Hyperemesis Gravidarum

By Dr. Abdel Magid M.Ahmed

Nov. 2015
 Background
 Nausea and vomiting are common in pregnancy,
occurring in 70-85% of all gravid women
 Hyperemesis gravidarum occurs in 0.5-2% of
pregnancies. Hyperemesis is the second leading
cause of hospitalization in pregnancy, second only
to preterm labor.
Definition
 Hyperemesis gravidarum is a severe and
intractable form of nausea and vomiting in
pregnancy associated with dehydration and
starvation ketonaemia (ketosis) and loss of body
weight
 Background
 It is a diagnosis of exclusion and may result in (5%) weight
loss ; nutritional deficiencies; and abnormalities in fluids,
electrolyte levels, and acid-base balance. The peak incidence
is at 8-12 weeks of pregnancy, and symptoms usually resolve
by week 20 in 90% of patients. Uncomplicated nausea and
vomiting of pregnancy is generally associated with a lower
rate of miscarriage, but hyperemesis gravidarum may affect
the health and well-being of both the pregnant woman and
the fetus.
PATHOPHSILOGY

 Reduced intake+ excessive vomiting

 ↓

 Starvation ketonaemia +ketonuria

 Dehydration

 Hypokaelmic alkalosis (Loss of

chloride)
 Hyponatraemia
Signs of Severe HG:

 Debilitating, chronic nausea//Frequent vomiting of

bile or blood

 Chronic ketosis and dehydration//Muscle weakness

and extreme fatigue//Medication does not stop
vomiting/nausea
 Inability to care for self (shower, prepare food)

 Loss of over 5-10% of your pre-pregnancy weight

 Inability to eat/drink sufficiently by about 14 weeks

Aetiology
The etiology is unknown. Some theories hold that elevated
human chorionic gonadotropin (hCG) or estradiol levels could
be causative, but this has not been demonstrated conclusively.
Psychological theories of the etiology are falling out of favor.
Multiple pregnancy and molar pregnancy are associated with
↑risk (why)
Race
Hyperemesis patients are more likely to be nonwhite.
Age
Patients younger than 30 years are more likely to experience
hyperemesis.
Others//Increase in serum thyroxine level// regurgitation of
duodenal content back into the stomach // deficiencies of
pyridoxine and zinc//physiological and immunological theories.
 Morbidity(complication) &
mortality

 Currently, mortality is exceedingly rare, but maternal

morbidities may include Wernicke encephalopathy from
vitamin B-1 deficiency, Mallory-Weiss tears,
esophageal rupture, pneumothorax, and acute renal
failure {acute tubular necrosis}. Additionally, many
women experience significant psychosocial morbidity,
occasionally interfering with assumption of the maternal role
and rarely leading to termination of the pregnancy.
 Other complications include Centeral pontine mylinolysis,
hypoglycemia, jaundice, Liver failure, DIC & Death
 Fetal complications include IUGR, & Preterm labour.
 Laboratory & Diagnostic
test
 Urine analysis mainly ketones & pus
cells
 CBC: elevated level of RBC &
hematocrit indicating dehydration.
 Liver enzyme: elevation of (AST) &
(ALT) are usually present.
 Laboratory & diagnostic
test
 RFTs (UREA,CREATININE) + Serum electrolyte
decrease levels of k, Na, Cl
 Urine specific gravity :grater than 1.025indicating
concentrated urine linked to inadequate fluid
intake
 Ultrasound :evaluation for molar or multiple
pregnancy
 OTHERS if suitable (B.F for malaria thyroid
function tests
 Management outlines
 Admit
 NPO initially to rest GIT
 I.V.F (normal saline or ringer lactate) & correction of
electrolyte imbalance. & Avoid glucose (Why)
 Diet Avoid fatty & Spicy foods/small frequent
meals/dry food.
 Anti-emetic (see later)
 Vitamines (thiamine & pyrodoxine)
 Steroids (see later)
 Total parenteral nutrition (see later)
 Enteral nutrition Via nasogasteric tube (NGT) {see
later}
 Termination of pregnancy (rarely) {see later}
 Pharmacological treatment

 vitamin B-6 10-25 mg 3-4 times

 Ginger capsules 250 mg 4 times daily can be added at
this point if the patient is still vomiting
 Metoclopramide 5-10 mg orally every 8 hours
Promethazine 12.5 mg orally or rectally q4h or
dimenhydrinate 50-100 mg orally q4-6h may be added
as well. Ondansetron 4-8 mg orally or IV q8h can be
used for further refractory cases. Methylprednisolone 16
mg orally or IV q8h for 3 days, tapered to the lowest
effective dose, can be used if persistent vomiting occurs
despite the above therapy. Steroids seem to increase
risk for oral clefts in first 10 weeks of gestation.
 doxylamine-pyridoxine (Diclegis) is FDA approved
 Correction of hypokaemia
& Avoiding Glucose
 If hypokalemia is severe or symptomatic, potassium should be
replaced parenterally. Before administering IV potassium,
renal function should be evaluated. Potassium is usually
added to intravenous fluid to achieve a concentration of 40
mEq/L (and not >80 mEq/L). An infusion rate of 10 mEq of
potassium per hour should be safe as long as urine output is
adequate.
 When administrating intravenous hydration to a patient who
has severe volume depletion in an effort to prevent the
development of Wernicke encephalopathy, avoid intravenous
glucose until intravenous thiamine has been administered.give
normal saline or ringer lactate.
 Total PARENTERAL
VS NGT
 If persistent dehydration, electrolyte loss, and/or
weight loss occur despite above therapy, nutrition
supplementation by either the parenteral or enteral
route is indicated. The standard method has been
via total parenteral nutrition (TPN). However,
documented risks of bacteremia, sepsis, and
thrombosis have been associated with the PICC
lines required for TPN supplementation. Nasogastric
tube placement and subsequent enteral feeding has
been shown in small series and reports to be a
valid alternative, with less complication risks,
similar efficacy, and similar outcomes in regard to
neonatal outcome when compared with TPN
Termination of the pregnancy
In some refractory severe cases of hyperemesis
gravidarum, if maternal survival is threatened, or
if hyperemesis gravidarum is causing severe
physical and psychological burden, termination
of the pregnancy should be considered.
PICC LINE
ENTERAL NUTRITION