[Inhalation of smoke causes hydrocyanic acid intoxication].
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Biomedical subjects
Publications and source records attributed to B Riou.
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No therapy has been proved to be effective for patients with severe chloroquine poisoning, which is usually fatal. In a retrospective study of 51 cases, we found that ingestion of more than 5 g of chloroquine was an accurate predictor of a fatal outcome, and therefore chose this dose as the criterion for severe chloroquine poisoning. We selected as a control group 11 consecutive patients who had ingested more than 5 g of chloroquine between July 1983 and December 1985. We then undertook a prospective study to determine whether a better outcome could be obtained with immediate mechanical ventilation and the administration of diazepam and epinephrine. Eleven consecutive patients who ingested more than 5 g of chloroquine in 1986 received this combination therapy. Ten of these patients survived, whereas only one control had survived (P = 0.0003). There was no significant difference between the combination-therapy and control groups in age (29 +/- 3 vs. 27 +/- 2 years), amount of chloroquine ingested (7.5 +/- 0.5 vs. 8.5 +/- 0.8 g), systolic arterial pressure (74 +/- 2 vs. 74 +/- 3 mm Hg), or QRS duration (0.14 +/- 0.01 vs. 0.14 +/- 0.01 second). In our combination-therapy group, blood chloroquine levels ranged from 40 to 80 mumol per liter, whereas a literature search showed that no patient in whom blood levels were more than 25 mumol per liter had survived. These preliminary data suggest that combining early mechanical ventilation with the administration of diazepam and epinephrine may be effective in the treatment of severe chloroquine poisoning.
The aim of this prospective study was to compare the results obtained with the non-protected lower respiratory tract secretions samples (LRS) with the protected specimen brushes (PSB) performed through a fiberoptic bronchoscope in mechanically ventilated patients, when pneumonia was suspected. The diagnosis of pneumonia was ultimately made at the end of the hospitalisation, in a double-blind manner by 2 members of the medical staff not aware of the bacteriologic results of LRS and PSB. LRS and PSB were performed in 24 patients. PSB culture was considered as positive at a level of 10(3) colony-forming units per milliliter (cfu/ml) microorganisms. Twenty-five samples from 24 patients were divided as follows: (1) LRS (-) and PSB (-) 5 samples: the clinical diagnosis of pneumonia was never established. (2) LRS (+) and PSB (+) 10 samples: the clinical diagnosis of pneumonia was always established, 2 microorganisms were involved 4 times and 1 microorganism 6 times. (3) LRS (+) and PSB (-) 10 samples: the clinical diagnosis pneumonia was retained in 3 with the possibility of false negative PSB. We conclude that (1) a negative LRS eliminated the diagnosis of pneumonia without PSB; (2) a positive LRS was not sufficient to diagnose pneumonia since PSB was negative in 50% of all LRS (+) cases; (3) the possibility of a false negative PSB must be kept in mind particularly in patients previously treated with antibiotics; (4) 2 microorganisms may be responsible for the pneumonia if the previously determined, as significant, bacteriological count (greater than or equal to 10(3) cfu/ml) appears to be accurate.
To assess the effects of diazepam in chloroquine poisoning, we studied pentobarbital anesthetized and mechanically ventilated pigs. All the pigs received 50 mg.kg-1 chloroquine given intravenously for 25 min. Eight pigs acted as control (group C). Another 7 were treated with diazepam given intravenously 5 min after the end of chloroquine infusion: 2 mg.kg-1 of diazepam for 2 min, then 1 mg.kg.h-1 for 25 min (group D). Thereafter, all pigs were sacrificed. In both groups the chloroquine infusion induced a large fall in arterial pressure, a decrease in heart rate, and an increase in QRS duration. No difference was observed between the 2 groups for weight, systolic and diastolic arterial pressures, heart rate, QRS and QT durations before diazepam. After diazepam, systolic and diastolic arterial pressures, heart rate, urine volume, urinary excretion of chloroquine, plasma and blood cell chloroquine levels were higher, whereas QRS duration was lower, in group D compared to group C. No difference was observed between the 2 groups for urinary concentration of chloroquine, the ratio between plasma and blood cell chloroquine levels, hepatic, cardiac, and skeletal muscle chloroquine levels, and QT duration. After diazepam, the slope of the regression curve between QRS duration and plasma chloroquine levels was reversed in group D compared to group C. We conclude that diazepam counteracts some haemodynamic and electrocardiographic changes, and increases urinary excretion of chloroquine, in acute experimental chloroquine poisoning.
We reviewed retrospectively from 1982 through 1984 35 cases of enterococcal bacteremia in a medical ICU. Of these, 27 patients acquired nosocomial infections; their mean previous hospital stay was 17 +/- 4 days. Thirteen had a serious debilitating disease; 20 received previous antibiotic therapy. The infection focus was not found in 16 patients. The deaths of nine patients were related directly to enterococcal bacteremia. Mortality was significantly lower in patients with nosocomial infections, with appropriate antibiotic therapy just after the start of the infection, without debilitation, and when the infection focus was discovered. In a medical ICU, some patients appear to be particularly predisposed to enterococcal bacteremia. When these patients develop a serious infection without obvious source, an appropriate antibiotic therapy for Enterococcus should be promptly initiated.
Nineteen trauma patients with either maxillofacial trauma or cervical spine fracture were orotracheally intubated over a guidewire percutaneously inserted through the cricothyroid membrane into the mouth in a retrograde fashion. In 13 patients, conventional techniques failed (average number of attempts 6 +/- 1, mean duration 18 +/- 1 min); in six patients, the initial method of choice was a retrograde technique. In all patients, retrograde technique succeeded on only one attempt (duration less than 5 min in all cases). No serious complication could be related to this technique; it is an easy, safe, efficacious method for difficult tracheal intubation in trauma patients.
Eighteen patients with life-threatening traumatic hemothorax received prehospital autotransfusion using a simple new device. During transfer to the hospital, they received 3.9 +/- 0.5 L of colloid fluid and 4.1 +/- 0.6 L of autotransfused blood, without anticoagulation. Hemorrhagic blood was not coagulable, had a hematocrit of 20 +/- 4 percent, few platelets, and low fibrinogen levels. Five patients died from irreversible hemorrhagic shock. Thirteen patients were alive upon admission to the hospital, underwent emergency surgery, and were discharged alive. During autotransfusion, hematocrit decreased from 24 +/- 3 to 19 +/- 3 percent, and systolic arterial pressure increased from 78 +/- 11 to 88 +/- 12 mm Hg. Upon admission to the hospital, platelet count was 90,800 +/- 21,400/cu mm, prothrombin time 48 +/- 3 percent, partial thromboplastin time 197 +/- 18 percent, plasma free hemoglobin levels 21 +/- 7 mg/100 ml, and serum potassium levels 3.6 +/- 0.5 mmol/L. No serious complication could be related to autotransfusion considered to be crucial to patients' survival. The preliminary results of this study suggest that autotransfusion might be developed in the prehospital setting since it appears simple and safe, and represents the only hope of survival for patients with life-threatening hemothorax.
Fatal asthma is rare but constitutes a serious public health problem on account of the raised prevalence of the disease. The incidence of fatal asthma is estimated at 3/100,000 people in France and the incidence of fatal asthma has not ceased to rise in the world despite therapeutic progress. The principal risk factors recognised are: 1. longstanding asthma, 2. unstable asthma, 3. acute severe asthma with a prior history, 4. insufficiently treated asthma or poorly compliant patient, 5. the absence of surveillance by peak flow measurements, etc. The socio-economic factors and above all the psychological factors play a role which is not negligible. A poor evaluation of the severity of the crisis by the asthmatic has been suggested as a factor, but it is possible that the rapidity of the progression of the crisis in fatal asthma may be responsible for the physical inability of the patient to react to the situation. There is no reason to incriminate beta-mimetic agents in fatal asthma. The prevention rests on an improvement in treatment, the education of the asthmatic and an improvement in medical teaching. However, only improvement in the speed of admission of emergency cases will effectively permit a reduction in the incidence of fatal asthma. The system of auto-admission of patients at risk should be reserved for co-operative patients but the systematic medicalization for urgent cases of asthma merits further development. A better definition of the asthmatic population at risk for fatal asthma is necessary.
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Two hundred and seventy-three acute hemorrhagic shocks were treated in 1984 in a pre-hospital emergency care unit. Twenty patients (7%) had a paradoxical bradycardia: they were conscious, 9 of them had an undetectable systolic arterial pressure with the sphygmomanometric method but the femoral pulse was still present. All of them recovered from bradycardia with fluid loading alone. The comparison between patients with paradoxical bradycardia and those with tachycardia showed that the former had more severe and rapid hemorrhages. During 1985, 7 new cases of acute hemorrhagic shock with paradoxical bradycardia were treated with an antishock trouser. These patients recovered from bradycardia more quickly (p less than 0.01) and with a less important fluid loading (p less than 0.01) than those previously treated without the antishock trouser. Two other patients were treated with atropine before antishock trouser inflation and experienced ventricular premature beats and one developed ventricular fibrillation. A paradoxical bradycardia can occur in hemorrhagic shock and denotes a rapid and severe hemorrhage requiring a massive and rapid fluid loading. The preliminary results of the antishock trouser in this setting are encouraging. The treatment of bradycardia per se may be deleterious and atropine must be avoided in conscious patients with hemorrhagic shock and paradoxical bradycardia.
Two cases of co-infection or very early superinfection of pneumococcal pneumonia with Staphylococcus aureus in one case, and Enterobacter cloacae in the other, are reported. The two patients were not fully immunocompetent, had leukopenia and a mild intravascular coagulation, and were bacteremic. Mixed infection probably accounted for the lethal outcome because initial antibiotherapy was only directed against Streptococcus pneumoniae. Accurate bacteriologic methods are required to delineate contaminating and infecting pathogens when another bacteria is found in initial bronchial samples of patients with pneumococcal pneumonia, and the antibiotherapy might be directed against the two pathogens until quantitative bacteriologic results would be available, especially in old and debilitated patients. The incidence of mixed infection in pneumococcal pneumonia seems low.
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Over a 32-month period, 980 calls from asthmatic patients were received at the switchboard office of a prehospital emergency care unit. A total of 90 patients (9 percent) died before receiving any medical help, and 216 (22 percent) patients were taken to the hospital with an emergency care ambulance where none of them died. We made the assumption that, when an asthmatic patient calls an emergency care unit, the attack is severe and might be fatal. A prospective study was performed during a six-month period to prevent these asthma deaths: 259 calls from asthmatic patients were received. For each emergency call from asthmatic patients, paramedical help (delay: 5.1 +/- 0.3 minutes) and an emergency care ambulance (delay: 9.7 +/- 0.6 minutes) were immediately sent. Only four patients died during this period. Emergency calls from asthmatic patients must be considered as related to a severe attack that might be fatal. Fatal asthma is often related to a severe attack that evolves rapidly. Some asthmatic patients are able to assess the severity of asthma attacks, and prehospital emergency care schemes for asthmatic patients are actually able to prevent some asthma deaths.