Bocio multinodular tóxico por intoxicación con monóxido de carbono / Toxic multinodular goiter due to poisoning by carbon monoxide

RESUMEN Paciente masculino de 53 años con antecedentes de alergia, trabajador artesanal que realiza serigrafías, con alta exposición a productos químicos que, al someterse a altas temperaturas desprenden gran cantidad de vapor. Acude a consulta refiriendo que desde aproximadamente 2 meses antes presenta decaimiento con calambres musculares, palpitaciones, enrojecimiento de la cara y, aumento de tamaño de la glándula tiroides. Se diagnostica un bocio multinodular tóxico, por cifras hormonales elevadas. Se realiza ultrasonido de tiroides que informa bocio multinodular, una biopsia por aspiración con aguja fina, con atipia de significado incierto, y lesión folicular del tiroides. Se separa de su centro de trabajo y se logra revertir la sintomatología a los 15 días del tratamiento. Frecuentemente aparecen enfermedades asociadas a intoxicaciones por químicos y medicamentos, donde la presencia de hipertiroidismo no es habitual. Se requiere una anamnesis exhaustiva y exámenes complementarios específicos para un diagnóstico y tratamiento adecuados(AU)

ABSTRACT 53 years old male patient with a history of allergy; he works as a craft worker (producing serigraphs) very exposed to chemicals, which when subjected to high temperatures emit large amount of steam. The patient attends to the consultation referring that from approximately 2 months before he has been presenting weakness with muscle cramps, palpitations, flushing of the face and, increase in the size of the thyroid glands. It is diagnosed by the high hormonal figures a toxic multinodular goiter. Thyroid ultrasound is performed that shows multinodular goiter; it is also conducted a biopsy by fine-needle aspiration resulting in atypia of uncertain significance, and follicular lesion of the thyroid. The patient was separated from his workplace and there were reversed the symptoms after 15 days of treatment. Frequently appear diseases associated to poisonings caused by chemicals and medicines, where the presence of hyperthyroidism is not usual. It requires a comprehensive anamnesis and complementary tests that are specific for a proper diagnosis and treatment(AU)

Characteristics of Children with Acute Carbon Monoxide Poisoning in Ankara: A Single Centre Experience

The purpose of the study was to define characteristics of children with acute carbon monoxide poisoning. Eighty children hospitalized with acute carbon monoxide poisoning were recruited prospectively over a period of 12 months. Sociodemographic features, complaints and laboratory data were recorded. When the patient was discharged, necessary preventive measures to be taken were explained to parents. One month later, the parents were questioned during a control examination regarding the precautions that they took. The ages of the cases were between one month and 16 yr. Education levels were low in 86.2% of mothers and 52.6% of fathers. All families had low income and 48.8% did not have formal housing. The source of the acute carbon monoxide poisoning was stoves in 71.2% of cases and hot-water heaters in 28.8% of cases. Three or more people were poisoned at home in 85.1% of the cases. The most frequent symptoms of poisoning were headache and vertigo (58.8%). Median carboxyhemoglobin levels at admission to the hospital and discharge were measured as 19.5% and 1.1% (P < 0.001). When families were called for re-evaluation, it was determined that most of them had taken the necessary precautions after the poisoning incident (86.3%). This study determined that children with acute childhood carbon monoxide poisoning are usually from families with low socioeconomic and education levels. Education about prevention should be provided to all people who are at risk of carbon monoxide poisoning before a poisoning incident occurs.

Atendimento às vítimas de lesão inalatória por incêndio em ambiente fechado: o que aprendemos com a tragédia de Santa Maria / Assistance of inhalation injury victims caused by fire in confined spaces: what we learned from the tragedy at Santa Maria

Em janeiro de 2013, uma catástrofe ocorrida em Santa Maria (RS), decorrente de um incêndio em ambiente fechado, resultou em 242 mortes, a maioria por lesões inalatórias. Em novembro de 2013, quatro vítimas necessitaram de suporte intensivo após inalação de fumaça em incêndio no Memorial da América Latina, em São Paulo (SP). Este artigo relata a evolução clínica e o manejo dos pacientes com lesão inalatória vítimas de uma catástrofe. Os pacientes ERL e OC apresentaram insuficiência respiratória precoce com broncoaspiração de material carbonáceo e intoxicação por monóxido de carbono. Foi instituído suporte ventilatório com oxigênio a 100%, retirada do material aspirado por broncoscopia, e terapia empírica com nitrito de sódio e tiossulfato de sódio para intoxicação por cianeto. O paciente RP apresentou tosse e queimação retroesternal. Evoluiu com insuficiência respiratória por edema de via aérea alta e infecção pulmonar precoce, manejados com ventilação pulmonar protetora e antimicrobianos. Foi extubado após melhora do edema no seguimento broncoscópico. O paciente MA, asmático, apresentou intoxicação por monóxido de carbono e broncoespasmo, sendo tratado com hiperóxia normobárica, broncodilatadores e corticoterapia. A estadia na unidade de terapia intensiva variou de 4 e 10 dias, e todos os pacientes apresentaram boa recuperação funcional no seguimento. Em conclusão, nos incêndios em ambientes fechados, as lesões inalatórias têm papel preponderante. O suporte ventilatório invasivo não deve ser postergado em caso de edema significativo de via aérea. A hiperóxia deve ser instituída precocemente como terapêutica para intoxicação por monóxido de carbono, bem como terapia farmacológica empírica para intoxicação por cianeto em caso de suspeita.

On January 2013, a disaster at Santa Maria (RS) due to a fire in a confined space caused 242 deaths, most of them by inhalation injury. On November 2013, four individuals required intensive care following smoke inhalation from a fire at the Memorial da América Latina in São Paulo (SP). The present article reports the clinical progression and management of disaster victims presenting with inhalation injury. Patients ERL and OC exhibited early respiratory failure, bronchial aspiration of carbonaceous material, and carbon monoxide poisoning. Ventilation support was performed with 100% oxygen, the aspirated material was removed by bronchoscopy, and cyanide poisoning was empirically treated with sodium nitrite and sodium thiosulfate. Patient RP initially exhibited cough and retrosternal burning and subsequently progressed to respiratory failure due to upper airway swelling and early-onset pulmonary infection, which were treated with protective ventilation and antimicrobial agents. This patient was extubated following improvement of edema on bronchoscopy. Patient MA, an asthmatic, exhibited carbon monoxide poisoning and bronchospasm and was treated with normobaric hyperoxia, bronchodilators, and corticosteroids. The length of stay in the intensive care unit varied from four to 10 days, and all four patients exhibited satisfactory functional recovery. To conclude, inhalation injury has a preponderant role in fires in confined spaces. Invasive ventilation should not be delayed in cases with significant airway swelling. Hyperoxia should be induced early as a therapeutic means against carbon monoxide poisoning, in addition to empiric pharmacological treatment in suspected cases of cyanide poisoning.

Contaminación por monóxido de carbono: un problema de salud ambiental / Carbon monoxide contamination: an environmental health problem

El monóxido de carbono es considerado uno de los mayores contaminantes de la atmósfera terrestre. Sus principales fuentes productoras responsables de aproximadamente 80 por ciento de las emisiones, son los vehículos automotores que utilizan como combustible gasolina o diesel y los procesos industriales que utilizan compuestos del carbono. Esta sustancia es bien conocida por su toxicidad para el ser humano. Sus efectos tóxicos agudos incluida la muerte han sido estudiados ampliamente; sin embargo, sus potenciales efectos adversos a largo plazo son poco conocidos. En los últimos años, los estudios de investigación experimentales en animales y epidemiológicos en humanos han evidenciado relación entre población expuesta en forma crónica a niveles medios y bajos de monóxido de carbono en aire respirable y la aparición de efectos adversos en la salud humana especialmente en órganos de alto consumo de oxígeno como cerebro y corazón. Se han documentado efectos nocivos cardiovasculares y neuropsicológicos en presencia de concentraciones de monóxido de carbono en aire inferiores a 25 partes por millón y a niveles de carboxihemoglobina en sangre inferiores a 10 por ciento. Las alteraciones cardiovasculares que se han descrito son hipertensión arterial, aparición de arritmias y signos electrocardiográficos de isquemia. Déficit en memoria, atención, concentración y alteraciones del movimiento tipo parkinsonismo, son los cambios neuropsicológicos con mayor frecuencia asociados a exposición crónica a bajos niveles de monóxido de carbono y carboxihemoglobina.

Carbon monoxide is considered to be a major factor contaminating earths atmosphere. The main sources producing this contamination are cars using gasoline or diesel fuel and industrial processes using carbon compounds; these two are responsible for 80 percent of carbon monoxide being emitted to the atmosphere. This substance has a well-known toxic effect on human beings and its acute poisonous effects (including death) have been widely studied; however, its long-term chronic effects are still not known. During the last few years, experimental research on animals and studies of human epidemiology have established the relationship between chronic exposure to low and middle levels of carbon monoxide in breathable air and adverse effects on human health, especially on organs consuming large amounts of oxygen such as the heart and brain. Harmful cardiovascular and neuropsychological effects have been documented in carbon monoxide concentration in air of less than 25 ppm and in carboxyhaemoglobin levels in blood of less than 10 percent. The main cardiac damage described to date has been high blood pressure, cardiac arrhythm and electrocardiograph signs of ischemia. Lack of memory, attention, concentration and Parkinson-type altered movement are the neuropsychological changes most frequently associated with chronic exposure to low levels of carbon monoxide and carboxyhaemoglobin.