To the Editor:
In the journal's last issue, Bretaudeau et al. retrospectively investigated the role of early gastrointestinal (GI) decontamination in improving the outcome of acute-on-chronic lithium-poisoned patients.Citation1 Using a multivariate analysis, they showed that early GI decontamination was associated with a significant reduction in overall Poisoning Severity Score (PSS), thus suggesting its usefulness in limiting the further need for hemodialysis.
Although we strongly believe that GI decontamination should be performed as early as possible in the absence of contraindications, we would like to highlight possible biases in this study that may limit its conclusions. Assessment of the effects of GI decontamination on lithium kinetics and resulting toxicity requires comparable groups regarding initial renal function and neurological features, which could be questioned in this studyCitation1 due to its retrospective methodology.
Patients’ serum creatinine concentrations and diuresis on hospital admission were not reported. Thus, given the significant difference in the time from lithium ingestion to hospital admission between the two groups (4.2 ± 2.5 h in the early GI decontamination group vs. 18.7 ± 21.9 h in the delayed or no GI decontamination group, p = 0.017), we cannot rule out significant alteration in renal function consequent to prolonged polyuria and vomiting/diarrhea occurring during the initial time course of lithium poisoning, influencing the patient's outcome. Interestingly, 11/44 patients in the group of delayed and no GI decontamination were hemodialyzed, probably in relation to renal injury (12/44 vs. 1/15 patients). Additionally, the amount of fluid resuscitation was not documented and could have been significantly larger in the early GI decontamination group, contributing to maintaining lithium elimination and consequently improving outcome. Lithium elimination depends entirely on renal clearance, supporting the importance of maintaining normal blood volume to preserve glomerular filtration.Citation2 Lithium is handled similarly to sodium in the proximal tubule, which accounts for up to 80% of its reabsorption.Citation2 Therefore, at least in patients with volume contraction, sodium load plays a key role in enhancing lithium elimination, as assessed in a rat model with low sodium diet leading to lithium reabsorption in the distal tubule in addition to its unique reabsorption in the proximal tubule in normal sodium diet animals.Citation3
A more detailed description of each patient's initial features according to Hansen and Amdisen's criteriaCitation4 was also lacking. Possible differences in neurological features on hospital presentation may have influenced not only the decision of the physicians in charge to perform GI decontamination but also directly influenced poisoning outcome.
Finally, improvement in patient outcome was based on a significant but relatively mild decrease in overall PSS (1.1 vs. 1.8, p = 0.001) and increase in Glasgow coma score (15 vs. 13, p = 0.038), while the percentage of mechanically ventilated and hemodialyzed patients, which represents pertinent toxicodynamic parameters in lithium poisoning, did not significantly differ between the groups, supporting the suggestion that the study was underpowered. Moreover, it would have been interesting to analyze the consequences of early GI decontamination on the length of hospital stay, which is also a determinant end point in lithium-poisoned patients at risk of prolonged toxic encephalopathy.Citation5
In conclusion, Bretaudeau's data clearly encourage early GI decontamination in lithium-poisoned patients.Citation1 However, as previously demonstrated,Citation2,Citation4 maintaining renal lithium clearance using saline infusion or enhancing lithium elimination using renal replacement therapy should be the early goal of management in order to improve outcome.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
- Bretaudeau Deguigne M, Hamel JF, Boels D, Harry P. Lithium poisoning: the value of early digestive tract decontamination. Clin Toxicol (Phila) 2013; 51:243–248.
- Waring WS. Management of lithium toxicity. Toxicol Rev 2006; 25:221–230.
- Thomsen K, Shirley DG. A hypothesis linking sodium and lithium reabsorption in the distal nephron. Nephrol Dial Transplant 2006; 21:869–880.
- Hansen HE, Amdisen A. Lithium intoxication. (Report of 23 cases and review of 100 cases from the literature). Q J Med 1978; 47:123–144.
- El Balkhi S, Megarbane B, Poupon J, Baud FJ, Galliot-Guilley M. Lithium poisoning: is determination of the red blood cell lithium concentration useful?. Clin Toxicol (Phila) 2009; 47:8–13.