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Biomedical subjects

F J Baud

Publications and source records attributed to F J Baud.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Acidosis and hyperlactatemia in acute sodium valproate poisoning].

OBJECTIVES: We searched for signs of metabolic acidosis and associated hyperlactatemia in case of sodium valproate overdose. PATIENTS AND METHODS: A retrospective study was conducted in the toxicology intensive care unit at the Fernand Widal hospital from 1990 to 1995. Patients retained for study had sodium valproate levels above the therapeutic range (> 600 mumol/l). Data collected included past history, intubation for mechanical ventilation, administration of catecholamines and infusion of bicarbonate or sodium lactate, and blood pressure. Laboratory tests included serum sodium valproate, pH, PCO2, bicarbonate, anion balance and lactate. RESULTS: The study included 22 consecutive patients. None had a history of liver disease. Thirteen patients were intubated before admission to intensive care. Two received catecholamines. None of the patients received bicarbonate or sodium lactate. Mean blood pressure was 118 +/- 16 mmHg, mean serum sodium valproate was 2668 +/- 2437 mumol/l, mean pH was 7.41 +/- 0.08, mean PO2 35.6 +/- 8.0, mean anion imbalance 23.2 +/- 6.0 mmol/l and mean lactate 5.0 +/- 2.1 mmol/l. There was a significant correlation between lactase and pH (p < 0.003). CONCLUSION: We found metabolic acidosis with major anion imbalance and high lactate levels in patients with acute sodium valproate intoxication. Hyperlactatemia could be due to the direct effect of sodium valproate or to an unknown mechanism.

Acidosis↗
PubMed1997

[New acute poisoning syndromes of drug origin].

The slow but constant modifications of the pharmacopeia and prescribing habits are at the origin of changes in the causes of intoxications by medications, which are reflected in the syndromes observed in daily practice. New syndromes have appeared: serotoninergic syndrome, adrenergic syndromes, toxic malignant hyperthermia, opioid toxic syndrome, intoxication by drugs with membrane-stabilizing effect. Recognizing these syndromes is not only useful to determine the possible causes of on intoxication, but also to direct appropriate, specific therapeutic interventions.

Adrenergic Agents↗
PubMed1997

Acetonitrile as a possible marker of current cigarette smoking.

Volatile nitriles are present in cigarette smoke. We tested the hypothesis that the presence of any of four nitriles in the blood can serve as a marker of recent cigarette smoking. We determined the sensitivity and specificity of these nitriles as indicators of daily cigarette smoking in 24 smokers (Group A) and 18 non-smokers (Group B), as well as the correlation between intensity of daily smoking and the blood concentration of acetonitrile. A new head space GLC assay method was used. Of the four nitriles, only acetonitrile was present in the blood of any study subject. Acetonitrile was moderately sensitive (67%) and entirely specific (100%) for self-reported daily smoking. There was fair correlation between blood acetonitrile concentration and the average daily number of cigarettes smoked (r2 = 0.39; P = 0.001), and the mean blood acetonitrile concentration was significantly higher (P = 0.03) among subjects with higher (> 10 cigarettes per day) current cigarette exposure (148.3 +/- 18.0 micrograms/l) than among smokers with low or minimal (1-10 cigarettes per day) exposure (43.3 +/- 6.0 micrograms/l). Thus, acetonitrile in blood appears to be highly specific and a moderately sensitive marker of cigarette smoking with a dose-effect relationship. As such, acetonitrile shows promise as a marker of current cigarette exposure.

Acetonitriles↗
PubMed1997

Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns.

OBJECTIVE: To evaluate the incidence of early pulmonary complications and the value of initial clinical signs and paraclinical investigations in victims of smoke inhalation not suffering from burns following structural fires. DESIGN: Retrospective chart review. SETTING: Thirteen-bed ICU. PATIENTS: Sixty-four victims of smoke inhalation following household fires were admitted to the ICU between January 1987 and December 1992. Exclusion criteria from the study were patients with cutaneous burns or multiple trauma or blast injury, and patients found in cardiac arrest. METHODS: Clinical, biological, and radiologic parameters were collected over a 5-day period. RESULTS: The mortality rate in relation to progressive respiratory failure was 3.1%. Mean ICU stay was 5.8 days (range, 1 to 33 days), and was longer in the patients presenting with soot deposits in the oropharynx (p = 0.02), dysphonia (D) (p = 0.05), or ronchi (R) (p = 0.0004) at the first examination, and in those having a positive sputum bacteriologic analysis (p = 0.003) or requiring parenteral bronchodilator agents for more than 24 h (p = 0.04). Thirty-five patients underwent mechanical ventilation (MV) for a mean of 101.2 h (range, 8 to 648 h). Mean MV duration was higher in the patients presenting initially with R (p = 0.003), high carbon monoxide (but not cyanide) levels (p = 0.02), or a positive bacteriologic sample (p = 0.0001). Positive bacteriologic sampling correlated with the presence of D (p = 0.02) or R (p = 0.04) and with immediate intubation (p = 0.0003). No correlation was found with chest radiograph. CONCLUSIONS: In this selected series of fire victims without cutaneous burns, respiratory injury was frequent. The initial clinical signs may be helpful to predict pulmonary complications.

Adult↗
PubMed1997

Value of C-reactive protein in the detection of bacterial contamination at the time of presentation in drug-induced aspiration pneumonia.

STUDY OBJECTIVES: To compare the plasma concentration of C-reactive protein (CRP) with traditional markers for diagnosis of bacterial pneumonia in patients with suspected aspiration. DESIGN: Prospective, nonrandomized, controlled study of consecutive hospital admissions. SETTING: Toxicology ICU in a university hospital. PATIENTS OR PARTICIPANTS: Acutely poisoned comatose patients admitted to the hospital with suspicion of aspiration pneumonia. INTERVENTIONS: Distal protected catheter sampling per fiberoptic bronchoscopy and bacteriologic culture were employed as a standard to detect the bacterial component of suspected aspiration pneumonia. Plasma CRP concentrations, temperature, and WBC count were measured on hospital day 1. MEASUREMENTS AND RESULTS: Sixty-six patients were evaluated. Thirty-two had bacterial contamination by positive culture (> or =10(3) cfu/mL). Multiple receiver-operating characteristic (ROC) curves were used to compare each parameter for detection of infection secondary to aspiration. The ROC curve of CRP concentrations showed that a CRP >75 mg/L is associated with bacterial contamination with a sensitivity of 87%, specificity of 76%, positive predictive value of 78%, and negative predictive value of 87%. ROC curves of temperature and WBC count demonstrated poor diagnostic value of these markers in indicating the bacterial component of suspected aspiration pneumonia. CONCLUSIONS: Early measurement of CRP is useful for the diagnosis of aerobic bacterial content of aspiration pneumonia and perhaps in determining the need for invasive bacteriologic sampling. Temperature and WBC count are poor indicators of bacterial infection of aspiration pneumonia in poisoned patients.

Adult↗
PubMed1997

Intravenous 4-methylpyrazole as an antidote for diethylene glycol and triethylene glycol poisoning: a case report.

Diethylene glycol (DEG) intoxication resembles that of ethylene glycol, with progressive inebriation, anion gap metabolic acidosis, renal failure, coma and death. DEG is oxidized by alcohol dehydrogenase (ADH) to more toxic byproducts, thus blockade of ADH might be beneficial. Triethylene glycol (TEG), also metabolized by ADH, is less toxic. A young female suicidally ingested DEG and TEG, presenting in metabolic acidosis with coma. Given 4-methylpyrazole (4-MP), an ADH inhibitor, the acidosis resolved, the patient recovered and was discharged without sequelae. 4-MP, if supported by further studies, may be useful in DEG poisoning.

Adolescent↗
PubMed1996

[Acute chloroquine poisoning].

Acute chloroquine intoxication is responsible for grave cardiovascular disturbances which may be rapidly life-threatening. For this reason, any suspicion of acute chloroquine intoxication requires hospitalisation in an intensive care unit for a minimum of 12 hours. Cardiovascular toxicity is linked to a potent membrane-stabilizing effect, which is also responsible for transfer-dependent hypokalemia, the degree of which is directly associated with the gravity of the intoxication. Blood chloroquine concentration confirms the intoxication and is likewise closely correlated to gravity. Treatment of this intoxication, based on vascular repletion, adrenalin, assisted ventilation and diazepam has markedly improved the prognosis of these intoxications, overall mortality for all degrees of intoxication nonetheless remains to the order of 10%.

Acute Disease↗
PubMed1996

Therapeutic trial of diazepam versus placebo in acute chloroquine intoxications of moderate gravity.

OBJECTIVE: Acute chloroquine intoxication is responsible for a membrane-stabilising effect which results in electrocardiographic (ECG) and hemodynamic disturbances. Diazepam is used in acute chloroquine intoxication on the basis of clinical and experimental observations, but its utility alone, in man, remains unproven. The goal of this study was to verify whether diazepam alone has an effect on the membrane-stabilising effect observed in moderately severe chloroquine intoxications. DESIGN: Prospective, multi-center, double-blind, placebo-controlled study. SETTING: Prehospital mobile intensive care units (Paris) and hospital intensive care units (paris and Dakar). PATIENTS AND PARTICIPANTS: Adults with moderately severe intoxication defined as: a suspected ingested dose of 2 or more but less than 4 g, systolic blood pressure (SBP) higher than 80 mmHg, QRS duration less than 0.12 s and the absence of dysrhythmia at inclusion. INTERVENTIONS: Patients received either a loading dose of 0.5 mg/kg diazepam followed by an infusion of 1 mg/kg over 24 h or an equivalent volume of placebo. MEASUREMENTS AND RESULTS: Outcome was measured by serial assessments of SBP, ECG (QRS and QT segments) and clinical deterioration. There were no significant differences observed in the initial or serial ECG or SBP measurements. There were no deaths and no patient had to be removed from the study due to clinical deterioration. CONCLUSIONS: Diazepam, at the dose studied, does not appear to reverse the chloroquine-induced membrane-stabilising effect in acute moderately severe chloroquine intoxication. Supportive intensive care of these intoxications appears to be all that is necessary.

Acute Disease↗
PubMed1996

Hyperthermia complicating tricyclic antidepressant overdose.

We observed a 51-year-old woman who was admitted for severe amitriptyline overdose. Besides major cardiovascular complications, the patient developed severe hyperpyrexia with a central body temperature of more than 43 degrees C for 5 h. The patient died on day 3 from cardiocirculatory collapse and arrhythmias. Hyperthermia was unresponsive to cooling with ice water, gastric lavage, muscle relaxation, and dantrolene and bromocriptine administration. The possible mechanisms of refractory hyperthermia are discussed.

Amitriptyline↗
PubMed1996

Empiric use of flumazenil in comatose patients: limited applicability of criteria to define low risk.

STUDY OBJECTIVE: To develop clinical rules for the safe and effective use of flumazenil in suspected benzodiazepine overdose. METHODS: We assembled a retrospective series of 35 consecutive comatose patients admitted between October 1992 and July 1993 to a toxicologic ICU with the presumptive diagnosis of drug overdose. These patients were divided into two groups. Group A (low-risk) patients had a clinical picture compatible with uncomplicated benzodiazepine intoxication (calm, without abnormalities in pulse or blood pressure, lateralizing signs, hypertonia, hyperreflexia, or myoclonus) in the absence of predefined electrocardiographic or clinical signs of tricyclic antidepressant or other proconvulsant overdose, and absence of an available history of long-term benzodiazepine treatment or an underlying seizure disorder. Group B ("non-low risk") comprised all other patients. Efficacy of flumazenil was categorized as complete awakening (with normal level of alertness), partial awakening, or no change in alertness level. The safety of flumazenil was defined on the basis of the absence of seizures or death. RESULTS: In group A (n=4), flumazenil was associated with complete awakening in three patients and partial awakening in one. No seizures were observed. In group B (n=31), flumazenil was associated with complete awakening in 4 patients, partial awakening in 5, and no response in 22. In group B, five seizures occurred. CONCLUSION: Comatose patients with clinical or ECG criteria thought to contraindicate the use of flumazenil have a reasonably high risk of seizures after administration of this drug. Low-risk patients may be able to receive flumazenil safely, but they may be only a small portion of comatose patients with suspected overdose.

Adolescent↗
PubMed1996

Treatment of acute chloroquine poisoning: a 5-year experience.

OBJECTIVE: To describe various aspects of prognostic and therapeutic importance in patients treated for acute chloroquine poisoning. DESIGN: Retrospective study. SETTING: Toxicology intensive care unit (ICU) of a university hospital. INTERVENTIONS: None. PATIENTS: One hundred sixty-seven consecutive patients with acute chloroquine overdose admitted to our toxicology ICU. MEASUREMENTS AND MAIN RESULTS: The mean amount ingested by history was 4.5 +2- 2.8 g. and 43 (26%) of 167 patients ingested > 5 g. The mean blood chloroquine concentration on admission was 20.5 +/- 13.4 mumol/L The majority (87%) of our patients received at least one arm of a combination therapy regimen (epinephrine, mechanical ventilation, diazepam). cardiac arrest occurred in 25 patients before hospital arrival; In seven of these patients, cardiac arrest occurred immediately after injection of thiopental. The mortality rate was 8.4% overall, and was 9.3% in patients with massive ingestions (NS vs. the group as a whole). We did not find a meaningful correlation between the amount ingested as estimated by history and the peak blood chloroquine concentration; the latter was highly correlated with the mortality rate. CONCLUSIONS: The mortality rate in patients with acute chloroquine poisoning, including those patients sick enough to be referred to a specialty unit such as ours, can be limited to < or = 10%. This finding appears to be true even in patients with massive ingestions. We were not able to correlate mortality with amount ingested by history, although the mortality rate does correlate with blood chloroquine concentration. While early use of diazepam, epinephrine, and mechanical ventilation in most of our patients may have contributed to the excellent overall results, these elements, either singly or in combination, do not appear to have a truly antidotal effect in acute chloroquine poisoning. Thiopental, on the other hand, should be used with great caution, if at all, in such cases.

Acute Disease↗
PubMed1996

Complexation of intracellular cyanide by hydroxocobalamin using a human cellular model.

1. The rational for administering hydroxocobalamin (OHCbl) as an antidote to cyanide poisoning is based on the high affinity of CN ion for cobalt compounds. However, only few data are available on the influence of OHCbl on the intracellular cyanide pool. 2. In human fibroblasts incubated for 10 min with 500 microM of [14C] cyanide, the accumulation ratio was 25 at 37 degrees C (10.45 +/- 1.51 mM) and 11.9 at 4 degrees C. 3. Using the monoblastic U-937 cell line, a rapid uptake of radioactive cyanide was observed with a maximum accumulation ratio of 1.97 at 5 min. 4. A linear relationship between cyanide uptake by U-937 cells and cyanide concentration in incubation medium (10-500 microM; 5 min) was found suggesting a first order process (k = 0.25 min-1). 5. After incubation of fibroblasts with 500 microM of OHCbl, a 75% decrease of intracellular cyanide was observed, with concomittant formation of intracellular cyanocobalamin CNCbl (intracellular/extracellular ratio: 158). 6. These findings suggest that OHCbl is able to penetrate into heavily cyanide loaded cells and to complex cyanide to the non-toxic CNCbl form.

Antidotes↗
PubMed1996

Markedly altered colchicine kinetics in a fatal intoxication: examination of contributing factors.

1. Colchicine poisoning, which is relatively rare, is associated with significant morbidity and mortality. Whilst a new treatment modality, in the form of colchicine-specific Fab fragments is on the horizon, currently available therapy is largely supportive. 2. The elimination of colchicine occurs primarily by hepatic metabolism, following a first-order process, with significant enterohepatic circulation. Renal extraction is responsible for approximately 20% of colchicine elimination. 3. We report a case of colchicine intoxication, complicated by the presence of co-ingestants, in which serum colchicine concentrations remained quasi-constant over the 3 days of the patient's survival, consistent with marked alterations both in metabolism and excretion. The initial presentation was relatively benign but the subsequent course was one of severe colchicine poisoning, resulting in death. 4. Severe colchicine toxicity appears to have resulted in a vicious cycle of progressive organ dysfunction and impaired elimination. 5. Josamycin, one of the co-ingestants and an inhibitor of P-glycoprotein, the membrane pump responsible for multidrug resistance, may have played a significant role in impeding the cellular and biliary elimination of colchicine. Co-ingested opioid and anticholinergic compounds may have altered colchicine absorption and gastrointestinal transit. 6. This case serves as a reminder of the need for attention to co-ingested drugs, to early aggressive therapy, and if available, to consideration of immunotherapy.

Adult↗
PubMed1996

Effects of mode of inhalation of carbon monoxide and of normobaric oxygen administration on carbon monoxide elimination from the blood.

1. The half-life of carbon monoxide (CO) in blood was studied retrospectively in 26 fire victims and in 19 cases of CO poisoning. Normobaric oxygen therapy was administered via mechanical ventilation in 19 fire victims, and by facial mask to the rest of the casualties. 2. Arterial pH was significantly lower (P < 0.05) and PaO2 significantly greater (P < 0.01) in the mechanically ventilated fire victims compared to the spontaneously breathing fire victims. 3. The blood CO half-lives were 91 +/- 38 min for the 26 fire victims and 87 +/- 40 min for the 19 pure CO intoxications. 4. The blood CO half-lives were 92 +/- 40 min for the 19 mechanically ventilated fire victims and 87 +/- 37 min for the 26 spontaneously breathing subjects. 5. We conclude that the elimination of CO from blood was a slow process with no significant effects on the blood CO half-life of either the cause of the CO poisoning or the mode of normobaric oxygen therapy. These data suggest that enhancement of the elimination of carbon monoxide by normobaric oxygen in both pure CO poisoning and fire victims is more difficult to achieve and more complex than has previously been reported.

Adolescent↗