Charpentier C, Audibert G, Dousset B, Weber M, Garric J, Welfringer P, Laxenaire M C
Department of Anesthesia and Surgical Intensive Care, Hôpital Central, Nancy, France.
Intensive Care Med. 1997 Oct;23(10):1040-8. doi: 10.1007/s001340050454.
(a) To investigate the relationship between gut ischemia parameters (gastric intramucosal pH [pHi], mucosal-arterial carbon dioxide difference [PCO2-gap]), and endotoxin or cytokine release during hemorrhagic shock; (b) to compare the predictive value of pHi, PCO2-gap and arterial lactate concentrations.
Prospective study.
Surgical intensive care unit of a university hospital.
20 multiple trauma patients with severe hemorrhagic shock.
Intramucosal measurements and blood samples were obtained on admission to the emergency room and repeatedly over 48 h.
Endotoxin was measured using a chromogenic limulus amoebocyte assay. Cytokine [tumor necrosis factor-alpha (TNF alpha) and interleukin-6 (IL-6)] values were evaluated by immunoradiometric assays. Only 3 patients had positive blood cultures but endotoxins were detected at least once in all patients. Endotoxin levels were similar in survivors and non-survivors over the study period and were not related to pHi or PCO2-gap. Initially, high levels of IL-6 were observed in both nonsurvivors and survivors [median 1778 pg/ml (range 435-44,540) vs 2068 pg/ml (range 996-92,300)]. IL-6 levels progressively decreased in the survivors but not significantly. On admission, TNF alpha concentrations were similar in nonsurvivors and survivors (42 +/- 35 vs 46 +/- 27 pg/ml). From the 24th h, TNF alpha values were higher in the nonsurvivors than in the survivors (24 h: 72 +/- 38 vs 34 +/- 17 pg/ml, p < 0.05). The greatest IL-6 levels were found for a pHi < 7.20 (28.5 +/- 36.5 vs 1.8 +/- 1.3 ng/ml, p < 0.05) or a PCO2-gap > 7.5 mmHg (1 kPa) (32.5 +/- 37.5 vs 1.7 +/- 1.3 ng/ml, p < 0.01). With the same pHi threshold, no difference was found in endotoxin levels. The lactate concentrations were predictive for outcome from the 12th h (9.5 +/- 5.9 vs 3.6 +/- 2.3 mmol/l, p < 0.05).
During severe hemorrhagic shock, endotoxin translocation from the gut was a common phenomenon that seemed independent of both pHi values and outcome. It could not explain IL-6 and TNF alpha release. In severe hemorrhagic shock, neither pHi nor PCO2-gap provides additional information to the lactate measurements.
(a) 研究失血性休克期间肠道缺血参数(胃黏膜内pH值[pHi]、黏膜 - 动脉二氧化碳差值[PCO2 - gap])与内毒素或细胞因子释放之间的关系;(b) 比较pHi、PCO2 - gap和动脉血乳酸浓度的预测价值。
前瞻性研究。
大学医院的外科重症监护病房。
20例严重失血性休克的多发伤患者。
在急诊室入院时及48小时内反复采集黏膜测量值和血样。
采用显色鲎试剂法测量内毒素。通过免疫放射分析评估细胞因子[肿瘤坏死因子 - α(TNFα)和白细胞介素 - 6(IL - 6)]值。仅3例患者血培养呈阳性,但所有患者至少有一次检测到内毒素。在研究期间,幸存者和非幸存者的内毒素水平相似,且与pHi或PCO2 - gap无关。最初,非幸存者和幸存者中均观察到高水平的IL - 6[中位数1778 pg/ml(范围435 - 44,540)对2068 pg/ml(范围996 - 92,300)]。幸存者中IL - 6水平逐渐下降,但无显著差异。入院时,非幸存者和幸存者的TNFα浓度相似(42±35对46±27 pg/ml)。从第24小时起,非幸存者的TNFα值高于幸存者(24小时:72±38对34±17 pg/ml,p<0.05)。当pHi<7.20(28.5±36.5对1.8±1.3 ng/ml,p<0.05)或PCO2 - gap>7.5 mmHg(1 kPa)(32.5±37.5对1.7±1.3 ng/ml,p<0.01)时,IL - 6水平最高。在相同的pHi阈值下,内毒素水平无差异。从第12小时起,乳酸浓度可预测预后(9.5±5.9对3.6±2.3 mmol/l,p<0.05)。
在严重失血性休克期间,肠道内毒素移位是一种常见现象,似乎与pHi值和预后均无关。它无法解释IL - 6和TNFα的释放。在严重失血性休克中,pHi和PCO2 - gap均未提供比乳酸测量更多的信息。