OBG

1. Hyper emesis gravidarum
Ms.Sasikalavathi Arunachalam MSc (N) OBG
PRINCIPAL
HARYANA COLLEGE OF NURSING

2. Definition
Excessive vomiting during pregnancy
Etiology
1st trimester
1st pregnancy
Family history
Hydatidiform mole
Multiple pregnancy
Unplanned pregnancies

3. Theories
Hormonal
Psychogenic
Neurogenic
Dietetic
deficiency ( Vit
B6, vit B1 &
proteins
Allergic or
immunological
Decreased
gastric motility

4. Pathophysiology
CHO
starvation
Ketoacidosis
Vomiting

5. Liver-centri lobular
fatty infiltration
Kidneys – fatty
changes
Heart – small
heart
subendothelial
haemorrhage
Brain – Wernick’s
encephalopathy

6. Metabolic changes
Glycogen
depletion
Ketone bodies
Acetone in urine
and breath
Increased
endogenous tissue
protein metabolism
Excessive excretion
of non protein
nitrogen in the urine

7. Biochemical changes
Loss of water & salt
Fall in plasma Na+, K+ & Cl-
Rise in BUN & uric acid
Hypoglycemia
Hypoproteinemia
hypovitaminosis

8. Circulatory changes
Loss of water
Haemoconcentration
Rise in Hb %, RBC count
Haematocrit values

10. Investigations
• Urinalysis
• Ophthalmoscopic examination
• ECG
• Ultrasonagraphy

11. Complications
Neurological
Wernicke’s
encephalopathy
Pontine
myelinolysis
Peripheral
neuritis
Korsakoff’s
psychosis
Stress ulcer
Esophageal tear
or rupture
Jaundice

12. Management
Principles
• Control vomiting
• To correct the fluid loss
• To prevent complications

13. • Hospitalization
• Oral feeding withheld for 24 hrs
• IV fluids
• Total amount of fluid 3 lrs – half is 5% D and half is Ringer’s
solution
• Extra amount 5% D equal to the amount of vomitus and urine
in 24 hrs
Drugs
• Antiemetic - metoclopramide or promethazine 25 mg
• Hydrocortisone 100 mg IV
Nutritional support
• Diet – Before IV stopped dry CHO foods gradually full diet
• Progress chart

14. If hyper emesis gravidarum is intractable or
associated with renal and neurological complications
Termination of pregnancy

15. Thank U