Sensitivity, specificity, and predictive values.
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Biomedical subjects
Publications and source records attributed to P Lheureux.
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During the years 1986 to 1990, an increasing number of cases of acute carbon monoxide (CO) poisoning were encountered in the Emergency Department Hacettepe University Hospital in Ankara, Turkey. Between January 1 and March 31, 1991, all the patients presenting with complaints compatible with CO poisoning were evaluated; the diagnosis was confirmed in 55 of the 5795 people who attended the Emergency Department during this period. In all cases the source of CO intoxication was determined. Among these patients, nausea or vomiting and headaches were the most common complaints (occurring in 100% and 85%, respectively). At least transient impairment of alertness was observed in 29% of cases. The carboxyhaemoglobin levels ranged from 3.80 to 48.1% (median 14.2%). Two comatose patients who developed a non-cardiogenic pulmonary oedema required mechanical ventilation. One of them was discharged from the hospital with mild cerebral disability. Another patient developed an acute myocardial infarction. In all the cases in this series, the source of CO poisoning was identified as improper combustion of recently marketed steam coal in inadequately ventilated bucket stoves.
Serious exposure to the herbicide paraquat usually results in death, either due to gastrointestinal caustic lesions, shock, and acute respiratory distress syndrome or related to the progressive development of pulmonary fibrosis associated with refractory hypoxemia. We report a case of suicidal paraquat ingestion in a 59-year-old man. Most of the indicators of poor prognosis were encountered in this patient. Treatment consisted of early digestive decontamination and hemodialysis, followed by antioxidant therapy, including the administration of deferoxamine (100 mg/kg in 24 h) and a continuous infusion of acetylcysteine (300 mg/kg/d during 3 weeks). The patient only developed a nonoliguric acute renal failure, a mild alteration of liver tests, and an impairment of CO transfer factor without any respiratory complaint. Renal and hepatic disturbances completely resolved within 1 month, whereas CO transfer factor remained altered 14 months later. This observation suggests that early administration of an antioxidant therapy, including deferoxamine and acetylcysteine could be usefully associated with measures that prevent digestive absorption or enhance elimination to limit systemic toxicity in potentially fatal paraquat poisoning.
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Acute urticaria represents the most commonly observed skin disorder (35%) presenting in an emergency department. We retrospectively analysed the records of 676 patients admitted for acute urticaria in order to know the particularities and the main aetiologies. The mean age was 28; females being more affected than males. Aetiologies varied according to age; drugs were involved in 50% of patients more than 50-years old and in only 19% of children less than 10 years old. Whilst causes are rarely known in the chronic forms, almost 60% of the acute cases were due to drugs or food. Amongst the former, antibiotics and NSAI were the most frequently met.
The ability of high doses of flumazenil to antagonize ethanol-induced sedation was assessed via ethanol-induced loss of the righting reflex (LRR) in rats. Ethanol (3.5-5 g kg-1 i.p) produces a dose-dependent increase in the proportion of animals presenting a LRR response. Flumazenil (0.1 to 1 mg kg-1 i.p) was ineffective in preventing the suppression of the righting reflex and even aggravated it for ethanol dosages of 3.5 and 4.0 g kg-1. These data support the view that flumazenil has no effective 'anti-ethanol' properties. Conversely, the prolongation of mean sleep time provoked by the antidote could be related to the suppression of a putative endogenous inverse-agonist activity at the benzodiazepine receptor, which could be implicated in the mechanism of the acute tolerance to ethanol.
Two very similar cases of drug-induced pneumonitis complicating treatment of rheumatoid arthritis with low-dose methotrexate are presented. Diagnosis was suggested by clinical history and findings, but the bronchoalveolar lavage showed a high percentage of neutrophils, an unusual feature in methotrexate-induced pneumonitis. Transbronchial lung biopsies (TBB) confirmed the diagnosis by showing interstitial lymphocytic infiltrate with microgranulomas. Although histologic findings are not strictly pathognomonic, when a differential diagnosis has to be made with infectious and rheumatoid lung disease, TBB appears to be of great promise.
This study evaluates the cardiac and neurologic risks associated with the antagonization of the benzodiazepine component of mixed drug overdoses, when cyclic antidepressants are also implicated. Twenty-four mongrel dogs were anesthetized and ventilated. Electroencephalogram, electrocardiogram, and tidal carbon dioxide and arterial pressure were continuously recorded. Amitriptyline (1 mg/kg/min) associated with midazolam (1 mg/kg + 1 mg/kg/h) was infused in 12 of the dogs. Midazolam was replaced by saline in the other 12. Drug administration was continued until signs of cardiotoxicity (QRS prolongation greater than 120 milliseconds or sustained arrhythmias) occurred. At that moment, midazolam effects were suddenly reversed by administration of flumazenil 0.2 mg/kg in six dogs out of each group. Placebo was administered in the others. Reactions were observed for the next 120 minutes. Midazolam-induced sedation efficiently protects (P less than .02) against seizures due to amitriptyline toxicity. This protective effect is counteracted by flumazenil. Midazolam has limited influence on the cardiac toxic effects of amitriptyline. The bolus of flumazenil is, however, associated with a significant worsening of electrocardiogram disturbances, and two sudden deaths were recorded. The mechanism of this effect remains unclear, as it could be unrelated to the antagonization of midazolam sedation. Given the problem of extrapolating animal data to humans, these results suggest that bolus administration of high doses of flumazenil in mixed intoxication implicating benzodiazepine and cyclic antidepressants has the potential to precipitate convulsions and/or arrhythmias. A slowly titrated administration of the antidote, as usually recommended, could prevent these effects.
A lifelong non-smoker who was the victim of a massive accidental exposure to anhydrous ammonia gas was followed up for 10 years. In the acute phase the patient presented with severe tracheobronchitis and respiratory failure, caused by very severe burns of the respiratory mucosa. After some improvement he was left with severe and fixed airways obstruction. Isotope studies of mucociliary clearance, computed tomography, and bronchography showed mild bronchiectasis. It is concluded that acute exposure to high concentrations of ammonia may lead to acute respiratory injury but also to long term impairment of respiratory function.
This preliminary study evaluates the cardiac and neurological risks associated with the sudden antagonism of benzodiazepine (BZD)--induced sedation in dogs intoxicated with tricyclic anti-depressants (TCA). Twelve dogs were anesthetized with midazolam and ventilated with room air. EEG, ECG, and arterial pressure were continuously recorded. An infusion of amitriptyline (6 dogs) or clomipramine (6 dogs) 1 mg/kg. min was maintained until signs of cardiotoxicity (QRS prolongation, hypotension or arrhythmias) occurred. The effects of a bolus of flumazenil 0.2 mg/kg were then observed until 120 minutes. In amitriptyline poisoning, BZD reversal was associated with development of convulsions in 3 dogs, with severe arrhythmias in 4 and with one death. In clomipramine intoxication, 2 dogs developed sudden fatal arrhythmias. These results show that BZD reversal may unmask the convulsant properties and increase the severity of arrhythmias induced by TCA.
Flumazenil acts as an antidote for pharmacological and toxic effects due to benzodiazepines. Several isolated observations and short uncontrolled series have also suggested a possible effect against the impairment of consciousness induced by pure alcohol intoxication. Patients admitted in the emergency department with coma related to acute alcohol (ALC) or pure benzodiazepine (BZD) intoxication were randomized and treated blindly with either placebo or 1 mg flumazenil. A modified Glasgow score was used to observe the evolution of consciousness. In the 18 ALC patients, 1 mg flumazenil was not more effective than placebo, whereas it appeared to be very active in the BZD group. However, an open administration of higher doses of flumazenil (2-5 mg) in 11 ALC patients, whose condition had not initially improved, was followed by clear improvement of consciousness in five of them. Flumazenil, administered at a dose usually active against BZD sedation, does not improve CNS depression induced by ALC intoxication. Higher doses could be more effective in some patients, but it should also be verified in a placebo-controlled trial.
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The purpose of this work is a review of usefulness, indications and handling of some antidotes which are at our disposal for therapeutic use since several years, especially naloxone, flumazenil, Fab fragments of digoxin specific antibodies, hydroxocobalamine, 4-methyl-pyrazole, N-acetylcystein or the new metal chelators. Older clinically relevant substances are also reviewed.
Zolpidem is a recently introduced sleep-inducer which is thought to act on the central-type benzodiazepine receptors. This observation is the first report of drug poisoning with this compound. The toxic response was characterized by the development of a profound but short-lasting coma, associated with pin-point pupils and respiratory depression, as observed in a narcotic overdose. These clinical signs were not influenced by the administration of naloxone, but responded dramatically to flumazenil. Some analytical data on zolpidem toxicokinetics are presented.
The authors analyze the contribution of flumazenil to the diagnosis and the management of common drug poisoning. This paper defines the guidelines and limits for its use, after a review of the literature and the personal experience on this topic.
Intentional benzodiazepine (BZD) overdose is usually a benign condition frequently encountered in the emergency department of hospital. Twenty-one patients, who were suspected of BZD overdose, were treated with the antagonist of the central type BZD-receptors Ro 15-1788. Samples for toxicological analysis were taken before and after treatment. The patients were divided into three groups. In the first group (pure BZD overdose, n = 9), rapid and complete awakening was observed in all the patients (9/9) with 3.5 +/- 1.5 mg Ro 15-1788. In the second group of patients with multiple drugs poisoning (including BZD, n = 6), CNS depression improved in all the patients despite incomplete awakening. In the last group (n = 6), where no BZD were detected in toxicological samples, none of the comatous patients improved significantly during Ro 15-1788 administration, except one patient with pure ethanol intoxication. No undesirable effects are reported, except mild transitory withdrawal syndrome in three cases following rapid injection. This study supports the introduction of Ro 15-1788 as a useful antidote in the diagnosis and the treatment of drug-induced coma.
We report the case of a 41-year-old patient with no history of abdominal symptoms who presented with an acute painful syndrome of the right flank and iliac fossa suggesting acute appendicitis. The diagnosis of panniculitis of the great omentum was suggested preoperatively by the particular aspect of omental fat observed by abdominal sonography and computed tomography. A subvoval omentum resection was performed and the outcome was uneventful.