastroesophageal reflux
Raise head of bed
Tx: oral antacids; milk – to buffer the acidity
H2 receptor antagonists: Cimetidine (Tagemet) and Ranitidine (Zantac); previously thought to be not safe for the pregnancy, but now it may be used (probably also because they usually have
GERD sa 3 rd trim na, tapos na ang organogenesis) twists on itself)
Pressure of growing uterus on intestinal adhesion intestinal obstruction
Dx: plain abdomen : fluid air-levels and dilated bowel loops
-High maternal and fetal mortality o Delay or error in diagnosis o Reluctance to operate o Inadequate preparation
Appendicitis
Difficult diagnosis: sx similar to pregnancy
Appendix moves upward and outward toward flank – pain/tenderness higher; significance of knowing where to palpate
Leukocytosis seen in normal pregnancy - up to
15,000 WBC
Appendiceal rupture more frequent because of delay in diagnosis
Infection less likely contained by omentum – this would be a poor prognosis for the patient
Increased risk of abortion and preterm labor
Fetal loss 15%
Treatment: surgery o Open surgery - traditionally o Laparoscopic: pneumoperitoneum with carbon dioxide similar perinatal outcome as laparotomy
Antibiotics
Silent appendicitis – stimulates pain
stimulates labor; gravid uterus contains infection
– but after
Postpartum – spillage of pus in the peritoneal cavity
Ruari and Abi OB: Gastrointestinal Disorders in Pregnancy page 1 of 4
St. Luke’s College of Medicine-William H. Quasha Memorial
Batch 2012
Liver Disease and Pregnancy
Coincidental with pregnancy o Viral hepatitis o Drug-induced hepatic failure
Induced by pregnancy and resolves postpartum o Intrahepatic cholestasis o Acute fatty liver of pregnancy o Severe preeclampsia o Hyperemesis gravidarum
Pregnancy superimposed on cirrhosis, chronic hepatitis, esophageal varices, liver transplant
Liver Function Test
Normal Changes during Pregnancy
Increased o Alkaline phosphatase o Hormone binding protein o Transferrin o Lipids o Cholesterol o Fibrinogen o Factors VII, VII, X
Unchanged o Aminotransferase o Lactic acid dehydrogenase o Bilirubin o Clotting times
Decreased o Albumin
Intrahepatic Cholestasis of Pregnancy
Recurrent jaundice, cholestatic hepatosis or icterus gravidarum or both
Manifestation will be jaundice and pruritus
Bile acids cleared incompletely by liver and accumulate in plasma
Intrahepatic cholestasis with centrilobular bile staining without inflammatory cells *
characteristic; not infectious
Hyperbilirubinemia
Liver biopsy o Mild cholestasis o Intracellular bile pigments o Canalicular bile plugging without necrosis
Generalized pruritus in last trimester from elevated serum bile salts
10% jaundice, dark urine, light stools
Impaired absorption of fat soluble vitamin - remember: it is the bile from the liver excreted into the colon that will absorb the vitamins, but since this is retained in the liver impairment
Impaired coagulation
Lab: increased bilirubin, bile acids and alkaline phosphatase (enzyme in bile duct and canalicular membrane of hepatocytes)
Tx: antihistamines ( Benadryl; to relieve the itching , cholestyramin)
Adverse pregnancy outcome o Meconium staining o Preterm delivery
Liver in Preeclampsia- Eclampsia
Periportal hemorrhage, fibrin deposition, hepatocyte disruption with necrosis
S/sx: RUQ pain – warning for the OB for
possible liver pathology
Increased SGOT/SGPT, thrombocytopenia
Lecture trans + Recording
HELLP syndrome: hemolysis, elevated liver enzyme, low platelet – severe prognosis for the
patient
If liver involvement ( see elevation in transaminases +RUQ pain) : prompt delivery
After delivery
Liver enzyme, LDH and platelet count normalize in 2-3 days
Intrahepatic or subcapsular hemorrhage o Diaphragmatic surface of right lobe o Liver rupture: packing, correction of coagulopathy, hysterotomy
Acute Fatty Liver of Pregnancy - extremely rare
Spectrum from subclinical hepatic dysfunction
(increased SGOT/SGPT) to hepatic failure and coma
Usually third trimester
Bleeding, jaundice, nausea/vomiting, coma
20-40% with preeclampsia
Biopsy: microvesicular fatty transformation of hepatocytes
Dx: high index of suspicion o Special stains for fat
Tx: terminate pregnancy =(
Acute Viral Hepatitis *favorite of MLE and local boards,,ahem,, therefore..^^
Most common serious liver disease in pregnancy
Viruses not hepatotoxic- immune response causes hepatocellular necrosis
5 types: Hepatitis A, B, C, D, E
S/Sx: nausea, vomiting, headache and malaise; jaundice with improvement of symptoms – pain and tenderness over liver
Labs: increase in serum aminotransferase
(SGPT/SGOT), bilirubin, antigen - antibody level
Chronic hepatitis B
- Asymptomatic carrier
- Chronic active hepatitis
- Ground glass hepatocyte
Sequela: Fulminant hepatic necrosis
- Fatal
- Usually hepatitis B
- Hepatic encephalopathy
- description of pic --- liver is smaller than normal, due to extensive areas of liver necrosis.
The liver is also soft with a wrinkled capsular surface
Hepatitis A
Fecal –oral route
Ingestion of contaminated food or water
Incubation of 2-7 weeks
IgM Anti HAV may persist for several months
IgG Anti HAV: immunity
Vaccine: 90% effective
Hepatitis A and Pregnancy
No teratogenic effect in fetus
Vertical intrapartal transmission – meaning at the time of delivery, the baby may acquire the
Hepatitis from the vaginal fluid of the mother
Increased preterm delivery
Exposed pregnant woman: should be given prophylaxis with 1 ml immune globulin
Ruari and Abi OB: Gastrointestinal Disorders in Pregnancy page 2 of 4
St. Luke’s College of Medicine-William H. Quasha Memorial
Batch 2012
Hepatitis B
Serious sequelae in infected adults (5-10%) and infants (70-90%) o Chronic hepatitis o Cirrhosis o Hepatocellular carcinoma
Transmission by infected blood/ blood products, saliva, vagina secretions and semen
HBsAg: 1st virologic marker
Anti HBsAg: 90%develops – which will protect the individual for life ; 10% (-)
on pic: ballooning cytoplasm in degenerating hepatocytes
HBeAg: infectivity & intact viral particles o (+) early acute hepatitis o Persistent: chronic infection o HBsAg and HBeAg (+): likely to transmit disease o HBsAg and HBeAg (-), Anti HBe (+): not
HBcAg transmit
Hepatitis B and Pregnancy
Course of hepatitis not altered
Treatment is supportive ( hydration, pain reliever, anti-pyretic)
Increased preterm delivery
Transplacental viral transfer with acute hepatitis:
80-90% in 3 rd trimester * the only one that can cross the placental blood barrier
Chronic hepatitis B: not transplacental
Chronic hepatitis: perinatal transmission thru ingestion during delivery, breastfeeding
85% infant: chronic carriers
Correlates with HBeAg – again measures the infectivity of the mother
HBsAg (+) mothers: o Infants given hepatitis B immune globulin after birth followed by hepatitis
B vaccine*
In the first 24-48h, it has been the policy of the government to give the baby Hepa B vaccine – studies show that this decreased hepatocellular carcinoma
Hepatitis B serological screening during prenatal care
If (-) and high risk: may vaccinate mother o Seroprotection lower (45% vs 60-70% when nonpregnant)
Hepatitis C - the dreaded hepatitis
Transmission as in hepatitis B
Anti- C antibody detected 15 weeks after acute infection
86% of antibody (+) Hep C: infectious
20-30% cirrhosis in 20-30 years
No adverse perinatal outcome
Vertical transmission: 3-6%
Portal inflammatory infiltrates frequently with lymphoid aggregates or lymphoid follicles
Steatosis is also present in HCV infections in contrast to HBV infection
Chronic Hepatitis (may be B, C or autoimmune)
Hepatic necrosis, active inflammation and fibrosis – cirrhosis and liver failure
Chronic inflammatory infiltrate in the portal areas extending beyond into the adjacent lobule
Many hepatocytes are undergoing degeneration and necrosis
Lecture trans + Recording
Either hepatitis B or C or autoimmune (ANA)
Asx; elevated serum transaminase
Interferon for antiviral, antiproliferative and immunoregulatory effects o After 6 mos: decrease viremia o Relapse rate 20%
Chronic Hepatitis and Pregnancy
Severe disease – anovulation
Asx chronic hepatitis: no pregnancy effect
Higher incidence of cholestatic jaundice
Autoimmune chronic hepatitis treated with corticosteroids +/- Azathioprine: increased fertility and survival
Cirrhosis
Irreversible chronic injury to lover parenchyma with extensive fibrosis and regenerative nodules
Lannec cirrhosis from chronic exposure to alcohol: most common
Young women/ pregnancy: from chronic B or C viral hepatitis
Hardly seen in the clinic, rarely become pregnant
On pic: Irregular depressed areas due to bands of fibrous scar tissue that separate nodules of regenerating liver parenchyma
Cirrhosis and Pregnancy
S/sx: jaundice, edema, coagulopathy, metabolic abnormalities, portal HPN
Cirrhosis associated with infertility
- High perinatal loss, maternal prognosis poor
Bleeding of esophageal varices: greater if no portal decompression shunting
Acute Acetaminophen Overdosage
Suicidal attempts with acetaminophen ( Tylenol) : nausea/vomiting, diaphoresis, malaise
In 1-2 days – liver failure – resolves in 5 days
Transplacental transfer
Antidote: N-acetylcysteine ( increases glutathione) if: o Plasma acetaminophen after 4 hrs: 120 ug/ml o Acetaminophen overdose > 7.5 grams
Cholelithiasis and Cholecystitis
Gallstones (GS) usually contain cholesterol
Non pregnant: risk for surgery of silent GS –
10% at 5 years; 18% at 15 yrs
Cholelithiasis and Pregnancy
Increased BG volume & residual volume – incomplete emptying - -cholesterol crystals – increased biliary sludge: precursor to gallstone
(GS)
GS in pregnancy: 2.5- 10%
Nonsurgical approaches to GS: no experience during pregnancy
Asx GS: no treatment
If acute symptoms: surgery
Cholecystitis
Obstruction of cystic duct with bacterial infection in 50-85%
S/sx; RUQ pain, anorexia, nausea, vomiting, low grade fever, leukocytosis
Ruari and Abi OB: Gastrointestinal Disorders in Pregnancy page 3 of 4
St. Luke’s College of Medicine-William H. Quasha Memorial
Batch 2012
Cholecystitis
Cholecystectomy: acute cholecystitis, biliary colic, jaundice and acute pancreatitis
Laparoscopic cholecystectomy: treatment of choice of most patients; increased morbidity
Open or laparoscopic cholecystectomy: equally acceptable in pregnancy
Pancreatitis
Triggered by activation of pancreatic trypsinogen autodigestion (cellular membrane disruption, proteolysis), edema, hemorrhage and necrosis
Nonpregnant: associated with GS ( to the cystic duct
duct of Vater
obstruction of the hormone secretion) and ROH abuse
Pregnant: cholelithiasis - most frequent cause
On pic – atrophy of most of the exocrine pancreatic glands and occasional preserved islets
Lecture trans + Recording
Pancreatitis during Pregnancy
S/sx: epigastric pain, nausea & vomiting, tenderness, increased amylase (3x normal), increased lipase
Tx: analgesia, hydration and food abstinence
Self limited within 3-7 days
Obesity
Quetelet’s Index: Body Mass Index
Wt (kg)/ Ht (m)2 = Kg/m2
20% increase in body weight o Or BMI > 85 th percentile o 27.3 for women 20-29 years old
Morbid Obesity and Pregnancy
Increased hypertension, diabetes, postterm pregnancy, cesarean section rate, large for gestational age babies, neural tube defects
Weight management
Praise GOD! Ahaha! Tapos na! *clap clap clap*
Dahil natapos mo na..you have a prize! Enjoy friend!
Ahahah…ang saya-saya! GOD bls everyone! -- abi
Ruari and Abi OB: Gastrointestinal Disorders in Pregnancy page 4 of 4