Journal of toxicology. Clinical toxicology最新文献

Background: Approximately 35% of patients acutely poisoned with organophosphates (OP) in developing countries like Sri Lanka require intensive care and mechanical ventilation. However, death rates remain high.

Objective: To study the outcomes and predictors of mortality in patients with acute OP poisoning requiring intensive therapy at a regional center in Sri Lanka over a period of 40 months.

Methods: Retrospective analysis of all intensive care records of patients with acute OP poisoning admitted to the Intensive Care Unit (ICU) between March 1998 and July 2001.

Results: During the study period, 126 subjects were admitted to the ICU with acute OP poisoning. Records of 10 patients were lost and those of 37 were incomplete and hence were excluded. All the remaining 71 patients (59 male) had required endotracheal intubation and mechanical ventilation for a period of four (median) days (range 1-27) in addition to gastric lavage and standard therapy with atropine and oximes and adequate hydration. Of these 71 patients, 36 (28 male) had died. Life table analysis demonstrated a steep decline in the cumulative survival to 67% during the first three days. Systolic blood pressure of < 100 mmHg and FiO2 of >40% to maintain a SpO2 of >92% within the first 24 h were recognized as poor prognostic indicators among mechanically ventilated patients.

Conclusion: Mortality following OP poisoning remains high despite adequate respiratory support, intensive care, and specific therapy with atropine and oximes. One-third of the subjects needing mechanical ventilation and reaching intensive care units die within the first 72 h of poisoning. Systolic blood pressure of less than 100 mmHg and the necessity of a FiO2>40% to maintain adequate oxygenation are predictors of poor outcome in patients mechanically ventilated in the ICU.

Objectives: To systematically review and summarize studies on the accuracy of ECG and tricyclic antidepressant (TCA) concentration as prognostic indicators of the risk of seizures, ventricular arrhythmia (VA) or death in patients with TCA overdose.

Methods: Articles were identified with MedLine and Cochrane register of controlled clinical trials searches and review of medical toxicology textbooks. Quality of the included studies was assessed. Pooled estimates of sensitivity, specificity, likelihood ratios and Summary Receiver Operating Characteristics (SROC) curves were generated.

Results: A total of 18 studies were included in the analysis. The pooled sensitivity (Se) and specificity (Sp) of the QRS for predicting seizures were 0.69 [95% CI 0.57-0.78] and 0.69 [95% CI 0.58-0.78] as compared to 0.75 [95% CI 0.61-0.85] and 0.72 [95% CI 0.61-0.81] for the TCA concentration. The Se and Sp of the QRS to predict VA were 0.79 [95% CI 0.58-0.91] and 0.46 [95% CI 0.35-0.59] compared to 0.78 [95% CI 0.56-0.90] and 0.57 [95% CI 0.46-0.67] for the TCA concentration. The Se and Sp of the QRS to predict death were 0.81 [95% CI 0.54-0.94] and 0.62 [95% CI 0.55-0.68] compared to 0.76 [95% CI 0.49-0.91] and 0.60 [95% CI 0.47-0.72] for the TCA concentration. Very few studies evaluated the accuracy of QTc, T 40 ms axis and the R/S ratio.

Conclusions: Overall, the studies suggested that the ECG and TCA concentration have similar but relatively poor performance for predicting complications, such as seizures, VA or death, associated with TCA overdose.

Background: Sources of cyanide exposure are many, including combustion of plastic and vinyl, such as in a house fire, laboratory or industrial exposures including exposure in the electroplating industry both of printed circuit boards and in jewelry work. Rapid and definitive diagnosis of cyanide poisoning is unavailable in the emergency department setting. It is desirable to make a definitive diagnosis in order to prevent potential complications of empiric treatment of presumptive cyanide poisoning from the cyanide antidote kit currently approved by the US Food and Drug Administration (FDA). We investigated a technique to detect cyanide currently utilized by water treatment facilities to determine if it can be applied to rapidly detect concentrations of cyanide in the clinically important range.

Methods: Varying standardized dilutions of KCN ranging from 0.25 microg/mL to 30 microg/mL were acidified with a drop of sulphuric acid in a closed system under a ventilation hood. Cyantesmo test strips were placed into the test tubes above the fluid level where liberated HCN gas interacted with the test strip to effect a color change. Color changes were compared to negative controls and to each other.

Results: The test strips demonstrated an incrementally increasing deep blue color change over a progressively longer portion of the test strip in less than 5 minutes for each concentration of KCN including 1, 3, 10, and 30 microg/mL. The concentrations of 0.25, 0.5, and 0.75 required more than 2 hours to begin demonstration of any color change.

Conclusion: The Cyantesmo test strips accurately and rapidly detected, in a semi-quantifiable manner, concentrations of CN greater than 1 microg/mL contained in each test sample. Future work to validate this test in blood and in clinical specimens is planned.

Gastric lavage should not be employed routinely, if ever, in the management of poisoned patients. In experimental studies, the amount of marker removed by gastric lavage was highly variable and diminished with time. The results of clinical outcome studies in overdose patients are weighed heavily on the side of showing a lack of beneficial effect. Serious risks of the procedure include hypoxia, dysrhythmias, laryngospasm, perforation of the GI tract or pharynx, fluid and electrolyte abnormalities, and aspiration pneumonitis. Contraindications include loss of protective airway reflexes (unless the patient is first intubated tracheally), ingestion of a strong acid or alkali, ingestion of a hydrocarbon with a high aspiration potential, or risk of GI hemorrhage due to an underlying medical or surgical condition. A review of the 1997 Gastric Lavage Position Statement revealed no new evidence that would require a revision of the conclusions of the Statement.

Ingestion of industrial-strength hydrogen peroxide is rare. Fatal outcomes have been reported with solutions of 35%. We report a six-year-old boy who unintentionally ingested an unknown quantity of hydrogen peroxide with a concentration of 60%. Upon admission to our Pediatric Intensive Care Unit he was intubated and received ventilatory assistance for 48h. Upper gastrointestinal endoscopy was performed soon after admission and laparoscopy was performed 24h later. Recovery was satisfactory, and the patient was discharged on day 18 with no evidence of pathological sequelae.

Single-dose activated charcoal (SDAC) is frequently administered to poisoned patients. The assumption is that toxin absorption is prevented and that toxicity (as defined by morbidity and mortality) of the poisoning is decreased. Yet there is no evidence that SDAC improves outcome. Risks of this procedure have not been determined. The reported adverse events following SDAC administration are reviewed and risk:benefit ratio for this procedure is discussed.

Background: Although it is a commonly held belief that the ingestion of drugs with an anticholinergic action would prolong the duration of time after drug ingestion for effective gastrointestinal decontamination, data are lacking to support this belief. The purpose of this study is to determine whether activated charcoal is more effective in the presence of concurrent anticholinergic activity.

Methods: A three-limbed randomized crossover study in 10 healthy volunteers was completed to determine the ability of a 50 g dose of activated charcoal to reduce the bioavailability of a simulated overdose of acetaminophen (12 x 325 mg tablets) in the presence and absence of a concurrently present anticholinergic drug, atropine (0.01 mg/kg I. M. administered 15 min prior to the acetaminophen ingestion).

Results: After the acetaminophen ingestion, median Cmax occurred at 1 h for all three exposures but was lower in the atropine-treated study arm (31+/-19 mg/L) than in the control or charcoal alone intervention arms (49+/-13 and 51+/-16 mg/L, respectively) (P<0.05). Compared to the control area under the serum concentration vs. time curve, a single dose of activated charcoal 1 h after drug ingestion reduced acetaminophen bioavailability by 20% (95% CI 4-36%) and by 47% (95% CI 35-59%) in the presence of atropine (P<0.05 atropine plus charcoal vs. charcoal alone).

Conclusions: Our data support the belief that activated charcoal is more effective in the presence of anticholinergic activity. Additional study is required to determine whether in patients with anticholinergic drug overdose, activated charcoal is effective at times beyond the recommendation for overdoses of drugs without this pharmacodynamic effect.

We present a 3-month-old female who developed fulminant hepatic failure after ingesting less than 8 mL of clove oil. Initial treatment involved gastrointestinal decontamination, supportive measures, and admission to hospital. She subsequently developed fulminant hepatic failure and was treated with intravenous N-acetylcysteine (N-AC) according to a protocol used for acetaminophen poisoning. Over the next 72 h her liver synthetic function and clinical status improved, and she made a complete recovery. Previous reported cases of clove oil toxicity and the potential role of N-AC therapy are reviewed.

Background: The Black Locust (Robinia Pseudoacacia) tree contain toxalbumins, robin and phasin, that exert their toxic effects by inhibition of protein synthesis. Despite the potential dangers of Black Locust intoxication, reports of human toxicity after ingestion are rare. We report the first human intoxication of Black Locust bark in North America in over one hundred years.

Case report: An eight-year-old male was brought to the emergency department 6 hours after chewing and expelling the Black Locust bark. He presented with emesis, which began approximately 2.5 hours after exposure. His vital signs were as follows: oral temperature, 97.5 degrees F; blood pressure, 128/75 mmHg; heart rate, 114 beats per minute; respiratory rate, 15 breaths per minute. Initial treatment included 4 mg i.v. ondansetron, which resolved the vomiting, one dose of activated charcoal, and intravenous fluids. He was then admitted to the intensive care unit (ICU) for observation of signs of toxicity. Laboratory findings were unremarkable except for a white blood cell of 18.4 K/uL and an elevated alkaline phosphatase of 183 U/L. The patient remained asymptomatic throughout his stay in the ICU and was discharged on the fifth day of admission with a normal white blood cell of 4.1 K/uL and an alkaline phosphatase of 251 U/L.

Conclusion: Patients with clinical toxicity following the ingestion of Black Locust are expected to do well with supportive care and observation.