Oral poisoning patients with a PSS

Oral poisoning patients with a PSS of 2 to 4 underwent gastriclavage. On admission to the emergency department, patientspresenting with shock, cerebral edema, or pulmonary edema receivedairway protection before lavage. In addition, patients with oralpoisoning received the established therapy: skin cleaning, gastriclavage, purges, catharsis, antidotes, and hemoperfusion, or hemodi-alysis when necessary.2.3. Outcome measuresThe primary outcome measurement was mortality from AOPPintoxication. The outcome measures also included the observedclinical manifestations, plasma cholinesterase activity [16,17],atropine adverse effects, complications (ie, liver, brain, kidney,and metabolic dysfunction), length of ICU stay, and the outcomefor each patient. All patients were followed up for 4 to 8 weeksafter discharge.2.4. Statistical analysisThe measurement data were expressed as the mean ± SD. Thecount data were analyzed using the χ 2 test, and the measurementdata were analyzed using a t test. All analyses were performed withSPSS 19.0 statistical software (Chicago, Illinois). P b .05 wasconsidered statistically significant.3. Results3.1. Baseline characteristics of the 2 groupsThe baseline characteristics of the patients in the 2 groups areillustrated in Table 1. There was no significant difference between the 2groups regarding the total dose of pralidoxime chloride; the dose ofatropinein group A was57.40 ± 15.14 mg, and the dosein groupB was308.26 ± 139.16 mg, with the group A dosage being significantly lower(P=.001).Theatropinewithdrawaltimewas3.98±2.16daysingroupA and 6.79 ± 4.19 days in group B. The withdrawal time wassignificantly shorter in group A (P = .003; Table 1). Dimethoate canpresent differently from other organophosphorus with cardiovascularcollapsebeforecholinergiccrises.However,only1ofthe16dimethoate-poisoned patients in our study demonstrated nodal tachycardia on anelectrocardiogram. No patient presented with the clinical manifesta-tions of cardiovascular collapse. No patient vomited during therapy.Only1patientpresentedwithanintermediatesyndromeingroupAand1 patient with atropine intoxication in group B.3.2. Atropine adverse effects in the 2 groupsAtropine adverse effects occurred in 3 of 36 severe cases in groupAand 11 of 27 severe cases in group B; fewer patients with severe casesin group A had atropine adverse effects (P = .002; Table 2). Atropineadverse effects occurred in 5 of 48 (PSS 0-2) patients in group A and 6of 51 in group B. In all group A patients, the rate of atropine adverseeffects was 8 of 74, whereas it was 17 of 78 in group B. There was nosignificant difference between the 2 groups in the rate of atropineadverse effects in other patients (P = .831) or all patients (P = .068).