Figure 1.
CONSORT flow diagram of progress through the RCT.
162 patients were excluded due to receiving pralidoxime in the referring hospital (151), being pregnant (7), or being less than 14 y old (4).
Table 1.
Baseline demographic and clinical characteristics.
Table 2.
Baseline analytical laboratory characteristics.
Figure 2.
Pharmacodynamics of oxime administration.
Time course of plasma pralidoxime concentration in patients allocated to receive pralidoxime chloride 2 g loading dose over 20 min followed by 0.5 mg/h until 7 d or until atropine no longer required (blue line, mean±SD; n≤85). A predicted time course (green line) was calculated for a 50 kg person using the kinetic data of Sidell and colleagues [42].
Figure 3.
Pharmacokinetics of oxime administration.
Red cell acetylcholinesterase activity (mean±SD) in patients poisoned by diethyl (blue) and dimethyl (red) OP insecticides, with (solid) and without (broken) pralidoxime chloride. Normal acetylcholinesterase activity is 600–700 mU/µmol Hb; an activity greater than 20%–30% of normal allows normal NMJ function [32]. Acetylcholinesterase was effectively reactivated after poisoning with diethyl insecticides but less so after dimethyl insecticide poisoning.
Figure 4.
Timing of deaths in the two study arms.
Cumulative percentage of patients who died. For the purposes of survival analysis, the clock has been started at randomisation and stops either at death or discharge (assumed to be 40 d if discharged alive sooner than 40 d).
Figure 5.
Timing of deaths during the first 6 d.
For the purposes of survival analysis, the clock has been started at randomisation and stops either at death or discharge (assumed to be 40 d if discharged alive sooner than 40 d).
Figure 6.
Forest plots of mortality for pralidoxime versus placebo for a priori defined study groups.
The relatively few events precluded plots of adjusted analyses.
Table 3.
Median red cell acetylcholinesterase activity (mU/µmol Hb) in patients surviving or dying, by study arm, at 1 and 24 h post-treatment.
Figure 7.
Timing of endotracheal intubation in the two study arms.
Cumulative percentage intubated postrandomisation during the first 7 d. For the purposes of survival analysis, the clock has been started at randomisation, or in the case of those who were intubated at randomisation, when the patient was first extubated. The clock stops either at the first postrandomisation intubation, or at death or discharge (assumed to be 40 d if discharged alive sooner than 40 d).
Figure 8.
Forest plots of mortality for pralidoxime versus placebo for exploratory study subgroups.
The relatively few events precluded plots of adjusted analyses.
Table 4.
Adverse effects reported in each arm after the pralidoxime chloride/placebo loading dose or during the first 3 d of the constant infusion.
Table 5.
Published RCTs of pralidoxime with more than 20 patients showing doses of the pralidoxime cation administered in each arm.