PRESENTER:
DR SHARWAJEET JHA
Table of Content
Definition Investigation
Prevalence Diagnosis
Etiology Severity
Risk factor Complications
Theories Management
Clinical Course Outcome
Differentials Reference
THE STORY BEGINS AS…..
DEFINITION
It is a severe type of vomiting of pregnancy which
has got deleterious effect on the health of mother
and/or incapacitates her in day to day activities. (Dutta
Obstetrics, 9th Edition)
Severe unrelenting nausea and vomiting-hyperemesis
gravidarum- is defined variably as being sufficiently
severe to produce weight loss, dehydration, ketosis,
alkalosis from loss of hydrochloric acid, and
hypokalemia. (Williams Obstetrics, 25th Edition)
PREVALENCE
According to the National Health portal 0.3%-
3% of pregnant women suffer from hyperemesis
gravidarum- being commonest cause of
hospitalization in first trimester.
There is marked fall in incidence during last 30
years . Reasons may be:
Better application of family planning knowledge-
reduces number of unplanned pregnancies
Early visit to the antenatal clinic
Potent antihistaminic and antiemetic drugs
ETIOLOGY
• Limited to first trimester
• More common in first pregnancy
• Younger age
• Low body mass
• History of motion sickness or migraine
• Familial history-mother or sister
• More prevalent in hyaditiform mole or multiple pregnancy
• Unplanned pregnancies
Age below 17 year and above 35 year
Risk Factors Primigravida
Asthma and other allergic disorder
Multiple pregnancy( increased placental mass)
Underweight (low BMI)
Psychological factors such as unwanted pregnancy, maritial problems
History of hyperemesis gravidarum
Trophoblastic diseases (increased β HCG)
Risk Factor
Risk of incidence of hyperemesis gravidarum decreases in:
Obesity
Smoking
Theories Behind Hyperemesis Gravidarum
1. Hormonal
◦ High HCG- H.Mole, multiple Pregnancies
◦ High Estrogen- higher BMI, 1st Pregnancy, OCP users
◦ High Progesterone- relaxation of cardiac sphincter
◦ Thyroxine- under high estrogen- increases TBG and transient
decrease in free T4 level
◦ Leptin-acts as afferent satiety hormone- reduces appetite
◦ Adreno cortisol hormone-overactivity of HPA axis-interpreted as
energy conservation mechanism in starving and dehydrating
patient
2. Psychogenic
It probably aggravates the
nausea once it begins, but
sometimes it triggers the
neurogenic element.
It could be resulting from
psychosocial stress, poverty or
marital conflicts.
3.Dietetic Deficiency
Probably due to low carbohydrate reserve, as it happens
after a night without food
Deficiency of vitamin B1, vitamin B6 and protein may be the
effect rather than cause
4. Allergic or Immunological Basis
During pregnancy ,changes in humoral or cell
mediated immune system occur.
Probably to Protect the fetus and decidua
from disruption by the maternal immune
system
5. Decreased Gastric Motility
During pregnancy,
sex steroids cause leading to slower slow gastric
abnormal activity small intestinal emptying that
in gastric and and colonic may cause nausea
colonic smooth transient time or vomiting.
muscle
Vomiting cycle
Initiation of
vomitting
vomiting,
features of
dehydration and
Ketoacidos carbohydrate
starvation
supervenes
Clinical Course
From management and prognostic point of view, the cases are grouped into;
EARLY LATE
NORMAL DAY TO DAY EVIDENCES OF
VOMITTING OCCURS
ACTIVITIES ARE DEHYDRATION AND
THROUGHOUT THE DAY
CURTAILED STARVATION
LATE(MODERATE TO SEVERE) PRESENTATION
SYMPTOMS
• INCREASED VOMITTING WITH RETCHING
• DIMINISHED URINE QUANTITY
• EPIGASTRIC PAIN
• CONSTIPATION
SIGNS
• FEATURES OF DEHYDRATION AND KETOSIS
• DRY COATED TONGUE
• SUNKEN EYES
• ACETONE SMELL IN BREATH
• TACHYCARDIA
• HYPOTENSION
• RISE IN TEMPERATURE
• JAUNDICE (LATER STAGE)
INVESTIGATIONS
1. URINE ANALYSIS
•Quantity- small( to see oliguria)
•Colour- dark (due to concentration)
•Sp. Gravity- high with acid reaction
•Presence of acetone- due to high accumulation of protein as incomplete
oxidation of fat reserve
•Protein occasionally present- due to increase endogenous protein metabolism
•Rarely bile pigments may be seen- due to centrilobular fatty infiltration in liver
•Diminished or absence of chloride- due to severe vomiting and dehydration
•Urine Dipstick: to quantify ketone as 1+ or more
2. Biochemical Findings
sodium, potassium and chloride- low
(due to loss of water and salt in vomiting)
Blood urea, uric acid, and ketone bodies-
due to hepatic dysfunction
Blood glucose – low or decreased
Hypoproteinemia- low
hypovitaminosis
2.Hematological Findings
Rise in hemoglobin percentage, RBC
count and hematocrit values due to
hemoconcentration
Slight increase in WBC with
eosinophils.
Concomitant reduction of ECF
Serum TSH or Free T4: women may
suffer from transient phase of thyroid
dysfunction( clinical or subclinical)
3. Ophthalmic Examination
In seriously ill patients,
retinal hemorrhage and
detachment of retina are
most unfavorable sign
4. ECG Findings:
Came positive when there is
abnormal potassium level
5. Sonography
To confirm pregnancy
To see viability of fetus
To look for Trophoblastic
disease (H.mole), Multiple
pregnacy
Diagnosis
Pregnancy is confirmed first
Associated causes of vomiting are excluded
USG- pregnancy, H.mole, Multiple pregnancy
Presenting feature: severe, protracted
nausea & vomiting a/o with weight loss >5%
of prepregnancy weight, dehydration and
electrolyte imbalances, presenting mostly in
first trimester
Severity
Complications
Complications
(1) Neurologic complications—
◦ (a) Wernicke’s encephalopathy ( ophthalmoparesis with
nystagmus, ataxia, and confusion.)
◦ (b) Pontine myelinolysis;
◦ (c) Peripheral neuritis;
(2) Stress ulcer in stomach;
(3) Esophageal tear (Mallory-Weiss syndrome);
(4) Jaundice, hepatic failure;
(5) Convulsions and coma;
(6) Hypoprothrombinemia due to vitamin K deficiency
(7) Renal failure.
Effect on Fetus
It depend on the severity of
vomiting
Mild to moderate vomiting
doesn’t effect on on fetus
But hyperemesis, leads to the
weight loss of mother and
starvation resulting in IUGR in third
of cases
Management
Principles of Management are:
Maintenance of hydration
To control vomiting
To correct the fluid and electrolyte imbalance
To correct metabolic disturbances( acidosis or alkalosis)
To prevent the serious complications of severe vomiting
Care of pregnancy
Primarily: supportive
1. Fluid and Nutrition
•Adequate and appropriate fluid and electrolyte is the
most important component of management
•Iv hydration (3L/day) and NPO for at least 24 hour
followed by reintroduction of oral intake (small liquid
or bland meals)
•Normal saline and Ringer Lactate is the fluid of choice
•NS (Nacl 0.9; Na:150 mmol/l) and Hartmann’s Solution
(Nacl 0.6%; Na:131 mmol/l)
Fluid and Nutrition
•Infusion of dextrose containing fluids (D5, D10) is
mistakenly thought by some to be desirable to
provide patient with calories, but these
assumption is erroneous and dangerous.
•Wernicke’s encephalopathy may be Precipitated
by carbohydrate, fruits or dextrose administration
intravenously
•Secondly, hyponatremia demands infusion of
sodium containing fluids
Fluid and Nutrition
•Vitamin supplementation
vitamin B1: Thiamine- to reduce risk of
Wernicke's encephalopathy (100 mg iv BD or TDS
for 2-3 days
Vitamin B6:pyridoxine 10-25 mg TDS PO given
with Doxylamine (antihistamine) to increase its
efficacy
Vitamin B12, Vitamin C are supplemented in
some cases
Non Pharmacologic Intervention
•Remove the triggers if any present or identified
•Supplements containing iron should be avoided
•Dietary changes:
Small liquid or bland foods
Frequent high carbohydrate,low fat, small meals
Avoid spicy and oily foods
Fluids are better tolerated if cold, clear,
carbonated or sour (eg; ginger ale, lemonade)
are tolerated taken in small amounts in between
meals.
Psychotherapy: for psychosocial causes
Pharmacologic Intervention
1. antiemetic drugs:
If All Failed!
Corticosteroids have been used in severe and refractory
cases , although mechanism is not well understood
Most obstetricians avoid its chronic use due to
◦ Increased risk of preterm premature rupture of
membrane(PPROM)
◦ Increased risk of oral cleft if administered before 10 WOG
if administered after 10 WOG
• methylprednisolone 16 mg po or iv every 8 hour for 3 days
• Stopped if no desired response is seen
• Stopped in tapering doses
Signs of Improvement
Subsidence of vomiting
Feeling of hunger
Normalization of blood Chemistry( electrolytes)
Disappearance of acetone from breath and urine
Normal pulse and blood pressure
Normal urine output
Outcome and Prognosis
The availability of parenteral nutrition and I.V.F has greatly reduced
morbidity, mortality is virtually non existent in patient who get treated.
If remain untreated, micronutrient deficiency, Wernicke's
encephalopathy and sequeale of malnutrition (immunosuppression,
poor wound healing) have been reported.
Esophageal tears and Malory Weiss tears are other complications.
If all measure failed and patient doesn’t improve, then patient are
counselled for termination of pregnancy
References
DC Dutta’s textbook of Obstetrics, 9th edition
Williams textbook of Obstetrics 25th edition
Creasy and Resnik’s maternal fetal medicine 7th edition
ACOG revised practice bulletin for hyperemesis gravidarum 2015
RCOG guidelines 2016
Pictures:
Google images
Dall-e 2.0
