PATHOGENESIS OF HYPEREMESISGRAVIDARUM

The etiology of hyperemesis in pregnancy is multifactorial.

Usually seen in first trimester of pregnancy.

HORMONAL

BIOLOGICAL

ENVIRONMENTAL

HORMONAL:

Mainly related to high rising serum levels of beta HCG.

During 8-12 weeks of gestation, beta HCG levels are highest at that time and decline afterwards.

Also common in multiple pregnancies and gestational trophoblastic disease due to very high levels of beta HCG.

Also related to rising levels of other hormones such as estrogen, progesterone, leptin, placental growth hormones, prolactin and adrenocortical hormones.

Metabolic,Biochemical and Circulatory changes:

Metabolic: Inadequate intake of food results in glycogen

depletion,hence the fat reserve is broken down for energy supply.

Due to low carbohydrate,there is incomplete oxidation of fat and accumulation of ketone bodies in the blood.The acetone is ultimately excreted through the kidneys and in breath.There is also increase in endogenous tissue protein metabolism resulting in excessive excretion of non-protein nitrogen in the urine.

Water and electrolyte metabolism are seroiusly affected leading to biochemial and circulatory changes.

Biochemical:Loss of water and salts in the vomitus results in fall in

plasma sodium,potassium and chlorides.

The urinary chloride may be well below the normal 5gm/dl or may even be absent.Hepatic dysfuction results in acidosis and ketosis with rise in blood urea and uric acid;hypoglycemia,hyponatremia;hypovitaminosis and rarely hyperbilirubinemia.

Circulatory:There is hemoconcentration leading to rise in

hemoglobin percentage.

RBC count and hematocrit values.There is slight increase in white cell count with increase in eosinophils.

There is concomitant reduction of extracellular fluid.

Changes in various organs:LIVER-Centrilobular fatty infiltration without necrosis.KIDNEYS-Fatty change in the cells of first convoluted

tubule.HEART-Small heart;Sub-endocardial hemorrhage.BRAIN-Small hemorrhages in the hypothalamic region

giving the manifestation of Wernicke’s encephalopathy;Vitamin B1 defeciency.

REFERENCE:Williams Obstetrics- 24th EditionD.C.Dutta’s Textbook of Obstetrics