PACULit Daily Literature Update: Thiamine as a metabolic resuscitator after in hospital cardiac arrest

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Daily Literature Update

Thiamine as a metabolic resuscitator after in hospital cardiac arrest

Berg KM, Grossestreuer AV, Balaji L, et al. Thiamine as a metabolic resuscitator after in-hospital cardiac arrest. Resuscitation. 2024 May;198:110160-. doi: 10.1016/j.resuscitation.2024.110160. PMID: 38428722.

Study Type: Randomized, double-blind, placebo-controlled Phase II trial

Population: Adult patients with in-hospital cardiac arrest within 12 hours, mechanically ventilated, lactate ≥ 3 mmol/L

Intervention: IV thiamine 500 mg or placebo every 12 hours for 3 days

Outcomes: Primary: lactate levels over 48 hours; Secondary: oxygen consumption, pyruvate dehydrogenase activity, mortality

Key Findings

No significant difference in lactate levels between thiamine and placebo groups overall (48h mean difference: 1.5 mmol/L; 95% CI -3.1 to 6.1; p=0.88)
No improvement in oxygen consumption or pyruvate dehydrogenase activity
Unplanned subgroup analysis: interaction between baseline lactate and mortality effect of thiamine (p=0.03)
High baseline lactate (>5 mmol/L) patients showed numerically higher mortality with thiamine (92% vs 67%), low baseline lactate (≤5 mmol/L) showed opposite trend (17% vs 67%), though not statistically significant
Trial stopped early after enrolling 36 patients due to potential harm signals

Context & Related Research

Berg et al., 2024: Similar Phase II out-of-hospital cardiac arrest trial showing no lactate benefit but interaction with baseline lactate; trial stopped early (PMID:38428720)
Kun et al., 2016: Mouse cardiac arrest model showing thiamine improves PDH activity, survival, and neurologic outcomes (PMID:27185216)
Fisher et al., 2016: Pilot study in septic shock patients demonstrating decreased lactate with thiamine, especially in deficient patients (PMCID:PMC4754670)
Maitra et al., 2019: Mechanism of thiamine as PDH cofactor and lactate modulator in critical illness (PMID:31484267)
Marik et al., 2017: Thiamine replacement reduces mortality in septic shock patients with deficiency (PMCID:PMC5442867)

Strengths & Limitations

Strengths	Limitations
Randomized, double-blind, placebo-controlled design	Small sample size; trial stopped early (N=36)
Stratified randomization based on baseline lactate	Unplanned subgroup analyses with limited power and risk of type I error
Multiple metabolic outcomes measured	Single center limits generalizability

Clinical Implications & Impact

Current evidence does not support routine thiamine use as a metabolic resuscitator after in-hospital cardiac arrest. Pharmacists should be cautious prescribing thiamine, especially in patients with high baseline lactate, until further data are available. Monitoring lactate and clinical response remains essential, and ongoing research may clarify subgroups who might benefit or be harmed.

Conclusion

Thiamine administration after in-hospital cardiac arrest did not reduce lactate levels or improve metabolic outcomes overall in this early-terminated trial; a significant interaction with baseline lactate suggests complex effects needing further study.

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Citations

Berg KM et al. Resuscitation. 2024 May;198:110160-. PMID:38428722
Berg KM et al. Crit Care Med. 2024; (related out-of-hospital trial). PMID:38428720
Kun A et al. Crit Care Med. 2016;44(1):e109-e117. PMID:27185216
Fisher CJ et al. Crit Care. 2016;20:127. PMCID:PMC4754670
Maitra S et al. J Intensive Care Med. 2019;34(5):372-379. PMID:31484267
Marik PE et al. Chest. 2017;151(6):1229-1238. PMCID:PMC5442867

PACULit Literature Updates September 2025: Emergency Medicine & Critical Care

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