The sudden onset of asthmalike symptoms and persistence of airway reactivity following an acute exposure to an irritant gas or vapor has been termed reactive airways dysfunction syndrome (RADS). A mixture of sodium hypochlorite (bleach, 40%) and hydrochloric acid (18%) is commonly used as a household cleaning solution in our region. From this mixture, chlorine gas is produced, which can cause airway damage and ensuing RADS. Here we describe findings of patients with RADS due to this cleaning mixture, and determine factors associated with a favorable outcome. Data were collected retrospectively on 55 symptomatic patients presenting to our emergency department after inhalation exposure to a mixture of bleach and hydrochloric acid. Symptoms, past medical and smoking history, details of the exposure, initial peak expiratory flow rate (PEFR) and oxygenation, and acute reversibility of airways obstruction were documented. All patients met previously defined criteria for the diagnosis of RADS, but did not undergo methacholine challenge testing and bronchoalveolar lavage or histopathologic study. Fifty patients were followed over the course of 3 mo. The majority of exposures (64%) occurred in the bathroom or kitchen. Only 21 of 55 (38%) patients showed an improvement in PEFR of 15% or greater following two beta(2)-agonist inhalation treatments. In follow-up, 48 patients (87%) improved clinically and functionally (FEV(1)). Seven patients (13%) deteriorated, with ARDS developing in two, one of whom died from respiratory failure. Advanced age, initial low PEFR, exposure in a small enclosed area, use immediately after mixing, and prolonged short- and long-term exposures were associated with a poorer prognosis. This descriptive study is the largest case series in the literature of RADS developing after exposure to a bleach-hydrochloric acid mixture. The optimum acute treatment and long-term outcomes for patients with RADS due to this combination still need to be determined.

Carbon monoxide (CO) poisoning is the leading cause of death from intoxication. In CO poisoning, it is important to know if there are any symptoms regarding myocardial damage, which are usually unobserved as a result of hypoxia. This study was planned to assess myocardial damage in young healthy patients with CO poisoning. Eighty-three young healthy cases who had been exposed to CO were included in this study. The demographic and clinical characteristics, the origin of CO gas and smoking habits of the patients were recorded. The evaluation of ECG, peripheral ABG, complete blood count and serial cardiac biomarkers (creatine kinase, creatine kinasemyocardial band and troponin I) measurements were performed in all cases. Additionally, echocardiogram (ECHO) and myocardial perfusion single-photon emission computed tomography (SPECT) were performed at the appropriate times in all cases. The mean age of the patients was 27.39 /10.9 years. The main complaint of the patients was loss of consciousness with a 62.7% rate. The average carboxyhaemoglobin level of the patients was 34.49 /15.9%. Sinus tachycardia was present in 26.5% of patients. Diagnostic ischaemic ECG changes were present in 14.4% of patients. In myocardial SPECT, myocardial ischaemic damage was observed in 9 cases, in 6 of whom ECHO findings were also confirmed. Myocar-dial damage due to CO poisoning should not be ignored. If patients are at risk in terms of myocardial damage, further studies, such as ECHO and scintigraphy are needed to determine myocardial damage resulting from CO poisoning. However, in the young adults of the risk group, if the baseline ECG and serial cardiac biomarkers are normal, further studies such as ECHO and scintigraphy, considering the length of exposure and the severity of poisoning, may not be necessary for the evaluation of myocardial damage due to CO poisoning.

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Neuropsychiatric sequelae may be observed in the late phases of carbon monoxide (CO) intoxication. Establishing a link between CO-related neuropsychiatric disorders and associated risk factors may decrease morbidity and mortality by means of appropriate treatment and counseling. The aim of the present study was to determine the relationship between neuropsychiatric outcomes of CO intoxication and demographic and clinical variables. Thirty patients who presented with CO intoxication and had no known neuropsychiatric disease, and 30 healthy controls were included. Physical examinations and laboratory tests were performed. Following the 1st therapy, they underwent mental and psychiatric tests 5 times (the time of discharge, during the 1st week, and during the 1st, 3rd, and 6th months). They underwent cerebral magnetic resonance imaging (MRI) at the end of the 1st month. They were evaluated by cognitive function tests at the 6th month. Lesions relevant to CO intoxication were detected in 46.7% of the patients via cranial computed tomography and in 13.3% via MRI. Evaluation of psychiatric tests revealed a clear decrease in cognitive functions, such as immediate memory, learning, reaching the criterion, spontaneous recall, attention, visual memory, and logical memory. It was found that the patients had anxiety within the 1st month, and the frequency of anxiety reached to the value of the control group by the end of the 6th month. In conclusion, we suggested that CO intoxication might lead to neuropsychiatric disorders. Our results emphasized that in addition to standard treatment, neuropsychiatric evaluation should also be performed in patients with CO intoxication.