Carbon monoxide poisoning in the 21st century

被引:61
作者
Chiew, Angela L. [1 ,2 ,3 ]
Buckley, Nicholas A. [1 ,2 ,3 ]
机构
[1] Prince Wales Hosp, Dept Emergency Med, Clin & Expt Toxicol Unit, Randwick, NSW 2031, Australia
[2] Univ Sydney, Sydney Med Sch, Sydney, NSW 2006, Australia
[3] Childrens Hosp, NSW Poisons Informat Ctr, Sydney, NSW 2145, Australia
来源
CRITICAL CARE | 2014年 / 18卷 / 02期
关键词
NEURON-SPECIFIC ENOLASE; HYDROGEN-RICH SALINE; SERUM S100B PROTEIN; HYPERBARIC-OXYGEN; RISK-FACTORS; CARBOXYHEMOGLOBIN LEVELS; TERM MORTALITY; BRAIN; MANAGEMENT; SEQUELAE;
D O I
10.1186/cc13846
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
The world has experienced some very large shifts in the epidemiology of carbon monoxide poisoning, but it remains one of the most important toxicological global causes of morbidity and mortality. The diagnosis can be quickly confirmed with blood gases (pulse oximeters lack both sensitivity and specificity). Several strong predictors for serious neurological sequelae (prolonged loss of consciousness and elevated S100B) and reduced life expectancy (elevated troponin) are now reasonably well established. Despite this clearly defined high-risk group and extensive research into the pathophysiology, there has been little translation into better treatment. Much of the pathophysiological research has focused on hyperbaric oxygen. Yet it is apparent that clinical trials show little evidence for benefit from hyperbaric oxygen, and the most recent even raises the possibility of harm for repeated courses. More logical and promising potential antidotes have been under-researched, although recently both animal and small human studies suggest that erythropoietin may reduce S100B and prevent neurological sequelae. Major breakthroughs are likely to require further research on this and other treatments that may inhibit post-hypoxic inflammatory responses and apoptosis.
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页数:8
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