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Lactate concentration, fibrinogen and fibrin(ogen) -- degradation-products in central venous blood were analysed in 35 unconscious patient with acute hypnotic drug poisoning (HDP) and compared with the results in 13 healthy control persons undergoing the same degree of forced diuresis via central venous catheters. Blood samples were taken on admission and at 12 h intervals up to 36 h after admission. Patients with HDP were attributed to the categories of moderate intoxications (n = 17) and severe intoxications (n = 18) according to their clinical condition. On admission, blood lactate was significantly higher in severe intoxication (3.90 +/- 2.94 mmol/l) as compared to the control group (1.25 +/- 0.17 mmol/l). Blood lactate was less elevated in moderate poisoning (2.74 +/- 1.22 mmol/l). Thirty-six hours after admission blood lactate was completely normalised in patients with moderate intoxication (1.19 +/- 0.69 mmol/l) but still significantly elevated in severely poisoned patients (2.26 +/- 1.48 mmol/l). Lactate concentration was above normal in 15 out of 17 patients with moderate and in 17 out of 18 patients with severe poisoning. A statistically significant linear correlation existed between the duration of unconsciousness and the maximal lactate concentration within 12 hrs after admission. For fibrinogen concentrations statistically significant differences were observed neither between groups nor across time. Titers of FDP were elevated in 9 out of 11 patients with moderate and to a higher degree in all patients with severe poisoning, indicating low rate DIC. Hyperlactatemia is a frequent finding in acute hypnotic drug poisoning. Blood lactate estimations may improve the evaluation of the severity of poisoning and the efficacy of therapeutic interventions.
Lactate concentration, fibrinogen and fibrin(ogen) -- degradation-products in central venous blood were analysed in 35 unconscious patient with acute hypnotic drug poisoning (HDP) and compared with the results in 13 healthy control persons undergoing the same degree of forced diuresis via central venous catheters. Blood samples were taken on admission and at 12 h intervals up to 36 h after admission. Patients with HDP were attributed to the categories of moderate intoxications (n = 17) and severe intoxications (n = 18) according to their clinical condition. On admission, blood lactate was significantly higher in severe intoxication (3.90 +/- 2.94 mmol/l) as compared to the control group (1.25 +/- 0.17 mmol/l). Blood lactate was less elevated in moderate poisoning (2.74 +/- 1.22 mmol/l). Thirty-six hours after admission blood lactate was completely normalised in patients with moderate intoxication (1.19 +/- 0.69 mmol/l) but still significantly elevated in severely poisoned patients (2.26 +/- 1.48 mmol/l). Lactate concentration was above normal in 15 out of 17 patients with moderate and in 17 out of 18 patients with severe poisoning. A statistically significant linear correlation existed between the duration of unconsciousness and the maximal lactate concentration within 12 hrs after admission. For fibrinogen concentrations statistically significant differences were observed neither between groups nor across time. Titers of FDP were elevated in 9 out of 11 patients with moderate and to a higher degree in all patients with severe poisoning, indicating low rate DIC. Hyperlactatemia is a frequent finding in acute hypnotic drug poisoning. Blood lactate estimations may improve the evaluation of the severity of poisoning and the efficacy of therapeutic interventions.
We prospectively studied 56 consecutive patients with severe tricyclic antidepressant ingestion to determine the incidence of associated pulmonary complications. Among the patients meeting the entrance criteria, the mean antidepressant level was 1136 ng/ml. Other characteristics were a QRS duration of greater than or equal to 0.1 seconds in 35 (63%) and seizures in 19 (34%). Seventeen patients (30%) developed 18 abnormal chest X-ray findings which included pulmonary edema in 8 cases and aspiration pneumonia in 10. Using logistic regression, we evaluated the influence of tricyclic antidepressant level, blood pressure, QRS interval, seizures, drug co-ingestion and the use of gastric lavage vs. ipecac-induced emesis on pulmonary complications. For patients with pulmonary edema, the only significantly associated factor was hypotension on emergency department presentation. For aspiration pneumonia, no significant associations were found. Co-ingestion of another drug had no apparent influence on the development of pulmonary abnormalities. Our findings suggest that pulmonary edema and aspiration pneumonia are frequent complications of severe ingestions of tricyclic antidepressants. Pulmonary edema appears to result from hypotension or its treatment. The etiology of aspiration pneumonia is unclear. A chest X-ray should be obtained in all victims of tricyclic antidepressant overdose.
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