OBJECTIVE: To describe a rare case of Wernicke encephalopathy (WE) as a result of hyperemesis gravidarum due to primary hyperparathyroidism (PHPT) in pregnancy. METHODS: We present the clinical presentation, supportive laboratory values, diagnostic dilemmas, treatment, clinical outcome, and supportive literature review of a patient with WE as a result of hyperemesis gravidarum due to PHPT in pregnancy. RESULTS: A 27-year-old previously healthy G1P0 female presented with initial symptoms of right upper-quadrant pain, nausea, vomiting, and paresthesias at 17.3 weeks of gestation. The patient later developed neurologic symptoms including acute encephalopathy, ataxia, and intranuclear ophthalmoplegia. The suspicion for WE was confirmed with characteristic findings on brain magnetic resonance imaging. WE was attributed to severe malnutrition from hyperemesis gravidarum and poor prenatal care. Hypercalcemia with an elevated parathyroid hormone level was identified following an unfortunate intrauterine fetal demise, raising suspicion for PHPT. PHPT was confirmed, and after undergoing successful parathyroidectomy, the patient regained normal neurologic function, with the exception of mild lower-extremity paresthesias. CONCLUSION: This case is an example where early recognition and treatment of hyperparathyroidism can be masked by severe malnutrition and present in an unusual way with neurologic symptoms of WE. Early recognition and suspicion are critical in preventing poor fetal outcomes and long-term consequences.
OBJECTIVE: To describe a rare case of Wernicke encephalopathy (WE) as a result of hyperemesis gravidarum due to primary hyperparathyroidism (PHPT) in pregnancy. METHODS: We present the clinical presentation, supportive laboratory values, diagnostic dilemmas, treatment, clinical outcome, and supportive literature review of a patient with WE as a result of hyperemesis gravidarum due to PHPT in pregnancy. RESULTS: A 27-year-old previously healthy G1P0 female presented with initial symptoms of right upper-quadrant pain, nausea, vomiting, and paresthesias at 17.3 weeks of gestation. The patient later developed neurologic symptoms including acute encephalopathy, ataxia, and intranuclear ophthalmoplegia. The suspicion for WE was confirmed with characteristic findings on brain magnetic resonance imaging. WE was attributed to severe malnutrition from hyperemesis gravidarum and poor prenatal care. Hypercalcemia with an elevated parathyroid hormone level was identified following an unfortunate intrauterine fetal demise, raising suspicion for PHPT. PHPT was confirmed, and after undergoing successful parathyroidectomy, the patient regained normal neurologic function, with the exception of mild lower-extremity paresthesias. CONCLUSION: This case is an example where early recognition and treatment of hyperparathyroidism can be masked by severe malnutrition and present in an unusual way with neurologic symptoms of WE. Early recognition and suspicion are critical in preventing poor fetal outcomes and long-term consequences.
Authors: C C Reading; J W Charboneau; E M James; P R Karsell; D C Purnell; C S Grant; J A van Heerden Journal: AJR Am J Roentgenol Date: 1982-09 Impact factor: 3.959
Authors: E Antunez; R Estruch; C Cardenal; J M Nicolas; J Fernandez-Sola; A Urbano-Marquez Journal: AJR Am J Roentgenol Date: 1998-10 Impact factor: 3.959