2. Objectives
1- Introduction about Nausea and vomiting
2- Hyperemesis gravidarum
3- Gastroesophageal reflux Diseases
4- Intrahepatic Cholestasis
3. Introduction
Nausea (with or without vomiting) occurs in up to 90% of pregnancies at any time of day,
despite the general term “morning sickness.”
Mean onset of symptoms is 5 to 6 weeks' gestation. While symptoms typically abate by 16 to
18 weeks of gestation, they continue into the third trimester in 15% to 20% of pregnant
women and until delivery in 5%
The cause appears to be either the effect of the rising levels of oestrogen, or the high levels of
human chorionic gonadotrophin (hCG) acting on the chemoreceptor trigger zone in the
midbrain.
Nausea and vomiting may be graded as MILD, MODERATE or SEVERE.
4.
5. Mild
Mild nausea (and occasional vomiting) affects 45% of pregnant women and is the most
common form. The nausea can occur in the morning (morning sickness), but may occur at
any time of the day and can be provoked by emotional stress.
Treatment
The patient should be advised to; eat frequent small meals during the day, to take fluid
between (not with) meals.
If the vomiting is distressing she can be prescribed pyridoxine 50 mg 6-hourly or
metoclopramide (Maxolon) 10 mg two to three times a day.
6. Treatment (Diet modification)
Eat when hungry, regardless of normal meal times.
Eat frequent small meals.
Avoid fatty and spicy foods.
High protein snacks are helpful.
Suggested foods include ginger.
Preconception use of prenatal vitamins may decrease nausea and vomiting associated
with pregnancy.
7. Moderate and Severe
Moderate nausea and vomiting
Affects 5% of all pregnant women. The symptoms may occur at any time of the day or night.
The patient feels miserable and may become mildly dehydrated.
Severe
This form is uncommon, affecting 1 in 1000 pregnant women. The nausea is continuous and
the vomiting. frequent The woman rapidly becomes dehydrated and ketoacidotic.
10. Hyperemesis gravidarum
Hyperemesis gravidarum is a severe form of nausea
and vomiting in pregnancy, characterized by
intractable vomiting, dehydration, alkalosis,
hypokalemia, and weight loss usually exceeding 5%
of prepregnant body weight.
It affects 0.3% to 2% of pregnancies and peaks
between the 8th and 12th weeks of pregnancy.
13. Morning sickness VS Hyperemesis gravidarum
Morning Sickness Hyperemesis Gravidarum (HG)
You lose little if any weight. You lose 5-20 pounds or more. (> 5% of prepregnancy
weight)
Do not interfere with your ability to eat or drink. Cause you to eat very little and get dehydrated if not
treated.
You vomit infrequently and the nausea is episodic but not
severe.
You vomit, or feel the need to, often and may vomit bile or
blood if not treated.
Traditional remedies like diet or lifestyle changes are
enough to help you feel better.
You will probably require fluid hydration through an IV
and/or medications to ease your symptoms.
Improve after the first trimester, but may be queasy at
times throughout pregnancy.
You usually feel some relief by mid-pregnancy, but may be
nauseous and/or vomit until late pregnancy.
16. Clinical picture (symptoms)
Main symptoms are nausea and vomiting, Other common symptoms include ptyalism, loss
of more than 5 percent of their pregravid weight, fatigue, weakness, and dizziness.
Patients may also experience the following:
1. Sleep disturbance
2. Hyperolfaction
3. Dysgeusia
4. Decreased concentration
5. Depression
6. Anxiety
7. Irritability
8. Mood changes
18. Labs
Initial lab studies for hyperemesis gravidarum should include the
following:
Urinalysis for ketones and specific gravity.
Serum electrolytes and ketones.
Liver enzymes and bilirubin.
Amylase/lipase.
TSH, free thyroxine.
Urine culture.
19. Labs
Calcium level: Some rare cases have been reported of hypercalcemia being associated with
hyperemesis gravidarum, resulting from hyperparathyroidism.
Hematocrit: This may be elevated because of volume contraction.
Hepatitis panel: If clinically indicated, hepatitis A, B, or C may be confused with hyperemesis
gravidarum.
20. Imaging Studies
Obstetric ultrasonography to evaluate for multiple gestations or trophoblastic disease.
Performing upper abdominal ultrasonography to evaluate the pancreas and/or biliary tree if
clinically indicated.
Abdominal MRI if appendicitis is under consideration as a cause of nausea and vomiting in
pregnancy.
21. Treatment
The initial therapy is focused on aggressive intravenous rehydration and restoration of
electrolyte deficiencies.
If hypokalemia is severe or symptomatic, potassium should be replaced parenterally. Before
administering IV potassium, renal function should be evaluated.
Avoid intravenous glucose until intravenous thiamine has been administered.
28. Introduction
During pregnancy, up to 80% of women experience heartburn at some
point, and 25% are affected daily.
The prevalence and severity progressively increase during pregnancy
and resolve after delivery.
The prevalence of heartburn symptoms is 22% for patients in the first
trimester, 39% for those in the second trimester, and 72% for patients
in the third trimester.
30. PATHOGENESIS
The resting lower esophageal sphincter (LES) pressure is decreased during pregnancy, and
progesterone mediates LES relaxation.
Other factors may include increased intra-abdominal pressure and decreased gastric
emptying (causing gastric fluid reflux), as well as ineffective esophageal motility to clear the
esophageal acid.
Thus, decreased motility, increased acidity of gastric secretions, and reduced function of the
lower esophageal sphincter contribute to the increased gastric reflux.
31.
32. DIAGNOSIS
Symptoms include:
Substernal burning,
epigastric discomfort,
dyspepsia,
mild dysphagia,
and regurgitation.
Patients may have extraesophageal manifestations, such as hoarseness, chronic cough, chronic
laryngitis, and asthma.
33. DIAGNOSIS
The diagnosis is usually made by clinical symptoms only.
There is no reason to do invasive diagnostic tests such as barium radiographs, esophageal pH
studies, or esophageal manometry studies.
Upper gastrointestinal endoscopy is rarely needed, EXCEPT in exceptional cases of symptoms
refractory to medical management.
34. MANAGEMENT
Lifestyle and dietary changes should be initiated for mild symptoms:
Patients should avoid eating within a few hours of bedtime, elevate the head of the bed 6
inches, sleep on the left shoulder, and avoid alcohol, cigarette smoking, caffeine, chocolate,
and peppermint.
Medication:
The use of medication in pregnancy is complicated by the theoretical risk for teratogenicity.
38. introduction
Intrahepatic cholestasis of pregnancy (ICP) is a condition characterized by accumulation of bile
acids in the liver with subsequent accumulation in the plasma, causing pruritus and jaundice.
ICP is the most common liver disorder unique to pregnancy.
ESTROGENS are considered to play a role in its etiology, probably by slowing the enzymes involved
in bile transport leading to incomplete bile acid clearance.
Risk factors include a personal or family history of ICP, multiple gestations, and chronic hepatitis C
infection.
39. Diagnosis
Initial diagnosis is clinical, with confirmation by laboratory testing.
The CARDINAL CLINICAL FINDING is total body itching involving the palms and soles that
worsens at night and Icterus.
Anorexia, malaise, steatorrhea, and dark urine are also common complaints.
develops in 15% of patients but resolves quickly after delivery.
Onset is usually late in pregnancy but occasionally occurs in the second trimester.
40. Labs
Increased levels of alkaline phosphatase, bilirubin, and serum bile acids (chenodeoxycholic
acid, deoxycholic acid, cholic acid).
Aspartate transaminase (AST) and alanine transaminase (ALT) levels may be mildly elevated.
Patients may be symptomatic weeks before the diagnosis laboratory abnormalities are noted.
It is advisable to perform a liver ultrasound examination to exclude biliary obstruction
42. Treatment
Symptomatic treatment of pruritus with antihistamines is useful:
Diphenhydramine, topical emollients, and dexamethasone (12 mg/day for 7 days).
Ursodeoxycholic acid (10–15 mg/kg/d in 2 divided doses) has been shown to inhibit absorption of
toxic bile acids and increase their biliary excretion.
Ursodeoxycholic acid (UDCA) is the only drug that has consistently been shown to improve the
maternal symptoms and biochemical features of ICP.
We can give cholestyramine but UDCA is the most used drug.
43. Treatment
Fat-soluble vitamins (A, D, E, and K) and prothrombin time should be checked periodically
for patients taking cholestyramine for extended treatment.
If the prothrombin time is elevated, 10 mg/day of oral vitamin K should be administered
until the coagulation profile normalizes.
Delivery should be performed no later than 38 weeks' gestation.
When cholestasis is severe, delivery at 36 weeks with or without fetal lung maturity can be
considered.
44. Treatment (Fetal concern)
No treatments have been shown to reduce fetal risks associated with ICP.
intrahepatic cholestasis of pregnancy is associated with fetal death, spontaneous preterm
birth, and postpartum hemorrhage.
Antenatal testing with a modified biophysical profile twice per week starting at the time of
diagnosis is suggested.
Patients may benefit from a diet that emphasizes salty liquids, soups, starches, and chicken, and avoids fatty foods, vegetables, and fibrous foods.
Increase intake of carbonated beverages.
Serum
electrolyte abnormalities include hyponatremia, hypocalcemia, and hypokalemia. Ketonuria may occur. Chronic vomiting of gastric contents may cause a hypochloremic metabolic acidosis. Inadequate nutrition can lead to vitamin or micronutrient deficiencies.
Urinalysis for ketones and specific gravity: A sign of starvation, ketones may be harmful to fetal development. High specific gravity occurs with volume depletion.
Serum electrolytes and ketones: Assess electrolyte status to evaluate for low potassium or sodium, identify hyperchloremic metabolic alkalosis or acidosis, and evaluate renal function and volume status.
Liver enzymes and bilirubin: Elevated transaminase levels may occur in as many as 50% of patients with hyperemesis gravidarum. Mild transaminitis often resolves once the nausea has resolved. Significantly elevated liver enzymes, however, may be a sign of another underlying liver condition, such as hepatitis (viral, ischemic, autoimmune), or some other etiology of liver injury.
Amylase/lipase: Amylase level is elevated in approximately 10% of patients with hyperemesis gravidarum. Lipase, when combined with amylase, can increase the specificity in diagnosing pancreatitis as an etiology.
TSH, free thyroxine: Hyperemesis gravidarum is often associated with a transient hyperthyroidism and suppressed TSH levels in 50-60% of cases. However, an elevated free thyroxine may suggest that overt hyperthyroidism is present, thus necessitating further workup and treatment.
Patients with epigastric or right upper quadrant pain should undergo an abdominal ultrasound, serum tests of liver function, serum amylase, and serum lipase to exclude gallbladder and pancreatic disease.
Patients with nausea and vomiting complicated by dysphagia or hematemesis may require EGD.
Patients with nausea and vomiting during pregnancy associated with heartburn and regurgitation should be instructed about antireflux measures of diet and lifestyle modifications, and should receive mild antireflux medications, as described later.
because glucose oxidation is a thiamine-intensive process that may drive the last reserves of circulating vitamin B-1 toward the intracellular compartment, thereby aggravating neurologic damage.
Start patients with mild cases of NVP on non-pharmacologic interventions. Dietary changes first.
Lifestyle modifications (could be disruptive to work day, so reserve for when feasible).
2. If diet and lifestyle changes alone are not working consider complementary and alternative medicine interventions. Acupressure (Note: Should be removed when sleeping at night).
Ginger supplement or ginger tea.
3. Patients with persistent NVP or moderate NVP to HG, initiate the non-pharmacologic interventions above plus pharmacotherapy.
Note: Use clinical judgment, if dehydration is suspected or inability to eat/drink for greater than 12 hours, then go directly to IV fluid replacement + ondansetron 4 mg IV q 8 hours. Otherwise follow a systematic approach, adding/substituting a new agent as indicated in the flow chart.
We prefer to treat outpatients with PO drugs, but IV drugs are also often feasible with home healthcare.
If the patient is not achieving control of NVP with one drug, then proceed to the next step in the algorithm.
We individualize regimens based upon the patient's side effects and response (control of NVP).
Pregnant women with NVP/HG may go on and off drug treatment and may switch back and forth among several different drugs and among oral, IM, PR, and IV routes of administration. We individualize therapy depending on how the patient is responding to her current treatment.
Pressure or massage at the P6 acupressure point is reported in some studies to relieve motion sickness. The point is found three of the patient's fingerbreadths proximal to the proximal wrist fold, between the palmaris longus and flexor carpi radialis tendons, shown in this picture by the tip of the pen.
The clinician should assess for medication use, including anticholinergics, calcium channel antagonists, antidepressants, and antipsychotics, that could aggravate her symptoms.
Endoscopy is considered if therapeutic measures are unsuccessful and symptoms are very severe.
Cholestasis may occur in conjunction with other liver diseases.
Ursodeoxycholic acid (10–15 mg/kg/d in 2 divided doses) has been shown to inhibit absorption of toxic bile acids and increase their biliary excretion. In doing so, the medication normalizes bile acids, improves liver function tests, and alleviates pruritus.