hyperemesis gravidarum.pptx

Table of Content
Definition
Prevalence
Etiology
Risk factor
Theories
Clinical Course
Differentials
Investigation
Diagnosis
Severity
Complications
Management
Outcome
Reference

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

Risk Factors
Age below 17 year and above 35 year
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
abnormal activity
in gastric and
colonic smooth
muscle
leading to slower
small intestinal and
colonic transient
time
slow gastric
emptying that may
cause nausea or
vomiting.

Vomiting cycle
Initiation of
vomiting,
features of
dehydration and
carbohydrate
starvation
supervenes
Ketoacidos
vomitting

Clinical Course
From management and prognostic point of view, the cases are grouped into;
EARLY
VOMITTING OCCURS
THROUGHOUT THE DAY
NORMAL DAY TO DAY
ACTIVITIES ARE
CURTAILED
LATE
EVIDENCES OF
DEHYDRATION AND
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

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

hyperemesis gravidarum.pptx

More Related Content

What's hot

Similar to hyperemesis gravidarum.pptx

Recently uploaded

In this document

hyperemesis gravidarum.pptx