Hyperbaric oxygen therapy mobilized circulating stem cells and improved delayed encephalopathy after acute carbon monoxide poisoning with up-regulation of brain-derived neurotrophic factor.

Background Delayed encephalopathy (DE) is the most severe complication after acute carbon monoxide (CO) poisoning, which seriously affects the outcome of patients and leads to a high disability rate. Prior studies have shown that hyperbaric oxygen (HBO2) therapy is therapeutic for DE due to reducing immune-mediated neuropathology and thus improving cognitive performance. Methods In our present perspective study, five DE patients were treated regularly with HBO2 therapy. The mini-mental state examination (MMSE) and Barthel index (BI) were intermittently collected during their hospitalization for mental and physical status evaluation, the peripheral bloods were serially sampled to determine the concentration changes of circulating stem cells, as well as corresponding BDNF and neural markers. Results MMSE and BI showed series of improvements after multiple HBO2 therapies. The CD34+/CD90+ and CD34+/CD133+ dual positive cells, which were categorized as circulating stem cells, were observed an overall up-regulation since the beginning of the DE onset upon the application of HBO2 therapy. Characteristic neurotrophin BDNF, neural markers such as nestin and synaptophysin (SYP) were also up-regulated after exposure of HBO2. Conclusion The application of HBO2 therapy is of significance in improving the cognition of DE patients, along with mobilized circulating stem cells. We primarily infer that the CD34+/CD90+ and CD34+/CD133+ cells were mobilized by HBO2 exposure and have played a positive role in cognition improvement on DE patients by up-regulation of BDNF, nestin and SYP. The altering amount of circulating stem cells mobilized in peripheral blood could be a potential marker on predicting the outcome of DE.

Gray matter nuclei damage in acute carbon monoxide intoxication assessed in vivo using diffusion tensor MR imaging.

OBJECTIVE: To observe the structural changes of gray matter nuclei in patients with acute carbon monoxide intoxication by diffusion tensor imaging (DTI), quantify the degree of deep gray matter damage in the brain by adopting imaging technology and research the characteristics of the damage and its pertinence with memory and cognitive impairment. METHODS: Twenty-five patients with acute carbon monoxide intoxication and 25 healthy volunteers matched in sex and age were examined by routine head MRI and diffusion tensor imaging (DTI). Bilateral hippocampus, dater nucleus, thalamus, amygdala, globus pallidus and putamen were taken as regions of interest. The mean diffusion coefficient (MD), anisotropic fraction (FA) and appearance of deep gray matter nucleus in patients with acute carbon monoxide intoxication were analyzed. It found that the change of diffusion coefficient (ADC) and its clinical correlation with cognitive impairment were generated by carbon monoxide intoxication. RESULTS: Compared with the healthy control group, the FA values of bilateral globus pallidus, hippocampus, dater nucleus and putamen decreased, while the FA values of amygdala and thalamus had no statistical significance; the MD values and ADC values of hippocampus, globus pallidus and putamen increased, while the MD and ADC values of dater nucleus, thalamus and amygdala had no statistical significance, either. CONCLUSION: DTI is capable of sensitively reflecting the damage of gray matter nuclei caused by acute carbon monoxide intoxication and quantifying the degree of hypoxic brain damage in a certain extent, and may be related to cognitive impairment.

Evaluation of changes in magnetic resonance diffusion tensor imaging after treatment of delayed encephalopathy due to carbon monoxide poisoning.

Diffusion tensor imaging of the brain tissue microstructure was performed to predict or diagnose the pathophysiological mechanism underlying delayed encephalopathy after carbon monoxide poisoning and the treatment effect was analyzed. The changes in the diffusion parameters (average diffusion coefficient and fractional anisotropy) in adult patients after hyperbaric oxygen therapy of delayed encephalopathy after carbon monoxide poisoning were not significant differences of the two lateral ventricles or anterior or posterior limb of the internal capsule. In the group exposed to hyperbaric oxygen therapy, the fractional anisotropy values of the white matter in the ventricles of the brain and anterior and posterior limbs of the internal capsule were higher than those recorded before therapy, while the average diffusion coefficient values were significantly lower. These finding provide important monitoring indicators for clinicians.

Targeting optimal time for hyperbaric oxygen therapy following carbon monoxide poisoning for prevention of delayed neuropsychiatric sequelae: A retrospective study.

OBJECTIVES: Delayed neuropsychiatric sequelae (DNS) are serious complications of carbon monoxide poisoning; neuropsychiatric disorders can occur within a few days of recovery from acute poisoning. Hyperbaric oxygen therapy (HBOT) has been the main treatment of carbon monoxide (CO) poisoning and was recommended as the treatment choice for CO poisoning by the American Undersea and Hyperbaric Medical Society and the Tenth European Consensus Conference on Hyperbaric Medicine of the European Underwater and Baromedical Society. However, the optimal timing for commencing HBOT in patients with CO poisoning remains unknown. We therefore conducted a retrospective study in an attempt to target the optimal time of HBOT for DNS prevention. METHODS: A retrospective review of patient files/medical records was conducted on all patients with CO poisoning admitted to the Emergency Department of Linkou Chang-Gung Memorial Hospital, Taiwan between January 1, 2009 and December 31, 2015. A total of 279 patients who received HBOT were eligible for further DNS detection. DNS was defined as the presence of one of the following neurological, cognitive, or psychological sequelae that were documented in the medical record during hospital stay or outpatient clinic follow-up for at least 6 months. A multivariable logistic regression analysis was employed to identify potential determinants of DNS after receiving HBOT for CO poisoning. A receiver operating characteristic (ROC) curve was used to analyse the influence of duration from CO exposure to HBOT on DNS development. RESULTS: A Glasgow coma score of <9 (odds ratio [OR], 3.20; 95% confidence interval [CI], 1.19-8.60) and a longer duration from CO exposure to HBOT (OR, 1.06; 95% CI, 1.03-1.09) were associated with a higher risk of DNS. By contrast, the presence of multiple victims from the same incident was associated with a lower risk of DNS. The ROC curve for the duration between CO exposure and HBOT in predicting DNS development demonstrated an area under the curve of 0.638 (95% CI, 0.575-0.698). The optimal cut-off point according to the Youden index was 22.5 h, with a sensitivity of 41.7% and a specificity of 85.9%. We also stratified the duration from CO exposure to HBOT into 5 intervals (< 6 h, 6-11 h, 12-23 h, 24-47 h and ≥ 48 h) and revealed a trend of increasing DNS risk with time. CONCLUSIONS: We identified several potential predictors of DNS in patients with CO poisoning who received HBOT. Multivariable logistic regressions further revealed that longer duration from CO exposure to HBOT, loss of consciousness, and the presence of multiple victims were independent predictors of DNS development. HBOT should be performed as early as possible and preferably within 22.5 h after CO poisoning.

Transient splenial lesion in a case with carbon monoxide poisoning: A clue supporting the excitotoxicity hypothesis?

Transient splenial lesions of the corpus callosum are uncommon radiologic findings seen in a number of clinical conditions. Awareness of these lesions is crucial to prevent further invasive investigation and intervention. We report a unique case of transient splenial lesion in a patient with carbon monoxide poisoning.

[Hyperbaric oxygen for carbon monoxide poisoning: case report of severe poisoning due to exhaust fumes]. / Hyperbare Oxygenierung bei Kohlenmonoxidintoxikation: Fallbericht einer schweren Intoxikation durch Autoabgase.

After rescue and transport a patient with severe carbon monoxide poisoning (CO-Hb concentration 82%) was treated by hyperbaric oxygen (HBO) therapy in a pressure chamber. During decompression the patient suffered cardiac arrest due to massive acidosis, hyperpotassaemia, haemoconcentration and elevated CO-Hb level. After successful resuscitation and cardiopulmonary diagnostics, HBO therapy was continued for prophylactic treatment of delayed neurological sequelae. Three months after completing treatment and discharge from hospital there were no neurological sequelae.

Unusual CT and MRI appearance of carbon monoxide poisoning.

Unilateral low attenuation areas within the right putamen, globus pallidus and thalamus were observed on CT in a patient after exposure to carbon monoxide. A transient bilateral appearance was found on subsequent CT examinations. Hemorrhagic infarction of the right putamen, and ischemic lesions in both thalami were visualized on MRI 2 weeks later.

Carbon monoxide poisoning and treatment with hyperbaric oxygen in the subacute phase.

The use of normobaric versus hyperbaric (>2 atm) oxygen in the treatment of carbon monoxide intoxication continues to be a matter of debate despite reports of increased efficacy with hyperbaric oxygen. When hyperbaric oxygen is used, immediate treatment is preferred for best results. The therapeutic window of time, however, is unknown. A patient presented with acute confusion and partial retrograde and total anterograde memory loss due to carbon monoxide poisoning. He was initially treated with normobaric oxygen and failed to show appreciable improvement. One month after carbon monoxide exposure the patient underwent treatment with hyperbaric oxygen and showed appreciable symptom relief confirmed by clinical findings and neuropsychological testing. This case shows that hyperbaric oxygen may be efficacious in the recovery of neuropsychiatric function up to 1 month after carbon monoxide induced brain injury.

Isotope brain scanning with Tc-HMPAO: a predictor of outcome in carbon monoxide poisoning?

Tc-HMPAO isotope brain scans were performed in three patients who received hyperbaric oxygen treatment following carbon monoxide poisoning. Cerebral perfusion imaging provides an index of severity of the initial cerebral damage which correlated with outcome.

Computed tomography of the brain in acute carbon monoxide poisoning.

Of 107 patients admitted to the South Western Hyperbaric Medical Centre with acute carbon monoxide poisoning for hyperbaric oxygen therapy 19 had cerebral imaging performed: 17 patients had CT, one patient had MRI and CT and one patient MRI alone. The role of brain CT is established in determining the prognosis from acute carbon monoxide poisoning. Brain imaging was indicated because of unconsciousness on admission and failure or delayed improvement in neurological status after initiation of hyperbaric oxygen therapy. Of the 18 patients who underwent brain CT, seven were found to have the characteristic changes of bilateral low attenuation areas within the globus pallidus and six had low attenuation changes within cerebral white matter. In two patients there were both globus pallidus and cerebral white matter changes. Out of the total of the 19 patients who were studied, four patients died, 10 recovered fully and five had variable disabilities ranging from short term memory loss to more severe cognitive impairment and physical disability. The role of CT and the practicalities of hyperbaric oxygen therapy for acute carbon monoxide poisoning are discussed in the light of the experience from a regional dedicated medical diving centre.

Brain computerized tomography after hyperbaric oxygen therapy for carbon monoxide poisoning.

The role of brain computerized tomography (CT) imaging in predicting clinical outcome was investigated in patients receiving hyperbaric oxygen therapy for serious carbon monoxide (CO) poisoning. From a series of 48 consecutive patients suffering loss of consciousness from CO exposures, the records of 40 selected patients were evaluated to determine how their CT findings correlated with clinical outcome. A neuroradiologist blinded to patient outcome confirmed the radiographic findings. CT abnormalities consisted of globus pallidus hypodensities (nine patients), subcortical white matter hypodensities (four), cerebral cortical lesions (one), cerebral edema (one), hippocampal lesions (one), and complete loss of gray-white differentiation (one). Of the patients with globus pallidus lesions, 44% manifested incomplete recovery, whereas white matter lesions reflected a 74% incidence of morbidity. Age, duration of CO exposure, and interval between CO exposure and treatment did not significantly relate to clinical outcome. The blood carboxyhemoglobin levels correlated with clinical prognosis (P < 0.05) and, importantly, CT results significantly predicted clinical outcome (P < 0.05). A normal scan correlated highly with a complete recovery, whereas an abnormal scan predicted incomplete recovery or death, despite prior HBO therapy. The current study establishes prognostic validity for brain CT imaging for evaluating clinical outcome after HBO therapy for CO poisoning.

Serial proton magnetic resonance spectroscopy in a patient with the interval form of carbon monoxide poisoning.

Serial proton magnetic resonance spectroscopy (1H-MRS) studies were performed from immediately after the appearance of sequelae in a patient with the interval form of carbon monoxide (CO) poisoning. The volume of interest was set over the frontal lobe white matter. In the early period a persistent increase in choline was found, which was thought to reflect the course of progressive demyelination. The appearance of lactate and decrease in N-acetylaspartate reflected the point at which neuron injury became irreversible. These were followed later by the finding of irreversible changes on MRI and single photon emission computed tomography. The findings suggest that 1H-MRS may be a useful modality to determine neuron viability and prognosis early in the course of the interval form of CO poisoning.

A positron emission tomography study of patients with acute carbon monoxide poisoning treated by hyperbaric oxygen.

Seven patients with an acute and severe carbon monoxide intoxication were treated with hyperbaric oxygen and underwent a positron emission tomographic examination 2-5 days after the acute event. Although the final clinical outcome was good in all patients, ischaemic changes were observed. Three patients with temporary sequelae after hyperbaric oxygen treatment showed the most severe changes, mainly in striatum and thalamus. Although positron emission tomographic examination cannot predict the final outcome, it can show the regions at risk for development of late complications following carbon monoxide poisoning.

Carbon monoxide poisoning: bilateral lesions in the thalamus on MR imaging of the brain.

Magnetic Resonance (MR) Imaging of the brain in a child with carbon monoxide poisoning revealed bilateral diffuse high signal in the centrum semiovale and the previously unreported finding of bilateral high intensity lesions in the anterior thalami. This case illustrates a previously unrecognized effect of carbon monoxide poisoning and demonstrates the superiority of MR imaging over computed tomography in cases of carbon monoxide poisoning.

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.