出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/06/28 22:12:58」(JST)
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.
When hyperemesis gravidarum is severe or inadequately treated, it may result in the following:[1]
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]
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 (hCG).[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]
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 |
|
Placenta |
|
|
Gastrointestinal tract | Helicobacter pylori | Increased steroid levels in circulation[15] |
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]
Diagnoses to be ruled out include the following:[13]
Type | Differential diagnoses |
---|---|
Infections
|
|
Gastrointestinal disorders
|
|
Metabolic |
|
Drugs |
|
Gestational trophoblastic diseases (rule out with urine β-hCG) |
|
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]
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]
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.
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 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]
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]
Acupuncture (both with P6 and traditional method) has been found to be ineffective.[23][29] 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]
If HG is inadequately treated, anemia,[1] hyponatremia,[1] Wernicke's encephalopathy,[1] kidney 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]
The effects of HG on the fetus are mainly due to electrolyte imbalances caused by HG in the 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]
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]
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]
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".
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 was hospitalised due to hyperemesis gravidarum during her first pregnancy, and was treated for a similar condition during her second pregnancy.[34]
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リンク元 | 「つわり」「妊娠悪阻」 |
関連記事 | 「hyperemesis」 |
妊娠5-6週 ~ 妊娠12週 (第2月初~第4月初)
.