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.
The onset of the nausea and vomiting in hyperemesis gravidarum is typically before the 20th week of pregnancy. Differential diagnosis
Diagnoses to be ruled out include the following:

Investigations
Common investigations include blood urea nitrogen (BUN) and electrolytes, liver function tests, urinalysis, and thyroid function tests. Hematological investigations include hematocrit levels, which are usually raised in HG. An ultrasound scan may be needed to know gestational status and to exclude molar or partial molar pregnancy. Management
Dry bland food and oral rehydration are first-line treatments. Due to the potential for severe dehydration and other complications, HG is treated as an emergency. If conservative dietary measures fail, more extensive treatment such as the use of antiemetic medications and intravenous rehydration may be required. If oral nutrition is insufficient, intravenous nutritional support may be needed. For women who require hospital admission, thromboembolic stockings or low-molecular-weight heparin may be used as measures to prevent the formation of a blood clot. Intravenous fluids
Intravenous (IV) hydration often includes supplementation of electrolytes as persistent vomiting frequently leads to a deficiency. Likewise, supplementation for lost thiamine (Vitamin B1) must be considered to reduce the risk of Wernickes encephalopathy. A and B vitamins are depleted within two weeks, so extended malnutrition indicates a need for evaluation and supplementation. In addition, electrolyte levels should be monitored and supplemented; of particular concern are sodium and potassium. After IV rehydration is completed, patients typically begin to tolerate frequent small liquid or bland meals. After rehydration, treatment focuses on managing symptoms to allow normal intake of food.