Hyperemesis gravidarum: Description, Causes and Risk Factors: Abbreviation: HG. Hyperemesis gravidarum is an uncommon disorder in which extreme, persistent nausea and vomiting occur during pregnancy. This condition might lead to dehydration. The cause of HG is unknown. The leading theories state that it is an adverse reaction to the hormonal changes of pregnancy. In particular, HG may be due to raised levels of beta HCG (human chorionic gonadotrophin) as it is more common in multiple pregnancies and in gestational trophoblastic disease. This theory would also explain why hyperemesis gravidarum is most frequently encountered in first trimester (often around 8 - 12 weeks of gestation), as HCG levels are highest at that time and decline afterward. It is thought that estrogen produces nausea and regurgitation of stomach acids in some women. There is also evidence that leptin (A helical protein secreted by adipose tissue and acting on a receptor site in the ventromedial nucleus of the hypothalamus to curb appetite and increase energy expenditure as body fat stores increase. Leptin levels are 40% higher in women, and show a further 50% rise just before menarche, later returning to baseline levels; levels are lowered by fasting and increased by inflammation) may play a role in HG. A positive correlation between the serum HCG elevation level and free T4 levels has been found, and the severity of nausea appears to be related to the degree of thyroid stimulation. hCG may not be independently involved in the etiology of hyperemesis gravidarum but may be indirectly involved by its ability to stimulate the thyroid. For these patients, HCG levels were linked to increased levels of immunoglobulin M, complement, and lymphocytes. Thus, an immune process may be responsible for increased circulating HCG or isoforms of HCG with a higher activity for the thyroid. Critics of this theory note that (1) nausea and vomiting are not usual symptoms of hyperthyroidism, (2) signs of biochemical hyperthyroidism are not universal in cases of hyperemesis gravidarum, and (3) some studies have failed to correlate the severity of symptoms with biochemical abnormalities. Some studies link high estradiol levels to the severity of nausea and vomiting in patients who are pregnant, while others find no correlation between estrogen levels and the severity of nausea and vomiting in pregnant women. Previous intolerance to oral contraceptives is associated with nausea and vomiting in pregnancy. Progesterone also peaks in the first trimester and decreases smooth muscle activity; however, studies have failed to show any connection between progesterone levels and symptoms of nausea and vomiting in pregnant women. Risk factors for hyperemesis gravidarum include multiple pregnancy, nulliparity, obesity, metabolic disturbances, a history of HG in a previous pregnancy, trophoblastic disorders, psychological disorders (for example, eating disorders such as anorexia nervosa or bulimia) and a history of migration. Symptoms: Signs and symptoms may include:

• Severe nausea and vomiting.
• Food aversions.
• Weight loss of 5% or more of pre-pregnancy weight.
• Decrease in urination.
• Dehydration.
• Headaches.
• Confusion.
• Fainting.
• Jaundice.
• Extreme fatigue.
• Low blood pressure.
• Rapid heart rate.
• Loss of skin elasticity.
• Secondary anxiety/depression.

Diagnosis: Initial lab studies for hyperemesis gravidarum should include the following:

• Urinalysis for ketones and specific gravity: A sign of starvation, ketones may be harmful to fetal development. High specific gravity occurs with volume depletion.
• Serum electrolytes and ketones: Assess electrolyte status to evaluate for low potassium or sodium, identify hyperchloremic metabolic alkalosis or acidosis, and evaluate renal function and volume status.
• Liver enzymes and bilirubin: Elevated transaminase levels may occur in as many as 50% of patients with hyperemesis gravidarum. Mild transaminitis often resolves once the nausea has resolved. Significantly elevated liver enzymes, however, may be a sign of another underlying liver condition, such as hepatitis (viral, ischemic, autoimmune), or some other etiology of liver injury.
• Amylase/lipase: Amylase level is elevated in approximately 10% of patients with hyperemesis gravidarum. Lipase, when combined with amylase, can increase the specificity in diagnosing pancreatitis as an etiology.
• TSH, free thyroxine: Hyperemesis gravidarum is often associated with a transient hyperthyroidism and suppressed TSH levels in 50-60% of cases. However, an elevated free thyroxine may suggest that overt hyperthyroidism is present, thus necessitating further workup and treatment.
• Urine culture: This may be indicated because urinary tract infection is common in pregnancy and can be associated with nausea and vomiting.
• Calcium level: Consider measuring Ca++ levels. Some rare cases have been reported of hypercalcemia being associated with hyperemesis gravidarum, resulting from hyperparathyroidism.
• Hematocrit: This may be elevated because of volume contraction.
• Hepatitis panel: If clinically indicated, hepatitis A, B, or C may be confused with hyperemesis gravidarum.

Imaging:

• Obstetric ultrasonography is usually warranted in patients with HEG to evaluate for multiple gestations or trophoblastic disease.
• Additional imaging studies generally are not needed unless the clinical presentation is atypical (eg, nausea and/or vomiting beginning after 9-10 wk of gestation, nausea and/or vomiting persisting after 20-22 wk, acute severe exacerbation) or another disorder is suggested based on history or physical examination findings.
• If indicated clinically, performing upper abdominal ultrasonography to evaluate the pancreas and/or biliary tree appears to be a low-risk study.
• In rare cases, abdominal CT scan or even MRI may be indicated if appendicitis is under consideration as a cause of nausea and vomiting in pregnancy.

Treatment: Treatment strategies for HG should be based on the severity of symptoms and multimodal in nature (advice, hydration, medication, hospitalization and psychosomatic counseling when necessary). The severity of the condition can be assessed by numerous questionnaires. Two of the most widely used questionnaires are the Pregnancy-Unique Quantification of Emesis and Nausea (PUQE) scoring index, which assesses nausea and vomiting over 12 h, and the PUQE-24, an extension of the original PUQE, which assesses symptoms over 24 h. Another recently developed score is the Hyperemesis Impact of Symptoms Questionnaire (HIS) that brings into focus not only physical but also psychosocial factors in order to assess the impact of HG holistically. In some cases hyperemesis gravidarum is so severe that hospitalization may be required. Hospital treatment may include some or all of the following: 1. Intravenous fluids (IV) - to restore hydration, electrolytes, vitamins, and nutrients 2. Tube feeding:

• Nasogastric - restores nutrients through a tube passing through the nose and to the stomach.
• Percutaneous endoscopic gastrostomy - restores nutrients through a tube passing through the abdomen and to the stomach; requires a surgical procedure.

3. Medications - Metoclopramide, antihistamines, and antireflux medications. NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.