Can initial lactate levels predict the severity of unintentional carbon monoxide poisoning?

Abstract

<jats:sec><jats:title>Introduction:</jats:title><jats:p> Accidental carbon monoxide (CO) intoxication is a major cause of unintentional poisoning. This study aimed to determine the value of initial lactate levels in patients with CO poisoning and to evaluate its utilization in the emergency department (ED). </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> A retrospective cross-sectional study was carried out among patients with CO intoxication, who were admitted to the ED between April 1, 2011 and April 1, 2012. The study data were extracted from a hospital database system using International Classification of Diseases-10 diagnosis codes. The patients were analyzed according to lactate levels, carboxyhemoglobin (COHb) levels, electrocardiographic manifestations, and clinical features at admission to the ED. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> A total of 74 patients with CO poisoning were enrolled in this study. The average COHb value of the patients was 21.5 ± 13.9%. A total of 50 patients (67.6%) received normobaric oxygen treatment and 24 patients (32.4%) received hyperbaric oxygen (HBO) treatment. The patients who received HBO treatment had increased lactate levels compared with patients receiving normobaric oxygen treatment (2.3 mmol/L vs. 1.0 mmol/L, p &lt; 0.001). The lactate levels were positively correlated with COHb values ( r = 0.738, p &lt; 0.001). We determined that a lactate level of 1.85 mmol/L has a sensitivity of 70.8% and a specificity of 78.0% to predict the HBO treatment needed in CO poisoning. </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> In evaluating patients with CO poisoning, an initial lactate level could be taken into consideration as an adjunctive parameter of severity, together with the clinical criteria and levels of COHb. </jats:p></jats:sec>

Clinical Uses of Lactate and Lactate Clearance in Carbon Monoxide Poisoning

“…Cervellin et al (11) and Icme et al (15) reported a more significant lactate increase among patients treated with HBOT. Doğan et al (9) found higher lactate levels in patients with mental status changes and the need for HBOT compared to those without; they also reported an AUC level of 0.83 for plasma lactate levels in predicting HBOT need (9). In agreement with the literature, we found a higher admission plasma lactate level among patients that received HBOT and found an AUC value of 0.708 for predicting HBOT need.…”

“…The efficacy of lactate clearance for treatment guidance in sepsis has led to the performance of studies to evaluate the feasibility of its use in critically ill patients with systemic involvement due to other diseases (7,8). Although several studies reporting a correlation between initial lactate levels and disease severity in CO exposure have been recently published, there are a limited number of studies examining lactate clearance in CO intoxication (9)(10)(11)(12).…”

Clinical use of plasma lactate concentration. Part 1: Physiology, pathophysiology, and measurement

“…Hyperlactatemia from carbon monoxide toxicity is suspected to result primarily from tissue hypoxia, although mitochondrial dysfunction and catecholamine effects, which will be discussed further in later sections, may also contribute . In keeping with a multifactorial pathogenesis, lactate concentration is variably correlated with carboxyhemoglobin concentrations as well as the duration of carbon monoxide exposure …”

“…22 In keeping with a multifactorial pathogenesis, lactate concentration is variably correlated with carboxyhemoglobin concentrations as well as the duration of carbon monoxide exposure. [117][118][119] Type B1 hyperlactatemia Hyperlactatemia associated with underlying disease: Malignancy A variety of potential mechanisms for malignancyassociated hyperlactatemia have been identified including: increased production of glycolytic enzymes by hypoxia-inducible factors 1 and 2, 120-122 increased production of glycolysis intermediates via upregulation of the pentose phosphate pathway, 22,123 mitochondrial dysfunction, reduced hepatic clearance, and malnutrition causing thiamine deficiency. 12,28 Malignant cells 90 preferentially use glycolytic pathways despite readily available oxygen, 22,122 and lactate may alter the tumor micro environment in a manner that inhibits destruction of neoplastic cells.…”

Lactate and carbon monoxide poisoning

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We read with interest the study by Dogan et al 1 and question the authors' interpretation.The study's primary outcome is to determine whether serum lactate correlates with hyperbaric oxygen (HBO) therapy. The main rationale for HBO in carbon monoxide (CO) poisoning is to reduce the risk of delayed neurologic sequelae.

2,3 However, HBO is a treatment modality and not a measurable clinical outcome.

…”