Hyperemesis Gravidarum with Neurologic Deterioration After Dextrose
A 32-year-old woman at 18 weeks gestation is admitted for hyperemesis gravidarum after 10 days of vomiting and minimal oral intake. She weighs 48 kg and has lost 4 kg. Initial laboratories show sodium 132 mmol/L, potassium 3.2 mmol/L, bicarbonate 18 mmol/L, glucose 88 mg/dL, and lactate 3.6 mmol/L. She is started on 5% dextrose in water at 125 mL/h. Forty-eight hours later, she becomes confused and disoriented. Examination shows horizontal nystagmus, bilateral ophthalmoplegia, and truncal ataxia. She has no history of alcohol use and no focal weakness. Blood glucose is now 112 mg/dL. The team considers whether to continue the dextrose infusion, add thiamine, or investigate for stroke. You are asked to explain the metabolic basis of her neurologic deterioration and choose the next step.
1. What is the most likely diagnosis, and why did the dextrose infusion precipitate it?
Read the worked answer
Wernicke encephalopathy due to thiamine deficiency. Pregnancy and prolonged vomiting increase thiamine requirement and reduce intake. Thiamine pyrophosphate is a cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, transketolase, and branched-chain ketoacid dehydrogenase. When thiamine is low, pyruvate cannot enter the Krebs cycle and accumulates; ATP production falls, and vulnerable regions such as the mammillary bodies, thalamus, and periaqueductal gray develop energy failure and edema. A dextrose load increases glycolytic flux and thiamine demand, so it can precipitate or worsen the encephalopathy. The triad of confusion, ophthalmoplegia or nystagmus, and ataxia is classic. The absence of alcohol use does not exclude the diagnosis because hyperemesis gravidarum is a recognized cause.
2. What is the immediate management, and why should thiamine not be delayed until laboratory confirmation?
Read the worked answer
Give intravenous thiamine immediately, before or alongside any glucose. A common regimen is 500 mg IV three times daily for 2–3 days, then 250 mg daily until deficits resolve; continue oral thiamine after discharge. Also replace magnesium because it is a cofactor for thiamine-dependent enzymes, correct potassium, and treat hyperemesis. Do not wait for blood thiamine levels, which are unreliable and usually unavailable acutely, because untreated Wernicke encephalopathy can progress to irreversible Korsakoff syndrome or death. Glucose should not be given alone in a malnourished or vomiting pregnant patient. Reassess ocular findings and mental status frequently, and involve obstetrics for antiemetic and fluid management.