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
