401/449. Treatment of severe thallium intoxication. CASE REPORT: We report a successfully treated case of severe thallium intoxication. In spite of very high serum thallium (5,240 micrograms/L), symptomatology was minor and recovery complete. Prussian Blue was administered, diuresis was enhanced by intravenous fluids and a prolonged hemodialysis was started early. High blood flows (300 mL/min) and intravenous potassium chloride supplements, to mobilize thallium from the tissues, resulted in good clearances (96 to 150 mL/min). In order to prevent the well known complications, we recommend aggressive treatment of severe thallium intoxication. ( info) |
402/449. pemoline induced acute choreoathetosis: case report and review of the literature. BACKGROUND: pemoline is an oxazolidine derivative that is structurally different from amphetamines and used in the treatment of attention deficit disorder. pemoline has not been commonly associated in the literature as a cause of acute movement disorders. The following case describes two children acutely poisoned with pemoline who experienced profound choreoathetosis. CASE REPORT: Two, 3-year-old male, identical twin siblings presented to the emergency department after found playing with a an empty bottle of pemoline originally containing 59 tablets. The children had a medical history significant for attention deficit disorder previously treated with methylphenidate without success. This was their first day of pemoline therapy. The choreoathetoid movements began 45 min to 1 h after ingestion. The children gave no history of prior movement disorders and there was no family history of movement disorders. The children received gastrointestinal decontamination and high doses of intravenous benzodiazepines in an attempt to control the choreoathetoid movements. Despite treatment, the children continued to have choreoathetosis for approximately 24 hours. Forty-eight hours after admission, the children appeared to be at their baseline and were discharged home. CONCLUSION: pemoline associated movement disorder has been rarely reported in the acute toxicology literature. The possibility of choreoathetoid movements should be considered in patients presenting after pemoline overdose. ( info) |
| OBJECTIVE: To define specific brain magnetic resonance features in methanol intoxicated patients and to evaluate the clinical relevance of monitoring these features. BACKGROUND: During the past decade magnetic resonance imaging has proven to be an exquisitely sensitive modality in depicting subtle water changes in diseased areas of the brain, allowing the definition of high-risk structures in numerous pathological conditions. METHOD: Four patients admitted to our institution for acute methanol intoxication were repeatedly evaluated by brain magnetic resonance imaging or a combination of computed tomography and magnetic resonance imaging. Common features of initial brain status were shown in all four cases and compared to those of patients presenting with other intoxications or critical deprivation states. RESULTS: Preferential localization of methanol-induced lesions within the putamina was observed in all four cases. This finding is specific compared to intoxication by other substances like carbon monoxide, or in the critical phase of metabolic disorders. The striking regression of the putaminal lesions on follow-up magnetic resonance examinations correlated with complete neurological recovery and the absence of extrapyramidal disturbance. Two patients exhibited discrete symmetric additional lesions in the medial areas of the parieto-occipital lobes. In a third one, the occipital lesions were severe. All three suffered from permanent visual impairment. The fourth patient, in whom magnetic resonance examinations failed to reveal any occipital lesion, never complained of visual disturbance though signs of optic neuropathy were detected in the visual evoked potentials. CONCLUSION: magnetic resonance imaging appeared as a well suited neuroimaging modality in methanol intoxicated patients both in revealing a specific pattern of brain lesions and in demonstrating valuable correlation between evolution of brain changes on magnetic resonance images and clinical outcome. ( info) |
404/449. Acute dapsone intoxication: a pediatric case report. INTRODUCTION: There are many case reports of dapsone overdose in adults but only a few reports of dapsone-induced methemoglobinemia in children. We report a case of a three-year-old boy who developed prolonged recurrent methemoglobinemia following an ingestion of dapsone. methods: Case report. ethics: Not applicable. statistics: Not applicable. RESULTS: This child developed significant symptoms of methemoglobinemia approximately two hours after ingesting dapsone 37.5 mg/kg. The initial methemoglobin level measured 2.5 hours after ingestion was 44%. The patient was treated with multiple doses of activated charcoal and methylene blue. Three doses of methylene blue reduced the methemoglobin level to 6% by approximately 16 hours after the overdose but the level rebounded to nearly 15% at 64 hours postingestion. DISCUSSION: dapsone is a drug that is being used for a wide variety of clinical conditions. The primary clinical manifestation of dapsone overdose is methemoglobinemia. An important aspect of dapsone poisoning is its ability to produce methemoglobinemia, which is long lasting and which may recur following methylene blue therapy. Because of this, dapsone-poisoned children need to be monitored for two to three days. ( info) |
405/449. Granulocyte-colony stimulating factor in the treatment of colchicine poisoning. 1. colchicine is a highly active alkaloid used in the treatment of gouty arthritis and pseudogout. In overdose colchicine inhibits cell division effecting organs with a high rate of cell turn-over, such as the gastrointestinal tract and bone marrow. Early fatality results from cardiovascular collapse and respiratory failure, however pancytopenia and overwhelming septicaemia can occur later. 2. We describe a case of suicidal ingestion of 25-30 mg of colchicine in a previously healthy 43-year-old woman. Initial symptoms were mainly gastrointestinal. By day 5 she had developed severe pancytopenia and early sepsis, which were successfully treated using granulocyte colony stimulating factor (G-CSF) 600 micrograms s.c. 3. in vitro G-CSF is produced by the haematopoietic system. However, G-CSF can now be produced by recombinant dna cloning technology and thus is available clinically. 4. There is no recognised antidote for colchicine poisoning and treatment is symptomatic. Fab fragments may have a promising future in eliminating colchicine from the body, but are currently not clinically available. In those patients that survive the initial phase of poisoning, G-CSF offers an effective method of treating the pancytopenia and preventing overwhelming septicaemia. Daily monitoring of the patient's haematological status is strongly recommended. ( info) |
406/449. hypertension and identification of toxin in human urine and serum following a cluster of mussel-associated paralytic shellfish poisoning outbreaks. Following four outbreaks of paralytic shellfish poisoning on Kodiak Island, alaska, during 1994, medical records of ill persons were reviewed and interviews were conducted. urine and serum specimens were analyzed at three independent laboratories using four different saxitoxin binding assays. High-performance liquid chromatography was used to determine the presence of specific toxin congeners. Among 11 ill persons, three required mechanical ventilation and one died. Mean peak systolic and diastolic blood pressure measurements were 172 (range 128-247) and 102 (range 78-165) mmHg, respectively, and blood pressure measurements corresponded with ingested toxin dose. All four different laboratory methodologies detected toxin in serum at 2.8-47 nM during acute illness and toxin in urine at 65-372 nM after acute symptom resolution. The composition of specific paralytic shellfish poisons differed between mussels and human biological specimens, suggesting that human metabolism of toxins had occurred. The results of this study indicate that saxitoxin analogues may cause severe hypertension. In addition, we demonstrate that saxitoxins can be detected in human biological specimens, that nanomolar serum toxin levels may cause serious illness and that human metabolism of toxin may occur. Clearance of paralytic shellfish poisons from serum was evident within 24 hr and urine was identified as a major route of toxin excretion in humans. ( info) |
407/449. Acute arsine intoxication as a consequence of metal burnishing operations. The report concerns a 30-year-old factory worker, employed in a small galvanizing plant for over ten years in the burnishing, copper- and nickel-plating of small metal articles for the shoe industry. Acute arsine poisoning was attributed to the use of a dilute solution of CuSO4 (3%), HCl (32%), and As2O3 (2%) for burnishing metal (Fe-Zn) shoelace eyelet holes, in the absence of local exhaust ventilation and with no respiratory protection. Arsine caused severe intravascular hemolysis with a rapid drop in hematocrit and hemoglobin levels. Other body organs were involved as a result of the hypoxic effect of anemia and hemolysis, or as a direct toxic effect of the arsine itself. Our experience confirms that exchange transfusion is capable of rapidly arresting the adverse effects of arsine. The importance of preventive measures and worker information to avoid acute arsine poisoning is emphasized. ( info) |
408/449. Diagnostic use of anion and osmolal gaps in pediatric emergency medicine. Analyzing anion and osmolal gaps can help in the diagnosis and management of clinically elusive cases. This article presents two such cases, and reviews the clinical use of gaps. ( info) |
409/449. Dystonic reaction associated with dextromethorphan ingestion in a toddler. INTRODUCTION: Accidental ingestions of cough and cold preparations containing dextromethorphan (DM) are common in the toddler age group and rarely have serious consequences. Even large intentional overdoses by adults seldom lead to serious morbidity. There have been no previous reports of an extrapyramidal reaction due to a DM ingestion. CASE REPORT: We report a 30-month-old girl who ingested approximately 38 mg/kg dextromethorphan. She presented with opisthotonus, ataxia, and bidirectional nystagmus. There was no change in her status with the administration of naloxone. The child was given diphenhydramine with clearing of her opisthotonus but persistence of her ataxia and nystagmus. DISCUSSION: A moderate ingestion of dextromethorphan in a toddler resulted in extrapyramidal symptoms with opisthotonus that responded to diphenhydramine. dextromethorphan is known to have complex CNS effects and, in sufficient doses, may have dopamine receptor blocking activity resulting in this dystonic reaction. ( info) |
410/449. Anticholinergic poisoning in colicky infants treated with hyoscyamine sulfate. hyoscyamine, one of the principal alkaloid components of belladonna, is a potent anticholinergic agent. Because of its anticholinergic properties, hyoscyamine sulfate drops are often prescribed for the treatment of colic in infants. Anticholinergic poisoning in infants is rare. However, five cases are reported of infants with anticholinergic toxicity following the administration of hyoscyamine drops for the treatment of colic. Common presenting symptoms included irritability, tachycardia, and erythematous flushed skin. These cases emphasize the need for a heightened awareness by emergency physicians and pediatricians of possible anticholinergic toxicity caused by the use of hyoscyamine for infant colic. ( info) |