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ABSTRACT: Superwarfarins have progressively replaced warfarin as rodenticides as they are more potent and have a longer anticoagulant activity. Human exposure may be complicated by spontaneous haemorrhage in various sites. We report the case of a 51-year-old woman who was admitted with spontaneous haemoperitoneum and intramural haematoma along the small intestine. After the evidence of a deficit of vitamin K1-dependent clotting factors (II, VII, IX, X), the patient admitted that she was chronically ingesting difenacoum. She was successfully treated with fresh frozen plasma and vitamin K1. Follow-up was not accepted.
European Journal of Emergency Medicine 01/2001; 7(4):305-7. · 0.90 Impact Factor
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Intensive Care Medicine 12/2000; 26(11):1715-6. · 5.40 Impact Factor
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ABSTRACT: Three fatalities caused by methanol ingestion are reported. Admission blood methanol concentrations ranged from 0.28 to 4.6 g/L. Two patients had been admitted after a significant delay (>20 hours), and one patient was observed within 90 minutes following ingestion. Formic acid levels were determined in blood samples at admission and ranged from 302 to 680 mg/L. The patients died 44, 55, and 82 hours after poisoning. Formic acid determinations in postmortem tissues were performed by a gas chromatograph method. The authors found great variability in formic acid distribution among the patients and among organs.
American Journal of Forensic Medicine & Pathology 12/2000; 21(4):335-8. · 0.88 Impact Factor
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ABSTRACT: Fatalities are still reported following methanol poisoning. Methanol is extensively metabolized by alcohol dehydrogenase to formaldehyde and by aldehyde dehydrogenase to formic acid which is the main toxic metabolite. Survival with extremely high blood methanol concentration is possible provided that aggressive symptomatic and specific therapy is applied. This is illustrated by the clinical observation of a 27-year-old man who was admitted 22 hours after poisoning and presented a peak blood methanol concentration of 12.9 g/l. Treatment included correction of metabolic acidosis, ethanol infusion, haemodialysis and peritoneal dialysis. The patient survived with moderate visual sequelae and oesophageal stenosis. The range of toxicity of methanol according to blood levels determination is discussed.
European Journal of Emergency Medicine 10/2000; 7(3):237-40. · 0.90 Impact Factor
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Transplantation Proceedings 04/2000; 32(2):491-2. · 1.00 Impact Factor
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ABSTRACT: Methanol ingestion is a cause of potentially life-threatening poisoning with numerous systemic manifestations. Clinicians may overlook the possibility of acute pancreatitis in this setting. The objective of this paper is to document the incidence of this complication in a series of 22 patients and to discuss the respective role of methanol and ethanol in its pathogenesis.
A 54-year-old woman developed acute necrotizing pancreatitis following acute methanol poisoning. She was treated by hemodialysis, ethanol infusion, and folinic acid, but, despite maximal supportive therapy, she died from multiple organ failure 54 hours after the ingestion.
In a series of 22 consecutive patients admitted with a diagnosis of acute methanol poisoning, we found evidence of pancreatic damage in 11 patients. The abnormalities were present from admission and before ethanol therapy in 7 cases and developed after ethanol therapy in 4 cases. Seven patients had a history of chronic ethanol abuse, but no patient had previously suffered from acute or chronic pancreatitis. Three patients presented moderate-to-severe acute pancreatitis according to clinical and radiological criteria and required aggressive supportive therapy including peritoneal dialysis. One patient died from the direct consequences of acute necrotizing pancreatitis and 2 fully recovered from this event. Three patients evolved to brain death; autopsy revealed hemorrhagic lesions in the pancreas in only 1 case.
Clinical, biological, and radiographic signs of acute pancreatic injury may be more common than previously realized. Acute methanol poisoning appears to produce pancreatic injury, although antidotal treatment with ethanol or prior chronic ethanol abuse may be contributing factors. Because ethanol treatment may complicate the pancreatic injury, fomepizole (4-methylpyrazole) may be the preferable antidote in acute methanol poisoning.
Journal of toxicology. Clinical toxicology 02/2000; 38(3):297-303.
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ABSTRACT: BACKGROUND: The poor prognosis of patients with persistent gastrointestinal radio-opacities after oral arsenic poisoning supports efficient gastrointestinal decontamination as critical for survival. In a case of massive arsenic ingestion, we performed repetitive gastric endoscopy and a continuous alkaline irrigation of the stomach over several days. CASE REPORT: A 41-year-old woman was admitted 4 hours after intentional ingestion of trivalent arsenic powder 5 g. The admission abdominal X-ray confirmed the presence of multiple gastric opacities. Initial treatment was gastric lavage with normal saline, dimercaprol chelation, and supportive therapy. Since gastric opacities persisted on the abdominal X-ray at 34 hours despite repeated gastric lavage, a gastroscopy was performed showing nonremovable agglomerates. In an attempt to achieve further gastric decontamination, we performed a continuous gastric alkaline irrigation. After 3 days of alkaline irrigation, the abdomen was normal on X-ray but the gastroscopy still showed arsenic concretions. Alkaline irrigation was continued for another 3 days until total disappearance of arsenic agglomerates at the gastroscopy. Admission urinary arsenic was 3663 microg/L. A total of 46.2 mg of inorganic arsenic, or less than 1% the ingested dose, was extracted from the stomach by this technique. The patient was discharged from the intensive care unit 20 days after admission without sequelae.
Journal of toxicology. Clinical toxicology 02/2000; 38(5):471-6.
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ABSTRACT: CASE REPORT: A 37-year-old man ingested in a suicide attempt 300 mL of a diquat solution (equivalent to 60 g diquat ion). The initial diquat serum concentration was 64 microg/mL 4 hours after poisoning. The clinical course was characterized by a progressive anuria and by neurological disorders (coma and seizures). The patient died 26 hours after poisoning from refractory cardiocirculatory collapse. Extracorporeal techniques removed 1.09 g of diquat which could be considered as significant in regard to the total amount that was likely absorbed, but they did not influence the clinical outcome. There was marked renal tubular damage at autopsy and the highest diquat tissue concentration was found in the kidneys.
Journal of toxicology. Clinical toxicology 02/2000; 38(2):149-52.
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ABSTRACT: To present results of electrophysiologic investigations of the visual toxicity observed during the early stage of methanol poisoning.
Retrospective, clinical study.
A 7-bed intensive care unit in a university hospital.
Nineteen patients admitted with a diagnosis of acute methanol poisoning.
Visual evoked potentials were obtained within the first 48 hrs after admission; a clinical follow-up examination was performed in 11 patients, and 12 patients were followed up by visual evoked potentials beyond the same delay. Correlations between the occurrence of an optic neuropathy and clinical, biological, and electrophysiological data were studied.
A significant correlation was found between arterial pH and blood formate concentration (r2 = 0.58, p = .003), between blood formate and bicarbonate concentrations (r2 = 0.36, p = .02), and between delay from ingestion and blood formate concentration (r2 = 0.44, p = .017). Clinical outcome was correlated not only with the bicarbonate (p = .007), formate (p = .018), and methanol (p = .03) concentrations and arterial pH (p = .004) but also with a well-defined electrophysiologic pattern during the acute stage. An index of global cortical functioning > or =3 was associated with death, whereas a global cortical functioning index < or =2 was associated with survival (p = .0058). Moreover, a statistically significant difference in long-term visual impairment was found between the subgroup with abnormal wave III morphology or a global cortical functioning index of 1-2 and the subgroup with normal wave III morphology and a global cortical functioning index <1 (p = .015). Results of the electrophysiologic studies were expressed as retinal dysfunction and optic nerve injury. Five patients had normal findings on electrophysiologic examination. Ten patients had early signs of retinal dysfunction that were fully reversed in the eight patients who were followed. Ten patients had persistent electrophysiologic signs of optic neuropathy.
Although reversible retinal dysfunction is evident in the early stage of human methanol poisoning, its absence does not preclude development of optic neuropathy. The occurrence of optic neuropathy and early electrophysiologic data are correlated.
Critical Care Medicine 01/2000; 27(12):2707-15. · 6.33 Impact Factor
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ABSTRACT: The necessity of defining brain death (BD) arose from technological development in medical science. The definition of this concept had practical consequences and opened the way to organ donation from BD patients. Nowadays, the imbalance between the number of organs available for transplantation and the size of the demand is becoming critical. In most laboratories, a BD diagnosis is made according to precise criteria and in a well-defined process. BD diagnosis should be improved, not only to assure the safety and to preserve the human dignity of the patient, but also in order to increase the rate of organ donation. By analysing some epidemiological parameters in BD diagnosis and organ donation, it appears that BD diagnoses can be made more often and more rapidly if one has a reliable, accurate, and safe confirmatory test, especially under misleading conditions (hypothermia, drugs, metabolic disturbances). In our experience, the use of multimodality evoked potentials (MEPs) to confirm a BD diagnosis has many advantages: MEPs can be rapidly performed at the patient's bedside, assess the brain stem as well as the cerebral cortex, and are innocuous for the patient. Moreover, their insensitivity to the aforementioned misleading factors is sufficient to distinguish BD from clinical and EEG states that mimic BD. They give an immediate diagnosis, and no delay is required in BD confirmation if there is sufficient cause to account for BD. MEPs are a safe, accurate, and reliable tool for confirming a BD diagnosis, and their use can improve the organ donation rate while preserving the safety of the patient.
QJM: monthly journal of the Association of Physicians 08/1999; 92(7):407-14. · 2.33 Impact Factor
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QJM: monthly journal of the Association of Physicians 08/1999; 92(7):415-8. · 2.33 Impact Factor
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Transplantation 08/1999; 68(1):165-6. · 4.00 Impact Factor
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ABSTRACT: Since the use of 4-methylpyrazole (4-MP) in the treatment of humans with methanol poisoning is poorly documented, we report two cases of acute methanol intoxication partially treated by this potent alcohol dehydrogenase (ADH) inhibitor.
Intensive Care Unit in a university hospital.
A 56-year-old man and an 18-year-old woman were observed, respectively, 41 and 16 h after the voluntary ingestion of an unknown amount of methanol.
In both cases, ethanol was used as the first antidote. In the first patient, hemodialysis was also performed on admission because a high methanol level (0.72 g/l) and visual impairment were noted. In the second patient, ethanol therapy was withdrawn after 12 h when clinical and biological signs of acute pancreatitis became evident. Both patients received multiple oral doses of 4-MP. No recurrence of metabolic acidosis occurred and the 4-MP therapy was well tolerated.
While the use of 4-MP is better documented in cases of ethylene glycol poisoning, it could also become an accepted option for the management of methanol poisoning since 4-MP offers advantages over ethanol therapy.
Intensive Care Medicine 06/1999; 25(5):528-31. · 5.40 Impact Factor
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ABSTRACT: To review the clinical and experimental data concerning the serious neurologic adverse events, and more particularly seizures, which could be related to the administration of recent antibiotics, with special reference to cephalosporins, monobactams, carbapenems, and fluoroquinolones.
We have searched in the MEDLINE database over the years 1966-1998 the pertinent publications dealing with antibiotics related neurotoxicity. We used the thesaurus function and the following key words: antibiotics, neurotoxicity, seizures. Additional references were found in the articles sorted by the MEDLINE search.
Neurotoxic manifestations following antibiotics administration are infrequently encountered under usual conditions. Experimental studies are helpful to demonstrate that these compounds might interact with a major component of the neurotransmission, the gamma aminobutyric acid (GABA) receptor complex. Structure-toxicity relationships can be described. For the clinician, the recognition of some predisposing factors related either to the patient (age, previous central nervous system disorder ...) or to the drug metabolism (reduced renal clearance, drug interactions ...) may help to minimise the risk of adverse neurologic manifestations. Several factors have to be taken into account before assessing causality: delay from administration, evolution, origin of the adverse event (risk factors, other drugs, non pharmacological origin), possibility of rechallenge, confirmation by biological testing or in vitro experiments....
Acta clinica Belgica 05/1999; 54(2):80-7. · 0.59 Impact Factor
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ABSTRACT: A 25-year-old woman developed "brain death" 48 h after acute methanol poisoning. After the elimination of methanol and the correction of metabolic disorders, organ donation was discussed. The lungs were transplanted into a 46-year-old woman suffering from cystic "emphysematous-like" lesions as a complication of lymphangioleiomyomatosis. The procedure was not complicated, and we have an uneventful follow-up of > 12 months. In addition to the lungs, the kidneys and the liver were also removed and transplanted with success.
Chest 05/1999; 115(5):1458-9. · 5.25 Impact Factor
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Clinical Transplantation 03/1999; 13(1 Pt 1):72-3. · 1.67 Impact Factor
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ABSTRACT: The main objective of this study was to evaluate the effect of switching from parenteral to enteral feeding on liver blood flow and propofol steady-state blood concentrations in patients in the intensive care unit (ICU).
Steady-state blood concentrations of propofol were measured in eight ICU patients before (on days D -3, D -2, and D -1) and after (on days D + 1, D + 2, and D + 3) switching from parenteral to enteral feeding (on day DO). All patients received a continuous intravenous infusion of propofol (4.5 mg x kg(-1) x h(-1)) from several days before the start of the study, continuing throughout the experimental period. Hepatic blood flow was estimated by measuring steady-state D-sorbitol hepatic clearance.
Hepatic blood flow was high and was not affected by switching from parenteral to enteral feeding: 33 +/- 8 ml x min(-1) x kg(-1) (mean +/- SD) and 33 +/- 10 ml min(-1) x kg(-1) on D -3 and D -1, respectively, as compared to 37 +/- 11 ml x min(-1) kg(-1) and 34 +/- 8 ml x min(-1) x kg(-1) on days D + 1 and D + 3, respectively. Systemic clearance of propofol was much higher than liver blood flow with average values on the six observation days ranging from 74.0 to 81.2 ml x min(-1) x kg(-1) and was not affected by switching from parenteral to enteral feeding.
Liver blood flow and systemic clearance of propofol were not affected by switching from parenteral to enteral feeding in the eight ICU patients studied. Extrahepatic clearance accounted for at least two thirds of the overall systemic clearance of propofol.
Intensive Care Medicine 09/1998; 24(8):795-800. · 5.40 Impact Factor
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ABSTRACT: A 19-year-old woman was admitted 45 min after ethylene glycol (EG) ingestion. The initial serum EG concentration was 1.34 g/l (21.6 mmol/l), the anion gap 14.5, and the osmolal gap 24. Renal function was preserved (serum creatinine 75.1 micromol/l). As the patient was seen soon after poisoning, before the development of metabolic acidosis, therapy with 4-methylpyrazole (4-MP) was proposed as an antidote. 4-MP was administered via the intravenous route (7 mg/kg as loading dose, followed by 3.6, 1.2, 0.6, and 0.6 mg/kg at intervals of 12 h). 4-MP alone was effective in preventing EG biotransformation to toxic metabolites (absence of metabolic acidosis and renal injury). Ethanol therapy, hemodialysis, and sodium bicarbonate administration were not required. The half-life of EG during 4-MP therapy was 11 h, with a mean EG renal clearance of 26.9 ml/min, and a total of 65.3 g EG was eliminated unchanged in the urine. 4-MP therapy was also well tolerated.
Intensive Care Medicine 08/1998; 24(7):736-9. · 5.40 Impact Factor
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Journal of toxicology. Clinical toxicology 02/1998; 36(4):375-7.
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Transplantation Proceedings 01/1998; 29(8):3345-6. · 1.00 Impact Factor
