Brote masivo de intoxicación por monóxido de carbono en los telespectadores de un partido de fútbol / Mass carbon monoxide poisoning among television viewers of a football match

Introducción. El objetivo fue estudiar un brote de intoxicación por monóxido de carbono (CO) y las características de los casos asintomáticos. Métodos. El 2 de febrero de 2015 un grupo de más de 30 telespectadores de un partido de fútbol contactó con el servicio de urgencias por una supuesta intoxicación por CO procedente de una estufa de butano. Se realizó una inspección ocular del local de la exposición y un estudio epidemiológico descriptivo. Según el tipo de variables, la existencia de una asociación estadística se estudió con la prueba exacta de Fisher o el test de Kruskal-Wallis. Resultados. Se vieron afectados 34 de 39 sujetos (87,2%). Los expuestos tenían una media de edad de 43,8años (DE=22,1) y el 28,2% (11/39) eran mujeres. El tiempo de exposición fue de 52,4min (DE=21,0) y la distancia a la estufa de 4,2m (DE=2,5). Los síntomas más frecuentes fueron cefalea (50%), náuseas (20,6%), pérdida de fuerza (20,6%) y vértigo (14,7%). Los niveles de carboxihemoglobina (COHb) fueron muy elevados (13,8%±5,8). El 97,1% precisó oxigenoterapia y el 39,4% tratamiento en cámara hiperbárica. Un 29,5% de los casos no presentaron síntomas, y respecto a los casos sintomáticos, estos mostraron niveles similares de COHb (13,6% vs. 15,3%, diferencia no significativa), pero un tiempo de exposición inferior (38,3min vs. 53,3min; p<0,036). Conclusiones. Casi una tercera parte de las personas expuestas fueron asintomáticas aun con niveles de COHb similares a los casos sintomáticos, e incluso la mayoría precisaron tratamiento con oxígeno en cámara hiperbárica (AU)

Background. The objective was to study a mass carbon monoxide (CO) poisoning and the characteristics of the asymptomatic cases. Methods. On the 2nd of February, 2015, a group of more than 30 television viewers of a football match contacted the emergency department due to suspected CO poisoning from a butane stove. A visual inspection of the location of the exposure and a descriptive epidemiological study were conducted. Based on the type of variable, the presence of a statistical association was studied with Fisher's exact test or the Kruskal-Wallis test. Results. Thirty-four of the 39 individuals were affected (87.2%). The exposed individuals had a mean age of 43.8 years (SD, 22.1), and 28.2% (11/39) were women. The time of exposure was 52.4min (SD, 21.0), and the mean distance from the oven was 4.2m (SD, 2.5). The most common symptoms were headache (50%), nausea (20.6%), weakness (20.6%) and dizziness (14.7%). The carboxyhaemoglobin (COHb) levels were very high (13.8% ±5.8%). Some 97.1% of the individuals required oxygen therapy, and 39.4% required hyperbaric chamber treatment. Some 29.5% of the cases had no symptoms but showed COHb levels similar to those that did have symptoms (13.6% vs. 15.3%, nonsignificant difference). The asymptomatic cases had a shorter exposure time (38.3min vs. 53.3min; P<.036). Conclusions. Almost a third of the exposed individuals were asymptomatic, even with COHb levels similar to those of the symptomatic patients, and the majority of these asymptomatic patients even required oxygen treatment in a hyperbaric chamber (AU)

Funciones neurocognitivas alteradas en paciente intoxicada por monóxido de carbono / Altered neurocognitive functions in a patient with carbon monoxide poisoning

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Sanguinate's effect on pial arterioles in healthy rats and cerebral oxygen tension after controlled cortical impact.

Sanguinate, a polyethylene glycol-conjugated carboxyhemoglobin, was investigated for cerebral vasoactivity in healthy male Sprague-Dawley rats (Study 1) and for its ability to increase brain tissue oxygen pressure (PbtO2) after controlled cortical impact (CCI) - traumatic brain injury (TBI) (Study 2). In both studies ketamine-acepromazine anesthetized rats were ventilated with 40% O2. In Study 1, a cranial window was used to measure the diameters of medium - (50-100µm) and small-sized (<50µm) pial arterioles before and after four serial infusions of Sanguinate (8mL/kg/h, cumulative 16mL/kg IV), volume-matched Hextend, or normal saline. In Study 2, PbtO2 was measured using a phosphorescence quenching method before TBI, 15min after TBI (T15) and then every 10min thereafter for 155min. At T15, rats received either 8mL/kg IV Sanguinate (40mL/kg/h) or no treatment (saline, 4mL/kg/h). Results showed: 1) in healthy rats, percentage changes in pial arteriole diameter were the same among the groups, 2) in TBI rats, PbtO2 decreased from 36.5±3.9mmHg to 19.8±3.0mmHg at T15 in both groups after TBI and did not recover in either group for the rest of the study, and 3) MAP increased 16±4mmHg and 36±5mmHg after Sanguinate in healthy and TBI rats, respectively, while MAP was unchanged in control groups. In conclusion, Sanguinate did not cause vasoconstriction in the cerebral pial arterioles of healthy rats but it also did not acutely increase PbtO2 when administered after TBI. Sanguinate was associated with an increase in MAP in both studies.

El monóxido de carbono y la neurología. Réplica / Carbon monoxide and neurology. Reply

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Intoxicaciones inadvertidas por monóxido de carbono: una epidemia oculta / Intoxications inadvertent carbon monoxide: an epidemic hidden

Diferentes autores afirman que existe un elevado volumen de intoxicaciones por monóxido de carbono que pasan inadvertidas para el personal sanitario, lo que representa un importante problema de salud. Para confirmar esta hipótesis en un área de salud determinada, sobre la que se dispone de reciente información en relación al volumen de intoxicaciones que sí son detectadas, se realizó este trabajo. Para ello, se seleccionó como población de estudio al conjunto de pacientes que acudieron al Servicio de Urgencias del Hospital do Salnes, por cualquier motivo, durante el mes de febrero de 2013. Se recogió una amplia muestra representativa de esta población por un sistema aleatorio sistemático, quedando constituida por 1501 pacientes. A todos ellos se les realizó una medición no invasiva de carboxihemoglobina mediante pulsicooximetría con el objetivo de detectar todas las intoxicaciones, tanto las sospechadas por el personal sanitario como las que pasarían inadvertidas. El número de intoxicaciones detectadas en la muestra fue de 10, lo que representa el 0,7% (± 0.34% p< 0.05) de las urgencias atendidas, siendo 18 (8,8-27,1) el número de casos esperados para la población de estudio. Esta cifra fue muy superior a la de intoxicados que se detectaron en el trabajo ordinario del personal sanitario durante los diez años previos, en el mismo mes de febrero y en el mismo centro sanitario, con una media anual de 1.3 casos (DS: 2.8), por lo que se concluye confirmando la hipótesis de que el número de intoxicaciones inadvertidas por monóxido de carbono es muy elevado (AU)

Different authors state that there is a high volume of carbon monoxide poisoning that go unnoticed for health workers, representing a major health problem. To confirm this hypothesis in a particular area of ​​health, on which recent information regarding the volume of poisonings that are detected itself, this work was performed. To do this, it was selected as study population to all patients presenting to the emergency department of Salnés Hospital, for any reason, during the month of February 2013. A broad cross-section of the population was collected by a systematic random system , it is composed of 1501 patients. All subjects underwent a noninvasive measurement of carboxyhemoglobin by pulsicooximetría in order to detect all poisonings, both suspected by medical personnel as they go unnoticed. The number of poisonings detected in the sample was 10, representing 0.7% (± 0.34% p <0.05) of emergencies attended, with 18 (8.8 to 27.1) for the number of expected cases the study population. This figure was much higher than that of intoxicated that were detected in the ordinary work of health workers during the previous ten years, in the month of February and at the same health center with an annual average of 1.3 cases (DS: 2.8) , so it is concluded confirming the hypothesis that the number of intoxications inadvertent carbon monoxide is very high

Intoxicación por monóxido de carbono: una patología poco valorada en urgencias / Carbon monoxide poisoning: an undervalued event in the emergency department

La intoxicación aguda por monóxido de carbono (CO) es una urgencia médica que, de no tratarse oportunamente, puede dejar considerables secuelas neurológicas o incluso provocar la muerte del paciente. El cuadro clínico depende de la intensidad de la exposición a este gas y varía según el grado de afectación de los distintos órganos involucrados. La administración de oxígeno normobárico (NBO) es el tratamiento utilizado en la mayoría de los servicios de urgencias hasta la resolución de los síntomas y la normalización de los niveles de carboxihemoglobina (COHb), siendo dados de alta los pacientes en la práctica común sin seguimiento posterior. Presentamos el caso de un paciente que acude a urgencias por síncope y nos cuestionamos si la utilización de oxigeno hiperbárico (HBO) frente a (NBO) disminuye las secuelas neurológicas, así como la existencia de indicaciones con evidencia científica para su uso (AU)

Carbon monoxide (CO) poisoning is a medical emergency, which if not treated properly could leave considerable neurological sequelae or even cause the death of the patient. The signs and symptoms depend on the intensity of the exposure to the gas and vary according to the degree to which the different organs are affected. Administration of normobaric oxygen (NBO) is the treatment used in most emergency services. This gas is administered until symptoms are resolved and carboxyhemoglobin (COHb) levels have returned to normal. The patient is then discharged with no subsequent follow-up. We present the case of a patient who came to the emergency department due to syncope. We ask ourselves whether the use of hyperbaric oxygen (HBO) compared to NBO decreases neurological sequelae, and if there is scientific evidence for its use in this indication (AU)

Modelo de cámara inhaladora para los estudios controlados sobre la toxicidad del humo del tabaco en los roedores / An Inhalation Chamber Model for Controlled Studies of Tobacco Smoke Toxicity in Rodents

Introducción: El tabaquismo constituye un grave problema de salud pública en todo el mundo. Los modelos animales actúan como un paso intermedio entre los estudios de laboratorio y los estudios en seres humanos. Los modelos aplicados son difíciles de reproducir debido al uso de diferentes tipos de cámaras inhaladoras y principalmente por la falta de una monitorización constante de la concentración del humo del tabaco.ObjetivoDesarrollar una cámara inhaladora para ratas (con la exposición exclusiva del hocico) en la que pueda mantenerse y monitorizarse constantemente la cantidad de monóxido de carbono (CO).Material y métodosSe expusieron ratas Wistar macho, de 250g de peso, a 50 partes por millón de CO producido por el humo del tabaco de un cigarrillo sin filtro. Los animales se sometieron a una exposición de 2h y, acto seguido, fueron sacrificados a las 0, a las 4, a las 24 y a las 48h. El grupo de control se dejó libre dentro de pequeñas cámaras perpendiculares y solo recibió 5l/min de aire comprimido.ResultadosEl modelo fue capaz de aumentar la concentración de carboxihemoglobina inmediatamente después del término de la exposición (p<0,001), observándose una disminución desde las 2h en adelante comparado con la concentración del grupo de control. La concentración plasmática de cotinina aumentó inmediatamente después de la exposición y todavía se detectó a las 2 y a las 4h (p<0,05).ConclusiónConcluimos que este sistema de cámara inhaladora puede mantener una concentración controlada de CO en un modelo en el que se expone a pequeños animales a la inhalación de humo de cigarrillos, lo que permite estudios adecuadamente controlados, al igual que investigaciones sobre otros gases tóxicos y contaminantes ambientales(AU)

Introduction: Smoking is a serious worldwide public health problem. Animal models act as a bridge between laboratory and human studies. The models applied are difficult to reproduce because of the use of different types of inhalation chambers and mainly because of the lack of continuous monitoring of smoke concentration.ObjectiveTo develop an inhalation chamber for rats (with only the nose exposed) in which the amount of carbon monoxide (CO) can be maintained and monitored constantly.Material and methodsMale Wistar rats weighing 250g were exposed to 50ppm CO produced by the smoke from a filter-free cigarette. The animals were submitted to a single 2-h exposure and then sacrificed at 0, 4, 24 and 48h. The control group was left restrained inside the small perpendicular chambers, receiving only 5L/min of compressed air.ResultsThe model was able to increase HbCO levels immediately after the end of exposure (p<0.001), with a decrease being observed from 2h onwards when compared to the levels of the control group. Plasma cotinine increased immediately after exposure, and showed still detectable levels at 2 and 4h (p<0.05).ConclusionWe conclude that the presented inhalation chamber system is able to maintain a controlled CO concentration in a model in which small animals are exposed to the inhalation of cigarette smoke, permitting well-controlled studies, as well as investigations involving other toxic gases and air pollutants(AU)

[Effects of low concentration carbon monoxide on human physiological function].

Human volunteers were exposed to various low concentrations of carbon monoxide (CO) in a closed cabin. The results showed that 35 mg/m3 of CO caused slight subjective symptoms and reduction in contrast vision, operating efficiency and T-wave of ECG. At 80 mg/m3 and 115 mg/m3 the above changes were more severe and a rise in hearing threshold level was observed. It demonstrated that an inhibitory effect on the CNS and heart were caused by low concentrations of CO. According to the absorption curves for human exposed to CO, it is suggested that the sense effect level and vision effect level for CO are 7% COHb, and the hearing effect level is 9% COHb.

National Association of Medical Examiners Pediatric Toxicology (PedTox) Registry Report 3. Case submission summary and data for acetaminophen, benzene, carboxyhemoglobin, dextromethorphan, ethanol, phenobarbital, and pseudoephedrine.

Data are presented from the National Association of Medical Examiners' (St. Louis, MO, U.S.A.) Pediatric Toxicology (PedTox) Registry. A total of 839 case reports have been submitted to the registry. Reported here are the concentrations of several drugs and potentially toxic substances observed in children who have died of various causes, often non-drug-related. Except for carbon monoxide, for each of the substances addressed in this report, there is insufficient information in the literature to distinguish "lethal" from "non- or sublethal" concentrations in children, and the data are presented only to provide a working frame of reference. For 30 infants whose deaths were attributed to causes other than phenobarbital, the median blood phenobarbital concentration was 7.8 mg/L, with a range of 0.1-22.4 mg/L. For eight infants whose deaths were not attributed to ethanol, the mean blood ethanol concentration was 0.029 gm/dl and ranged from 0.011 gm/dl to 0.050 gm/dl. Blood dextromethorphan concentrations in seven infants showed a mean of 0.38 mg/L and ranged from 0.10 mg/L to 0.95 mg/L. In 15 infants, blood pseudoephedrine concentrations ranged between 0.07 mg/L and 13.0 mg/L, with a mean concentration of 3.55 mg/L. Blood carboxyhemoglobin saturations for 38 children aged < or = 5 years, who died in fires and were dead on the scene and not resuscitated, ranged between 29% and 94%, with a mean saturation of 64%. Blood benzene concentrations in eight children aged < or = 6 years who died in fires and were dead on the scene showed a mean concentration of 2.3 mg/L and a range of 0.2-4.9 mg/L. For 33 children aged < or = 5 years whose deaths were attributed to nondrug causes, the mean blood acetaminophen concentration was 9.9 mg/L, and the range was 1.0-34.5 mg/L. These data are not well controlled in terms of testing methodology or cause of death determinations and should not be used as the sole source of information when assessing whether or not a death is caused by one of these substances. Further data and controlled studies are needed to work toward establishing lethal concentrations of certain drugs and toxic substances in children, and the reporting of cases to the PedTox Registry is encouraged.