Wernicke's Encephalopathy in Hyperemesis Gravidarum

Hyperemesis gravidarum causes severe, persistent vomiting in pregnancy, which can rapidly deplete water-soluble vitamin stores — particularly thiamine (vitamin B1), a vitamin with very limited body reserves (only 2–3 weeks' worth). Prolonged vomiting, poor oral intake, and administration of intravenous dextrose without thiamine supplementation (which accelerates thiamine consumption in glucose metabolism) precipitate an acute deficiency state.

This thiamine deficiency damages the mammillary bodies, periaqueductal grey matter, and medial thalami, producing the classic triad of Wernicke's encephalopathy: ophthalmoplegia/nystagmus, ataxia, and confusion. If untreated, it can progress to Korsakoff's psychosis. Management requires prompt parenteral thiamine replacement before or alongside glucose administration.

Option Analysis

• Vitamin B1 (correct): Thiamine deficiency is the well-established cause of Wernicke's encephalopathy in hyperemesis gravidarum due to depleted reserves and increased utilization from vomiting and glucose-containing IV fluids.
• Vitamin B6 (incorrect): Pyridoxine deficiency is not linked to Wernicke's encephalopathy; B6 is actually used therapeutically to help control the nausea and vomiting of hyperemesis gravidarum itself, not implicated in this neurological complication.
• Vitamin B12 (incorrect): Cobalamin deficiency causes subacute combined degeneration of the spinal cord and megaloblastic anemia, not Wernicke's encephalopathy, and its body stores last for years, making acute deficiency from vomiting alone unlikely.
• Vitamin B4 (incorrect): This is not a recognized/established vitamin in current nomenclature and has no association with Wernicke's encephalopathy.

Hence, the correct answer is vitamin B1 (thiamine).