HYPEREMESIS

GRAVIDARUM
AND
WERNICKE’S
ENCEPHALOPATHY
SYNDROME

R. Atika Fitria Permadi

4151161429
 CHAPTER I
INTRODUCTION

Nausea Hyperemesis
& vomiting Gravidarum
Vit B1
deficiency
Wernicke’s Triad:
Encephalopathy - Confusion
Syndrome - Ataxia/motor problems
- Oculomotor abnormalities

An Emergency !
 CHAPTER II
LITERATURE REVIEW

1. Definition
– Hyperemesis gravidarum (HG) is a persistent and excessive
vomiting starting before the end of the 20 weeks of
gestation, if severe  associated with malnutrition &
metabolic disturbances.
– Wernicke’s encephalopathy (WE) is an acute
neuropsychiatric disorder caused by prolonged thiamine
(vitamin B1) deficiency. The disorder characterized by a
triad of signs (a change in mental status, ocular
abnormalities, and motor problems).
 CHAPTER II
LITERATURE REVIEW
2. Epidemiology
– Nausea and vomiting affects up to 80% of pregnant woman, 0,3-2
% experience Hyperemesis Gravidarum
– Wernicke’s encephalopathy  Uncommon diagnose. Over 25
cases published between 2012-2015. Only 28% of patients had a
resolution of symptoms.
– WE present as a triad of signs, however all three are present in
only 49% of cases.
– The rate of fetal loss associated with WE in the same review was
48%.
– 71-85% of WE cases remain undiagnosed until postmortem
evaluation
 CHAPTER II
LITERATURE REVIEW
3. Ethiology
– The ethiology of HG  multifactorial, but one popular theory says
it’s related to trophoblastic activity and gonadotropin (hCG) levels.
– Wernicke’s encephalopathy is an acute neuropsychiatric disorder
caused by thiamine deficiency. Thiamine deficiency can be
precipitated by three pregnancy-related conditions: hyperemesis
gravidarum (0,1-0,5 %), diabetic ketoacidosis, and IV administration
of glucose in the presence of chronically inadequate thiamine
intake.
– The body stores of thiamine only last about 18-21 days 
Wernicke’s encephalopathy may occur quite rapidly in patients with
very poor oral intake or persistent vomiting lasting 3-4 weeks.
 CHAPTER II
LITERATURE REVIEW
4. Pathophysiology
– High trophoblastic activity and gonadotropin (hCG) levels  Nausea &
vomiting in HG  poor intake  malnutrition
– The body stores of thiamine only last about 18-21 days, thus very poor
oral intake or persistent vomiting lasting 3-4 weeks  may cause
Wernicke’s encephalopathy
– Free thiamine, which is converted into thiamine diphosphate after going
through the blood-brain-barrier  known as one of the cofactors which
aid in energy metabolism within the brain.
– Thiamine deficiency  Pyruvic acid and lactic acid accumulate within
the brain  changes in the energy metabolism, activation of cellular
membranes, and concentration of nerve conduction molecules 
damaging the nervous system
 CHAPTER II
LITERATURE REVIEW

4. Pathophysiology (continued)
– Lesion of the sixth and third
nerve nuclei  The ocular
muscle and gaze palsies Wernicke’s
Encephalopathy
– Lesion of the cerebrum
syndrome
cortex  Change in mental
status
– Lesion of the cerebellum 
Ataxia/Gait abnormalities
 CHAPTER II
LITERATURE REVIEW

5. Diagnosis
– HG characterized by prolonged and severe nausea and vomiting,
dehydration, large ketonuria, and more than 5% body weight loss.
– WE as a complication of HG is typically identified by the symptom
triad of ataxia or motor problems, confusion, and oculomotor
abnormalities.
– There is no specific laboratory test to diagnose WE. Serum
thiamine levels do not precisely reflect the total body thiamine
status and they can be within normal range.
– Advanced WE signs  elevated transaminase levels, diffuse
background slowing on EEG, seizure activity, and high CSF protein
levels.
 CHAPTER II
LITERATURE REVIEW
5. Diagnosis (continued)
Figure 2 showed bilateral symmetric
edematous high-signal changes in medio-
posterior thalami (arrow) and fornices (large
arrowhead) (A,B). Fluid-attenuated inversion
recovery imaging showed high-signal-
intensity lesions in medio-posterior thalami
(arrow), fornices (large arrowhead) and
mammillary bodies (small arrowhead) (C, D).
(A) T2-weighted imaging of both medio-
posterior thalami and fornices. (C) Fluid-
attenuated inversion recovery imaging of
both medio-posterior thalami and fornices.
(D) Fluid-attenuated inversion recovery
imaging of both mammillary bodies.
 CHAPTER II
LITERATURE REVIEW
6. Treatment
– Prevention of thiamine deficiency is important, the daily
requirement of thiamine in pregnancy increases by about one
third (1,5 mg/day)
– All women with HG who require IV hydration and have been
vomiting for more than three weeks, dehydration, and/or weight
loss should get thiamine supplementation (100mg/day IV or oral
for three days)
 CHAPTER II
LITERATURE REVIEW
6. Treatment (continued)
– Thiamine should be given prior to the administration of glucose
containing fluids. But, patients with hypoglycemia should be
restored to normoglycemia as quickly as possible (repeated dosing
of dextrose 50% in adults until normoglyecemia is achieved).
– Patients with WE should be treated immediately with a minimum
of 500 mg of thiamine dissolved in 100 mL of saline administered
intravenously 3x/day for 2-3 days  After assessing the response,
250 mg of thiamine per day should be given intravenously for 3-5
days or until the clinical signs resolve.
– Oral thiamine dosing should follow parenteral when an HG patient
is asymptomatic  Given its short-life, thiamine should be taken at
least twice daily for 3 months or more in 30-50 mg doses
 CHAPTER II
LITERATURE REVIEW

7. Complication
– The impact of maternal thiamine deficiency on the unborn
baby and neonate is not well studied. Chiossi et al. observed an
increase in the rate of fetal demise by 48% and only 28% of
pregnant women had a resolution of symptoms.
– Another cases showed that if patients with WE receive
inappropriate or delayed treatment  potentially fatal and
provoke several problems such as neurologic sequelae in the
mother, miscarriage, preterm birth, and IUGR
– WE may progress to Korsakoff’s amnestic syndrome which is
associated with severe memory impairment or result in death.
 CHAPTER II
LITERATURE REVIEW

8. Prognosis
– Although Wernicke’s encephalopathy is a rare disorder in
pregnancy  a high index of suspicion for this condition
should be maintained in any pregnant woman suffering
with hyperemesis gravidarum who develops acute
neurological symptoms.
– Early diagnosis and treatment led to favorable maternal
and fetal outcome.
 CHAPTER III
DISCUSSION
– WE is most common in alcoholics, but it also occurs in patients
with malnutrition due to hyperemesis, starvation, renal
replacement therapy, malignancy, and gastric surgery.
– The diagnosis of WE may be difficult because of the high rate at
which patients present with nonspecific symptoms and neurologic
signs. There is no specific laboratory test to diagnose Wernicke’s
encephalopathy.
– Glucose supplementation without thiamine can increase the
thiamine requirement so care is needed. However, because risk of
prolonged hypoglycemia include coma and death  Patients with
hypoglycemia should be restored to normoglycemia as quickly as
possible  then the patient should be given thiamine
intravenously or intramuscularly as soon as possible after
restoration of normoglycemia.
 CHAPTER IV
SUMMARY

– Nausea and vomiting are common symptoms in early pregnancy

during the first trimester. Nausea and vomiting affects up to 80%
of pregnant woman, and 0,3-2,0% experience Hyperemesis
Gravidarum (HG).
– HG can lead to Wernicke’s encephalopathy (WE). WE is an acute
neuropsychiatric disorder caused by thiamine deficiency due to
prolonged vomiting and poor intake.
– The disorder characterized by a triad of signs  a change in
mental status, ocular abnormalities, and motor problems.
– There is no specific laboratory test to diagnose WE. Serum
thiamine levels do not precisely reflect the total body thiamine
status and they can be within normal range in Wernicke’s
encephalopathy. Brain MRI is helpful to eliminate other DDs.
 CHAPTER IV
SUMMARY

– WE should be treated immediately with a minimum of 500 mg of

thiamine dissolved in 100 mL of saline administered intravenously
3x/day for 2-3 days  After assessing the response, 250 mg of
thiamine per day should be given intravenously for 3-5 days or
until the clinical signs resolve
– Prevention of thiamine deficiency  the daily requirement of
thiamine in pregnancy increases by about one third (1,5 mg/day),
due to the increased demand by the fetus and the hypermetabolic
state of pregnancy.
– Early diagnosis is important because if patients with WE receive
inappropriate or delayed treatment, it can be potentially fatal and
provoke several problems such as neurologic sequelae in the
mother and miscarriage, preterm birth, and intrauterine growth
retardation in the fetus
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 THE END

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