Journal of toxicology. Clinical toxicology最新文献

A case of a 27-year-old woman who ingested 9000 mg arsenic trioxide (As2O3) is reported. Classical symptoms of an acute arsenicum (As) poisoning such as gastrointestinal cramps, vomiting, diarrhea, ECG changes and disturbed liver function tests were observed. The absorption of the ingested As was minimalized by a continuous gastric irrigation with highly concentrated NaHCO3 and intestinal cleansing with NaHCO3 and polyethyleneglycol was performed. Forced diuresis, BAL (2,3-dimercaptopropanol) and DMSA (meso-2,3-dimercaptosuccinic acid) were started and therapy to enhance the formation of methylated As derivatives, which are potentially less toxic and which can be excreted more easily, was then administered. The patient survived this massive dose of ingested inorganic As with only polyneuropathy one year later.

Study objective: To determine if pharmacologic trapping of ingested toxins in the stomach using cholecystokinin (CCK) in addition to activated charcoal (AC) decreases the absorption of ingested toxins.

Methods: We performed a two-phase study that was prospective, randomized, blinded, and placebo-controlled, using a subtoxic acetaminophen (APAP) animal model. Eight adult beagle dogs were studied to detect a 20% decrease in 4h APAP levels with a power of 80%. A control arm using APAP at 100 mg/kg without AC or CCK was first performed. APAP levels were drawn at 0.5, 1, 1.5, 2, 4, 8, and 24 h. This was repeated in a CCK dose finding phase using a 60-min CCK infusion (4 vs. 8 pmol/kg/min) starting at 30 min post-APAP ingestion. Once the optimal CCK dose was established, animals in the treatment phase received AC and a 1 h infusion of CCK (vs. placebo). The efficacy of CCK when started at 30 and 60 min post-APAP ingestion was tested.

Results: In the dose finding arm 8 pmol/kg/min was well tolerated and also reduced maximum APAP levels by a mean of 49% from control. This dose was then used for the treatment phase. Four-hour APAP levels, maximum APAP levels, and area under the curve (AUC) were measured. No significant differences were found between placebo and CCK arms at either the 30 or 60 min postingestion interventions.

Conclusions: In this model, CCK infusion did not decrease the absorption of APAP. Adding charcoal to the model overcame the suggested beneficial effect of CCK alone in the dosing arm.

Background: Organochlorine insecticides are highly toxic compounds that are responsible for a number of severe intoxications worldwide with several deaths. Despite their widespread use in agriculture during the 1940s to 1960s and the well-known signs and symptoms of intoxication, the clinical picture in case of poisoning varies. We report two cases of acute intentional endosulfan intoxication with cerebral edema and cardiac failure.

Case reports: Both cases developed life-threatening signs like epileptic state, respiratory insufficiency and hemodynamic instability soon after ingestion. The survivor developed severe myocardial insufficiency and pulmonary edema documented by echocardiography and x-ray of the chest. The deceased patient developed severe cerebral edema and multiorgan failure ten days after ingestion of Thiodan 35. The peak serum concentration of endosulfan in the survivor was 0.12 mg/L approximately 23 hours after ingestion, whereas the peak blood concentration in the fatal case was 0.86 mg/L approximately 25 hours post-ingestion. Post-mortem endosulfan levels in different organs were determined.

Conclusion: Endosulfan is a highly toxic organochlorine insecticide that produces well-known neurological symptoms of tonic-clonic convulsions, headache, dizziness and ataxia but also can cause gastrointestinal symptoms and metabolic disturbances. Life-threatening cerebral edema and hemodynamic instability may occur. Treatment is symptomatic and supportive.

Objective: To report a case of D-lactic acid acidosis owing to massive oral ingestion of propylene glycol.

Case report: A 72-year old man with known congestive failure was admitted to the ICU with encephalopathy. Twelve hours prior to admission he had erroneously ingested a large amount of propylene glycol (PG). The laboratory revealed high anion gap (anion gap = 27 meq/l) acidosis (arterial pH = 7.16) and an increased osmolal gap. Toxicological analysis revealed a low serum propylene glycol level. Biochemical analysis indicated that very high amounts of D-lactic acid (up to 110 mmol/l), but not of the usual type of L-lactic acid, were responsible for the metabolic acidosis. Hemodialysis was initiated and associated with a decline of both the acidosis and D-lactic acid levels. The patient regained conciousness.

Conclusion: Ingestion of massive doses of propylene glycol, previously not reported as a cause of D-lactic acidosis, should be added to the differential diagnosis of this rare condition.

Micrurus snakes (coral snakes) may produce severe envenomation that can lead to death by peripheral respiratory paralysis. Only few laboratories produce specific antivenoms, and despite the cross-reactivity found in some Micrurus species venoms, the treatment is not always effective. To test two therapeutic antivenoms against the venom of four species of Micrurus from Southern America, North of South America, Central America, and North America, the determination of the lethal potency of the venoms, the study of some biochemical and immunochemical characteristics, and the determination of the neutralizing activity of both antivenoms were studied. North American and South American antivenoms neutralized well venoms from Micrurus species of the corresponding hemisphere but displayed lower effectiveness against venoms of species from different hemispheres. It was concluded that the neutralization of Micrurus venoms by regional antivenoms could be useful to treat the envenomation by some Micrurus snakes but is necessary to evaluate carefully the antivenoms to be used with the venoms from the snakes of the region. Also, considering the difficulties for coral snake antivenom production, the development of a polyvalent antivenom is useful to treat the envenomation by coral snakes from different regions is necessary.

Background: While routine immunizations are very safe, their administration to healthy children requires minimization of immunization programmatic errors. In order to estimate the incidence and ascertain the nature of reported immunization errors in the Greek childhood population, we have undertaken a study using data from the National Poison Information Center in Greece, which also has the responsibility to address medication-induced errors.

Methods: All immunization errors concerning children and reported to the National Poison Information Center during the 2-yr period 1999-2000 were retrieved and the conditions of their occurrence were examined. The incidence of reported errors was calculated under the assumption that during each year 100,000 children are born in Greece, and during their childhood they receive a total of about 20 immunization doses of all childhood immunizations.

Results: There were 40 immunization errors reported, corresponding to a reported incidence of about 11 per million immunization doses. Of these errors, 20 concerned OPV, 13 DTP, 5 MMR, 1 Haemophilus influenza and 1 Hepatitis B immunizations. In 12 instances an erroneous route was used (out of which 11 concerned OPV), whereas overdose was documented in 13 instances (out of which 8 concerned OPV). The third most common error was administration of DTP instead of the recommended Td vaccine. No adverse patient outcomes were reported.

Conclusions: In Greece, reported errors in immunization practice are relatively rare. Packaging modifications (about one in three errors in this study) of the OPV and DTP could further reduce their incidence.

There is increasing evidence of permanent sequalae from acute organophosphate poisoning. We report on accidental diazinon overexposure with acute organophosphate poisoning through cutaneous absorption and inhalation followed by persistent neurological effects. In addition, we observed skeletal and endocrine effects likely attributable to the diazinon poisoning. A family of seven was exposed to diazinon in June 1999 over a two-day period. The pesticide company mistakenly used diazinon to heavily spray the inside of the home instead of permethrin. The applicator applied the pesticide over the entire surface of the floor, carpeting, furniture, and clothing in closets to eradicate an infestation of fleas. Acute symptoms in the family members included headaches, nausea, skin irritation, runny nose, and vomiting. The family was first evaluated at 3 months and then 3 years after the acute poisoning. There were persisting neurological symptoms of memory loss, decreased concentration, irritability, and personality changes of varying degrees in all family members. Objective neurological findings of impaired balance, reaction time, color vision, slotted pegboards and trials making were present in the three older children who could be tested. Neuropsychological evaluation revealed evidence of organic brain dysfunction in all seven family members. Bone growth difficulties are present in four of five children. One child has delayed menarche.

Background: Tizanidine is a centrally acting muscle relaxant with a novel mechanism of action and structurally related to clonidine. There are no large case series of tizanidine exposure.

Methods: Retrospective review of all ingestions involving tizanidine reported to a poison control center from January 2000 through February 2003. Exclusion criteria were polydrug ingestion, no follow-up or lost to follow-up.

Results: There were 121 cases of which 45 patients met entrance criteria. Mean age was 32 years (range 1 to 80). Thirty-seven patients were evaluated in a health care facility of which 27 were admitted for medical care. Clinical effects included lethargy (n = 38), bradycardia (n = 14), hypotension (n = 8), agitation (n = 7), confusion (n = 5), vomiting (n = 3), and coma (n = 2). Mean dose ingested by history was 72 mg (S.D. + 86). The lowest dose associated with hypotension was 28mg, which occurred in a 63-year-old female with a BP of 88/52 and a HR of 54. The lowest dose associated with coma was between 60 mg and 120 mg, which occurred in a 30-year-old female with a HR of 30 and BP of 81/48. There were 6 patients < 6 yrs. The lowest dose with bradycardia and drowsiness in a small child was 16 mg in a 2 YO (weight unknown). All other cases in children < 6 yrs involved ingestion of a single tablet (2 or 4 mg) with only mild drowsiness reported. Therapy in this series was primarily supportive and included pressors in 3 cases and intubation in 3 cases. Naloxone was administered to 7 patients. There was no response to naloxone in 5 patients, poor documentation of response in one, and arousal in one patient. All patients recovered without residual complications.

Conclusion: Clinical manifestations of tizanidine overdose include alterations of mental status, bradycardia, and hypotension. In this series, outcome was good with supportive therapy.

We describe a case of a 43-yr-old female with severe multiorgan injury after accidental poisoning with Colchicum autumnale, which was mistaken for wild garlic (Allium ursinum). Both plants grow on damp meadows and can be confused in the spring when both plants have leaves but no blossoms. The autumn crocus contains colchicine, which inhibits cellular division. Treatment consisted of supportive care, antibiotic therapy, and granulocyte-directed growth factor. The patient was discharged from the hospital after three weeks. Three years after recovery from the acute poisoning, the patient continued to complain of muscle weakness and intermittent episodes of hair loss.