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M Shannon

Publications and source records attributed to M Shannon.

At least 19 recordsLinked to original sources

Anticonvulsant effects of intracerebroventricular adenocard in theophylline-induced seizures.

STUDY OBJECTIVE: To evaluate the potential anticonvulsant effects of Adenocard in theophylline-induced seizures, we developed a rodent model of theophylline neurotoxicity with resultant convulsions. We used this model to investigate the actions of intracerebroventricular (ICV) Adenocard on seizure onset. PARTICIPANTS: Male Sprague-Dawley rats. INTERVENTIONS: Surgical cannulation of the jugular veins of the rats was followed by stereotaxic placement of a catheter in the right lateral ventricle. The rats then received 15 micrograms (5 microL) ICV Adenocard or an equivalent. Ten seconds later, continuous infusion of IV aminophylline was begun at a rate of 75 mg/minute until the appearance of generalized convulsions with maximal hindlimb extension. RESULTS: Compared with vehicle-injected controls, rats that received ICV Adenocard had a significant delay in mean time to seizure (162.1 seconds versus 107.4 seconds; P < .001). There was a corresponding increase in the weight-adjusted convulsant dose of aminophylline after the ICV administration of Adenocard (311.4 mg/kg versus 470.4 mg/kg; P < .003). CONCLUSION: Our data indicate that ICV Adenocard ameliorates theophylline-induced seizures. Potential anticonvulsant benefits of Adenocard and other adenosinergic compounds for victims of severe theophylline poisoning should be investigated further.

Adenosine

Efficacy of magnesium citrate cathartic in pediatric toxic ingestions.

STUDY OBJECTIVE: To investigate the efficacy of magnesium citrate in reducing gastrointestinal transit time of activated charcoal in children. DESIGN: A prospective, randomized, clinical comparison of four magnesium doses. SETTING: Urban children's hospital emergency department. PARTICIPANTS: Children aged 1 month to 6 years who presented for management of an acute toxic ingestion. INTERVENTION: Each child received 1 g/kg activated charcoal combined with a randomly assigned dose of a 6% solution of magnesium citrate: 0 mL/kg, 4 mL/kg (standard recommended dose), 6 mL/kg, or 8 mL/kg. The primary outcome measure was the interval to first activated charcoal-containing stool, which was determined by follow-up telephone call or review of the medical record. RESULTS: Sixty-four children were enrolled. Median times to first charcoal stool were 19.5 hours (0 mL/kg), 13.0 hours (4 mL/kg), 14.0 hours (6 mL/kg), and 12.0 hours (8 mL/kg). Intergroup differences were significant by Kruskal-Wallis analysis of variance (P = .0035). CONCLUSION: Magnesium citrate reduces gastrointestinal transit times of activated charcoal stools when administered to children who receive activated charcoal for a toxic ingestion. Further study is needed to determine the clinical value of this reduction.

Antacids

Effect of acute versus chronic intoxication on clinical features of theophylline poisoning in children.

OBJECTIVES: To determine whether the method of intoxication influences the metabolic disturbances and pattern of life-threatening events that occur after theophylline intoxication in children. METHODS: Five-year prospective observational study of consecutive pediatric patients referred to a regional poison control center with a theophylline concentration (theo) greater than or equal to 30 micrograms/ml. At the time of referral, intoxication was categorized as acute (single toxic exposure), chronic (long-term toxic exposure), or acute-on-therapeutic (single toxic exposure superimposed on maintenance therapy). RESULTS: One-hundred twenty-five patients were monitored. Mean age was 12 years (range, 3 days to 20 y). Seventy-four patients (59%) had acute intoxication, 31 (25%) had chronic intoxication, and 20 (16%) had acute-on-therapeutic intoxication. Mean peak serum (theo) was 55 micrograms/ml. Life-threatening events occurred in 12 patients (10%). Patients with acute intoxication had a significantly lower serum potassium level (3.04 vs 3.80 mmol/L; p less than 0.001) and higher serum glucose level (10.8 vs 7.0 mmol/L (194 vs 127 mg/dl); p less than 0.001) than did children with chronic intoxication. Although life-threatening events (seizures or arrhythmias) occurred at a similar rate across categories, the (theo) at which these events occurred was significantly higher in patients with acute intoxication than in those with chronic intoxication (100 vs 42 micrograms/ml; p = 0.02). Among children with chronic intoxication, those who had life-threatening events had (theo) similar to those who remained well (42 vs 47 micrograms/ml) but were significantly younger (1.6 vs 8.0 years; p less than 0.001). CONCLUSIONS: These data indicate that method of intoxication has significant effects on the metabolic and clinical consequences of theophylline poisoning. Life-threatening events occur in those with acute theophylline intoxication at significantly higher (theo) than in those with chronic intoxication. After chronic intoxication, peak (theo) does not identify patients at risk for life-threatening events; young age appears to be the primary risk factor. These findings potentially complicate the management of theophylline poisoning, given the difficulty of extracorporeal drug removal in young infants.

Acute Disease

Pharmacokinetics of drugs in overdose.

The pharmacokinetics of drugs may be altered following an overdose. The degree of absorption depends on the physical characteristics of the drug; the rate of dissolution may delay or broaden peak serum concentrations. The pathophysiological effects of a drug may also limit or augment absorption. Altered distribution of drugs in overdose results from changes in the extent of protein binding and size of the volume of distribution. Saturation of hepatic enzyme systems in overdose is manifested by delayed metabolism or elimination of many drugs; renal elimination of unchanged drug may take on greater importance in this instance. Familiarity with the toxicokinetic profile of a given drug enables the physician to exploit these principles in order to limit toxicity. Delayed or prolonged absorption allows for late decontamination. Multiple doses of activated charcoal are effective in interrupting both entero-enteric and enterohepatic recirculation. Alkalinisation-induced ion trapping enhances renal elimination of unchanged drugs which normally undergo hepatic transformation. For several drugs, chronic overdose due to altered distribution is associated with a greater severity of toxic manifestations despite relatively low serum drug concentrations. Conversely, with some drugs, induction of metabolic pathways may lead to more rapid drug elimination in chronic overdose. Knowledge of the pharmacokinetic alterations which occur in drug overdose enables the physician to predict toxicity with greater accuracy and to institute optimum therapy in a timely manner.

Absorption

Unsuspected quinine intoxication presenting as acute deafness and mutism.

A case of unsuspected quinine overdose is reported in a 14-year-old girl. Presenting symptoms included deafness and mutism. Diagnosis was delayed for approximately 4 hours because of the absence of an accurate history. Case details, laboratory values, and hospital course are discussed. Signs of cinchonism and common ototoxins are discussed. Strategies for the management of quinine overdose are reviewed.

Adolescent

Accidental and intentional poisonings with ethylene glycol in infancy: diagnostic clues and management.

Ethylene glycol has long been recognized as a potentially lethal poison and remains available today as automotive antifreeze and windshield deicer fluids. Ethylene glycol is rapidly absorbed from the gastrointestinal tract, with peak levels measured one to four hours after ingestion. Metabolism of the parent compound and the production of several organic acids are responsible for the metabolic acidosis observed in ethylene glycol poisoning. Target organ cellular damage is seen in the kidney, brain, myocardium, pancreas, and blood vessel walls. Renal tubular deposition of calcium oxalate crystals is felt to be responsible for the development of the severe renal injury which may accompany ethylene glycol ingestion. The clinical course is quite varied and includes inebriation, hematuria, cardiorespiratory compromise, and neurologic effects. Prompt diagnosis and initiation of treatment, including ethanol therapy and hemodialysis, is necessary to ameliorate the effects of ethylene glycol ingestion. Two cases of ethylene glycol poisoning, one accidental and one intentional, are reviewed.

Accidents, Home

Ten cases of acute lead intoxication among bridge workers in Louisiana.

We report the cases of ten construction workers who developed acute lead intoxication while repairing a bridge in Louisiana. All but one patient received a five-day course of edetate calcium disodium (calcium EDTA) chelation therapy; one patient received five doses instead of five days of treatment. Calcium EDTA 25 mg/kg q12h was administered for ten consecutive doses by intravenous infusion over two hours. Each dose was diluted in NaCl 0.9% 500 mL. No adverse drug effects were observed during treatment. The posttreatment mean whole blood lead (PbB) concentration was significantly reduced compared with the pretreatment mean PbB (1.48 +/- 0.70 vs. 3.8 +/- 1.68 mumol/L; p = 0.0012, Student's paired t-test). This indicates that the body lead burden of these patients was effectively reduced with calcium EDTA. Eight patients had complaints on admission that were suggestive of lead intoxication. These included malaise, numbness of the extremities, arthralgia, myalgia, abdominal discomfort, sleep disturbance, and lower back pain. Patients had no complaints on discharge. Eight patients had mild anemia that was consistent with acute lead intoxication (mean pretreatment hemoglobin (+/- SD), 128.6(+/- 17.2 g/L), but calcium EDTA therapy did not appear to effect any change in the pretreatment hemoglobin values. The Occupational Safety and Health Administration (OSHA) lead standard requires that manufacturers provide employees at risk for occupational lead exposures with proper respirators and medical surveillance to prevent lead intoxication. The construction industry is exempted from these standards except in Maryland. We believe that amendment of the OSHA lead standards, to provide specific lead regulation of the construction industry, would be helpful in preventing similar cases of occupational lead intoxication.

Acute Disease