ESSENTIALS OF DIAGNOSIS
Hyperemesis gravidarum is defined as unexplained intractable nausea, retching, or vomiting beginning in the first trimester, resulting in dehydration, ketonuria, and typically a weight loss of > 5% of prepregnancy weight.
Symptoms typically start between 3 and 5 weeks of pregnancy and 80% resolve by 20 weeks.
Treatment frequently includes avoidance of noxious stimuli, medications to relieve nausea and vomiting, hydration, and possibly hospitalization.
Hyperemesis gravidarum (HEG) affects 0.3–2% of pregnant women. The pathogenesis is largely unknown, with possible contributing factors being increased levels of human chorionic gonadotropin (hCG), estradiol, and possible progesterone. It is more common among younger mothers and those with a history of motion sickness, migraines, and nausea and vomiting associated with oral contraceptives. It is more commonly seen in women carrying multiple gestations, and patients with siblings or a mother with HEG are more likely to be affected.
HEG is associated with severe nausea and vomiting that may result in dehydration, weight loss, and frequently social isolation and negative impacts on relationships with family and friends. Patients with HEG, rather than nausea and vomiting of pregnancy, tend to have an earlier onset and longer duration. Excess salivation (ptyalism) may also be seen in a subset of women with HEG.
Suppressed thyroid-stimulating hormone/elevated free thyroxine and elevated liver enzymes, bilirubin, amylase, and lipase may all be noted in patients with severe nausea and vomiting; these are transiently abnormal and resolve with improvement of HEG.
No imaging studies are needed for the diagnosis of hyperemesis; however, they can be used to exclude other conditions such as pancreatitis, cholecystitis, or intracranial lesions.
Other medical conditions should be suspected if the onset of severe nausea and vomiting is after 9 weeks of gestational age. The differential diagnosis for late HEG should include gastroenteritis, gastroparesis, biliary tract disease, hepatitis, peptic ulcer disease, pancreatitis, appendicitis, pyelonephritis, ovarian torsion, diabetic ketoacidosis, migraines, drug toxicity or withdrawal, psychological conditions, acute fatty liver of pregnancy, and preeclampsia.
Maternal complications of HEG can include Wernicke’s encephalopathy, acute tubular necrosis, central pontine myelinolysis, Mallory-Weiss tear of the esophagus, pneumomediastinum, and splenic avulsion. Additionally, significant psychological burden of the disease has been reported, with depression, anxiety, and lost work frequently seen among those with persistent or severe HEG. Fortunately, no clear fetal complications have been associated with HEG. One study did show that women with HEG who gain < 7 kg during the entire pregnancy have a slightly higher risk of low birth weight and preterm birth. However, there are no congenital anomalies or increased risk of miscarriage or stillbirth noted.
Treatment of HEG begins with supportive measures including hydration and vitamin supplementation (in particular thiamine to prevent Wernicke’s encephalopathy). Nonpharmacologic measures such as acupuncture, hypnotherapy, avoidance of defined nausea ...