Shoshin Beriberi in Critically-Ill patients: case series

Abstract

Thiamine plays a fundamental role in cellular metabolism. The classical syndrome caused by thiamine deficiency is beriberi, and its fulminant variant, once considered an uncommon finding, is now encountered among the critically ill.We present a case series of four critically ill non-septic non-alcoholic patients with severe lactic acidosis and refractory cardio-circulatory collapse caused by acute fulminant beriberi, which drastically responded to thiamine administration.In critical care settings, increased awareness of this life-threatening but reversible condition is a requirement, especially among patients receiving parenteral nutrition and those with unexplained recalcitrant lactic acidosis.

Fig. 1

The four charts represent the trend of MAP along with the vasopressor doses prior and following Thiamine infusion. In the four charts the x- Axis is hours and the Arrow points at the time of the initial Thiamine infusion.1.a. Case # 1. 1.b. Case # 2, 1.c.: Case # 3, 1.d.: Case # 4. In the charts Epinephrine (Adrenaline) and Norepinephrine are shown in milliliters per hour, conversion to mg per hour is 0.25 mg/ml and 0.2 mg/ml respectively

Fig. 2

Carbohydrate metabolism and role of thiamine. The inability to use the Krebs cycle is the major underlying pathophysiological feature of thiamine deficiency. Thiamine pyrophosphate (TPP), is an essential component of aerobic metabolism. A decrease in its activity may lead to the tissue accumulation of toxic intermediates such as pyruvate and lactate. TPP: Thiamine Pyrophosphate, Glucose 6-P: Glucose 6 Phosphate, Glyceraldehyde 3 P: D-Glyceraldehyde 3 Phosphate, RNA Synthesis: Ribonucleic Acid Synthesis, Acetyl CoA: Acetyl Co-enzyme A, Succinyl CoA: Succinyl Co-enzyme A