(P107) Muscle Atrophy, Nystagmus, and Confusion in Pregnancy: Think Wernicke Encephalopathy

Chief Complaint : Nausea and vomiting

History of Present Illness : A 19yo G2P0010 female at 20 weeks gestational age with remote D&C and no medical problems presented for lethargy, confusion. Speaking in short sentences, she endorsed abdominal pain, vomiting, bilateral leg paresthesias. Friend noted multiple recent ED visits for nausea/vomiting.

Pertinent Physical Exam: Toxic-appearing. Loose hanging skin on arms and abdomen with poor turgor. Cracked lips. Intermittent nystagmus. Regular rhythm. Clear lungs. Mild tenderness diffusely to gravid abdomen. A&Ox3, slow speech. Thenar/hypothenar muscle atrophy. Moving all extremities weakly.

Pertinent Laboratory Data: Labs: Na 128, K 2.7, Cl 82, Cr 2.37, pH 7.4, CO2 26, anion gap 20, Lactate 7.2. WBC 8.9, Hgb 13.8. EKG with sinus tachycardia, prolonged QTc. Ultrasound with IUP, EGA 17 weeks, fetal HR 143, no free fluid.

Case Discussion: Given exam ,there was concern for Wernicke Encephalopathy. Patient received electrolyte repletion, IV fluids with dextrose, IV B1 and B9 for presumed WE. MRI with abnormal T2 signal intensity along medial thalami consistent with WE (fig 1&2).

Nausea and vomiting occurs in the majority of pregnancies with 0.3-2% diagnosed with hyperemesis gravidarum (HG), which may be associated with weight loss or electrolyte derangements. In severe cases, development of thiamine (B1) can lead to Wernicke Encephalopathy (WE). While rare with less than 200 cases reported. WE should be considered in pregnant patients with HG with neurologic findings. WE, usually described in patients with chronic alcohol use or bariatric surgery, classically consists of ophthalmoplegia, altered mental status and ataxia; however, rarely do patients present with all three. In pregnancy, poor oral intake, vomiting and higher metabolic demand increase risk for thiamine deficiency in as little as 18 days, with nystagmus being the most common finding. Thiamine is a vital co-factor in glucose metabolism; deficiency increases anaerobic metabolism and lactate production. Prompt treatment with 500mg IV Thiamine improves maternal and fetal morbidity and mortality.

Signs of malnutrition (eg. muscle atrophy) and neurologic findings in pregnant patients should prompt consideration of thiamine deficiency and WE. If high suspicion, immediate empiric IV Thiamine, fluids with dextrose and electrolyte repletion should be administered. Emergency providers play a critical role in the evaluation and management of these high-risk patients.

References and Acknowledgements (Optional): Tucker R, Platt M, “Chapter 38: Obstetric and Gynecological Emergencies and Rape” in Tintinalli J, Cline D, Ma O, Fitch M, Joing S, Wang V. Tintinalli's Emergency Medicine Manual 7e. McGraw Hill, 2016
Goodwin TM. “Hyperemesis gravidarum” Obstet Gynecol Clin North Am 2008;35(3):401–417
Oudman E, Wijnia JW, Oey M, et al “Wernicke's encephalopathy in hyperemesis gravidarum: A systematic review.” Eur J Obstet Gynecol Reprod Biol. 2019;236:84-93.
Donnino MW, Vega, J., Miller, J., et al. “Myths and Misconceptions of Wernicke’s Encephalopathy: What Every Emergency Physician Should Know.” Ann Emerg Med 2007; 50: 715-21.
Chataway JE, Hardman EL “Thiamine in Wernicke’s syndrome--how much and how long?” Postgrad Med J. 1995, 71:249. 10.1136/pgmj.71.834.249