Hyperemesis gravidarum is the most severe form of nausea and vomiting during pregnancy and is characterized by intractable nausea and vomiting that leads to dehydration, electrolyte and metabolic disturbances, and nutritional deficiency that may require hospitalization. Hyperemesis gravidarum is a clinical diagnosis; most of physicians diagnose it by its typical presentation and exclusion of other causes of nausea and vomiting in the pregnant woman. Onset of vomiting typically starts between 6 and 8 weeks’ gestation and peaks by 12 weeks. It is a disease of high prevalence among pregnant women. It is a common experience affecting 50% to 90% of all women. It is the most common indication for hospitalization during the first half of pregnancy. Hyperemesis gravidarum are usually limited to first trimester but 20% of women continue throughout pregnancy. It causes economic burden upon families and countries. There are many lines of treatment of Hyperemesis gravidarum, some lines are well studied. Moreover, studies regarding drug safety were done to determine incidence of congenital anomalies in babies of mothers received these drugs. Other lines are still experimental. In this article, we are going to discuss those lines using recent statistics and studies regarding each line of treatment.

The most important intervention is fluid and electrolyte replacement. This pregnant woman is in a catabolic condition and sufficient caloric requirements must be administered through our treatment strategy. The volume of fluid should be enough to replace the deficit and continuing loss through vomiting as well as to meet normal fluid and electrolyte requirements. RCOG guidelines of 2016 recommend that saline with potassium chloride with daily monitoring of electrolytes is the most beneficial parenteral hydration. Dextrose solutions are not preferred except if the serum sodium levels are normal and thiamine has been given to avoid precipitation of Wernicke’s encephalopathy. A randomised controlled trial comparing the use of 5% dextrose and 0.9% sodium chloride with 0.9% sodium chloride in women with Hyperemesis gravidarum showed no difference after 24 hours in terms of persistent ketonuria, quality of life, nausea, vomiting or resolution of electrolyte imbalance. But higher concentration sodium chloride (for example 1.8%) should be avoided even if the patient is significantly hyponatraemic because too rapid correction of serum sodium level may cause osmotic demyelination syndrome. Potassium intake is often necessary and should be given according to the serum potassium level.

With Regards,
Sara Giselle
Associate Managing Editor
Journal of Critical Care Obsestrics & Gynocology