Abstract

Introduction: Thiamine is an essential enzyme cofactor in cellular metabolism. Its deficiency can manifest as wet beriberi with high-output heart failure. Its more severe and fulminant form is known as shoshin beriberi, characterized by cardiogenic shock, hemodynamic collapse, and multiorgan failure. Case Description: A 67-year-old male presented with dyspnea on exertion and orthopnea. On exam, he was tachycardic and cold to the touch. Initial workup showed metabolic acidosis, elevated lactate, acute kidney and liver injury, and elevated NT proBNP. ECG showed atrial fibrillation with RVR. His past medical history included heavy alcohol use and a similar presentation two years prior with new-onset heart failure complicated by shock and acute kidney injury, requiring CRRT. At that time, he improved with high-dose thiamine and decompensation was attributed to shoshin beriberi. Shortly after admission, the patient developed worsening shock, with liver failure, renal failure, and DIC. He was started on pressors, broad-spectrum antibiotics, high-dose thiamine and CRRT. TTE showed biventricular dysfunction and global hypokinesis with LVEF of 20%. Hemodynamic monitoring was consistent with cardiogenic shock. Infectious workup was negative. Within 96h of the initiation of thiamine, the patient’s mental status and hemodynamics significantly improved, with resolution of cardiogenic shock. He remained hemodynamically stable, his laboratory abnormalities improved, and he was started on GDMT. He required intermittent HD for several months, after which it was discontinued. He later underwent LHC that showed nonobstructive CAD. Discussion: The diagnosis of shoshin beriberi is challenging and requires a high index of suspicion for presumed thiamine deficiency, particularly in critically ill patients with many comorbidities. An empiric therapeutic trial of thiamine supplementation in this group of patients can lead to improvement of hemodynamics within hours to days, as in this case. Even though his LVEF has not yet fully recovered, we suspect that his presentation was due to an acute-on-chronic insult, in the setting of alcohol-induced cardiomyopathy. To the best of our knowledge, this is the first report of recurrent shoshin beriberi in the literature.

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