HYPEREMESIS

GRAVIDARUM

INTRODUCTION
At least 80% of women experience
nausea &vomiting.
The term morning sickness is often used
to describe this condition when
symptoms usually disappear after the
first trimester.
severe form ( hyperemesis gravidarum )
Dehydration
Electrolyte imbalance
Need for hospitalization

Definitions
o Morning sickness: is the nausea felt by about 50% of
pregnant women on getting up in the morning.
o Emesis gravidarum: Actual vomiting in the morning.
o These two conditions usually start between the 4th and
6th weeks of pregnancy and improves or disappears
about the 12 th week.
o Hyperemesis gravidarum: The vomiting is not confined
to the morning but it is repeated throughout the day
until it affects the general condition of the patient.

 Hyperemesis gravidarum (HG) is a condition

of pregnancy characterized by
intractable nausea
vomiting
dehydration and is estimated to affect 0.5-2.0%
of pregnant women.

Malnutrition and other serious

complications such as fluid or electrolyte
imbalances may result.

SIGNS AND SYMPTOMS

Loss of 5% or more of pre-pregnancy body
weight
Dehydration, causing ketosis, and constipation
Nutritional disorders such as Vitamin B1
(thiamine) deficiency, Vitamin B6 deficiency or
Vitamin B12 deficiency
Metabolic imbalances such as metabolic
ketoacidosis or thyrotoxicosis
Physical and emotional stress of pregnancy on
the body
Difficulty with activities of daily living

 Symptoms can be aggravated by hunger,

fatigue, prenatal vitamins (especially those
containing iron), and diet
Hyperemesis gravidarum tends to begin
somewhat earlier in the pregnancy and last
significantly longer than morning sickness.
Hyperemesis gravidarum will experience severe
symptoms until they give birth to their baby,
and sometimes even after giving birth

Diagnosis
Symptoms:
o The patient cannot retain anything in her
stomach, vomiting occurs through the day
and night even without eating.
o Thirst, constipation and oliguria.
o In severe cases, vomitus is bile and/ or
blood stained.
o Finally, there is manifestations of
Werniches encephalopathy as drowsiness,
nystagmus and loss of vision then coma.

Diagnosis
Signs:
Manifestations of starvation and
dehydration:
* Loss of weight.
* Sunken eyes.
* Dry tongue and inelastic skin.
* Pulse: rapid and weak.
* Blood pressure: low.
* Temperature: slight rise.

Differential diagnosis
Other causes of vomiting as:
* cholecystitis,
* appendicitis,
* pyelonephritis,
* gastroenteritis,
* gall bladder diseases,
* complicated ovarian tumours.

Risk Factor Hyperemesis

Gravidarum

CAUSES
While there are numerous theories
regarding the cause of HG, the cause
remains controversial.
It is thought that HG is due to a
combination of factors which may
vary between women and include:
genetics, body chemistry, and overall
health.

 One factor is an adverse reaction to the

hormonal changes of pregnancy, in particular,
elevated levels of beta human chorionic
gonadotropin.
This theory would also explain why
hyperemesis gravidarum is most frequently
encountered in the first trimester (often around
8 12 weeks of gestation), as hCG levels are
highest at that time and decline afterward.
Another postulated cause of HG is an increase
in maternal levels of estrogens (decreasing
intestinal motility and gastric emptying leading
to nausea/vomiting).

Aetiology
1. Hormonal: high human chorionic
gonadotrophin (hCG) stimulates the
chemoreceptor trigger zone in the brain
stem including the vomiting center. This is
the most accepted theory and proved by
the higher frequency in the conditions
where the hCG is high as in:a. early in pregnancy,
b. vesicular mole and
c. multiple pregnancy.

Aetiology
2.Allergy: to the corpus luteum or the
released hormones.

Aetiology
3. Deficiency of:
a. adrenocortical hormone
and /or,
b. vitamin B6 and B1

Aetiology
4.Nervous and psychological:
a.due to psychological rejection of
an
unwanted pregnancy,
b. fear of pregnancy or labour so it
is
more common in
primigravidae.

PATHOPHYSIOLOG
Y

Although the pathophysiology of HG is

poorly understood, the most
commonly accepted theory suggests
that levels of hCG are associated with
it.
Leptin may also play a role
Possible pathophysiological processes
involved are summarized in the
following table

SOURCE

AETOLOGY

PLACENTA
CORPUS
LUTEUM

hCG

PLACENTA

OESTROGEN
PROGESTERONE

PATHOPHYSIOLOGY

GIT

Distention of
gastrointestinal tract
Crossover with TSH,
causing gestational
thyrotoxicosis
Decreased gut mobility
Elevated liver enzymes
Decreased lower
esophageal sphincter
pressure
Increased levels of sex
steroids in hepatic
portal system

HELICOBACTER
PYLORI

Increased steroid levels

in circulation

PSYCHOLOGICAL

Possible effect of
culture and
environment

COMPLICATIONS
1. Weight loss
2. Dehydration
3. Metabolic acidosis from
starvation
4. Alkalosis from loss of HCL
5. Hypokalemia (electrolyte
imbalance)

Pathological Changes
These are the same as in prolonged
* Liver: small fatty infiltration.
* Kidney: fatty degeneration of the convoluted
tubules.
* Heart: small subendocardial and subpericardial
haemorrhages.
* Brain: congestion and petechial haemorrhages in
the brain stem resembling that of Wernickes
encephalopathy.
Eye: optic neuritis and retinal haemorrhage.
* Peripheral nerves: degeneration

Pathological Changes
Blood:
Hypovolaemia and haemoconcentration.
Hyponatraemia, hypokalaemia and hypochloraemia.
Increased blood urea.
Hyperbilirubinaemia (due to liver damage).
Acidosis.
Urine:
Oliguria.
Increased specific gravity.
Decreased chloride.
Albuminuria.
Ketonuria.

Laboratory & Diagnostic test

Liver enzyme: elevation of (AST) & (ALT) are
usually present.
CBC: elevated level of RBC & hematocrit indicating
dehydration.
Urine ketones: positive when the body breaks
down fat to provide energy in the absence IIT
BUN: increase in the presence of salt &water
depletion
Urine specific gravity: grater than 1.025indicating
concentrated urine linked to inadequate fluid intake
Serum electrolyte decrease levels of k, Na, Cl
Ultrasound: evaluation for molar or multi
pregnancy

MANAGEMEN
T

1. Promoting Fluid & Nutrition

balance
Maintain NPO status to allow GI tract
to rest
Administer antiemetic drugs like :
promethazine, prochlorperazine,
ondansetron.
Administer IV fluid like 5% dextrose
in lactated ringer
Administer electrolyte replacement
therapy

Management
Intravenous fluids
* Oral feeding is prevented for 24-48 hours.
* Three litres of glucose 5% is given by
rapid infusion over 2-3 hours.
* Maintain intravenous glucose 5% and
saline therapy.
* When vomiting is controlled frequent
gradual small carbohydrate diets are
started.

Management
Drugs
* Adrenocortical preparations.
* Vit. B6 and Vit. B1.
* Antihistaminics that have antiemetic effect as
meclozinehydrochloride 25-50 mg twice daily. A
preparation contains both meclozine
hydrochloride + pyridoxine hydrochloride (vit.
B6) is of good benefit.
* Phenothiazine (chlorpromazine=largactil) 5-10
mg three times daily has a tranquilliser and
antiemetic effect.

2.promoting comfort
Hygiene measures and oral care
Pay special attention to the
environment making sure to keep
the area free of pungent odors
As the Client's nausea and vomiting
subside, gradually introduce oral
fluid & foods in small amounts
Monitor intake and output

 Avoid tight waistband

Eat small frequent meals (6 meals)
Separate fluid from solid by
consuming fluid In between meals
Use high protein supplement
Avoid lying down for at least 2
hours after eating
Avoid food high in fat drink herbal
tea
eat food that settle the stomach
such as toast or soda

Observation
* Vomiting: frequency, amount, colour and
contents.
* Vital signs: pulse, temperature and blood
pressure.
* Fluid: intake and output.
* Urine analysis: specific gravity, albumin,
ketone bodies,chloride and bile pigments.
* Blood: urea, electrolyte and liver function
tests.
* Eye: examination of the fundus.

GEJALA
Tingkatan I

Keadaan umum lemah, compos mentis

Mual., muntah, tidak mau makan, BB turun
Nyeri epigastrium, nadi sekitar 100x/m, TD trn
dehidrasi

Tingkatan II

Keadaan umum tambah lemah, apatis

Dehidrasi bertambah berat, hemokonsentrasi
Nadi kecil, cepat, suhu badan naik
Ikterus ringan
TD trn, asetonuria

Tingkatan III
Keadaan umum jelek, somnolen, koma
Syok
Kx : encefalopathy Wernicke

TERIMA KASIH