Emesis

HYPEREMESIS
IN
PREGNANCY
Causes:
A. Early Pregnancy
B. Late pregnancy
Related to pregnancy
Simple vomiting(morning
sickness, emesis gravidarum)
Hyperemesis gravidarum
(pernicious vomiting)
Associated with pregnancy
Related to pregnancy
Continuation or reappearance of
simple vomiting of pregnancy

Acute fulminating preeclampsia
Associated with pregnancy
Medical-surg-gynecological causes
in early pregnancy
Hiatus hernia
Medical:
Intestinal infestation
Urinary tract infection
Hepatitis
Diabetic ketoacidosis
Pyelonephritis
uremia
Surgical:
Appendicitis
Peptic ulcer
Intestinal obstruction
Cholecystitis
Pancreatitis
Gynecological:
Twisted ovarian tumor
Red degeneration of fibroid
EMESIS GRAVIDARUM
Patient complains of nausea & occasional sickness on rising in morning.
Vomitus is small & clear or bile-stained
No impairment of health nor any restriction of normal activities of
women
Disappears by 12-14th week of pregnancy with or without pregnancy
High level of serum hCG, estrogen & altered immunological states are
considered responsible for initiation of manifestation which is
aggravated by the neurogenic factor.
MANAGEMENT
Assurance is important
Dry toast or biscuits & avoidance of fatty and spicy foods are enough to
relieve the symptoms in majority

Vit B1 supplementation 100 mg daily is helpful
If simple measures fail, antiemetic drugs- trifluoperazine 1 mg twice
daily is effective
Promethazine & ondansetron can be used.
Patient is advised to take plenty of fluids 2.5 L in 24 hours and fruit
juice.
HYPEREMESIS GRAVIDARUM
Definition: it is a severe type of vomiting of pregnancy which has got
deletrious effect on the health of the mother and/or incapacitates her in

day-to-day activities.
The adverse effects of severe vomiting are- dehydration,
metabolic acidosis(from starvation) or alkalosis(from loss of
hydrochloric acid), electrolyte imbalance(hypokalemia) & weight loss.
Incidence: marked fall in incidence in last 30 years. Now a rarity in
hospital practice(less than 1 in 1000 pregnancies)
reasons: 1) better family planning which reduces number of unplanned
pregnancies 2) early ANC 3)potent antihistaminic & antiemetic drugs.
ETIOLOGY:
Mostly limited to 1st trimester
More common in first pregnancy wirh 15% tendency to recur in
susequent pregnancies
Younger age
Low body mass
History of motion sickness or migraine
Familial history
More prevalent in h mole & multiple pregnancy
More common in unplanned pregnancies
THEORIES:
HORMONAL: excess of hCG. Proved by frequency of vomiting at the
peak level of hCG & also increased association with h.mole or multiple
pregnancy when hCG titer is very much raised.
2. PSYCHOGENIC: probably aggravates nausea once it begins.
Evidenced by shifting of the patient from home surroundings.
Conversion disorder, somatization, excess perception of senses are
other theories.
3. DIETETIC DEFICIENCY: probably due to low carbohydrate reserve.
Deficiency of vit B6, B1 & proteins may be effect rather than cause.
1.
4. Allergic or immunological basis

5. Decreased gastric motility is found to cause nausea.
VICIOUS CYCLE OF VOMITING

VOMITING
CARBOHYDRATE STARVATION
KETOACIDOSIS
VOMITING
PATHOLOGY
As described by SHEEHAN :
LIVER: liver enzymes are elevated. Centrilobular fatty infiltration
without necrosis.
KIDNEYS: usually normal with occasional findings of fatty change in
the cells of first convoluted tubule, which may be related to acidosis.
HEART: a small heart is a constant finding. There may be subendocardial hemorrhage.
BRAIN: small hemorrhages in hypothalamic region giving manifestation
of wernickes encephalopathy. The lesion may be related to vit B1
deficiency.
METABOLIC, BIOCHEMICAL & CIRCULATORY CHANGES

METABOLIC:
inadequate intake of food

Glycogen depletion
fat reserve is broken down

Incomplete oxidation of fat &
ketonemia
Acetone is excreted through kidneys
& in breath
endogenous tissue protein metabolism

excess excretion of nonprotein
nitrogen in urine
water & electrolyte metab disrupted
BIOCHEMICAL:
Acidosis from starvation.
Alkalosis from loss of hydrochloric acid & hypokalemia.
Loss of water & salts in vomitus results in fall in plasma Na+, K+ & ClUrinary chloride may be below 5g/L or may even be absent.
Hepatic dysfunction results in ketosis with rise in blood urea & uric acid.
Patient suffers from hypoglycemia, hypoproteinemia & hypovitaminosis.
CIRCULATORY: hemoconcentration with rise in Hb%, RBC count &
hematocrit values. Slight increase in WBC count with increase in
eosinophils. Concomitant reduction in ECF.
CLINICAL COURSE
EARLY: Vomiting occurs throughout day. Normal day-to day activities
are curtailed. No evidence of dehydration or starvation.

LATE:
Symptoms- vomiting is increased in frequency with retching. Urine is
diminished to the stage of oliguria. Epigastric pain, constipation may
occur.
Signs: features of dehydration & ketoacidosis- dry coated tongue, sunken
eyes, acetone smell in breath, tachycardia, hypotension, rise in
temperature may be noted. Jaundice is a late feature. Vaginal exam & usg
is done to confirm the diagnosis of pregnancy.
INVESTIGATIONS:
URINALYSIS: quantity- small
colour dark
high specific gravity with acid reaction
presence of acetone, occasional protein & bile pigments
diminished or even absent chloride
BIOCHEMICAL & CIRCULATORY CHANGES
SERUM TSH, T3 & FREE T4: transient phase of thyroid
dysfunction( clinical or subclinical)
OPHTHALMOSCOPIC EXAM: if pt is seriously ill. Retinal
hemorrhage & detachment of retina are the most unfavourable signs.
ECG: if abnormal serum potassium levels.
DIAGNOSIS:
Confirm pregnancy first
Thereafter all associated causes of vomiting are to be excluded.
USG is helpful not only to confirm pregnancy but also to exclude
obstetric( h mole, multiple pregnancy), gynecologic, surgical or medical

causes of vomiting
COMPLICATIONS:
MATERNAL: The majority of clinical manifestations are due to effects of
dehydration & starvation with resultant ketoacidosis. The following are

the rare nowadays:
1. Neurologic complications: a) wernickes encephalopathy
b) pontine myelinolysis c) peripheral neuritis d) korsakoffs psychosis
2. Stress ulcer in stomach
3. Esophageal tear( mallory weiss syndrome)
4. Jaundice, hepatic failure
5. Convulsions & coma
6. Hypoprothrombinemia due to vit K deficiency
7. Renal failure
EFFECTS ON FETUS: Fetus usually remains unaffected once the
problem is resolved.
fetal risks may be due to low birth weight.
MANAGEMENT:
The principles in the management are :
Maintenance of hydration
To control vomiting
To control fluids & electrolyte imbalance
To correct metabolic disturbances
To prevent serious complications of severe vomiting
Care of pregnancy
HOSPITALIZATION: A case of hyperemesis gravidarum when admitted
surprisingly improves rapidly with the same diet & drugs used at home.
FLUIDS: oral feeding is withheld for atleast 24 hours after cessation of
vomiting. During this period fluid is given through intravenous drip.
Amount of fluid to be infused in 24 hrs is calculated as follows:
Total fluid= 3 liters ( half as 5% dextrose & half as RL)
Extra amount of crystalloids equal to amount of vomitus & urine in 24 hrs
is to be added.
With this regime-dehydration, ketoacidosis, water & electrolyte imbalance
are rectified. Serum electrolyte sholud be estimated & corrected if there is
any abnormality. Enteral nutrition though NG route may be given.
DRUGS
Antiemetics promethazine(phenargan 25mg) or prochlorperazine 5mg
or triflupromazine 10 mg may be administered BD or TDS daily i.m.
2. Trifluoperazine 1 mg BD i.m. is a potent antiemetic. Vit B6 &
doxylamine are also safe & effective. Metoclopramide stimulates
gastric & intestinal motility without stimulating secretions & is found
useful
3. Hydrocortisone 100 mg i.v. in drip in a case with hypotension or
intractable vomiting. Oral method prednisolone is also used in severe
cases
4. Nutritional supplementation with vit B1 100 mg daily, vit B6, vit C &
vit b12 are given
1.
Nursing care: sympathetic but firm handling of the patient is essential.

Hyperemesis progress chart to assess the progress of patient while in hospital.
Daily record of pulse, temp, BP at least twice daily, intake-output, urine for
acetone, protein, bile, blood chemistry & ECG.

Clinical features of improvement are evidenced by:
a) subsidence of vomiting,
b) feeling of hunger,
c) better look,
d) disappearance of acetone from breath & urine,
e) normalization of blood chemistry,
f) normal pulse & BP,
g) normal urine output
DIET: before iv fluid is omitted, foods are given orally. At first, dry
carbohydrate foods like biscuits, bread & toast are given. Small but
frequent feeds are recommended. Gradually full diet is restored.
Termination of pregnancy is rarely recommended.
Intractable hyperemesis gravidarum inspite of therapy is rare these
days.
THANK YOU!

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HYPEREMESIS

simple vomiting of pregnancy

relieve the symptoms in majority

Definition: it is a severe type of vomiting of pregnancy which has got

deletrious effect on the health of the mother and/or incapacitates her in

4. Allergic or immunological basis

VICIOUS CYCLE OF VOMITING

METABOLIC, BIOCHEMICAL & CIRCULATORY CHANGES

inadequate intake of food

fat reserve is broken down

endogenous tissue protein metabolism

are curtailed. No evidence of dehydration or starvation.

obstetric( h mole, multiple pregnancy), gynecologic, surgical or medical

dehydration & starvation with resultant ketoacidosis. The following are

EFFECTS ON FETUS: Fetus usually remains unaffected once the

HOSPITALIZATION: A case of hyperemesis gravidarum when admitted

Nursing care: sympathetic but firm handling of the patient is essential.

acetone, protein, bile, blood chemistry & ECG.

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