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Heyer L, Madadaki C, Rezlan E, Welschbillig S, Mateo J, Payen D. Int Care Med. 2006;32(Supp 1):S254. Abstract 0982.
Introduction: We study the micro-oxygenation dysfunction in septic and haemorrhagic shock patients.
Methods: 29 consecutive septic shock patients (SEPSIS) and 13 severe post-partum haemorrhagic shock women (HAEMORRHAGE) were studied at ICU admission. Tissue oxygenation and perfusion of thenar muscle were assessed using near infrared spectrometry technique (NIRS). Tissue O2 saturation was measured at baseline (StO2) and following forearm arterial occlusion. The slope of the decrease in StO2 during occlusion (S-Occ), the slope of the increase in StO2 following occlusion release (S-Release) and the deficit of post-ischemic oxygenation recruitment (Deficit) were used to characterise micro-vascular pathway function. Values obtains in a control group of 10 subjects (CONTROL) were used for comparison. The severity of post-partum haemorrhagic shock was defined by a Troponin I value above 0.08 ng/ml.
Results: StO2 values were lower in both groups of patients with shock:* p< 0.05 ** p<0.01 *** p<0.0001 between CONTROL and HAEMORRHAGE; § p<0.001 §§ p<0.0001 between CONTROL and SEPSIS; £ p < 0.01 between HAEMORRHAGE and SEPSIS.
Table 1:
|
CONTROL mean (SD) |
HAEMORRHAGE mean (SD) |
SEPSIS mean (SD) |
Anova p | |
|
StO2 (%) |
91 (3) |
77 (12) * |
80 (9) § |
< 0.01 |
|
S-Occ (%/s) |
-0.4 (0.2) |
-0.2 (0.1) ** |
-0.4 (0.2) £ |
< 0.004 |
|
S-Release (%/s) |
10 (2) |
3 (2) *** |
2 (1) §§ |
< 0.0001 |
|
Deficit (%) |
2 (0) |
10 (11) * |
9 (10) § |
< 0.08 |
Conclusion: StO2 measurements in combination to a transient arterial occlusion test demonstrate differential micro-vascular pathway adaptation accordingly to shock aetiology. In septic shock patients, the decrease in StO2 remains normal while it is impaired in haemorhagic shock patients. This discrepancy support evidence of an oxygen delivery failure at the muscle level as it could also be inferred from Troponin I elevation. The reperfusion is impaired in the two groups of patients with a decrease of vascular post-ischemic recruitment.
Grant acknowledgement: supported by HUTCHINSON Technology Inc.