| Hyperemesis gravidarum |
| Classification and external resources |
| ICD-10 |
O21.1 |
| ICD-9 |
643.1 |
| MedlinePlus |
001499 |
Hyperemesis gravidarum (HG) is a complication of pregnancy characterized by intractable nausea, vomiting, and dehydration and is estimated to affect 0.5–2.0% of pregnant women.[1][2] Malnutrition and other serious complications, such as fluid or electrolyte imbalances, may result.
Hyperemesis is considered a rare complication of pregnancy, but because nausea and vomiting during pregnancy exist on a spectrum, it is often difficult to distinguish this condition from the more common form of nausea and vomiting experienced during pregnancy known as morning sickness.
Contents
- 1 Signs and symptoms
- 2 Causes
- 3 Pathophysiology
- 4 Diagnosis
- 4.1 Differential diagnosis
- 4.2 Investigations
- 5 Management
- 5.1 Intravenous fluids
- 5.2 Medications
- 5.3 Nutritional support
- 5.4 Alternative medicine
- 6 Complications
- 6.1 Pregnant woman
- 6.2 Infant
- 7 Epidemiology
- 8 History
- 9 Notable cases
- 10 References
Signs and symptoms
When hyperemesis gravidarum is severe or inadequately treated, it may result in the following:[1]
- Loss of 5% or more of pre-pregnancy body weight
- Dehydration, causing ketosis,[3] and constipation
- Nutritional disorders such as Vitamin B1 (thiamine) deficiency, Vitamin B6 deficiency or Vitamin B12 deficiency
- Metabolic imbalances such as metabolic ketoacidosis[1] or thyrotoxicosis[4]
- Physical and emotional stress of pregnancy on the body
- Difficulty with activities of daily living
Symptoms can be aggravated by hunger, fatigue, prenatal vitamins (especially those containing iron), and diet.[5] Some women with hyperemesis gravidarum lose as much as 10% of their body weight.[6] Many sufferers of HG are extremely sensitive to odors in their environment; certain smells may exacerbate symptoms. This is known as hyperolfaction. Ptyalism, or hypersalivation, is another symptom experienced by some women suffering from HG.
Hyperemesis gravidarum tends to occur in the first trimester of pregnancy[3] and lasts significantly longer than morning sickness. While most women will experience near-complete relief of morning sickness symptoms near the beginning of their second trimester, some sufferers of HG will experience severe symptoms until they give birth to their baby, and sometimes even after giving birth.[7]
Causes
There are numerous theories regarding the cause of HG, but the cause remains controversial. It is thought that HG is due to a combination of factors which may vary between women and include: genetics,[1] body chemistry, and overall health.[8]
One factor is an adverse reaction to the hormonal changes of pregnancy, in particular, elevated levels of beta human chorionic gonadotropin.[9][10] This theory would also explain why hyperemesis gravidarum is most frequently encountered in the first trimester (often around 8–12 weeks of gestation), as 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).[1]
Pathophysiology
Although the pathophysiology of HG is poorly understood, the most commonly accepted theory suggests that levels of hCG are associated with it.[11] Leptin may also play a role.[12]
Possible pathophysiological processes involved are summarized in the following table:[13]
| Source |
Etiology |
Pathophysiology |
|
|
hCG |
- Distention of gastrointestinal tract
- Crossover with TSH, causing gestational thyrotoxicosis[11]
|
| Placenta |
|
- Decreased gut mobility
- Elevated liver enzymes
- Decreased lower esophageal sphincter pressure
- Increased levels of sex steroids in hepatic portal system[14]
|
| Gastrointestinal tract |
Helicobacter pylori |
Increased steroid levels in circulation[15] |
Diagnosis
Hyperemesis gravidarum is considered a diagnosis of exclusion.[1] HG can be associated with serious maternal and fetal morbidity, such as Wernicke's encephalopathy, coagulopathy, peripheral neuropathy,[11] fetal growth restriction, and even maternal and fetal death.
Women experiencing hyperemesis gravidarum often are dehydrated and lose weight despite efforts to eat.[16][17] The onset of the nausea and vomiting in hyperemesis gravidarum is typically before the twenty-second week of pregnancy.[1]
Differential diagnosis
Diagnoses to be ruled out include the following:[13]
| Type |
Differential diagnoses |
Infections
- (usually accompanied by fever or associated neurological symptoms)
|
- Urinary tract infection
- Hepatitis
- Meningitis
- Gastroenteritis
|
Gastrointestinal disorders
- (usually accompanied by abdominal pain)
|
- Appendicitis
- Cholecystitis
- Pancreatitis
- Fatty liver
- Peptic ulcer
- Small bowel obstruction
|
| Metabolic |
- Thyrotoxicosis (common in Asian subcontinent)[11]
- Addison's disease
- Diabetic ketoacidosis
- Hyperparathyroidism
|
| Drugs |
- Antibiotics
- Iron supplements
|
| Gestational Trophoblastic diseases(rule out with urine β-hCG) |
- Molar pregnancy
- choriocarcinoma
|
Investigations
Common investigations include blood urea nitrogen (BUN) and electrolytes, liver function tests, urinalysis,[17] and thyroid function tests. Hematological investigations include hematocrit levels, which are usually raised in HG.[17] An ultrasound scan may be needed to know gestational status and to exclude molar or partial molar pregnancy.[18]
Management
Dry bland food and oral rehydration are first-line treatments.[19] 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.[3] 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.[13]
Intravenous fluids
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 Wernicke's encephalopathy.[20] 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 in general progress to frequent small liquid or bland meals. After rehydration, treatment focuses on managing symptoms to allow normal intake of food. However, cycles of hydration and dehydration can occur, making continuing care necessary. Home care is available in the form of a PICC line for hydration and nutrition (called total parenteral nutrition).[21] Home treatment is often less expensive than long-term or repeated hospitalizations.
Medications
A number of antiemetics are effective and safe in pregnancy including: pyridoxine/doxylamine, antihistamines (such as diphenhydramine), and phenothiazines (such as promethazine).[22] With respect to effectiveness, it is unknown if one is superior to another,[22] and there is even limited evidence of significant effect at all of pharmacological therapy in hyperemesis gravidarum.[23]
While pyridoxine/doxylamine, a combination of vitamin B6 and doxylamine, is effective in nausea and vomiting of pregnancy,[24] some have questioned its effectiveness in HG.[25] Ondansetron (Zofran) may be beneficial, however, there are some concerns regarding an association with cleft palate,[26] and there is little high quality data.[22] Metoclopramide is also used and relatively well tolerated.[27] Evidence for the use of corticosteroids is weak; there is some evidence that corticosteroid use in pregnant women may slightly increase the risk of oral facial clefts in the infant and may suppress fetal adrenal activity.[1][28] However, hydrocortisone and prednisolone are inactivated in the placenta and may be used in the treatment of hyperemesis gravidarum.[1]
Nutritional support
Women not responding to IV rehydration and medication may require nutritional support. 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.[23] Hyperalimentation may be necessary in certain cases to help maintain volume requirements and allow weight gain.[18] A physician might also prescribe Vitamin B1 (to prevent Wernicke's encephalopathy) and folic acid supplementation.[13]
Alternative medicine
Acupuncture (both with P6 and traditional method) has been found to be ineffective.[29][23] The use of ginger products may be helpful, but the evidence of effectiveness is limited and not consistent, though two recent studies support ginger over placebo.[23]
Complications
Pregnant woman
If HG is inadequately treated, anemia,[1] hyponatremia,[1] Wernicke's encephalopathy,[1] renal failure, central pontine myelinolysis, coagulopathy, atrophy, Mallory-Weiss tears,[1] hypoglycemia, jaundice, malnutrition, pneumomediastinum, rhabdomyolysis, deconditioning, deep vein thrombosis, pulmonary embolism, splenic avulsion, or vasospasms of cerebral arteries are possible consequences. Depression is a common secondary complication of HG and emotional support can be beneficial.[1]
Infant
The effects of HG on the fetus are mainly due to electrolyte imbalances caused by HG in mother.[13] Infants of women with severe hyperemesis who gain less than 7 kg (15.4 lb) during pregnancy tend to be of lower birth weight, small for gestational age, and born before 37 weeks gestation.[3] In contrast, infants of women with hyperemesis who have a pregnancy weight gain of more than 7 kg appear similar to infants from uncomplicated pregnancies.[30] There is no significant difference in the neonatal death rate in infants born to mothers with HG compared to infants born to mothers who do not have HG.[1]
Epidemiology
Vomiting is a common condition affecting about 50% of pregnant women, with another 25% suffering from nausea.[31] However, the incidence of HG is only 0.3–1.5%.[11] After preterm labor, hyperemesis gravidarum is the second most common reason for hospital admission during the first half of pregnancy.[1] Factors such as infection with Helicobacter pylori, a rise in thyroid hormone production, low age, low body mass index prior to pregnancy, multiple pregnancies, molar pregnancies, and a past history of hyperemesis gravidarum have been associated with the development of HG.[1]
History
Thalidomide was prescribed for treatment of HG in Europe until it was recognized that thalidomide is teratogenic and is a cause of phocomelia in neonates.[32]
Etymology
Hyperemesis gravidarum is from the Greek hyper-, meaning excessive, and emesis, meaning vomiting, and the Latin gravidarum, the feminine genitive plural form of an adjective, here used as a noun, meaning "pregnant [woman]". Therefore, hyperemesis gravidarum means "excessive vomiting of pregnant women".
Notable cases
Author Charlotte Brontë is often thought to have suffered from hyperemesis gravidarum. She died in 1855 while four months pregnant, having been afflicted by intractable nausea and vomiting throughout her pregnancy, and was unable to tolerate food or even water.[33]
Catherine, Duchess of Cambridge (also known as Kate Middleton) was hospitalized due to hyperemesis gravidarum during her first pregnancy.
References
- ^ a b c d e f g h i j k l m n o p q Summers, A (July 2012). "Emergency management of hyperemesis gravidarum.". Emergency nurse 20 (4): 24–28. doi:10.7748/en2012.07.20.4.24.c9206. PMID 22876404.
- ^ Goodwin, TM (September 2008). "Hyperemesis gravidarum.". Obstetrics and gynecology clinics of North America 35 (3): 401–17, viii. doi:10.1016/j.ogc.2008.04.002. PMID 18760227.
- ^ a b c d Ahmed KT, Almashhrawi AA, Rahman RN, Hammoud GM, Ibdah JA (November 2013). "Liver diseases in pregnancy: diseases unique to pregnancy". World J Gastroenterol 19 (43): 7639–46. doi:10.3748/wjg.v19.i43.7639. PMC 3837262. PMID 24282353.
- ^ Matthews, DC; Syed, AA (June 2011). "The role of TSH receptor antibodies in the management of Graves' disease.". European journal of internal medicine 22 (3): 213–216. doi:10.1016/j.ejim.2011.02.006. PMID 21570635.
- ^ Carlson, Karen J., MD; Eisenstat, Stephanie J., MD; Ziporyn, Terra, PhD (2004). The New Harvard Guide to Women's Health. Harvard University Press. pp. 392–3. ISBN 0-674-01343-3.
- ^ "Extreme Weight Loss and Extended Duration of Symptoms Common in Hyperemesis Gravidarum" (pdf). Retrieved 26 July 2012.
- ^ "Do I Have Morning Sickness or HG?". H.E.R. Foundation. Retrieved 6 December 2012.
- ^ "HG Theories & Research". helpher.org. Retrieved 25 December 2012.
- ^ Cole, LA (August 2010). "Biological functions of hCG and hCG-related molecules.". Reproductive biology and endocrinology 8 (102). doi:10.1186/1477-7827-8-102. PMC 2936313. PMID 20735820.
- ^ Hershman JM (June 2004). "Physiological and pathological aspects of the effect of human chorionic gonadotropin on the thyroid". Best Pract. Res. Clin. Endocrinol. Metab. 18 (2): 249–65. doi:10.1016/j.beem.2004.03.010. PMID 15157839.
- ^ a b c d e Sheehan, P (September 2007). "Hyperemesis gravidarum--assessment and management". Australian Family Physician 36 (9): 698–701. PMID 17885701. Retrieved 25 January 2012.
- ^ Aka N, Atalay S, Sayharman S, Kiliç D, Köse G, Küçüközkan T (2006). "Leptin and leptin receptor levels in pregnant women with hyperemesis gravidarum". The Australian & New Zealand journal of obstetrics & gynaecology 46 (4): 274–7. doi:10.1111/j.1479-828X.2006.00590.x. PMID 16866785.
- ^ a b c d e Handbook of early pregnancy care. London: Informa Healthcare. 2006. pp. 149–154. ISBN 9781842143230.
- ^ "Hyperemesis gravidarum, a literature review.". Human reproduction update 11 (5): 527–539. September–October 2005. doi:10.1093/humupd/dmi021. PMID 16006438.
- ^ Bagis, T; Gumurdulu, Y; Kayaselcuk, F; Yilmaz, ES; Killicadag, E; Tarim, E (November 2002). "Endoscopy in hyperemesis gravidarum and Helicobacter pylori infection.". International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics 79 (2): 105–9. doi:10.1016/s0020-7292(02)00230-8. PMID 12427393.
- ^ "Hyperemesis Gravidarum (Severe Nausea and Vomiting During Pregnancy)". Cleveland Clinic. 2012. Retrieved 23 January 2013.
- ^ a b c Medline Plus (2012). "Hyperemesis gravidarum". National Institutes of Health. Retrieved 30 January 2013.
- ^ a b Manual of obstetrics (7th ed. ed.). Philadelphia: Wolters Kluwer / Lippincott Wiliams & Wilkins. 2007. pp. 265–268. ISBN 9780781796965.
- ^ Office on Women's Health (2010). "Pregnancy Complications". U.S. Department of Health and Human Services. Retrieved 27 October 2013.
- ^ British National Formulary (March 2003). "4.6 Drugs used in nausea and vertigo – Vomiting of pregnancy". BNF (45 ed.).
- ^ Tuot, D; Gibson, S; Caughey, AB; Frassetto, LA (March 2010). "Intradialytic hyperalimentation as adjuvant support in pregnant hemodialysis patients: case report and review of the literature". International urology and nephrology 42 (1): 233–237. doi:10.1007/s11255-009-9671-5. PMC 2844957. PMID 19911296.
- ^ a b c Jarvis, S; Nelson-Piercy, C (June 2011). "Management of nausea and vomiting in pregnancy.". BMJ (Clinical research ed.) 342: d3606. doi:10.1136/bmj.d3606. PMID 21685438.
- ^ a b c d Matthews, Anne; Haas, David M; O'Mathúna, Dónal P; Dowswell, Therese; Doyle, Mary; Matthews, Anne (2014). Interventions for nausea and vomiting in early pregnancy. doi:10.1002/14651858.CD007575.pub3.
- ^ Tan, PC; Omar, SZ (April 2011). "Contemporary approaches to hyperemesis during pregnancy.". Current Opinion in Obstetrics and Gynecology 23 (2): 87–93. doi:10.1097/GCO.0b013e328342d208. PMID 21297474.
- ^ Tamay, AG; Kuşçu, NK (November 2011). "Hyperemesis gravidarum: current aspect.". Journal of obstetrics and gynaecology : the journal of the Institute of Obstetrics and Gynaecology 31 (8): 708–12. doi:10.3109/01443615.2011.611918. PMID 22085059.
- ^ Koren, G (October 2012). "Motherisk update. Is ondansetron safe for use during pregnancy?". Canadian family physician Medecin de famille canadien 58 (10): 1092–3. PMC 3470505. PMID 23064917.
- ^ Tan, PC; Omar, SZ (April 2011). "Contemporary approaches to hyperemesis during pregnancy.". Current Opinion in Obstetrics and Gynecology 23 (2): 87–93. doi:10.1097/GCO.0b013e328342d208. PMID 21297474.
- ^ Poon, SL (October 2011). "Towards evidence-based emergency medicine: Best BETs from the Manchester Royal Infirmary. BET 2: Steroid therapy in the treatment of intractable hyperemesis gravidarum.". Emergency medicine journal : EMJ 28 (10): 898–900. doi:10.1136/emermed-2011-200636. PMID 21918097.
- ^ Matthews, A; Dowswell, T; Haas, DM; Doyle, M; O'Mathúna, DP (September 2010). "Interventions for nausea and vomiting in early pregnancy.". Cochrane database of systematic reviews (Online) (9): CD007575. doi:10.1002/14651858.CD007575.pub2. PMID 20824863.
- ^ Dodds L, Fell DB, Joseph KS, Allen VM, Butler B. (2006). "Outcomes of pregnancies complicated by hyperemesis gravidarum.". Obstet Gynecol. 107 (2 Pt 1): 285–92. doi:10.1097/01.AOG.0000195060.22832.cd. PMID 16449113.
- ^ Niebyl, Jennifer R. (2010). "Nausea and Vomiting in Pregnancy". New England Journal of Medicine 363 (16): 1544–1550. doi:10.1056/NEJMcp1003896. PMID 20942670.
- ^ Cohen, (Ed.) Wayne R. (2000). Cherry and Merkatz's complications of pregnancy. (5th ed. ed.). Philadelphia: Lippincott Williams & Wilkins. p. 124. ISBN 9780683016734.
- ^ McSweeny, Linda (2010-06-03). "What is acute morning sickness?". The Age. Retrieved 2012-12-04.
|
Pathology of pregnancy, childbirth and the puerperium (O, 630–679)
|
|
| Pregnancy |
|
Pregnancy with
abortive outcome
|
- Ectopic pregnancy
- Abdominal pregnancy
- Cervical pregnancy
- Interstitial pregnancy
- Ovarian pregnancy
- Molar pregnancy
- Miscarriage
|
|
|
Oedema, proteinuria and
hypertensive disorders
|
- Gestational diabetes
- Gestational hypertension
- Pre-eclampsia
- Eclampsia
- HELLP syndrome
|
|
|
Other, predominantly
related to pregnancy
|
|
Digestive system
|
- Acute fatty liver of pregnancy
- Hepatitis E
- Hyperemesis gravidarum
- Intrahepatic cholestasis of pregnancy
|
|
|
Integumentary system /
dermatoses of pregnancy
|
- Gestational pemphigoid
- Impetigo herpetiformis
- Intrahepatic cholestasis of pregnancy
- Linea nigra
- Prurigo gestationis
- Pruritic folliculitis of pregnancy
- Pruritic urticarial papules and plaques of pregnancy (PUPPP)
- Striae gravidarum
|
|
|
Nervous system
|
|
|
|
Blood
|
- Gestational thrombocytopenia
- Pregnancy-induced hypercoagulability
|
|
|
|
Maternal care related to the
fetus and amniotic cavity
|
- amniotic fluid
- Oligohydramnios
- Polyhydramnios
- Braxton Hicks contractions
- chorion / amnion
- Amniotic band syndrome
- Chorioamnionitis
- Chorionic hematoma
- Monoamniotic twins
- Premature rupture of membranes
- Obstetrical hemorrhage
- placenta
- Circumvallate placenta
- Monochorionic twins
- Placenta praevia
- Placental abruption
- Twin-to-twin transfusion syndrome
|
|
|
| Labor |
- Amniotic fluid embolism
- Cephalopelvic disproportion
- Dystocia
- Fetal distress
- Locked twins
- Obstetrical hemorrhage
- placenta
- Preterm birth
- Postmature birth
- Umbilical cord prolapse
- Uterine rupture
- Vasa praevia
|
|
| Puerperal |
- Breastfeeding difficulties
- Agalactia
- Fissure of the nipple
- Galactorrhea
- Breast engorgement
- Diastasis symphysis pubis
- Peripartum cardiomyopathy
- Postpartum depression
- Postpartum thyroiditis
- Puerperal fever
- Puerperal mastitis
|
|
| Other |
- Concomitant conditions
- Diabetes mellitus
- Systemic lupus erythematosus
- Thyroid disorders
- Maternal death
|
|
|
|
|
