ABSTRACT
Objective: Although much is known about acute carbon monoxide (CO) poisoning, little is known about chronic CO poisoning. Chronic CO poisoning is often diagnosed based on the patient’s living environment and medical history. Herein, we report the case of an older patient who presented with repeated unconsciousness due to chronic CO poisoning.Case presentation: A 90-year-old man was brought to the emergency department after being found at home with a disturbance of consciousness. Arterial blood gas measurements in room air revealed a carboxyhemoglobin level of 18.0%. Impaired consciousness was caused by chronic CO poisoning. The patient received high-flow oxygen therapy, which promptly improved his condition. According to his family, briquette kotatsu was the cause of chronic CO poisoning.Conclusion: Although high-flow oxygen therapy has been said to be less effective than hyperbaric oxygen therapy in CO poisoning treatment, recent studies have demonstrated that high-flow oxygen has similar effects and benefits. Thus, in institutions that do not have hyperbaric oxygen, high-flow oxygen may be sufficient to treat patients with CO poisoning, as seen in the present case. It should be noted that briquette kotatsu can lead to CO poisoning. This case highlights the need for clinicians to consider patients’ living conditions.
ABSTRACT
Objective To investigate the effect of Xing-Zhi-Yi-Nao (XZYN) particles on the expressions of Nogo and OMgp proteins in brain of rats after acute carbon monoxide (CO) poisoning.Methods A total of 120 Sprague-Dawley rats were randomly divided into normal group,CO poisoning group and XZYN particles treatment group (40 rats in each group).The rats in CO poisoning group and treatment group of acute CO poisoning were established by using an animal chamber,and then received hyperbaric oxygen therapy.Meanwhile,rats in treatment group were further given additional XZYN particles twice a day by gavage.At 1 day,1 week,1 month and 2 months after CO poisoning,the neurobehavioral score of rats was evaluated by a Morris water maze test and a shuttle box test,and the expressions of neurite outgrowth inhibitor (Nogo) and oligodendrocyte-myelin glycoprotein (OMgp) were investigated in rat brain tissue by immunohistochemistry staining and western blotting assay,respectively.Results Compared with those in normal control group((11.6±8.4)s,(41.8±4.4)%,(16.1±2.3)s,and (1.2±0.2)s),the escape latency in CO group was significantly prolonged ((14.1±6.1)s),and the T1/ T total was obviously decreased (23.6±2.4) %,the escape time ((26.3±3.8)s),the active escape latency ((2.3±0.3)s) were notably extended at 1 d (P1 week) in Xing-Zhi-Yi-Nao treatment group (P0.05).Conclusion The expression of Nogo and Omgp proteins may be associated with brain injury and demyelination in rats induced by CO poisoning.XZYN particles can down-regulate the expression of Nogo,and pave a way for the treatment of acute brain damage and delayed encephalopathy after CO poisoning.
ABSTRACT
The clinical cases of 6 patients suffering with chorea after acute carbon monoxide (CO) poisoning were reviewed. There were 2 men and 4 women, and the age at onset ranged from 11 to 60 (mean 33.0) years. All the patients except one were associated with mild delayed CO encephalopathy. The latency period between CO poisoning and the onset of chorea was 10 to 30 (mean 21.7) days. The duration of chorea after CO poisoning was 14 to 90 (mean 39.8) days. The brain CT findings were bilateral low- density lesions in the basal ganglia and/or in the white matter of the cerebral cortex, and there was no correlation between the lesion sites on the imagings and the development of chorea. Neuroleptic agents alleviated the chorea and the patients did not relapse after neuroleptic agents were halted.
Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Acute Disease , Brain Diseases/etiology , Carbon Monoxide Poisoning/complications , Chorea/etiology , Tomography, X-Ray ComputedABSTRACT
Objective To evaluate CT and MRI features of brain lesions in CO poisoning and to compare the ability of detecting rate of lesions by CT and MRI.Methods CT and MRI appearances in 52 cases with CO poisoning were analysed and compared.Results Necroses and degenerations of globus pallidus in 9 cases,cerebral white matter demyelination in 3 cases and brain atrophy in 3 cases were showed by CT.The detecting rate was 28.8% by CT while,necroses and degeneration of glodus pallidus were observed in 24 cases and white matter change in 7 cases were observed by MRI,the detecting rate was 59.6% which was higher than that of CT (?
ABSTRACT
PURPOSE: This study was conducted to develop field triage, transportation, distribution, and prehospital care at a fire disaster by analyzing the victims of the fire that broke out at a bar in Incheon. METHOD: We analyzed the cases of the victims of a fire in Incheon in Oct. 1999. We determined the primary care hospital, the arrival time, the burn size, the outcome, and the injury type from the medical records, the concerned organ records, and interviews with concerned persons. RESULT: The total number of victims was 137: 56 prehospital deaths, 1 hospital death, and 80 survivals. The Pearson correlation coefficient between the burn size and the severity was -0.175. There were 121 (89.6%) cases of inhalation injury, 59 (43.7%) cases of flame burns, 66 (48.9%) cases of hypoxic brain damage, and 16 (11.9%) cases involving other types of injury. CONCLUSION: The causes of death of the fire victims were inhalation injury and hypoxic brain damage due to CO poisoning and other toxic inhalants. We propose the use of a simple triage and rapid treatment (START) system and a reassessment the delayed category in fire disasters.
Subject(s)
Humans , Beer , Burns , Cause of Death , Disasters , Fires , Hypoxia, Brain , Inhalation , Medical Records , Poisoning , Primary Health Care , Transportation , TriageABSTRACT
A 45-year-old Korean woman visited our hospital complaining of poor vision after carbon monoxide (CO) poisoning. We have confirmed the presence of a point mutation at position 11778 in the ND4 gene of mitochondrial DNA. This case suggests that CO poisoning may precipitate the clinical expression of Leber's hereditary optic neuropathy (LHON). To our knowledge, this would be the first case report of clinical expression of LHON precipitated by CO poisoning.
Subject(s)
Female , Humans , Middle Aged , Carbon Monoxide/adverse effects , Carbon Monoxide Poisoning/complications , DNA Damage , DNA, Mitochondrial/genetics , Optic Atrophies, Hereditary/etiology , Point Mutation , Visual AcuityABSTRACT
This study was performed to observe the changes of blood sugar levels in 200 cases with acute Carbon monoxide (CO) poisoning. Successive tests of blood sugar on the day of onset and the lst, 2nd, 3rd & 4th day after anoxic insult were done in 12 patients with acute CO poisoning. In addition, to determine the derangement of thyroid function, blood levels of triiodothyronine(T3), tetraiodothyronine(T4), thyroid-stimulating hormone (TSH) were measured on the day of admission in 29 with C0 poisoning. The blood levels of T3, T4 and TSH were within normal ranges, but over two-thirds were distributed in lower range of normal mean values. This lower tendency within normal range was especially prominent in the blood level of T3. The blood level of sugar was increased, and 79.5% was higher than the upper limit of normal range. The blood levels of T3 and T4 were significantly decreased as CO exposure time period- prolonged. There was significant negative correlation between blood T3 levels and consciousness levels. Blood TSH levels were not significantly affected in acute CO poisoning. As consciousness levels were depressed and exposure time period were prolonged, blood sugar was increased. There found a rapid increase in blood sugar, followed by a abrupt dropping, and then progressive decrease to normal level over a period of 5 days after exposure to CO. In conclusion, acute CO poisoning obviously changes the thyroidal physiology. Even though blood TSH levels were variable, there was an obvious decrease in T3. The assumed CO-induced decrease in thyroid hormone secretion is seemingly not mediated by depressed TSH secretion but thyroid hormone metabolic dysfunction or extrathyroidal cotiverslon defect The alterations of blood sugar were also found to be acute and temporal which may be the result of physiologic compensation to hypoxic state caused by CO poisoning.
Subject(s)
Humans , Blood Glucose , Carbon Monoxide Poisoning , Carbon Monoxide , Carbon , Compensation and Redress , Consciousness , Physiology , Poisoning , Reference Values , Thyroid Gland , Thyroid Hormones , ThyrotropinABSTRACT
A new method of determination of COHb is reported in this paper by two- wavelength second-derivative spectrophotometry.Blood was diluted with a solution of THAM containing Na_2S_2O_4.The second-derivative spectrum was measured in the region of 500-600 nm and the derivative absorbance differerce ?Ax was deter mined at the wavelengths of 564 nm and 576 nm.Then the solution was satura- ted with CO gas.The second-derivative spectrum of COHb was measured in the same region.The derivative absorbance difference ?A_(100) was determined at the same wavelengths.The COHb in blood was calculated by the ratio of ?Ax to ?A_(100).The results of determination of COHb in standard blood samples were in good agreement with the theoretical values.