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WIC 301 Hyperemesis Gravidarum
Hyperemesis Gravidarum (HG) is defined as severe and persistent nausea and vomiting during pregnancy which may cause more than 5% weight loss and fluid and electrolyte imbalances (1). This nutrition risk is based on a chronic condition, not single episodes. HG is a clinical diagnosis, made after other causes of nausea and vomiting have been excluded.
Presence of condition diagnosed, documented, or reported by a physician or someone working under a physician’s orders, or as self-reported by applicant/participant/caregiver. See Clarification for more information about self-reporting a diagnosis.
Nausea and vomiting are common early in gestation; 50-80% or more of pregnant women experience some vomiting. However, pregnant women diagnosed with HG are at risk of weight loss, dehydration, ketonuria, and electrolyte imbalances such as hypokalemia. HG affects approximately 0.3-3.0% of pregnancies and may lead to adverse fetal consequences and hospitalization in some cases. HG is the second most common reason for hospitalization for pregnant women, with preterm labor being the most common (2).
Risk Factors for HG
Biological, physiological, psychological and sociocultural factors are thought to be influential in HG (3). The various risk factors for HG include maternal underweight, multiple pregnancy, nulliparity, previous history of HG and trophoblastic disorders (see clarification). A history of eating disorders, such as anorexia nervosa or bulimia, is also a risk factor associated with HG (4, 5). Helicobacter pylori infection may be a contributing factor for HG (6). Studies indicate that offspring or siblings of women with HG, and/or women pregnant with a female fetus, have increased chances of having HG. A history of motion sickness and/or migraine headaches are also risk factors for HG (7).
Various hormones such as estrogen, progesterone, adrenocorticotropic hormone, cortisol, growth hormone, prolactin and human chorionic gonadotropin (HcG) play an influential role in HG. Increased levels of HcG, which may occur in molar (see clarification) or multi fetal pregnancies may be associated with HG. Studies indicate that HG increases when HcG level reaches its peak at 9 weeks of gestation (8). It should be noted that thyroid function is affected in pregnancy. For pregnant women with hyperthyroidism, decreased levels of thyroid stimulating hormone may be implicated for HG (9, 10).
HG an Adverse Maternal Outcomes
HG can adversely affect maternal outcomes and, if inadequately managed, can lead to malnutrition, dehydration, electrolyte imbalances, thrombosis, and Wernicke’s encephalopathy (a very rare but potentially life-threatening complication of HG, caused by thiamine deficiency) (11). Vitamin K deficiency has also been reported with HG and may be implicated in neonatal hemorrhage (12). Other serious complications include esophageal rupture (caused by severe vomiting), peripheral neuropathy, coagulopathy and Mallory-Weiss syndrome (acute increase in esophageal pressure due to vomiting) (8).
Studies indicate that pregnant women with HG in the second trimester are also at an increased risk for placental disorders, such as placental abruption (13). Pregnant women with HG are at an increased risk for any autoimmune disorder, and in extreme cases this may lead to organ damage manifesting as oliguria and abnormal liver function tests (14). In addition, pregnant women with HG are at increased risk for psychological distress therefore leading to an increased risk for depression and anxiety (15). Other concerns associated with HG include severe distress, social dysfunction and loss of time from work (16, 17).
Malnourishment may develop over a period of time in women suffering with HG, which may lead to refeeding syndrome (RFS). RFS includes severe metabolic abnormalities and electrolyte disturbances due to the change from catabolic to anabolic metabolism that occurs when refeeding (orally, parentally, or enterally) occurs too quickly after severe malnourishment. RFS requires multidisciplinary nutrition team management as it is a life-threatening condition (18).
HG and Adverse Birth Outcomes
Systematic review and meta-analysis indicate that HG is frequently associated with adverse birth outcomes (19). Women with HG have an increased risk of giving birth to low birth weight, small for gestational age, and premature infants (20). Infants born to mothers suffering from HG have increased risk of colic, irritability, and growth restrictions (21). There is a scarcity of data examining the long-term effect on fetuses exposed to HG in utero. However, some studies indicate that there is an increased risk of psychological disorders and reduced insulin sensitivity for infants born to women with HG (22, 23)
WIC nutrition staff can provide the following nutrition services to women with HG:
- Refer to a health care provider for appropriate monitoring and treatments as necessary.
- Provide education on how to recognize symptoms of dehydration such as: Increased thirst, dry mouth, low urine output or urine that is darker in color than normal.
- Offer suggestions to help with nausea such as:
Avoid foods and smells that seem to trigger nausea (e.g., fried or greasy foods, spicy foods, foods of a certain texture).
Eat crackers or dry cereal before getting out of bed to curb nausea in themorning.
Avoid large fluid intakes in the morning. Drink liquids between meals instead of with meals.
Choose foods carefully. Select foods that are high in carbohydrates or protein, low in fat, and easy to digest. Salty foods are sometimes helpful, as are foods that contain ginger — such as ginger lollipops. Avoid greasy, spicy and fatty foods. Consume foods that settle the stomach and calm the nausea. (24)
Eat several small meals throughout the day instead of three large meals. Meals should contain more carbohydrate than fat and acid. Protein-rich meals also decrease symptoms. Lighter snacks, including nuts, dairy products, and beans, are recommended. (25)
Take prenatal supplement at night or before bedtime.
- Review weight gain goal and weight gain pattern. If weight loss is a problem, discuss nutrient and calorie-dense food choices and refer to the health care provider.
- Encourage women to take prenatal vitamins if considering becoming pregnant again. Studies indicate that taking prenatal vitamins a month before conception may help alleviate the symptoms of HG during pregnancy (26).
Self-reporting of a diagnosis by a health care provider should not be confused with self-diagnosis, where a person simply claims to have or to have had a medical condition without any reference to professional diagnosis. A self-reported medical diagnosis (“My doctor says that I have/my son or daughter has…”) should prompt the CPA to validate the presence of the condition by asking more pointed questions related to that diagnosis.
Gestational Trophoblastic Disease (GTD) may be defined as a condition in which a tumor develops in the uterus that would normally develop as a placenta. Molar pregnancy or a hydatidiform mole may be classified as a form of noninvasive tumor under GTD. A molar pregnancy results from an abnormal fertilization of the egg lacking in maternal tissues. It should be noted that although the tumor is considered benign they have potential to become malignant. The symptoms include vaginal bleeding, hyperemesis, preeclampsia, and hyperthyroidism. (27)
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2. Schiff MA, Reed SD, Daling JR. The sex ratio of pregnancies complicated by hospitalisation for hyperemesis gravidarum. BJOG: An International Journal of Obstetrics & Gynaecology. 2004 Jan 1;111(1):27-30.
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7. Basso O, Olsen J. Sex ratio and twinning in women with hyperemesis or pre-eclampsia. Epidemiology. 2001 Nov and 12(6):747-9.
8. Sheehan P. Hyperemesis gravidarum: assessment and management. Australian Family Physician. 2007 Sep 1;36(9):698.
9. Chan NN. Thyroid function in hyperemesis gravidarum. The Lancet. 1999 Jun 26;353(9171):2243.
10. Blankenstein TJ, Kainer F, Friese K, Mylonas I. Extended hyperemesis gravidarum in a patient after total thyroidectomy. Archives of Gynecology and Obstetrics. 2009 Dec 1;280(6):1029.
11. Dodds L, Fell DB, Joseph KS, Allen VM, Butler B. Outcomes of pregnancies complicated by hyperemesis gravidarum. Obstetrics & Gynecology. 2006 Feb 1;107(2, Part 1):285-92.
12. Toriello HV, Erick M, Alessandri JL, Bailey D, Brunetti-Pierri N, Cox H,Maternal vitamin K deficient embryopathy: association with hyperemesis gravidarum and Crohn disease. American Journal of Medical GGenetics Part A. 2013 Mar 1;161(3):417-29.
13. Bolin M, Åkerud H, Cnattingius S, Stephansson O, Wikström AK. Hyperemesis gravidarum and risks of placental dysfunction disorders: a population-based cohort study. BJOG: An International Journal of Obstetrics & Gynaecology. 2013 Apr 1;120(5):541-7.
14. Ahmed KT, Almashhrawi AA, Rahman RN, Hammoud GM, Ibdah JA. Liver diseases in pregnancy: diseases unique to pregnancy. World Journal of Gastroenterology: WJG. 2013 Nov 21;19(43):7639.
15. McCarthy FP, Khashan AS, North RA, Moss-Morris R, Baker PN, Dekker G, Poston L, Kenny LC, SCOPE consortium. A prospective cohort study investigating associations between hyperemesis gravidarum and cognitive, behavioral and emotional well-being in pregnancy. PloS one. 2011 Nov 18 and 6(11):e27678.
16. Piwko C, Ungar WJ, Einarson TR, Wolpin J, Koren G. The weekly cost of nausea and vomiting of pregnancy for women calling the Toronto Motherisk Program. Current Medical Research and Opinion. 2007 Apr 1;23(4):833-40.
17. Piwko C, Koren G, Babashov V, Vicente C, Einarson TR. Economic burden of nausea and vomiting of pregnancy in the USA. J Popul Ther Clin Pharmacol. 2013;20(2):e149-60.
18. Stokke G, Gjelsvik BL, Flaatten KT, Birkeland E, Flaatten H, Trovik J. Hyperemesis gravidarum, nutritional treatment by nasogastric tube feeding: a 10-year retrospective cohort study. Acta Obstetricia et Gynecologica Scandinavica. 2015 Apr 1;94(4):359-67.
19. London V, Grube S, Sherer DM, Abulafia O. Hyperemesis Gravidarum: A Review of Recent Literature. Pharmacology. 2017;100(3-4):161-71.
20. Veenendaal MV, van Abeelen AF, Painter RC, van der Post JA, Roseboom TJ. Consequences of hyperemesis gravidarum for offspring: a systematic review and meta-analysis. BJOG: An International Journal of Obstetrics & Gynaecology. 2011 Oct 1;118(11):1302-13.
21. Mullin PM, Ching C, Schoenberg F, MacGibbon K, Romero R, Goodwin TM, Fejzo MS. Risk factors, treatments, and outcomes associated with prolonged hyperemesis gravidarum. The Journal of Maternal-Fetal & Neonatal Medicine. 2012 Jun 1;25(6):632-6.
22. Mullin PM, Bray A, Schoenberg F, MacGibbon KW, Romero R, Goodwin TM. Prenatal exposure to hyperemesis gravidarum linked to increased risk of psychological and behavioral disorders in adulthood. Journal of Developmental Origins of Health and Disease. Aug, 2011 and 2(4):200-4.
23. Ayyavoo A, Derraik JG, Hofman PL, Biggs J, Bloomfield FH, Cormack BE, Stone P, Cutfield WS. Severe hyperemesis gravidarum is associated with reduced insulin sensitivity in the offspring in childhood. The Journal of Clinical Endocrinology & Metabolism. 2013 Aug and 98(8):3263-8.
24. Mayo Clinic [Internet]. Minneapolis: Patient Care and Health Information; [Sep 2014: cited 2018 May 1] Morning Sickness. Available from: https://www.mayoclinic.org/diseasesconditions/morning-sickness/diagnosis-treatment/drc-20375260.
25. Wegrzyniak LJ, Repke JT, Ural SH. Treatment of hyperemesis gravidarum. Rev Obstet Gynecol. 2012;5(2):78-84. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410506/.
26. Committee on Practice Bulletins-Obstetrics. ACOG Practice Bulletin No.189.Nausea and Vomiting of Pregnancy. Obstet Gynecol. 2018 Jan 1;131(1):15-30.
27. Garner EI, Goldstein DP, Feltmate CM, Berkowitz RS. Gestational trophoblastic disease. Clin Obstet Gynecol. 2007 Mar;50(1):112-22.