An MRI-Based Quantification for Correlation of Imaging Biomarker and Clinical Performance in Chronic Phase of Carbon Monoxide Poisoning

PURPOSE: The purpose of this study was to determine the relation between quantitative magnetic resonance imaging biomarkers, and clinical performances in chronic phase of carbon monoxide intoxication. MATERIALS AND METHODS: Eighteen magnetic resonance scans and cognitive evaluations were performed, on patients with carbon monoxide intoxication in chronic phase. Apparent diffusion coefficient (ADC) ratios of affected versus unaffected centrum semiovale, and corpus callosum were obtained. Signal intensity (SI) ratios between affected centrum semiovale, and normal pons in T2-FLAIR (fluid-attenuated inversion recovery) images were obtained. The Mini-Mental State Exam, and clinical outcome scores were assessed. Correlation coefficients were calculated, between MRI and clinical markers. Patients were further classified into poor-outcome and good-outcome groups based on clinical performance, and imaging parameters were compared. T2-SI ratio of centrum semiovale was compared, with that of 18 sex-matched and age-matched controls. RESULTS: T2-SI ratio of centrum semiovale was significantly higher in the poor-outcome group, than that in the good-outcome group and was strongly inversely correlated, with results from the Mini-Mental State Exam. ADC ratios of centrum semiovale were significantly lower in the poor outcome group than in the good outcome group, and were moderately correlated with the Mini-Mental State Exam score. CONCLUSION: A higher T2-SI and a lower ratio of ADC values in the centrum semiovale, may indicate presence of more severe white matter injury and clinical impairment. T2-SI ratio and ADC values in the centrum semiovale, are useful quantitative imaging biomarkers for correlation with clinical performance in individuals with carbon monoxide intoxication.

Cognitive Intervention in a Patient with Carbon Monoxide Intoxication

BACKGROUND: Cognitive intervention (CI) is a nonpharmacological approach used to compensate for cognitive impairment. It is categorized into cognitive training, cognitive stimulation and cognitive rehabilitation. Several studies showed that CI could induce cognitive enhancement and reduction of risk for future cognitive decline in patients with brain injury. We investigated effects of CI on cognitive functions and brain glucose metabolism based on serial cognitive assessments and [18F]-Fluorodexoxyglucose positron emission tomography (FDG-PET) in a patient with carbon monoxide (CO) intoxication. METHODS: A 40-year-old man presented with memory impairment and abnormal behaviors such as apathy, indifference, and perseveration 2-month after CO intoxication. Brain magnetic resonance image (MRI) demonstrated high signal changes in the bilateral basal ganglia, hippocampus and the subcortical white matter on T2 weighted images. FDG-PET also showed glucose hypometabolism in the bilateral hippocampus, basal ganglia, and the subcortical white matter. A detailed neuropsychological evaluation revealed multiple cognitive impairments in memory, language and frontal functions. He received twice a week sessions of 60-minute group-based cognitive intervention for 12 weeks. Several neuropsychological examinations and FDG-PETs were conducted at baseline and after CI. RESULTS: After CI, he showed improvements in memory and frontal functions compared with baseline performances. These cognitive improvements persisted by the 7-month follow-up. The extent of glucose hypometabolism was decreased 1-month after CI, however increased 8-month after CI. CONCLUSIONS: This case study suggested that CI could enhance cognitive functions and improve glucose metabolism in a patient with CO intoxication. Also, the effects of CI on cognitive functions seem to be last at least 7-month after training.

CO Intoxication in the Car: Case Report / 대한법의학회지

A man and a woman were found dead in their parked car. The car was placed in a deep embankment. The windows were rolled up. Since it was cold winter the engine and heater was running while soil surrounded the rear of the automobile. The cause of death was 87%, 85% carbon-monoxide blood saturation respectively. The source of the CO was a defective exhaust system, The tail pipe outlet was blocked by the soil, and fumes could not escape adequately. Carbon monoxide fumes might entered the vehicle through the rusted floorboards, air conditioning, and through the dash board. It is important to know that unintened carbon monoxide deaths from motor vehicle exhaust can occur outdoors in older vehicles with defective exhaust system. We suggest the public need to be aware of the potential for this life threatening hazard to occur so that there can be proper prevention of fatalities.

Delayed-onset Movement Disorders after Carbon Monoxide Intoxication

BACKGROUND: Presently, it is well known that there are neurological and systemic complications after carbon monox-ide (CO) intoxication. Until recently, delayed-onset movement disorders after CO intoxication were rarely reported. We analyzed 32 patients with delayed onset movement disorders after CO intoxication. METHODS: We reviewed the medical records of 242 patients admitted to the Yonsei University Medical Center from January 1986 to December 1996 due to CO intoxication. Patients were analyzed with respect to movement disorders, onset, latency, and radiological findings. RESULTS: Among the 242 patients of CO intoxication, 32 (13.2%) patients had delayed-onset movement disorders. Of these, 23 (71.9%) had parkinsonism, 5 (15.6%) had dystonia, 3 (9.4%) had chorea, and 1 (3.1%) had myoclonus. The mean age of the patients was 46.66 +/-16.91 years. Among the 4 patients with CO intoxication occuring at age 17 or younger (Childhood group), 2 had parkinsonism and 2 had focal dystonia. The mean age of the Childhood group was 1 7 . 7 5 +/-6.99 years. Among the 28 patients with CO intoxication occuring at age 18 or older (Adult group), 21 (75%) had parkinsonism, 3(10.7%) dystonia, 3(10.7%) chorea, and 1(3.6%) myoclonus. Among the 3 patients with dystonia in the Adult group, 1 had focal dystonia and 2 had segmental dystonia. The mean age of the adult group was 50.79 +/-1 3 . 4 6 years. The mean latency between CO intoxication and the onset of movement disorders was 27.20 +/-27.94 weeks in the Childhood group and 9.60 +/-14.97 weeks in the Adult group. The mean latency between CO intoxication and the onset of movement disorders was 6.44 +/-6.76 weeks in parkinsonism, 41.76 +/-27.99 weeks in dystonia, 4.0 weeks in chorea, and 8.0 weeks in myoclonus. The mean latency in dystonia was longer than in the others. Among the 23 patients who underwent brain computed tomography, 12 (52.2%) had abnormal findings. Low density lesions were found in the globus pallidus (13.0%), cerebral white matter (13.0%), and both globus pallidus and cerebral white matter (17.4%). One (14.3%) patient showed cortical atrophy while another patient showed both cortical atrophy and low density in cerebral white matter. CONCLUSIONS: The development of a delayed-onset movement disorder after CO intoxication is not rare. In our research, the radiological findings of patients with delayed-onset movement disorders after CO intoxication were inconsistant. The findings revealed no correlations with the various types of delayed-onset movement disorders.

Hematologic changes in acute carbon monoxide intoxication

This study was performed to investigate the hematologic changes and its pathogenesis in acute carbon monoxide (CO) intoxication. Serial complete blood counts (CBC) were obtained in 17 patients with acute CO intoxication five times in two weeks. Peripheral blood smear, bone marrow aspiration and biopsy were obtained in 7 patients within the first week. We analyzed the results of serial CBC's. Levels of hemoglobin and hematocrit rose only initially, probably due to dehydration and hemoconcentration rather than hypoxia. Leukocytosis, mainly neutrophilic, observed during the first few days seemed to be a physiological phenomena due to a stressful situation, such as hypoxia. Levels of platelet increased steadily after a initial decrease. We found no specific findings in bone marrow.

A clinical study of acute carbon monoxide intoxication / 영남의대학술지

To obtain the basic data of prognosis of acute carbon monoxide (CO) intoxication, one hundred and sixteen cases of CO intoxication defined by carboxyhemoglobin (COHb) and admitted via emergency room of Yeungnam University Hospital from Oct. '85 to April' 89 have been clinically analyzed and evaluated, including delayed postanoxic encephalopathy (DPE) and the following results were obtained. 1. The ratio of male to female was 1:1.5 and mental state was drowsy mostly (26.2% of 116 cases) 2. The more disturbed the mental state, the more decreased was the arterial pH and PaCO₂, which may be the result of metabolic acidosis. 3. The early laboratory findings in patients of CO intoxication were as follows: leukocytosis-65.5%, increase of hematocrit-23.3%, hyperglycemia-19.8%, increase of GPT-19.8% increase of creatinine-0.9% and glucosuria-12.1%. 4. The early findings of EKG were abnormal in 35.3%: change of rhythm-25.0%, abnormal ST segment 15.5% (change of rhythm and abnormal ST segment-5.2%) but the conduction disorder was not present. 5. The abnormal EEG above mild degree was 93.1%, of which moderate was most frequent (80.2%). 6. The incidence of DPE was 7.8% among all admitted CO patients. DPE cases had long duration of exposure time (8 hours), severe leukocytosis (20,000) and an abnormal EEG (MA).

Electron Microscopic Study on Mitochondria and Cytochrome Oxidase Activity Following Acute Carbon Monoxide Exposure in Rat Myocardium

The problem of carbon monoxide intoxication has been increasing since 1950s and it is still regarded as one of the most serious public health problem in Korea. If the patients survives the acute episode, elimination of carbon monoxide occurs in the rate of a halt-time of 3 to 4 hours. Nevertheless, there may remain after effect. Therefore, the present study was desinged to elucidate the change of myocardial tissue caused by acute carbon monoxide poisoning were evaluated by electrton microscopic observation of the severity of the mitochondrial swelling and cytochrome oxidase activity, which was demonstrated by histochemical staining with diaminobenzidine(DAB). Male Sprague-Dawley rats were exposed to the carbon monoxide of 1500 ppm for 150 minutes. They were divided into two groups ; one group were treated with hyperbaric oxygenation 15 minutes after carbon monoxide exposure, the other were not treated. Rats were sacrified 6 hours, 12 hours, 1 day, 3 days, 7days, 14 days, and 21 days after carbon monoxide exposure. The specimens were collected from the apex of the heart. In the group without hyperbaric oxygenation, mitochondrial swelling subsided 21 days after carbon monoxide exposure accompained by restoration of cytochrome oxidase activity. On the other hand, with hyperbaric oxygenation, healing process was shortened. Cytochrome oxidase activity was restored 7 days after carbon monoxide exposure.

Clinical Study on Carbon Monoxide Intoxication in Children

Carbon monoxide intoxication has long been one of the most serious public health problems in Korea. This is mainly due to the wide use of anthracite coal briquettes as domestic fuel for cooking and under-the floor heating. One hundred and seven cases of CO intoxicated children hospitalized at Yonsei Medical center from January 1970 to December 1986 have been investigated clinically. The sex ratio was 1.3:1 (male 60 cases, female 47 cases) with the peak incidence occuring in patients between 12 and 14 years of age (28%). The most common symptoms were vomiting convulsions and headache; and the most frequent signs were altered mental state, increased deep tendon reflex and a positive Babinski sign. The outcome of patients was as follows: 4 cases (3.7%) expired, 77 cases (72.0%) recovered without neurologic sequelae and 26 cases (24.3%) survived with neurologic sequelae. The neurologic sequelae included persistent convulsions (7 cases), cortical blindness (3 cases), peripheral neuropathy (2 cases) and delayed neurologic sequelae (11 cases). Neurologic sequelae occurred most frequently in comatose patients (45.5%) and least often in mentally alert patients (6.1%), more frequently m patients exposed to CO gas for more than 8 hours than in those exposed for less than 8 hours, and in patients who did not receive hyperbaric oxyen therapy(29.4%) than in those who did(19.6%). Delayed neurologic sequelae were mental retardation (72.7%), epilepsy (36.4%), mutism (18.2%) etc. The lucid interval in 11 cases of delayed neurologic sequelae ranged from 2 to 20 days. The results of this study suggest that every patient exposed to CO gas should receive prompt and efficient oxygenation including hyperbaric oxygen therapy and that expeditious reduction of cerebral edema maybe of value. The importance of providing follow-up facilities in anticipation of a relapse of the delayed neurologic sequelae has been established.