OUT

NIGUSI .A
 Outline
 Definition of HEG
 Epidmeology HEG
 Cause of HEG
 Risk factor of HEG
 Clinical presentation of HEG
 Investigation of HEG
 Management of HEG
 Complication of HEG

03/07/2016 HEG
 Definition

It is a severe type of vomiting of pregnancy

which has got deleterious effect on the health of
the mother and/or incapacitates her in day-to-day activities.

03/07/2016 HEG
 Epidmeology

• Nausea and vomiting of pregnancy appears to be more

common in Western countries and urban areas and less
common in Africa and Asia.
• Younger, primigravid individuals are more likely to be affected
than older, multiparous individuals, but data are inconsistent.

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 Risk factor
Multiple gestation
Symptoms in a prior pregnancy
Hydatidiform molar pregnancy
Overweight
Young age
Primigravidity
Acid reflux or other gastrointestinal disorders
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 Etiology
 The etiology is obscure but the following are the known facts:
 It is mostly limited to the first trimester
 It is more common in first pregnancy, with a tendency torecur
again in subsequent pregnancies
 It has got a familial history — mother and sisters alsosuffer
from the same manifestation
 It is more prevalent in hydatidiform mole and multiple
pregnancy
 It is more common in unplanned pregnancies

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 Common theory
Hormonal :
• Excess of chorionic gonadotropin or higher biological
• activity of hCG is associated. This is proved by the frequency
• of vomiting at the peak level of hCG and also the increased
• association with hydatidiform mole or multiple pregnancy
• when the hCG titer is very much raised

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A. High serum level of estrogen

B. Progesterone excess
• leading to relaxation of the cardiac sphincter and
simultaneous retention of gastric fluids due to impaired
gastric motility.

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 Other hormones involved are
thyroxin
prolactin,
 leptin and
adrenocortical hormones
Psychogenic:
• It probably aggravates the nausea once it begins.

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• But neurogenic element sometimes plays a role, asevidenced
by its subsidence after shifting the patient from the home
surroundings.
 Conversion disorder, somatization,excess perception of
sensations by the mother are the other theories.

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Dietetic deficiency:
• Probably due to low carbohydrate reserve, as it happens after a
night without food.
•Deficiency of vitamin B6, Vit B1 and proteins may be the effects
rather than the cause.

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Allergic or immunological basis.
Decreased gastric motility is found to cause
nausea
• Whatever may be the cause of initiation of
vomiting, it is probably aggravated by the
neurogenic element

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 Clinical presentation
• Symptoms typically start at 5 to 6 weeks of gestation
• Peak at approximately 9 weeks
• usually subside by 16 to 20 weeks.
• However, symptoms may continue until the third trimester in
15 to 20 percent of patients and until delivery in 5 percent.

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 Con...
• Sixty percent of patients are asymptomatic six weeks after
onset of nausea .
• If vomiting begins in the latter half of pregnancy and/or
persists beyond a few days postpartum
• other etiologies should be investigated

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• Although the lay term for mild pregnancy-related nausea and
vomiting is "morning sickness
• The symptoms may occur at any time of day,
• May only occur in the evening, and often (80 percent) persist
throughout the day

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• Excessive vomiting, loss of appetite, sign of dehydration, low
BP, increase pulse rate, weight loss
• In severe cases acidotic pattern of breathing (deep and
shallow) may ensue.
• In addition the clinician should look for other medical and
surgical causes like hyperthyroidism, food poisoning, diabetes,
appendicitis, etc.

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 Diagnosis and Investigation
The diagnosis of hyperemesis is considered in
the presence of severe nausea and vomiting
after exclusion of other causes of nausea and
vomiting during pregnancy

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• The standard initial basic evaluation of all pregnant patients
with persistent nausea and vomiting includes:
• Serum electrolytes
• Urine ketones and specific gravity
• Creatinine
• Complete blood count

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 Investigation
• Ketonuria, Elevated AST and ALT
• Screen the patient for UTI and other medical causes
• Ultrasound examination to look for GTD, Multiple gestation
• Serum electrolytes
• Creatinine
• Complete blood count

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 Management of Principles
• Correction of fluid and electrolyte deficits
• Identification and treatment of any co-
morbidities
• Identification and management of
complications

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Outpatient management
• IV fluids:
• Infuse one liter over 1-2 hours and then 1000
mL over 4 hours (i.e. 2 litres over 5 to 6 hrs),
followed by further assessment, including urine
ketone testing.
• Discharge the patient from outpatient care with
PO medications and dietary advice.
• Or, admit for inpatient care
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 Medications:
• Vitamin B6 (pyridoxine):- 10–25mg PO BID-
QID and Meclizine 25 mg PO TID, or
• Metoclopramide:- 5-10 mg PO TID, or
• Promethazine:- 12.5-25 mg PO TID to QID, or
• Ondansetron 4-8 mg PO TID, or
• Chlorpromazine 12.5 mg IM BID

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Dietary advice:
• Avoiding of empty stomach,
• Advise intake of small and frequent diet,
• Restriction of coffee, and spicy, odorous, high fat,
acidic and very sweet foods,
• Counsel on preferably taking protein rich, salty
(e.g. nuts), low fat, tasteless and dry snacks/meals.
• Encourage on fluid intake (better tolerated if cold,
clear, and carbonated or sour).
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• Advise on taking peppermint containing
products (e.g. chewing gum, candy) to reduce
postprandial nausea.
• Advise not to take drugs that may cause
nausea and vomiting, e.g. iron supplement
should be temporarily discontinued.
• Advise on taking ginger or ginger containing
preparations

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• Counsel on avoiding of environmental
triggers:
• stuffy rooms
• strong odors (e.g.perfume, chemicals, food,
smoke)
• heat, humidity, noise
• visual or physical motion (e.g. flickering lights,
driving).
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tient management
ications for admission:
ight loss > 5% from pre-pregnancy
tonuria above +2
ctrolyte imbalance
ranged renal and liver function tests
rsistent vomiting / failed OPD management

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 Fluid management:

• Oral feeding withheld for 24 to 48 hrs.

• Give 1 to 2 liters of isotonic saline or ringer lactate
within 1 - 2 hrs.
• Continue fluid repletion at a rapid rate (1-2 L over
the next 2-3 hrs) until the clinical signs of
hypovolemia improves (e.g. low blood pressure, low
urine output, and / or impaired mental status,).
• Avoid dextrose containing fluid until thiamine is
supplemented with the initial rehydration fluid.

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Give maintenance fluid after deficit is
corrected:-
o 4 ml / kg / hr- for the first 10 hrs
o 2 ml / kg / hr for the next 10 hrs
o 1 ml / kg / hr for the rest
In addition replace ongoing loss

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• Vitamins:
• Thiamine (vitamin B1):
• Give 100 mg IV with the initial rehydration
fluids before administration of dextrose
containing fluids and another 100 mg daily for
the next two or three days i.e. 10 ampoules of
Vita. B complex containing 10 mg of thiamine
per 24 hrs (3 ampoules / liter).

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• Vitamin B6:
• Give 10-25 mg in every liter (i.e. at least 5
ampoules of vitamin B complex containing 2
mg of vitamin B-6 in each bag of fluid).

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Electrolyte management:
• Depends on the electrolyte abnormality
detected on lab tests.
• Potassium supplementation:
• For mild to moderate hypokalemia (serum
potassium 2.5-3.5 meq)
• Give potassium - 20-80 meq / 24 hrs.
• Add 1vial of KCL in each bag of maintenance
fluid
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• For severe hypokalemia (serum potassium
<2.5 meq/l) or symptomatic hypokalemia.
• Give potassium – 20 meq/2-3 hrs with careful
monitoring every 2-4 hrs,
• Add 2-3 vials of KCL (40-60 meq) in each bag
of maintenance fluid.
• Adjust the amount based on the serum
potassium level.

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Antiemetics
First line
Meclizine 25mg IV TID, or
Metoclopramide- 5–10 mg IV TID, or
Promethazine 5-10 mg IM every 6-8 hrs
Second line:
Serotonin antagonists - Ondansetron 4-8 mg IV or
PO, TID
Third line: Chlorpromazine 25mg IV or IM QID.
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• NOTE:
• Combinations of different drugs should be
considered in women who do not respond to
a single antiemetic.
• Shift to the next line of antiemetic drugs if
emesis continues without improvement after
24 hrs of therapy.

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• PO diet can be resumed after a short period of
gut rest.
• Dietary recommendations stated above for
outpatient management similarly applies for
in patient cases.
• If the patient has acid reflux or PUD
administer anti-acid suspensions or H2
receptor blockers as needed.

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 Follow up:
• Vital signs (twice daily)
• Weight (at presentation, then daily)
• Features of dehydration
• In put & out put
• Urine ketone (daily)
• Appetite

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Criteria for Discharge
• Improvement of ketone level in the urine
• Tolerating oral fluids and possibly food for at
least 24 hrs hours after urine is free for ketone
and with PO antiemetic.

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 COMPLICATIONS

Maternal
• Esophageal tear or rupture
• Peripheral neuropathy due to B6 and B12
deficiency
• Wernicke's encephalopathy
• Liver and renal failure

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 Fetal
• Preterm deliveries
• Stillbirths
• Miscarriages
• Fetal growth retardation
• Fetal death

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