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Biomedical subjects

F J Baud

Publications and source records attributed to F J Baud.

At least 55 records · Page 3Linked to original sources
PubMed1996

Pharmacokinetics of hydroxocobalamin in smoke inhalation victims.

OBJECTIVE: Hydroxocobalamin has been proposed as a cyanide antidote. Little is known, however, about its pharmacokinetics in human cyanide poisoning. METHODS: We prospectively studied the pharmacokinetics of hydroxocobalamin in 11 smoke inhalation victims of whom all but one had objective evidence of cyanide exposure. Serum hydroxocobalamin levels were followed from just before drug administration to six days after a single 5 g dose of hydroxocobalamin. RESULTS: The results (mean +/- standard error) suggest a two compartment model. Distribution half-life is on the order of 1.86 +/- 0.34 h and the elimination half-life 26.2 +/- 2.7 h. The apparent volume of distribution is 0.45 +/- 0.03 L/kg. Renal and total body clearance are 0.31 +/- 0.06 and 0.83 +/- 0.07 L/h, respectively. CONCLUSION: The apparent volume of distribution suggests a predominantly extracellular partitioning of the antidote, even in the presence of cyanide, an important factor in terms of its antidotal effect. Hydroxocobalamin's elimination half-life in these cyanide-exposed patients far exceeds those found in previous studies of dogs and minimally-exposed humans. If confirmed, this half-life suggests that a single dose of hydroxocobalamin, sufficiently large enough to bind the cyanide present, should be adequate.

Adult↗
PubMed1996

Pulmonary dysfunction in survivors of acute paraquat poisoning.

Five patients survived acute paraquat ingestion, despite developing restrictive pulmonary dysfunction. Of these, 2 patients with documented long-term follow-up had progressive functional improvement. A literature review revealed 29 other patients surviving restrictive pulmonary dysfunction following acute paraquat poisoning. Some patients who survive an acute paraquat poisoning may develop pulmonary fibrosis, yet progressively improve over time.

Adolescent↗
PubMed1996

Acute cyanide poisoning: clinical spectrum, diagnosis, and treatment.

Cyanide poisoning presents in many forms. Industrial intoxications occur due to extensive use of cyanide compounds as reaction products. Smoke inhalation, a polyintoxication, is most often responsible for domestic cyanide poisonings. Suicidal poisonings are rare. Cyanogenic compounds may produce acute or subacute toxicity. Signs of cyanide poisoning include headache, vertigo, agitation, confusion, coma, convulsions and death. Definitive laboratory confirmation is generally delayed. Elevated plasma lactate, associated with cardiovascular collapse, should suggest cyanide intoxication. Immediate treatment includes 100% oxygen, assisted ventilation, decontamination, correction of acidosis and blood pressure support. Antidotes include oxygen, hydroxocobalamin, di-cobalt EDTA and methaemoglobin-inducers. Hydroxocobalamin is an attractive antidote due to its rapid cyanide binding and its lack of serious side-effects, even in the absence of cyanide intoxication. Sodium thiosulphate acts more slowly than other antidotes and is indicated in subacute cyanogen poisoning and as an adjunct to acute cyanide poisoning. Initial evaluation of antidotal efficacy is based on correction of hypotension and lactic acidosis; the final analysis rests on the degree of permanent central nervous system injury.

Acute Disease↗
PubMed1995

Hypokalaemia related to acute chloroquine ingestion.

Large doses of chloroquine can cause poisoning. Our aim was to determine the possible relation between the plasma potassium concentration on admission with the severity of acute chloroquine poisoning and to assess the mechanism of chloroquine-induced hypokalaemia. We conducted a retrospective study of 191 consecutive cases. The main data included the occurrence of vomiting before admission, plasma, and urinary potassium concentration at admission, whole blood chloroquine concentration on admission, haemodynamic parameters and ECG, administration of catecholamines and outcome. Mean blood chloroquine level was 20.1 mumol/L (SD 14.3) (therapeutic level < or = 6 mumol/L). Mean plasma potassium concentration was 3.0 mmol/L (0.8) and was lower in the subjects who died than in those who survived (p = 0.0003). Plasma potassium varied directly with the systolic blood pressure and inversely with the QRS and QT. Plasma potassium varied inversely with the blood chloroquine (p = 0.0001; tau = -0.42). Acute chloroquine intoxication is responsible for a hypokalaemia which correlates with the gravity of the intoxication and may be due to a transport-dependent mechanism. Plasma potassium concentrations should be carefully observed, particularly among patients who also receive catecholamine infusions. We should keep in mind, however, that overzealous repletion invokes the risk of subsequent hyperkalaemia and thus should be avoided.

Acute Disease↗
PubMed1995

Relation of blood cyanide to plasma cyanocobalamin concentration after a fixed dose of hydroxocobalamin in cyanide poisoning.

Hydroxocobalamin combines with cyanide to form cyanocobalamin. We hypothesised that the amount of cyanocobalamin formed after a fixed dose of hydroxocobalamin given for cyanide poisoning would correlate with initial blood cyanide concentration. We determined blood cyanide concentration in 12 patients exposed to residential fires, and compared this with markers of the amount of cyanocobalamin formed after treatment with 5 g intravenous hydroxocobalamin. All relationships were highly correlated (r2 0.79-0.95), for the whole group, and there appeared to be an almost linear relationship for the 9 patients with initial cyanide concentration below 40 mumol/L. Above this concentration, no further cyanocobalamin was formed from a single 5 g dose of hydroxocobalamin. In one patient with initial blood cyanide concentration of 96 mumol/L, however, plasma cyanocobalamin concentration approximately doubled after a second 5 g dose of hydroxocobalamin. 5 g of hydroxocobalamin appears capable of binding all available cyanide ions for blood cyanide concentrations up to about 40 mumol/L. Beyond this, more hydroxocobalamin must be given for remaining cyanide ions to be bound. This information will allow clinicians to use rapidly measurable plasma cyanocobalamin concentrations to gauge severity of exposure and evaluate adequacy of treatment.

Adult↗
PubMed1995

Simultaneous determination of hydroxocobalamin and its cyanide complex cyanocobalamin in human plasma by high-performance liquid chromatography. Application to pharmacokinetic studies after high-dose hydroxocobalamin as an antidote for severe cyanide poisoning.

Hydroxocobalamin (OHCbl) is a powerful antidote for cyanide poisoning, via the formation of non-toxic cyanocobalamin (CNCbl). Plasmatic cobalamins were measured at 361 nm, after enrichment and purification on a short C18 precolumn (1% acetic acid; 1 ml min-1; 2 min), by back-flush elution on a C18 ODS-2 column [0.1 M sodium dihydrogenphosphate-methanol (63:27, v/v) (pH 4.0); 0.80 ml min-1]. The precision was 3.21 and 3.54% for 10 microM OHCbl and CNCbl, respectively. The method was used to study the pharmacokinetics of OHCbl and the formed CNCbl in severely poisoned patients.

Antidotes↗
PubMed1995

4-methylpyrazole monitoring during haemodialysis of ethylene glycol intoxicated patients.

4-methylpyrazole (4-MP) was administered IV during haemodialysis of two ethylene glycol-intoxicated patients with anuric renal failure. The plasma 4-MP concentration decreased after each pass through the dialyser, indicating its dialysability in humans. In these two cases, the extraction coefficient was 0.78 and 0.71, and the mean dialysance was calculated to be 137 and 117 ml.min-1, corresponding to a 4-MP removal rate of 83 and 50 mg.h-1, respectively. The results imply that a higher rate of 4-MP infusion would be needed to replace 4-MP lost due to metabolism and to haemodialysis. The treatment of two ethylene glycol poisoned patients who were haemodialysed raised the problem of the dialysance of 4-MP. A recent study in pigs indicated that the amount of 4-MP removed by haemodialysis was significant [8]. No data were available for man. The aim of the study was to evaluate the dialysability of 4-MP in the two intoxicated patients, and to estimate how to compensate for 4-MP elimination during haemodialysis.

Acute Kidney Injury↗
PubMed1995

A case of life-threatening lactic acidosis after smoke inhalation - interference between beta-adrenergic agents and ethanol?

A 49-year-old male developed bronchospasm and severe lactic acidosis after exposition to fire smoke. The correction of lactic acidosis following beta-adrenergic agents withdrawal, and the transitory increase in lactate after salbutamol reintroduction are consistent with hypersensitivity to salbutamol. However, the plasma lactate concentration (32.6 mmol/l) that we observed 9.5 h after admission is far above those currently seen after administration of beta-adrenergic agents. We searched for causes able to potentiate the adverse effects of these drugs and we noticed that our patient had a high plasma ethanol level (2.4 g/l). Alcohol metabolism in the liver results in generation of high NADH/NAD+ ratios, thus reducing lactate liver clearance. This observation suggests that plasma lactate levels should be monitored closely in alcoholic patients treated with beta-mimetic agents.

Acidosis, Lactic↗
PubMed1995

Mercury oxycyanide and mercuric cyanide poisoning: two cases.

BACKGROUND: Although cyanide poisoning can be serious or fatal, it is typically described as mild when the cyanide is ingested in the form of either mercuric cyanide or mercury oxycyanide. METHODS: We studied two patients with acute cyanide poisoning following ingestion of one of these two agents in each case. RESULTS: Both patients demonstrated features of life-threatening cyanide poisoning, including hemodynamic instability, severe lactic acidosis, and high blood cyanide concentration. One of the patients died, while the second demonstrated signs of mercury intoxication (acute renal failure and severe gastrointestinal symptoms), in addition to cyanide intoxication. CONCLUSION: Ingestion of either mercuric cyanide or mercury oxycyanide can result in life-threatening cyanide intoxication.

Administration, Oral↗
PubMed1995

Modifying toxicokinetics with antidotes.

Five approaches may be described through which antidotes can modify toxicokinetics: (1) Decreased bioavailability of the toxins; (2) Cellular redistribution of the toxin in the organism; (3) Promotion of elimination in an unchanged form; (4) Slowing of metabolic activation pathways; (5) Acceleration of metabolic deactivation pathways. However, the ability to modify toxicokinetics with a new treatment, while demonstrating an understanding of the mechanism of action, must never be construed to be, in and of itself, the goal of therapy. The ultimate evaluation of an antidote modifying toxicokinetics is strictly clinical.

Animals↗
PubMed1995

Pharmacokinetics of lithium in plasma and red blood cells in acute and chronic intoxicated patients.

Lithium disposition in plasma, red blood cells (RBC) and urine was studied in acute self-poisoned patients upon chronic lithium therapy (n = 4) and in chronic intoxicated patients receiving oral lithium (n = 10). Following acute intoxication upon chronic lithium therapy, lithium pharmacokinetics did not differ from previous reports. Terminal plasma half-life ranged from 19.0-29.0 h and RBC/plasma ratio was 0.32 +/- 0.11. The distribution volume of the terminal phase, Vz, was estimated at 0.84 +/- 0.32 l/kg and renal clearance was 0.38 +/- 0.11 ml/mn/kg. After chronic intoxication lithium pharmacokinetics differed from those of the acute patients. Terminal plasma half-life ranged from 36.5-79.4 h and zero-order decline appeared in 8 of the 10 patients. The RBC/plasma ratio was 0.87 +/- 0.22 on admission. Vz was estimated at 0.71 +/- 0.27 l/kg and renal clearance was 0.16 +/- 0.07 ml/mn/kg. These modifications in lithium elimination kinetics could be related to the decrease in the glomerular filtration rate with age or renal dysfunction in this group of patients.

Administration, Oral↗
PubMed1994

An analysis of the factors implicated in fire deaths in children.

The aim of this study was to determine: 1) the factors implicated in fire deaths in children, 2) the relevance of blood carbon monoxide (CO) and hydrogen cyanide (CN) concentrations in child fire victims. 34 child fire victims (17 males: 17 females) were studied. Mean age was 4.5 years. In 12 cases medico-legal autopsies were performed, but no toxicological analyses were done (group A). In 14 cases autopsies were not performed, but blood CO and CN concentrations were measured in the victims (group B). In the remaining 8 cases both toxicological analyses and medicolegal autopsies were done (group C). In 29 cases out of 34, children had been left alone by their parents. In 20 cases out of 34, children had 80% burns of their body surface. In groups A and C autopsies enabled violence or other criminal cause of deaths to be excluded. All victims had smoke inhalation. The mean blood CN concentration in the 22 fire victims (groups B and C) was 70.67 +/- 14.11 micromol/l (0-207). The mean blood CO concentration was 1.89 +/- 0.51 mmol/l (0.11-5.89). There was no significant correlation between CN and the CO blood concentrations. There was no significant correlation between the burn surface area and the blood concentration of either CN or CO. In 11 cases, one or both gases concentrations were in the potential toxic range (CN: 40-<100 micromol/l; CO: 1-<5.8 micromol/l) but below the lethal range. Therefore these deaths were considered to be due to the combined effect of gas toxicity. It is concluded that: 1) In case of fire death, a medico-legal autopsy should be performed to confirm that victims suffered smoke inhalation and to exclude violence or other criminal cause of deaths; 2) Blood CN and CO measurements identify the exact contribution of each to the death; 3) Immediate blood sampling at the scene of death should be done because CN may disappear rapidly from body tissue after death.

Journal Article↗
PubMed1994

Elemental mercury vapour toxicity: treatment and levels in plasma and urine.

1. We report two cases of acute mercury vapour intoxication in humans. The mercury vapour was released from smelting alloys (gold-mercury amalgam). The alloy was apparently contaminated with an unknown amount of mercury. 2. Within half an hour of the incident, the victims began having moderate headache, nausea, lumbar pain and shortness of breath at rest. The patients were treated with BAL (2,3 dimercaptopropanol), followed by DMSA (2,3 dimercaptosuccinic acid). 3. Serial measurements of mercury metal in plasma and in urine were made for ten days. 4. The results suggest that in spite of the treatment, relatively high concentrations of mercury remain in the plasma for a very long time, and this could be explained by the progressive release of mercury from red blood cells and tissues after oxidation. However, BAL and DMSA did not seem to be the most efficient antidotes. They reduce the plasma inorganic mercury uptake at concentrations of < 50 micrograms I-1.

Administration, Oral↗
PubMed1993

Clinical features and management of digitalis poisoning--rationale for immunotherapy.

The intensity of gastrointestinal and visual symptoms together with hyperkalemia and the characteristic ECG features make diagnosis of acute digitalis intoxication relatively easy. Death results mainly from ventricular fibrillation or from ventricular asystole or pump failure. Mesenteric infarct may also occur in elderly patients. Previous assessment of outcome has shown that mortality increases in patients exhibiting five prognostic factors: 1) advanced age; 2) heart disease; 3) male sex; 4) high-degree atrioventricular block; 5) hyperkalemia. Conventional treatment includes gastric lavage, activated charcoal and supportive care. First-line antiarrhythmic therapy is usually atropine, because of bradycardia-induced arrhythmia. Ventricular pacing is a toxicodynamic treatment that may be helpful in both bradycardia-induced arrhythmia and high-degree atrioventricular block. Pacing is difficult to handle and can result in serious adverse effects. Immunotherapy has two advantages. First, a strong toxicodynamic effect due to quick reversal of digitalis-induced dysrhythmias, hyperkalemia, and myocardial depression, by reactivation of membrane ATPases. Second, a toxicokinetic effect due to accelerated renal excretion of Fab-digitalis complexes. Since this therapy is well tolerated and efficient, we recommend early administration of Fab fragments as soon as poor prognostic factors are identified.

Animals↗