cardiology

1. Wernicke’s Encephalopathy following Hyperemesis Gravidarum
Dr.MOHAN
Deparment of General Medicine,JJM Medical College,Davangere,Karnataka
INTRODUCTION
CASE HISTORY
Wernicke’s encephalopathy (WE) is rare nuerological
disorder due to thiamine defienciency and is precipate
by administration of glucose containing fluids before
thiamine supplementation.alomost 80%cases remain
undiagnosed as the majority are during on autopsy.
Many cases of WE in pregnancy with hyperemesis gravi
darum were first reported in 1914.There is no specific
Laboratory test available to support the diagnosis.Can
further be complicated by life threatening condition like
Central pontine myelinolysis(CPM) due to electrolyte
fluctuations.In our study case of WE following HG where
Clinical findings were supported by magnetic resonance
imaging of brain
A 23-year-old woman at 22 weeks gestation,presented
to bapui hospital attached to JJMMedical College ,Dava
ngere with excessive vomiting for several weeks followed by
by progressive weakness of lower limbs,altered sensorium,
and blurred vision.On admission,she had stable vitals with
7/15 Glasgow Coma Scale.Physical examination revealed
Sluggishly reacting puils with papilledema,left sided faci
-al twitching with ptosis of eye,bilateral conjugate palsy
With nystagmusand flaccid paralysis of all four limbs with
Bilateral plantar flexor reflexes.she had no significant past
history and not hypertensive,diabeticor rosk factors.On
General physical exmination ,BP-120/70mmhg,PR-88bpm,
No significant per abdomen findings
Investigations
RADIOLOGICAL INVESTIGATIONS
Tests Normal Range Day1 Day15 Day30
(per litre)
s.chloride 98-107MMOL 96 98 106
s.sodium 137-145MMOL 129 131 140
s.pottasium 3.5-5.1MMOL 3.4 3.9 4.5
s.creatinine 0.7-1.8MG 0.6 1.6 1.8
s.urea 10-50MG 32 42 45
s.magnesium 1.6-2.3MG 1.8 2.1 2.0
s.phosphate 0.7-1.4MMOL 1.2 0.9 0.8
s.albumin 3.5-5.0MG 3.0 4.5 4.2
Bilateral symmetrical
increased signal intensity
of the posteromedial
aspect of both thalami
CONCLUSION
MANAGEMENT
She was electively intubated and ventilated and was
administered intravenous thiamine 100 mg thrice
daily along with other vitamins, electrolytes, and
trace elements. Gradually, her ocular signs
disappeared and she showed neurological recovery
with improvement in muscle power.
DISCUSSION
WE occurs due to deficiency of thiamine which is an
essential cpfactor in various stages of carbonate metab
-olism.If the cells with high metabolic requirements hav
e inadequte stores of thiamine ,energy production drop
and nueronal damage ensues .Body stores B1 of falls
rapidly during fasting.Intravenous dextrose adminitered
before correction of thimaine will aggravate matters
further .In pregnancy it happens due to excessive
vomiting,poor intake and increased metabolic demand
.Sequestration of the vitamin by the fetus and placenta
,can have devastating complications like spontaneous
abortion ,fetal loss.Lab assesment of blood tranketolas
activity and thiamine pyrophosphate are not very reliab
le .MRI is the imaging modality of choice .Our pat
-ient had a signoficant history of of severe vomiting
during pregnancy with poor intake which led to WE.she
present ed with acute mental confusion ,encephalopat
-hy and opthalmoplegia.MRI of the brain was diagnostic
and treatment was started without any delay
WE is a potentially reversible condition if treated early. Thiamine
supplementation is crucial for women with HG.We would like to
emphasize the importance of prompt thiamine supplementation
in pregnant women with prolonged vomiting in pregnancy,
especially before starting intravenous or parenteral nutrition
REFFERENCES
1.Harper C. The incidence of Wernicke's encephalopathy in
Australia
2.Harrison 20th edition