Early predictors of brain injury in patients with acute carbon monoxide poisoning and the neuroprotection of mild hypothermia.

INTRODUCTION: Carbon monoxide (CO) poisoning can cause serious neurological sequelae. However, there is neither effective treatment strategy nor reliable indicators to determine the prognosis of patients with CO poisoning. The present study aimed to observe the changes of neurological function score, disease severity score, cerebral oxygen utilization (O2UCc), bispectral (BIS) index and neuron-specific enolase (NSE) concentration, and to elucidate the clinical significance of these potential indicators and the neuroprotective effect of mild hypothermia on brain injury in patients with severe acute CO poisoning. MATERIALS AND METHODS: A total of 277 patients with acute severe CO poisoning from 2013 to 2018 were enrolled in our hospital. Patients were divided into three groups according to their body temperature on the day of admission and their willingness to treat: a fever group (n = 78), a normal temperature group (NT group, n = 113), and a mild hypothermia group (MH group, n = 86). All patients were given hyperbaric oxygen therapy, while those in the MH group received additional mild hypothermia treatment. The severity of the disease, the neurobehavioral status, the incidence of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), and other indicators including BIS, O2UCc, NSE were further evaluated in all patients at given time-points. RESULTS: Mild hypothermia therapy improved the prognosis of patients with CO poisoning, significantly decreased the value of O2UCc and NSE, and up-regulated BIS. The incidence of DEACMP at 6 months was 27% in the fever group, 23% in the NT group, and 8% in the MH group. The values of Glasgow-Pittsburgh coma scale (G-P score), BIS index and NSE were closely related to the occurrence of DEACMP, the cutoff values were 12.41, 52.17 and 35.20 ng/mL, and the sensitivity and specificity were 79.3%, 77.6%, 79.3% and 67.6%, 89.5%, 88.6% in the receiver operating characteristic curve (ROC), respectively. CONCLUSIONS: Early mild hypothermia treatment could significantly reduce the severity of brain injury after CO poisoning, and might be further popularized in clinic. G-P scores, NSE and BIS index can be regarded as the prediction indicators in the occurrence and development of DEACMP. CLINICAL TRIAL REGISTRATION: The study protocol was granted from Qingdao University Research Ethics Committee (Clinical trial registry and ethical approval number: QD81571283).

Corrigendum to "Clinical Characteristics of Visual Dysfunction in Carbon Monoxide Poisoning Patients".

[This corrects the article DOI: 10.1155/2020/9537360.].

Clinical Characteristics of Visual Dysfunction in Carbon Monoxide Poisoning Patients.

PURPOSE: The aim of the present study was to analyze the clinical characteristics of visual dysfunction in patients with carbon monoxide (CO) poisoning. METHODS: A total of 436 patients with CO poisoning were enrolled in our hospital from October 2012 to December 2018, including 193 patients with moderate poisoning (MP group), 165 with severe poisoning (SP group), and 78 with delayed encephalopathy (DE group). The clinical characteristics of visual dysfunction in patients with CO poisoning were analyzed through the collection of medical history, regular physical examination, brain magnetic resonance imaging (MRI), ophthalmological examination, the National Eye Institute Visual Function Questionnaire (NEI-VFQ), and its influencing factors. RESULTS: Some patients in the three groups had visual dysfunction. The main ocular symptoms were local pain, eye movement disorder, and visual field defect. The key pathological factors were keratopathy, retinal nerve cell damage, optic nerve damage, retinal vascular disease, macular disease, and occipital visual center damage. The clinical symptoms of visual dysfunction after CO poisoning lasted for a long time (>12 months) and were not completely consistent with the positive results of the ophthalmological examination. A few sequelae of ophthalmology were still left after the help of medicine. CONCLUSION: The incidence of visual dysfunction in patients with CO poisoning was high, the clinical symptoms were rich and diverse, the duration of disease was long, and the prognosis was poor. Thus, the relevant ophthalmological examination and intervention treatment should be perfected as soon as possible.

Feasibility analysis of external application of Xiao-Shuan-San in preventing PICC-related thrombosis.

PURPOSE: We aim to analyze the feasibility of external application of Xiao-Shuan-Santo prevent peripherally inserted central catheter (PICC) -related thrombosis. METHODS: A total of 218 patients with PICC catheterization were randomly divided into a control group (n = 103) and a treatment group (n = 115). Patients in the treatment group received additional external application of Xiao-Shuan-San. The changes of coagulation index, the incidence of PICC-related thrombosis and other complications, and the maximum blood flow rate (Vmax) of axillary vein were observed at 1 day before catheterization and 30 days after PICC. RESULTS: At 30 days after PICC, the incidence of PICC-related thrombosis and other adverse events in the treatment group were obviously lower than that in the control group (P < 0.05), and the decreased Vmax value of axillary vein in the control group (11.75±1.91 cm/s) was more visible than that in the treatment group (14.63±3.03 cm/s), accompanied by a statistical significance (P < 0.05). CONCLUSIONS: External application of Xiao-Shuan-San could reduce the incidence of PICC-related thrombosis and other complications.

Edaravone attenuates brain damage in rats after acute CO poisoning through inhibiting apoptosis and oxidative stress.

Acute carbon monoxide (CO) poisoning is the most common cause of death from poisoning all over the world and may result in neuropathologic and neurophysiologic changes. Acute brain damage and delayed encephalopathy are the most serious complication, yet their pathogenesis is poorly understood. The present study aimed to evaluate the neuroprotective effects of Edaravone against apoptosis and oxidative stress after acute CO poisoning. The rat model of CO poisoning was established in a hyperbaric oxygen chamber by exposed to CO. Ultrastructure changes were observed by transmission electron microscopy (TEM). TUNEL stain was used to assess apoptosis. Immunohistochemistry and immunofluorescence double stain were used to evaluate the expression levels of heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf-2) protein and their relationship. By dynamically monitored the carboxyhemoglobin (HbCO) level in blood, we successfully established rat model of severe CO poisoning. Ultrastructure changes, including chromatin condensation, cytoplasm dissolution, vacuoles formation, nucleus membrane and cell organelles decomposition, could be observed after CO poisoning. Edaravone could improve the ultrastructure damage. CO poisoning could induce apoptosis. Apoptotic cells were widely distributed in cortex, striatum and hippocampus. Edaravone treatment attenuated neuronal apoptosis as compared with the poisoning group (P < 0.01). Basal expressions of HO-1 and Nrf-2 proteins were found in normal brain tissue. CO poisoning could activate HO-1/Nrf-2 pathway, start oxidative stress response. After the administration of Edaravone, the expression of HO-1 and Nrf-2 significantly increased (P < 0.01). These findings suggest that Edaravone may inhibit apoptosis, activate the Keapl-Nrf/ARE pathway, and thus improve the ultrastructure damage and neurophysiologic changes following acute CO poisoning.