Hyperbaric treatment for decompression sickness: current recommendations

被引:0
|
作者
Moon, Richard E. [1 ,2 ]
Mitchell, Simon [3 ,4 ]
机构
[1] Duke Univ, Med Ctr, Ctr Hyperbar Med & Environm Physiol, Dept Anesthesiol, Durham, NC 27710 USA
[2] Duke Univ, Med Ctr, Ctr Hyperbar Med & Environm Physiol, Dept Med, Durham, NC 27710 USA
[3] Auckland City Hosp, Dept Anaesthesia & Perioperat Med, Auckland, New Zealand
[4] Univ Auckland, Fac Med & Hlth Sci, Auckland 3, New Zealand
关键词
decompression sickness; bends; hyperbaric oxygen; CENTRAL-NERVOUS-SYSTEM; DELAYED TREATMENT; AIR; ACTIVATION; OXYGEN; TABLES; INVOLVEMENT; COMPLEMENT; DYSBARISM; EMBOLISM;
D O I
暂无
中图分类号
Q17 [水生生物学];
学科分类号
071004 ;
摘要
Rationale Decompression sickness (DCS, "bends") is caused by formation of bubbles in tissues and/ or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation) [1]. This may occur when ambient pressure is reduced during any of the following: ascent from a dive; depressurization of a hyperbaric chamber; rapid ascent to altitude in an unpressurised aircraft or hypobaric chamber; loss of cabin pressure in an aircraft [2] and during space walks. In diving, compressed gas breathing is usually necessary, although rarely DCS has occurred after either repetitive or very deep breath-hold dives [3, 4]. Although arterial gas embolism due to pulmonary barotrauma can occur aftera dive as shallow as 1 meter, the threshold depth for DCS in compressed-gas diving is around 20 feet of seawater (fsw) [5]. DCS after a dive can be provoked by mild altitude exposure, such as a commercial aircraft flight [6, 7], but without a preceding dive the threshold altitude for DCS occurrence in unpressurized flight is 18,000-20,000 feet [8, 9]. Several mechanisms have been hypothesized by which bubbles may exert their deleterious effects. These include: direct mechanical disruption of tissue [10]; occlusion of blood flow, platelet deposition and activation of the coagulation cascade [11]; endothelial dysfunction [12-13]; capillary leakage [14-18]; endothelial cell death, complement activation [19, 20]; inflammation [21]; and leukocyte-endothelial interaction [22]. Recent evidence suggests that circulating microparticles may play a pro-inflammatory role in DCS pathophysiology [23, 24].
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页码:685 / 693
页数:9
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