This is the first nationwide population-based study with a relatively large number to investigate the one-year mortality of survivors after CI poisoning. Chronic renal failure, hemodialysis, and respiratory failure requiring mechanical ventilation were significantly associated with a poor outcome. For those survivors after CI poisoning, the one-year mortality rate of survivors after CI poisoning was 6.7%, and age, pneumonia, and mechanical ventilation were independent risk factors for one-year mortality among survivors of cholinesterase inhibitor poisoning. A recent prospective population-based cohort study in Unite State showed hospital mortality of pneumonia was 6.5%, but the one-year mortality was up to 30.6%.  The result is similar in our study that pneumonia is a predictive factor for the one-year mortality after CI poisoning.
Several strengths of this study are worth highlighting. First, this was a nationwide population-based study, meaning that a relatively large number of CI intoxication patients were included, and this sample was considered representative of the general population. Second, the study cohort was largely selected from a computerized database comprising all Taiwanese CI intoxication patients diagnosed between January 1, 2003, and December 31, 2012, thus decreasing the potential for selection bias.
The disease burden of OP and CM toxicity differs between Taiwan and most western countries . Because OP and CM are easily accessed and highly lethal, this type of toxicity is one of the most frequent causes of poisoning in Taiwan . Previous epidemiologic data of 1985–2006 indicate that most cases of OP exposure involve a single OP (80.37%), and the overall mortality rate is 12.71% , which is similar to that (13.2%) in our study.
Respiratory failure is one of the most important complications of CI poisoning. This may be due to respiratory muscle weakness, aspiration, hypersecretion, pneumonia, sepsis, or acute respiratory distress syndrome. . A retrospective study of 155 patients reported that 59% of patients with CI poisoning developed respiratory failure . In our study, 29.4% of patients had respiratory failure with mechanical ventilation. The mortality rate was 33.4% among the patients who were mechanically ventilated, whereas it was 4.7% among the patients who were not mechanically ventilated. (95% CI of the difference between percentages was 26.54 to 30.89%, p < 0.0001) These findings demonstrate that CI intoxication patients who require mechanical intubation had a higher mortality rate than those without mechanical intubation. This information aids clinical physicians in realizing that respiratory failure is a useful prognostic indicator in patients with CI poisoning.
In the previous reports, several prognostic factors were associated with CI poisoning, including age, serum cholinesterase and bicarbonate levels, and acute physiology and chronic health evaluation II scores [12, 19]. A retrospective study of 118 patients with OP poisoning reported that the DM status did not increase mortality . This result is consistent with our findings that diabetes is not associated with both hospital mortality and one-year mortality. Sungur revealed that among patients with OP insecticide poisoning, the mortality rate was 50% in patients requiring mechanical ventilation and 21% in those not mechanically ventilated . In the current nationwide study of 6832 patients, the hospital mortality rate was 33.4% among those with mechanical ventilation. A recent study demonstrated that acute renal failure was associated with mortality in organophosphorus poisoning. . Our study showed that when patients with CI poisoning received hemodialysis during hospitalization, the hospital mortality rate was higher (OR; 6.332, 95% confidence interval: 4.419–9.074).
In our study, the prescription percentage of PAM and atropine was significantly higher in nonsurvivors than in survivors. This could be due to one of the two following reasons. First, the survivors may have experienced less CI toxicity and may have had less severe clinical symptoms. Therefore, PAM and atropine were not prescribed, according to clinical judgement. Second, most of the survivors may have experienced CM intoxication. Because PAM is not suggested for use in CM intoxication, the percentage of PAM use may have been lower in the survivors.
The findings of this study should also be interpreted in light of its limitations. First, serum laboratory data were not available in the NHIRD. Thus, we could not obtain the level of acetylcholinesterase activity, which is a direct biomarker for toxicity of organophosphorus. However, not all hospitals check acetylcholinesterase activity to the patients. Second, we could not categorize the precise intensity of the intoxication because NHIRD may not provide the detailed clinical course, such as clinical symptoms, the cause of intoxication (exposure to organophosphate or carbamates), the dose of toxin, the dose and length of antidote, or time to doctors. Third, the present study is a retrospective cohort study. Despite the meticulous design and control of some confounding factors, biases could remain because of possibly unmeasured or unknown confounding factors. We were unable to consider the severity of the diseases, which reduced our chances of showing the severity related effects of comorbidities. Finally, causes of death for the patients cannot be reported in the study because we have no death certificate databases.