Patients might receive parenteral nutrition (intravenous feeding via a PICC line) or enteral nutrition (via a nasogastric tube or a nasojejunal tube). There is only limited evidence from trials to support the use of vitamin B6 to improve outcome. An oversupply of nutrition (hyperalimentation) may be necessary in certain cases to help maintain volume requirements and allow weight gain. A physician might also prescribe Vitamin B1 (to prevent Wernickes encephalopathy) and folic acid. Alternative medicine
Acupuncture (both with P6 and traditional method) has been found to be ineffective. The use of ginger products may be helpful, but evidence of effectiveness is limited and inconsistent, though three recent studies support ginger over placebo. Complications
Pregnant woman
If HG is inadequately treated, anemia, hyponatremia, Wernickes encephalopathy, kidney failure, central pontine myelinolysis, coagulopathy, atrophy, Mallory-Weiss tears, hypoglycemia, jaundice, malnutrition, pneumomediastinum, rhabdomyolysis, deconditioning, deep vein thrombosis, pulmonary embolism, splenic avulsion, or vasospasms of cerebral arteries are possible consequences. Depression and post-traumatic stress disorder are common secondary complications of HG and emotional support can be beneficial. Infant
The effects of HG on the fetus are mainly due to electrolyte imbalances caused by HG in the mother. Infants of women with severe hyperemesis who gain less than 7 kilograms (15 lb) during pregnancy tend to be of lower birth weight, small for gestational age, and born before 37 weeks gestation. In contrast, infants of women with hyperemesis who have a pregnancy weight gain of more than 7 kilograms appear similar to infants from uncomplicated pregnancies.
It is thought that HG is due to a combination of factors which may vary between women and include genetics. Women with family members who had HG are more likely to develop the disease.One factor is an adverse reaction to the hormonal changes of pregnancy, in particular, elevated levels of beta human chorionic gonadotropin (β-hCG). This theory would also explain why hyperemesis gravidarum is most frequently encountered in the first trimester (often around 8–12 weeks of gestation), as β-hCG levels are highest at that time and decline afterward. Another postulated cause of HG is an increase in maternal levels of estrogens (decreasing intestinal motility and gastric emptying leading to nausea/vomiting).More recently, another cause of HG was discovered: "Evidence suggests abnormal levels of the hormone GDF15 are associated with HG. The validation of a second risk variant, rs1054221, provides further support for GDF15s role in the etiology of HG. Additionally, maternal genes appear to play a more significant role than paternal DNA in contributing to the severity of NVP." Pathophysiology
Although the pathophysiology of HG is poorly understood, the most commonly accepted theory suggests that levels of β-hCG are associated with it. Leptin, a hormone that inhibits hunger, may also play a role.Possible pathophysiological processes involved are summarized in the following table:

Diagnosis
Hyperemesis gravidarum is considered a diagnosis of exclusion. HG can be associated with serious problems in the mother or baby, such as Wernickes encephalopathy, coagulopathy and peripheral neuropathy.Women experiencing hyperemesis gravidarum often are dehydrated and lose weight despite efforts to eat.