Gestational malnutrition, hyperemesis gravidarum, and Wernicke's encephalopathy: What is missing?

Abstract Hyperemesis gravidarum (HG), or the severe nausea and vomiting of pregnancy, is one of the most dreaded complications of gestation, affecting between 1.5% and 3.0% of pregnant women. From the late 1800s to the mid‐1980s, the etiology was frequently cited to have psychological and/or—later—perhaps hormonal origins, which have numbered at least 10. Current research has unearthed a genetic basis for HG that implicates growth differentiation factor 15, insulin‐like growth factor binding protein 7, and hormone receptors (namely, glial cell line–derived neurogenic factor family receptor alpha‐like and the progesterone receptor). Whatever the origins of this disease, it has caused immeasurable physiological and psychological damage to women, their fetuses, and their families. The psychological trauma includes a high rate of suicidal ideation as well as posttraumatic stress disorder. Whereas the healthcare costs are substantial for the mother with HG, the lifetime costs to the neonate include that which accompanies reduced employment earnings related to cognitive compromise. Another devastating outcome of severe HG can be Wernicke's encephalopathy (WE), which has a high fetal and maternal mortality rate. Our study explored 18 current reports of HG and WE. We highlighted additional presenting features we believe also accompany, and sometimes replace, the classically taught triad components of WE: ataxia, confabulation, and nystagmus. We agree with the conclusion made by Sheehan and Ironside in 1939 that thiamin alone may not reverse WE, and we offer possible explanations. Lastly, we offer suggestions for remediation.