Hyperemesis gravidarum

Captain Ala’a Ababneh

RN, Msc
Introduction

 Nausea and vomiting during pregnancy is a common

experience affecting 50% to 90% of all women.
 Nausea and vomiting are usually limited to the first
trimester, but 20% of women have symptoms that
continue throughout pregnancy.
 The spectrum of nausea and vomiting in pregnancy
can range from mild to severe and can involve
persistent and excessive vomiting.
 Hyperemesis gravidarum (HG) is the most severe
form of nausea and vomiting in pregnancy and is
characterized by intractable nausea and vomiting
that leads to dehydration, electrolyte and metabolic
disturbances, and nutritional deficiency that may
require hospitalization.
 Hyperemesis gravidarum has also been defined as
severe vomiting with onset at less than 16 weeks of
estimated gestational age that causes 5% weight
loss and considerable ketonuria.
Incidence

 Hyperemesis gravidarum has an incidence

varying from 0.3% to 2% of all pregnancies.
 Deuchar noted 8.6 million hours of paid
employment and 5.8 million hours of
housework are lost each year because of this
condition.
Etiology
 The cause of HG is not well understood but appears to have
both physiologic and psychologic components. Estrogen,
progesterone, adrenal, and pituitary hormones have been
proposed as causes but currently there is no conclusive
evidence implicating any of them.
 One popular theory is that nausea and vomiting of
pregnancy is related to trophoblastic activity and gonadotropin
production, possibly secondary to elevated
serum human chorionic gonadotropin (hCG) levels.
 Recently, Helicobacter pylori infection has been implicated as a
possible cause of HG. In a prospective study, Helicobacter serum IgG
concentrations in patients with HG were compared with those in
asymptomatic gravidas matched for week of gestation. Positive IgG
concentrations were found in 95/105 hyperemesis patients compared
with 60/129 controls. The authors conclude that infection with H. pylori
may cause HG.
 A psychosomatic etiology has been proposed for HG. Zechnich and
Hammer reported, “pregnant women have been shown to have a
significantly higher level of anxiety than nonpregnant women and are
known to be readily influenced by suggestion and by reassurance.”
Other authors have suggested that HG has been linked to stress and
emotional tension and is found more commonly among “immature,
dependent, hysteric, depressed, or anxious” women, although this has
not been studied.
 Other mechanisms that have been proposed
for HG include changes in gastrointestinal
tract motility, thyroid dysfunction,
hypofunction of the anterior pituitary and
adrenal cortex, and abnormalities of the
corpus luteum.
Associated Risks

 Various risk factors have been theorized to be

associated with HG. These include increased body
weight, multiple gestations, trophoblastic disease, HG
in a prior pregnancy, and nulliparity
 Also, metabolic disorders associated with HG could
possibly contribute to an increased risk, including
hyperthyroidism, hyperparathyroidism, altered lipid
metabolism, and liver dysfunction.
 Another associated risk factor for hyperemesis
gravidarum may be a previous diagnosis of an eating
disorder.
Diagnosis
 The diagnosis of HG rests in careful observation of the signs
and symptoms of pregnant patients with excessive vomiting.
Symptoms of HG typically present during the first trimester of
pregnancy, usually beginning between the 4th and 10th weeks
of gestation, peaking between the 8th and 12th week, and
resolving by the 20th week. In only the rare case, symptoms
persist into the second half of gestation.
 Patients usually present with signs of dehydration, ketosis,
electrolyte and acid-base disturbances. Weight loss of greater
than 5% of body weight may occur.
 Work-up must always start with confirmation of a
viable, intrauterine pregnancy. When HG is
diagnosed, the associated conditions of multiple
gestations and hydatidiform mole should be
excluded.
 The diagnosis of HG should exclude other causes of
vomiting, such as gastroenteritis, cholecystitis, acute
pancreatitis, gastric outlet obstruction, pyelonephritis,
primary hyperthyroidism, primary
hyperparathyroidism, or liver dysfunction.
 Laboratory tests to help with diagnosis and treatment may
include electrolytes, liver function tests, amylase, lipase, thyroid
function tests, B-HCG, creatinine, blood urea nitrogen,
urinalysis, and CBC.
 Ultrasound examination should be considered to rule out
multiple gestation and molar pregnancy. Laboratory findings at
presentation of HG may include increased ketones and
increased specific gravity in urine with an associated increase
in blood urea nitrogen.
 Also, the hematocrit may be elevated indicating a contracted
fluid volume. Electrolytes values that may be associated with
HG include decreased sodium, potassium, and chloride, and
possibly increased liver function tests.
Prognosis

 The effect of nausea and vomiting of pregnancy on

maternal and neonatal outcome has been
controversial. Several studies suggest that nausea
and vomiting of pregnancy is a favorable prognostic
sign with a decreased risk of miscarriage, stillbirth,
fetal mortality, preterm delivery, low birth weight,
perinatal mortality, or growth retardation. Thus the
outcome of nausea and vomiting in pregnancy is
considered excellent with no adverse fetal outcome.
 Severe and untreated HG was found to be associated with a poor
outcome. In one particular study, the hyperemetic pregnant patients
were at severe nutritional risk as the mean dietary intake of most
nutrients fell below 50% of the recommended dietary allowances and
differed significantly from that of controls.
 In selected cases where greater than 5% weight loss and long-term
malnourishment were of concern, adverse pregnancy outcomes have
been reported including low birth weight, antepartum hemorrhage,
preterm delivery, and an association with fetal anomalies.
 Prolonged vomiting also carries the risk of Wernicke’s encephalopathy
secondary to thiamine (vitamin B1) deficiency. Also, hyponatremia and
its rapid reversal may cause fatal central pontine myelinosis.
Treatment
 The main treatment of HG is supportive care.
 Various lifestyle and diet changes can help patients tolerate oral
intake. Patients should try to avoid unpleasant odors; eat a bland, dry,
carbohydrate diet; eat small, frequent meals; and separate solid and
liquid foods by at least 2 hours.
 Immediate correction of fluid and electrolyte deficits and acid-base
disorders must be acomplished. If this cannot be done using oral
therapy, intravenous fluids may be considered. The patient should
initially have nothing by mouth until deficits are corrected. Once this is
done, an attempt may be made to restart oral intake using the
recommend diet. One study found that treatment with intravenous
rehydration led to cessation of vomiting and increase tolerance to oral
intake within 24 hours in HG patients.
 In cases that are refractory to intravenous fluid treatment,
parentaral nutrition and even feeding tubes have been
necessary. Nutritional support is reserved for patients who
continue to have intractable symptoms and weight loss despite
appropriate therapy. Without nutritional support, the mother and
hence the fetus are at significant nutritional risk. Hsu and
colleagues report successful use of nasogastric tube feeding in
the management of HG, as compared with total parenteral
nutrition. Tube feeding is less invasive, carries fewer risks,
provides nutrition more physiologically, and is easier to use.
 The safety of antiemetic therapy is questionable, especially
during the first trimester. Examples of antiemetics used for
treatment of HG include doxylamine (Unisom),
metoclorpramide (Reglan), promethazine (Phenergan),
prochlorperazine (Compazine), trimethobenzamide (Tigan),
dimenhydrinate (Dramamine), droperidol (Inapsine),
diphenhydramine (Benadryl), and ondansetron (Zofran). All the
mentioned medications are FDA class B (presumed safety
based on animal studies) or class C (uncertain safety as animal
studies show an adverse effect and no human studies have
been performed).
 Oral corticosteroid use has been studied in the
treatment of HG and may be beneficial. The
mechanism by which corticosteroids suppress the
severe vomiting is probably a direct effect on the
vomiting center in the brain.
 Vitamin B6 has been postulated to have a beneficial
effect on HG treatment. Unfortunately, studies have
not shown a proven medical benefit. Ginger has also
been used in HG treatment.
Prevention

Prevention of hyperemesis has been studied

using oral multivitamin therapy. A randomized
double-blind controlled trial of peri-
conceptional multivitamin supplementation
found a significant reduction in the occurrence
of HG, 3% in the supplemented group versus
6.6% in the unsupplemented group. There was
a significant decrease in the rate of moderate
nausea and vomiting.