Wernicke Encephalopathy Secondary to Hyperemesis Gravidarum
OBJECTIVES
To review the clinical manifestations and differential diagnosis of Wernicke encephalopathy.
To summarize the basic neuropathological findings of Wernicke encephalopathy.
To list the most frequent conditions associated with Wernicke encephalopathy.
To review management guidelines for Wernicke encephalopathy.
VIGNETTE
A 34-year-old woman was diagnosed with hyperemesis gravidarum. About 4 weeks after its onset, she started to complain of intermittent oscillopsia and dizziness. A month later, she had gallbladder surgery and induction of a stillborn child at 17 weeks of pregnancy.
CASE SUMMARY
Our patient had intractable vomiting due to hyperemesis gravidarum resulting in Wernicke encephalopathy. Wernicke encephalopathy results from a deficiency in vitamin B1 or thiamine. Because the body’s reserves of thiamine are only 30 to 50 mg, they become depleted in approximately 4 to 6 weeks in the absence of thiamine intake. Global confusional state (greater than 60%), gait ataxia (50%), and a variety of ocular abnormalities (40%) are the hallmark of this disorder, although the occurrence of this triad in combination is unusual. Ocular findings most commonly encountered are vertical nystagmus, bilateral CN VI
palsies, and conjugate gaze palsies, reflecting lesions of the vestibular nuclei, anterior and superior cerebellar vermis, abducens nuclei, and paramedian pontine reticular formation (PPRF).
palsies, and conjugate gaze palsies, reflecting lesions of the vestibular nuclei, anterior and superior cerebellar vermis, abducens nuclei, and paramedian pontine reticular formation (PPRF).