Pathophysiology and Treatment of Carbon Monoxide Poisoning

Abstract

Carbon monoxide poisoning is the leading cause of poisoning deaths in the US, and published reports of carbon monoxide related morbidity and mortality can vary widely. Common morbidity involves myocardial and/or neurologic injury including delayed neurologic sequelae. The pathophysiology of this entity is complex, involving hypoxic stress on the basis of interference with oxygen transport to the cells and possibly impairing electron transport. Carbon monoxide can also affect leukocytes, platelets and the endothelium, inducing a cascade of effects resulting in oxidative injury. Carboxyhemoglobin levels are valuable for confirming carbon monoxide exposure but cannot be used to stratify severity of poisoning, predict prognosis, or indicate a specific treatment plan. Oxygen therapy is the key treatment of carbon monoxide intoxication, and hyperbaric oxygen has been shown to interdict and improve clinical outcome in some patients. Immediate treatment with a high fraction of inspired oxygen and careful clinical evaluation are mandatory. Timely referral for hyperbaric oxygen is indicated for patients with any history of unconsciousness, cardiovascular instability or ischemia, and persistent mental and/or neurologic deficits. Hyperbaric oxygen should also be considered in certain other patient subsets.     

Confirmation of correct tracheal tube placement in newborn infants

Tracheal intubation remains a common procedure during neonatal intensive care. Rapid confirmation of correct tube placement is important because tube malposition is associated with serious adverse outcomes. The current gold standard test to confirm tube position is a chest radiograph, however this is often delayed until after ventilation has commenced. Hence, point of care methods to confirm correct tube placement have been developed. The aim of this article is to review the available literature on tube placement in newborn infants. We reviewed books, resuscitation manuals and articles from 1830 to the present with the search terms “Infant, Newborn”, “Endotracheal intubation”, “Resuscitation”, “Clinical signs”, “Radiography”, “Respiratory Function Tests”, “Laryngoscopy”, “Ultrasonography”, and “Bronchoscopy”. Various techniques have been studied to help clinicians assess tube placement. However, despite 85 years of clinical practice, the search for higher success rates and quicker intubation continues. Currently, chest radiography remains the gold standard test to confirm tube position. However, rigorous evaluation of new techniques is required to ensure the safety of newborn infants.     

活性炭对氟康唑氯化钠注射液含量的影响

目的：探讨炭处理过程中活性炭用量对氟康唑氯化钠注射液中氟康唑含量的影响。方法：在同一温度下加入不同量的活性炭，在不同的温度下加入等量的活性炭，在同一温度、不同pH值下加入等量的活性炭，进行炭处理后测定氟康唑含量的变化。结果：随着活性炭用量的增加，主药含量明显降低；随温度升高，活性炭吸附作用减小；pH值对活性炭吸附作用的影响不明显。结论：在炭处理过程中应控制炭用量，并适当增加氟康唑的投料量。     

水药酢浆草对四氯化碳致小鼠肝损伤的保护性研究

目的 探讨水药酢浆草对四氯化碳CCl4诱导的小鼠肝损伤的保护作用。方法 将40只小鼠随机分为5组,正常组、CCl4模型组、酢浆草低、中、高剂量组,每组8只。正常组和CCl4模型组给予生理氯化钠溶液,酢浆草低、中、高剂量组给分别给100、300及600 mg/kg酢浆草灌胃,连续5 d。于末次给药2 h后,除正常组外,其余各组小鼠给予0.3% CCl4花生油溶液稀释、按0.02 ml/g的剂量皮下注射,在中毒后16 h取血和肝脏组织,分别检测各组小鼠肝功能相关的生化指标。结果 与CCl4模型组小鼠比较,不同剂量酢浆草治疗组小鼠肝脏指数、血清ALT、AST及TNF-α水平不同程度降低（P <0.05）;肝组织中CAT、GSH及SOD水平不同程度升高（P <0.05）,MDA水平不同程度降低（P <0.05）。结论 水药酢浆草对CCl4所致小鼠肝损伤具有明显的保护作用,其机制可能与酢浆草降低氧化酶活性和抗脂质过氧化作用有关。     

维生素C碳点对口腔鳞状细胞癌KB细胞增殖、自噬和凋亡的影响

目的：研究维生素C碳点对口腔黏膜鳞状细胞癌（口腔鳞癌）KB细胞的杀伤作用,探讨其相关作用机制。方法：以不同浓度（5、10、20、40和80 mg·L^-1）维生素C碳点体外处理口腔鳞癌KB细胞作为实验组,以0 mg·L^-1维生素C碳点组作为空白对照组。MTT法检测各组细胞增殖率,克隆形成实验检测各组细胞克隆形成能力,Western blotting法检测各组细胞中自噬相关蛋白LC3蛋白表达水平,流式细胞术检测KB细胞的凋亡率。结果：与空白对照组比较,20、40和80 mg·L^-1维生素C碳点组KB细胞的增殖率及克隆形成能力均明显降低（P<0.01）,40 mg·L^-1维生素C碳点组KB细胞中LC3 Ⅱ蛋白表达水平和细胞凋亡率明显升高（P<0.05或P<0.01）。结论：维生素C碳点能够有效地杀伤口腔鳞癌KB细胞,抑制KB细胞的增殖并减弱其克隆形成能力,其杀伤作用可能与KB细胞自噬和凋亡的发生有关。     

重组人MG53对CCl4诱导的急性肝损伤的保护作用

目的 研究重组人MG53(rhMG53)对四氯化碳(CCl4)诱导的急性肝损伤的保护作用及其相关机制.方法 40只雄性C57小鼠采用完全随机化分组法分成4组:正常对照组、rhMG53组、CCl4组、rhMG53+CCl4组,每组10只.CCl4组、rhMG53+CCl4组小鼠予0.1％ CCl4花生油溶液2 mL/kg腹腔内注射,rhMG53+CCl4组在注射CCl4前30 min予rhMG53 1 mg/kg肌肉注射.rhMG53组予rhMG53 1 mg/kg肌肉注射.正常进食进水24 h后眼球取血分离血清,测定谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)活性.取小鼠肝脏,观察肝脏的组织学改变.以体外培养的人肝癌细胞(HepG2)为靶细胞,观察rhMG53对CCl4诱导的细胞损伤的保护作用.结果 rhMG53降低小鼠血清ALT、AST、LDH水平,病理镜检显示rhMG53可改善肝脏的病理结构,差异均有统计学意义(P＜0.05);rhMG53可以修复HepG2细胞膜,保护CCl4对HepG2细胞的损伤.结论 rhMG53改善CCl4诱导的急性肝细胞损伤,保护肝脏功能.     

Soda lime temperatures during low-flow sevoflurane anaesthesia and differences in dead-space

BACKGROUND: Sevoflurane degrades during low-flow anaesthesia to compound A, and high carbon dioxide absorbent temperatures cause increased degradation. The purpose of this investigation was to determine if larger tidal volumes, without increasing alveolar ventilation, decrease the temperature in the carbon dioxide absorber during low- and minimal-flow sevoflurane anaesthesia. METHODS: Prospective, randomized study, including 45 patients (ASA 1-2), scheduled for elective general or urology surgery. The patients were randomly assigned to one of three treatments. Patients in group 1 (NDS) received fresh gas flow of 1 litre/min without using additional dead-space volumes. In group 2 (DS + 1.0), the patients received fresh gas flow of 1 litre/min using additional dead-space volumes, placed between the Y-piece and the HME, and patients in group 3 (DS + 0.5) received the same technique with a fresh gas flow of 0.5 litre/min. The soda lime temperatures, dead-space volumes, end-tidal carbon dioxide, sevoflurane concentrations, ventilation volumes and pressures, absorbent weight and ear temperatures were measured. RESULTS: The maximum temperature of the soda lime was 44.1 +/- 1.1 degrees C in the NDS group, 37.8 +/- 0.8 degrees C in the DS + 1.0 group and 38.5 +/- 2.7 degrees C in the DS + 0.5 group (P<0.0001). The dead-space volume between the Y-piece the tracheal tube was 164 +/- 69 ml in the DS + 1.0 group and 196 +/- 15 ml in the DS + 0.5 group (P<0.05). The ventilator pressure were higher in the DS groups compared with the NDS group (P<0.001). Soda lime weight increased in all groups. End-tidal carbon dioxide, sevoflurane concentrations and ear temperatures were similar between the groups. CONCLUSION: Increasing dead-space volumes can reduce carbon dioxide absorber temperature during low- and minimal-flow sevoflurane anaesthesia.     

脑血管反应性检测方法的临床评价

目的对二氧化碳吸入、屏气及过度换气等3种不同的脑血管反应性检测方法进行比较,拟为临床应用探索一种有效且简便的方法。方法70例健康体格检查者通过经颅多普勒(TCD)超声技术常规检测颅底及颈部各动脉,然后分别进行二氧化碳吸入试验、过度换气试验和屏气试验,记录试验前后双侧大脑中动脉血流速度变化数据和趋势,检测脑血管反应性。结果吸入二氧化碳后,大脑中动脉平均血流速度明显加快,增加率为(44.86±10.18)%;过度换气时,平均血流速度明显减慢,于过度换气20～30s后降至平台期,平均下降率为(33.63±8.62)%,直至过度通气结束血流速度无明显变化。70例受试者平均屏气时间为(41.66±9.51)s,其中男性屏气时间(42.05±9.23)s,女性(40.63±10.47)s,男女之间差异无统计学意义(P>0.05);屏气后大脑中动脉平均血流速度明显加快,增加率为(46.53±11.83)%;平均屏气指数为1.16±0.37;屏气后血流速度增加率和屏气指数之间呈高度正相关(r=0.865,P<0.01);当屏气时间>30s时,无论采用屏气后血流速度增加率或屏气指数作为分析指标,均可准确地反映脑血管反应性变化。对二氧化碳吸入试验、过度换气试验及屏气试验3种不同方法进行比较显示,过度换气试验与二氧化碳吸入试验、屏气试验间差异有统计学意义(P<0.01);而二氧化碳吸入试验与屏气试验之间差异无统计学意义(P>0.05)。结论二氧化碳吸入试验、屏气试验和过度换气试验均可有效地评价脑血管反应性,其中以屏气试验评价脑血管反应性更为简便。     

Fibrinolytic responses of human peritoneal fluid in laparoscopic cholecystectomy: a prospective clinical study

Background The reduction in peritoneal fibrinolysis is believed to be the pathogenetic mechanism of adhesion formation. The general conclusion based on previous clinical and experimental studies is that laparoscopic procedures produce less adhesion formation. The association between this beneficial effect of laparoscopic cholecystectomy and peritoneal fibrinolytic changes is not clear. Therefore, the authors aimed to compare the effects of open and laparoscopic cholecystectomy on peritoneal fibrinolysis. For this purpose, fibrinolytic parameters in peritoneal fluid were investigated 24 h after laparoscopic and open cholecystectomies. Methods In a prospective clinical study, peritoneal fluid was sampled via a drain 24 h after laparoscopic (n = 10) and open (n = 9) cholecystectomies. Activities and concentrations of tissue plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), and tPA/PAI-1 complex were determined by enzyme-linked immunosorbent assay (ELISA) kits. Results In peritoneal fluids, tPA and tPA/PAI-1 complex concentrations were higher in the open cholecystectomy group (p = 0.009 and p < 0.001, respectively), but tPA activity and PAI-1 concentrations did not differ between the groups (p = 0.514 and p = 0.716, respectively). Conclusions Fibrinolytic changes in peritoneal fluid have several similarities in open and laparoscopic cholecystectomies with regard to tPA activity and PAI-1 levels. However, higher tPA levels after the open procedure probably are secondary to more intense tissue handling leading to mesothelial release of tPA.