HYPEREMESIS

GRAVIDARUM

DR.A. RATHNA ., M.S ( O&G )

1 ST YR PG

Nausea and vomiting of pregnancy

commonly termed as morning sickness
It is common phenomenon in pregnancy
Occurring in 70 % of all pregnancies
HYPEREMESIS GRAVIDARUM
It is severe type of vomiting in pregnancy
which has got delirious effect on the health
of mother or incapacitates her in day to day
activities

Cont .
It is mostly limited to the first trimester
More common in first pregnancy with
tendency to recur in subsequent pregnancy.
Younger age
Low body mass
History of motion sickness of migraine
Family history of mother and sisters suffers
same
More prevalent in hydatiform mole and
multiple pregnancy .

History

When obtaining history from the patient,

discuss present symptoms. Obtain
information pertaining to the timing, onset,
severity, pattern, and alleviating and
exacerbating factors (eg, relationship to
meals, medications, prenatal vitamins,
stress, other triggers).

Physical examination

Pay attention to the vital signs, including

standing and lying blood pressure and
pulse, volume status (eg, mucous
membrane condition, skin turgor, neck
veins, mental status), general appearance
(eg, nutrition, weight), thyroid examination
findings, abdominal examination findings,
cardiac examination findings, and
neurologic examination findings.

Theories
Endocrine theory :high levels of hCG &
estrogen during pregnancy
Metabolic theory :low carbohydrate
reserve . vitamin B6 deficiency
Psychological theory : Psychological stress
increase the symptoms

Theories
Elevated Level OF HCG are present in all
pregnant women during early pregnancy,
usually declining after 12 week .this
corresponds to the usual duration of morning
sickness .In hyperemesis gravidarum ,the
decrease fluid intake& prolonged vomiting
cause dehydration which increase serum
concentration of hCG
Raised level of estrogen , which is more
common in women using combined oral pills
in the past

Cont
Increased progesterone level , which
results in smooth muscle relaxation
This leads to oesophageal , gastric and
small bowel motility impairment , which
results in nausea and vomiting.
Other hormones- throxine , prolactin , leptin
and adrenocortical hormones

Pathology
Metabolic changes
Starvation

Depletion of glycogen stores and metabolism of

fat stores leads to increaed production of ketone
bodies.
Increased protein metabolism leads to increased
production of blood urea and nitrogen
Results in hypoglycemia , hypoproteinemia
and hypovitaminosis

Biochemical changes
Patient develop acidosis ( due to
starvation ) and alkalosis ( from loss of HCL
and hypokalemia .
Loss of water and salt in vomitus results in
decrease in sodium , potassium and
chlorides

Clinical features

Begins at 4 weeks

Peaks at 8 12 weeks

Decreases at 20 weeks

Signs and symptoms

When vomiting is severe it may result in the
following:
Loss of 5% or more of pre-pregnancybody weight
Shrunken eye , dry tongue , ketotic odour .
Loss of skin elasticity , tachycardia and
hypotension
Epigastic pain , constipation
Oliguria
Physical and emotionalstress of pregnancy on the
body
Difficulty withactivities of daily living

DDx
It is important to consider other diagnoses
in cases of severe refractory nausea and
vomiting during pregnancy, especially if the
presentation is atypical or other symptoms
are present
Other conditions to consider in the
differential diagnosis of patients with
suspected hyperemesis gravidarum include
the following:

Ddx
Infection
Urinary tract infection
Hepatitis
Meningitis
Gastroenteritis
Gastrointestinal disorders(usually
accompanied by abdominal pain)
Appendicitis
Cholecystitis
Pancreatitis
Fatty liver
Peptic ulcer

Ddx
MetabolicThyrotoxicosis (common in Asian
subcontinent)
Addison's disease
Diabetic ketoacidosis
Hyperparathyroidism
DrugsAntibiotics
Iron supplements
Gestational trophoblastic diseases (rule out
with urine -hCG)Molar pregnancy
choriocarcinoma

Investigations
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.

Urine culture: This may be indicated because

urinary tract infection is common in
pregnancy and can be associated with nausea
and vomiting.
Calcium level: Consider measuring Ca +
+levels. 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.

Imaging studies

Obstetric ultrasonography is usually warranted in

patients with hyperemesis gravidarum to evaluate
for multiple gestations or trophoblastic disease.
Additional imaging studies generally are not
needed unless the clinical presentation is atypical
(eg, nausea and/or vomiting beginning after 9-10
wk of gestation, nausea and/or vomiting persisting
after 20-22 wk, acute severe exacerbation) or
another disorder is suggested based on history or
physical examination findings.

complications
Dehydration
electrolyte imbalance
renal failure

Wernickes Encephalopathy
(Thiamine deficiency)

Vitamin K deficiency : maternal

coagulopathy or fetal intracranial
hemorrhage

Complications
Mallory Weiss tears
. Characterized by upper gastro-intestinal
bleeding secondary to longitudinal mucosal
lacerations at the gastroesophageal
junction or gastric cardia.

Diet
Initial suggestions for dietary modification in
patients with nausea and vomiting associated with
pregnancy include the following:
Eat when hungry, regardless of normal meal times.
Eat frequent small meals.
Avoid fatty and spicy foods and emetogenic foods
or smells. Increase intake of bland or dry foods.
Eliminate pills with iron.
High protein snacks are helpful.
Preconception use of prenatal vitamins may
decrease nausea and vomiting associated with
pregnancy.

Treatment

Intravenous (IV) hydration often includes

supplementation ofelectrolytesas
persistent vomiting frequently leads to a
deficiency. Likewise, supplementation for
lostthiamine(Vitamin B1) must be
considered to reduce the risk ofWernicke's
encephalopathy. In addition, electrolyte
levels should be monitored and
supplemented.

If hypokalemia is severe or symptomatic,

potassium should be replaced parenterally.
Before administering IV potassium, renal
function should be evaluated. Potassium is
usually added to intravenous fluid to
achieve a concentration of 40 mEq/L (and
not >80 mEq/L). An infusion rate of 10 mEq
of potassium per hour should be safe as
long as urine output is adequate.

If persistent dehydration, electrolyte loss,

and/or weight loss occur despite above
therapy, nutrition supplementation by
either the parenteral or enteral route is
indicated. The standard method has been
via total parenteral nutrition (TPN)

Nasogastric tube placement and

subsequent enteral feeding has been shown
in small series and reports to be a valid
alternative, with less complication risks,
similar efficacy, and similar outcomes in
regard to neonatal outcome when compared
with TPN.[5

TREATMENT

pharmacologic therapy is necessary,

treatment may be initiated by giving
vitamin B-6 10-25 mg 3-4 times daily;
doxylamine 12.5 mg 3-4 times daily can be
used in addition. Ginger capsules 250 mg 4
times daily can be added at this point if the
patient is still vomiting; this has been shown
to be effective in randomized trials.

Treatment cont .

Metoclopramide 5-10 mg orally every 8

hours may be used next. Promethazine 12.5
mg orally or rectally q4h or dimenhydrinate
50-100 mg orally q4-6h may be added as
well. Ondansetron 4-8 mg orally or IV q8h
can be used for further refractory cases

Treatment cont.
The only FDA-approved drug for treating
nausea and vomiting in pregnancy is
doxylamine-pyridoxine combinations.
The new dosage form approved in April
2013 is a delayed-release tablet that, when
taken at bedtime, is at its peak serum
concentrations in the morning, when
nausea and vomiting may be worse.

Treatment

Evidence for the use ofcorticosteroidsis

weak; there is some evidence that
corticosteroid use in pregnant women may
slightly increase the risk of oral facial clefts
in the infant and may suppress fetal adrenal
activity.However,hydrocortisoneandpredni
soloneare inactivated in the placenta and
may be used in the treatment of
hyperemesis gravidarum after 12 weeks.