RESUMEN
The underlying mechanisms of behavioral functions at different levels of organization of the nervous system are not yet fully understood. No satisfactory answers have been supplied to the question of how do brain subsystems operate to ensure the adaptive behavior of the organism. In our view the answer to these complex questions lies in the physical chemistry of colloidal systems and moving boundaries. The latter coordinate metabolic, transport, and signal functions, while glial cells are active modulatory elements in signal transmission. This paper shows both theoretically and experimentally that optimal functioning of the brain at all its levels is determined by and based on the laws of thermodynamics of colloidal-electrolyte systems.
Asunto(s)
Adaptación Fisiológica , Conducta/fisiología , Encéfalo/fisiología , Modelos Neurológicos , Potenciales de Acción , Animales , Células Cultivadas , Fenómenos Químicos , Química Física , Coloides , Decapodiformes , Electrólitos/metabolismo , Transporte Iónico , Músculos/citología , Músculos/metabolismo , Neuroglía/fisiología , Neuronas/metabolismo , Dinámicas no Lineales , Ratas , TermodinámicaRESUMEN
BACKGROUND: Volatile substance abuse is practiced mainly by adolescents and young adults. Its effects are central nervous system excitation followed by central nervous system depression, at times accompanied by seizures. It may cause sudden death as a result of ventricular arrhythmias, reflex vagal inhibition, respiratory depression, and anoxia. Chronic toxicity may involve the nervous system, heart, kidney, and liver. Toluene-based adhesives are among the most commonly inhaled substances. CASE REPORT: A 14-year-old female presented with confusion, hallucinations, and intermittent laughing and crying after having inhaled contact glue several times daily in the course of 5 days. Her condition improved within 3 h. Urinary hippuric acid was 93.9 g/g creatinine indicating heavy toluene exposure (biological exposure index, BEI, is 1.6 g/g creatinine). CONCLUSION: In this patient, urinary hippuric acid was a biomarker for her toluene abuse.
Asunto(s)
Hipuratos/orina , Detección de Abuso de Sustancias , Tolueno , Adolescente , Biomarcadores , Cromatografía Líquida de Alta Presión , Femenino , Humanos , Trastornos Relacionados con SustanciasRESUMEN
BACKGROUND: Ecbalium elaterium is a plant endemic to the Mediterranean basin. Its roots and cucumber-shaped fruit have been used in folk medicine since antiquity. The alleged uses of the fruit juice are as a potent cathartic, analgesic, and antiinflammatory agent. Cucurbitacin B, a triterpene derivative is the active antiinflammatory principal. PATIENTS: We present a series of 13 patients who were exposed to the juice of Ecbalium elaterium in its natural form. In 3 patients, exposure was intranasal for the treatment of sinusitis or liver cirrhosis. In 3 other cases, children ingested the fruit unwittingly. In 6 patients, exposure was ocular and, in one, dermal. Within minutes of exposure, the patients exhibited irritation of mucous membranes at various degrees of severity manifested as edema of pharynx, dyspnea, drooling, dysphagia, vomiting, conjunctivitis, corneal edema, and erosion, depending on the route of the exposure. Recovery began within several to 24 hours after administration of oxygen, steroids, antihistamines, and beta-2-agonists. Ocular exposures responded to topical steroid and antibiotic eyedrops within a few days. The toddler with the dermal exposure remained asymptomatic. CONCLUSION: Exposure to the juice of Ecbalium elaterium, mainly in its undiluted form, may cause irritation of mucous membranes, supposedly of inflammatory nature. Patients exposed orally or intranasally should be closely followed for upper airway obstruction. Patients exposed ocularly should have their eyes promptly irrigated to prevent corneal and conjunctival injury.
Asunto(s)
Cucurbitaceae/envenenamiento , Cucurbitaceae/uso terapéutico , Fitoterapia , Adolescente , Adulto , Antiinflamatorios no Esteroideos/envenenamiento , Antiinflamatorios no Esteroideos/uso terapéutico , Niño , Preescolar , Conjuntivitis/inducido químicamente , Edema Corneal/inducido químicamente , Trastornos de Deglución/inducido químicamente , Disnea/inducido químicamente , Femenino , Humanos , Cirrosis Hepática/tratamiento farmacológico , Masculino , Membrana Mucosa/efectos de los fármacos , Membrana Mucosa/patología , Extractos Vegetales/envenenamiento , Extractos Vegetales/uso terapéutico , Intoxicación/terapia , Estudios Retrospectivos , Sinusitis/tratamiento farmacológico , Triterpenos/envenenamiento , Triterpenos/uso terapéutico , Vómitos/inducido químicamenteRESUMEN
BACKGROUND: When ingested, concentrated paraquat can cause either rapid death from multisystem failure and cardiovascular shock or delayed death from progressive pulmonary fibrosis. Diquat ingestion does not usually cause pulmonary fibrosis, but produces early onset acute renal failure. CASE REPORT: A 52-year-old male ingested approximately 50 mL of a solution containing 13% paraquat and 7% diquat (about 6650 mg of paraquat and 3500 mg of diquat), and subsequently developed adult respiratory distress syndrome and pulmonary fibrosis. Survival prediction employing the criteria of Hart et al. for paraquat plasma levels was 30%. From the probable amount of paraquat ingested, severe toxicity was expected. The clinical course was not consistent with significant diquat toxicity. Treatment included oral Fuller's earth, forced diuresis, hemofiltration, N-acetylcysteine, methylprednisolone, cyclophosphamide, vitamin E, colchicine, and delayed continuous nitric oxide inhalation. The patient recovered and pulmonary function was subsequently normal. CONCLUSION: It is unclear which, if any, of the above treatments contributed to recovery, but the encouraging outcome suggests a possible benefit of nitric oxide inhalation in paraquat poisoning which deserves further study.
Asunto(s)
Broncodilatadores/uso terapéutico , Disnea/tratamiento farmacológico , Herbicidas/envenenamiento , Pulmón/efectos de los fármacos , Óxido Nítrico/uso terapéutico , Paraquat/envenenamiento , Fibrosis Pulmonar/tratamiento farmacológico , Síndrome de Dificultad Respiratoria/tratamiento farmacológico , Administración por Inhalación , Broncodilatadores/administración & dosificación , Terapia Combinada , Diquat/sangre , Diquat/envenenamiento , Disnea/inducido químicamente , Disnea/diagnóstico por imagen , Herbicidas/sangre , Humanos , Pulmón/diagnóstico por imagen , Masculino , Persona de Mediana Edad , Óxido Nítrico/administración & dosificación , Paraquat/sangre , Fibrosis Pulmonar/inducido químicamente , Fibrosis Pulmonar/diagnóstico por imagen , Radiografía , Síndrome de Dificultad Respiratoria/inducido químicamente , Síndrome de Dificultad Respiratoria/diagnóstico por imagen , Pruebas de Función Respiratoria , Intento de Suicidio , Resultado del TratamientoRESUMEN
A fatal case of poisoning due to ingestion of an apparently innocuous household product is described. A healthy 28-year-old man accidentally drank floor polish (Cristalizador, a Spanish import). On arrival at the emergency room a few hours later he passed large amounts of bloody stool and lost consciousness. A call to the Spanish Poison Center revealed that although not indicated on the label, the polish contained a highly poisonous salt, fluoro-silicate. Blood gas analysis revealed severe metabolic acidosis. Serum calcium was 3.8 mg/dL. The post-resuscitation ECG showed subendocardial ischemia and ST-elevation in the anteroseptal wall and prolonged QT-interval. In the intensive care unit he received large amounts of fluids, dopamine, sodium bicarbonate and calcium. Despite the treatment, his condition continued to deteriorate: VPB's appeared, there was a short run of ventricular tachycardia and then atrial fibrillation developed. Further treatment included lidocaine, verapamil, amiodarone, and electrical cardioversion. Blood pressure remained low and 11 hours after admission he died of myocardial infarction, severe arrhythmia and multi-organ failure.
Asunto(s)
Intoxicación por Flúor , Productos Domésticos/envenenamiento , Ácido Silícico/envenenamiento , Adulto , Electrocardiografía , Resultado Fatal , Intoxicación por Flúor/sangre , Intoxicación por Flúor/fisiopatología , Fluoruros , Humanos , Masculino , ResucitaciónRESUMEN
A 15-year-old girl took 3 g of isoniazid (15 tablets) in a suicide attempt and was brought unconscious to the emergency room. She was in respiratory failure, with seizures that could not be stopped with diazepam. Severe metabolic acidosis with normal serum lactate developed (pH 6.85), but did not improve after infusion of bicarbonate. Intravenous administration of pyridoxine led to prompt cessation of the seizures and to gradual improvement of acid-base status. She recovered consciousness after several hours and was discharged a week later.
Asunto(s)
Acidosis/inducido químicamente , Acidosis/tratamiento farmacológico , Isoniazida/envenenamiento , Piridoxina/uso terapéutico , Convulsiones/inducido químicamente , Convulsiones/tratamiento farmacológico , Adolescente , Sobredosis de Droga , Femenino , Humanos , Infusiones Intravenosas , Resultado del TratamientoRESUMEN
Obidoxime is an oxime used in several countries as an antidote in organophosphate intoxication. Its pharmacokinetics were studied in a 20 year-old female with severe and complicated methamidophos intoxication. Obidoxime elimination half life was 6.9 h, volume of distribution 0.845 L/kg, total body clearance 85.4 mL/min, and renal clearance 69 mL/min (creatinine clearance 54 mL/min). Eighty percent of the dose was excreted in the urine over 5 h. Possible reasons for the different pharmacokinetic values as compared with values previously reported in healthy volunteers are discussed. Obidoxime dose should be adjusted according to renal function. More studies are needed to establish the therapeutic window of obidoxime in patients with organophosphate intoxication.
Asunto(s)
Lesión Renal Aguda/inducido químicamente , Insecticidas/envenenamiento , Cloruro de Obidoxima/farmacocinética , Cloruro de Obidoxima/uso terapéutico , Compuestos Organotiofosforados/envenenamiento , Lesión Renal Aguda/tratamiento farmacológico , Adulto , Electrocardiografía , Femenino , Humanos , Infusiones Intravenosas , Tasa de Depuración Metabólica , Cloruro de Obidoxima/sangre , Intento de SuicidioRESUMEN
Out of 859 consecutive cases treated for exposure to organophosphate (PO) insecticides, 53 were included in the study. Criteria for inclusion were severe OP poisoning necessitating artificial ventilation, intensive care monitoring and treatment according to a standard protocol. The protocol was based on relatively high doses of obidoxime, relatively low doses of atropine and overriding with a pacemaker in cases of ventricular arrhythmias and prolonged Q-T interval. Seven patients died during hospitalization. Thirty-two patients (60%) had major central nervous system (CNS) involvement. Five (9.4%) presented severe psychiatric sequelae. Twenty-two patients (41.5%) presented cardiac arrhythmias. Five (9.4%) had liver dysfunction. High frequency of cardiac arrhythmias was observed in patients who received high cumulative doses of atropine and obidoxime; impairment of liver functions was significantly higher in patients who received high cumulative doses of obidoxime. We conclude that each drug should be titrated separately: atropine dosage should be adjusted to the severity of tracheobronchial secretions and bronchospasm, while full doses of obidoxime are justified for the period before "aging" sets in.
Asunto(s)
Atropina/uso terapéutico , Insecticidas/envenenamiento , Cloruro de Obidoxima/uso terapéutico , Compuestos Organofosforados , Oximas/uso terapéutico , Adolescente , Adulto , Anciano , Arritmias Cardíacas/inducido químicamente , Atropina/administración & dosificación , Atropina/efectos adversos , Niño , Preescolar , Estudios de Evaluación como Asunto , Femenino , Humanos , Lactante , Masculino , Persona de Mediana Edad , Estudios Multicéntricos como Asunto , Cloruro de Obidoxima/administración & dosificación , Centros de Control de IntoxicacionesRESUMEN
Larvae of the caterpillar Thaumetopoea wilkinsoni are widely distributed in pine groves throughout Israel. Erucism is defined as urtication by Lepidoptera larvae. Both irritating effects on contact with skin and eyes and toxic effects on ingestion have been described after exposure to several species of Lepidoptera. We report the case of a 4-year-old child who vomited repeatedly and developed symmetrical swelling of both hands after touching a larva of Thaumetopoea wilkinsoni.
Asunto(s)
Lepidópteros , Urticaria/etiología , Animales , Preescolar , Antagonistas de los Receptores Histamínicos H1/uso terapéutico , Humanos , Masculino , Urticaria/tratamiento farmacológicoRESUMEN
A case of group poisoning from the consumption of the fish Sarpa salpa, caught in the Mediterranean coastal waters of Israel, is presented. Mullets and rabbitfish caught at the same site caused no harm. This is the third case of ciguatera poisoning in the region and the first to be transferred by a fish which is not a Red Sea immigrant. It implies that toxic algae dinoflagellates, originating from the Red Sea, crossed the Suez Canal and found their way to the Mediterranean coastal waters.
Asunto(s)
Intoxicación por Ciguatera , Peces , Enfermedades Transmitidas por los Alimentos/etiología , Toxinas Marinas/envenenamiento , Adulto , Animales , Femenino , Humanos , Masculino , Mar MediterráneoAsunto(s)
Intoxicación/epidemiología , Adolescente , Adulto , Niño , Preescolar , Femenino , Humanos , Israel , Masculino , Intoxicación/etiologíaRESUMEN
Sodium fluoroacetate (compound "1080") was injected intravenously, 3 mmol/kg, to artificially-ventilated anesthetized cats. Blood pressure, ECG, acid-base parameters and serum ionized calcium were monitored in four groups of cats. Group A served as control. Group B cats were treated with calcium chloride to restore normal values of serum ionized calcium. Group C was given monoacetin (glyceryl monoacetate), 0.5 ml/kg every 30 min. Both monoacetin and calcium chloride were given to cats in group D. Fluoroacetate poisoning caused significant decrease in ionized calcium and severe metabolic acidosis with increased levels of lactate and pyruvate. The lactate to pyruvate ratio remained normal as long as there was no significant drop in blood pressure. Correction of blood ionized calcium prolonged survival from 94 to 166 min (group B). Monoacetin prolonged average survival time to 166 min. Metabolic acidosis was aggravated in monoacetin-treated animals (group C). Combined treatment with monoacetin and calcium chloride did not prolong mean survival time above 166 min.