2. INTRODUCTION
HYPER : EXCESSIVE
EMESIS : VOMIT
GRAVIDARUM : PREGNANCY
Nausea/vomit of moderate intensity are especially
common until about 16 week.
Hyperemesis gravidarum occurs when vomiting becomes
intractable in early pregnancy & cause fluid & electrolyte
imbalances & nutritional deficiency.
Women usually needs to be hospitalized.
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4. DEFINITION
HYPEREMESIS GRAVIDARUM IS DEFINED
VARIABLY AS VOMITING SUFFICIENTLY SEVERE
TO PRODUCE WEIGHT LOSS, DEHYDRATION,
ACIDOSIS FROM STARVATION, ALKALOSIS FROM
LOSS OF CHLORIDE IN VOMIT & HYPOKALAMIA.
SEVERE VOMITING IN PREGNANCY PARTICULARLY
DURING EARLY PREGNANCY CAUSING
DELETERIOUS AFFECTION ON MOTHER’S
HEALTH SUCH AS WEIGHT LOSS, DEHYDRATION,
ACIDOSIS OCCURING FROM STARVATION.
5. ETIOLOGY
Unknown
More common risk factors are-
o Trophoblastic disease
o Multiple pregnancy
o Nulliparity
o Female fetus
o Age > 30year
o Maternal obesity
o Smoking
o Those who had Hyperemesis in previous pregnancy
o Has got familial history.
6. THEORIES
HORMONALTHEORY :
-excess of HCG & oestrogen → trigger vomiting centre
-progesterone excess → i)relaxation of cardiac sphincter →
retention of gastric fluid.
ii) decreased gastric and intestinal motility.
INFECTION
-Helicobacter pylori, a gram negative bacteria, associated
with the development of peptic ulcer where similar symptoms
are seen.
-This organism has been isolated in severe hyperemesis
PSYCHOGENIC THEORY:
It is associated with AGGRAVATED NAUSEA RELATED
NEUROGENIC ELEMENTS.
7. Theories
DIETARY DEFICIENCY: Due to low Chloride reserve
-deficiency of vitamin B1, B6 & protein may be the effect
rather than cause.
GENETIC
ALLERGIC OR IMMUNOLOGICAL BASIS
ANY PATHOLOGY OF :
Vestibular System
Liver
Kidney
Heart
Brain
10. CLINICAL FEATURE
SIGN:
• Dehydration
•Muscle wasting
•Ketosis
•Weight loss > 5% of pregnancy weight
•Tachycardia
•Postural hypotension
•Dry coated tongue
•Sunken eyes
•Acetone smell in breath
11. Pathology
Metabolic changes
Glycogen depletion- incomplete oxidation of fat- ketone
bodies
Biochemical- Loss of K, Na, Cl in the vomitus causes
acidosis and ketosis along with increase in blood urea,
uric acid
Circulatory-
Haemoconcentration- rise in Hb,RBC count, haematocrit
12.
13. INVESTIGATION
URINE ANALYSIS
• dark coloured, oliguria, acidic PH
• high specific gravity with acid reaction
• presence of ketones
• Diminished or absent chlorides
CBC: haemoconcentration- rise in Hb,RBC count, haematocrit
LIVER FUNCTIONTEST(LFT)
THYROID FUNCTIONTEST
SERUM ELECTROLYTES
ULTRASOUND SCAN
ECG- when there is hypokalemia
OPHTHALMOSCOPIC EXAMINATION -retinal haemorrhages &
detachment
14. MANAGEMENT
Principles of management:-
To control vomiting.
To correct fluid & electrolyte imbalance.
To correct metabolic disturbance.
To prevent serious complications of severe vomiting.
Care of pregnancy.
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16.
17.
18. Cold meals reduce smell related nausea.
Avoid caffeine & alcohol as these can enhancer dehydration.
Meal high in Carbohydrates & low in fat is better.
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21.
22. General Consideration
Oral Medications will not be effective if the woman is
dehydrated.
With severe Hyperemesis, the risk of using certain
medicines is less than the risk of malnutrition and
significant weight loss
Always ask a health care provider before taking any
medications.
23. MEDICAL MANAGEMENT
DRUGS:
Antihistaminics:
Meclizine 50 mg I/V, I/M or orally
Dimenhydrinate
Diphenhydramine
Doxylamine 10 mg BD or TDS
Phenothiazines
Promethazin(phenargan) 25mg IM bd or tds maximum 150mg/day
Prochlorperazine(stemetil) 50 mg/day in divided doses
Chlorpromazine
Trifluopromazine 10mg IM
Drug stimulating gastric and intestinal motility without stimulating the secretions
Metachlopromide 10mg IM TDS
Nutritional support:- Vitamin B1, vitamin B6, vitamin B12 & vitamin C
24. MEDICAL MANAGEMENT
Drugs decreasing stomach acid production and reflux
Ranitine
Famotidine
Lansoprazole
Drugs decreasing stimulation of the vomiting centre in the brain
Ondencetron
Granisetron
Dolasetron
Steriods
Hydrocortisone:- 100mg IV in drip or I/M (for hypotension or intractale vomiting)
Pridnisolone orally maximum 60mg/day.
25. OTHER MANAGEMENT
FLUID: (Oral Fluid restricted)
• 3 liters-5% dextrose & RL infusion in 24 hrs.
• K+ supplement fluid (Correct Serum Electrolytes)
NURSING MANAGEMENT:-
Initiate measures to alleviate nausea including medication
therapy. If unsuccessful on weight loss & electrolyte
imbalances correction occur, IV administration of fluid &
electrolyte replacement or total parenteral nutrition may be
necessary.
Monitor lab data & look for sign of dehydration & electrolyte
imbalances.
26. NURSING MANAGEMENT
Monitor urine for ketone.
Monitor fetal heart rate, fetal activity & fetal growth.
Encourage intake of small proportion of food.
Liquid should be taken b/w meals to avoid distending
stomach & triggering vomit.
Encourage patient to sit upright after meal.
27. OBSTETRIC CARE
No therapeutic abortion is indicated if patient improve on
therapy.
Therapeutic abortion is seldom indicated on-
o Vomiting doesn’t stop on therapy
o if there is risk of complication.
29. COMPLICATIONS
Mallory Weiss tears
Characterized by upper gastro-intestinal bleeding
secondary to longitudinal mucosal lacerations at the
gastroesophageal junction or gastric cardia.
Stress ulcers in Stomach
30.
31. COMPLICATIONS
Boerhaave syndrome - characterized by upper
gastrointestinal bleeding secondary to transmural
perforation of the esophagus
Renal Failure, Convulsions, Coma.
32.
33. HYPEREMESIS GUIDELINES
A doxylamine/pyridoxine combination should be the standard
of care, since it has the greatest evidence to support its efficacy
and safety. (I-A)
H1 receptor antagonists should be considered in the
management of acute or breakthrough episodes of NVP. (I-A)
Pyridoxine monotherapy supplementation may be considered
as an adjuvant measure. (I-A)
Phenothiazines are safe and effective for severe NVP. (I-A)
SOGC 2002, ACOG 2010
34. HYPEREMESIS GUIDELINES
Metoclopramide is safe to be used for management of
NVP, although evidence for efficacy is more limited. (II-
2D)
Corticosteroids should be avoided during the first
trimester because of possible increased risk of oral clefting
and should be restricted to refractory cases. (I-B)
When NVP is refractory to initial pharmacotherapy,
investigation of other potential causes should be
undertaken. (III-A)
SOGC 2002, ACOG 2010