(Also see FAQ: What is the relationship between InSpectra StO2and base deficit or excess?)
Summary
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InSpectra StO2 |
Lactate |
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Direct measure of the adequacy of oxygen available to tissues? |
Yes, percent hemoglobin oxygen saturation measured primarily in the microcirculation, where oxygen is delivered to tissue cells |
No, accumulates in tissue and blood as a result of inadequate oxygen available to tissue and physiological events unrelated to impaired oxygenation e.g. impaired liver function |
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Noninvasive? |
Yes |
No, blood sample, often arterial |
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Continuous measurement? |
Yes |
No |
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Measurement update frequency? |
Continuous measurement with 2-second updates |
Measurement availability variable dependent on hospital practice e.g. 15-minute to 4-hour intervals |
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Used for clinical assessment of |
Oxygen availability to tissue cells, i.e. tissue perfusion status or tissue oxygenation |
Systemic accumulation of anaerobic metabolite caused by tissue hypoperfusion somewhere in the patient |
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Predicts bad patient outcome? |
Yes, <75% InSpectra StO2 in the first hour of ED arrival predicts MODS and death in trauma patients 8 |
Yes, lactate values that fail to clear in 24 hours are predictive of mortality 5 |
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Changes with onset of shock? |
Yes, InSpectra StO2 changes real-time with changes in tissue perfusion 9 |
Yes, lactate changes as a result of inadequate oxygen available to tissue cells and restoration of adequate oxygen. There may be a lag in both the accumulation and clearance of lactate that does not reflect the patient’s status real-time |
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Responds to interventions targeted at improving tissue perfusion status? |
Yes, immediate, real-time response to interventions that improve perfusion status9 |
Yes, but lactate may continue to increase and/or take minutes to hours to clear after restoration of adequate tissue oxygenation |
Background
InSpectra StO2 is a measure of percent hemoglobin oxygen saturation primarily in the capillaries, venules, and arterioles of the microcirculation of peripheral tissue, usually in the muscle of the thenar eminence (muscle at base of thumb). The microcirculation is where oxygen leaves hemoglobin to meet the oxygen demand of tissue cells. InSpectra StO2 therefore changes dynamically with changes in oxygen delivery to the tissue and oxygen consumption by the tissue. Changes in tissue perfusion status caused by reduced blood flow to peripheral muscle, such as hemorrhage, result in direct, real-time changes in InSpectra StO2.9
Lactate is a natural byproduct of glycolysis and is normally present in the blood in unstressed patients at a concentration of 1.0±0.5mmol/L.1,2 Blood lactate elevations in hemorrhagic shock patients have been associated with tissue hypoperfusion, inadequate tissue oxygenation and anaerobic metabolism.3 Serum lactate levels >5mmol/L indicate lactic acidosis and are associated with major metabolic dysregulation. However, hyperlactatemia (2-5mmol/L) may also occur in critically-ill patients (trauma, burns and sepsis) whose tissues are adequately oxygenated.2
There are a variety of confounding factors that affect lactate levels. Luchette and colleagues found that elevated blood lactate during hemorrhage and resuscitation may result from increased levels of epinephrine not just tissue hypoxia or anaerobic metabolism.3 Lactic acidosis has been classified into two categories: Type A in association with poor tissue perfusion and Type B when there is adequate tissue oxygenation. Diabetes mellitus, liver disease, sepsis, alcohol (ethanol), epinephrine, and cocaine are among the causes of lactic acidosis when there is adequate tissue oxygenation (Type B).2
Despite the potential confounding factors in interpreting elevated lactate, it is commonly used to assess hypoperfusion and as a marker for adequate resuscitation in trauma patients. Abramson found that patients whose lactate levels cleared (returned to normal range) within 24 hours had a higher probability of survival.5 Mizock also showed that patients who did not survive failed to clear lactate in the first 18 hours after injury.2 Interestingly, Mizock also found that it took 18 hours for lactate to decrease to half it’s initial value after fluid resuscitation completion in hypovolemic and septic shock patients.
Resuscitating patients solely to lactate values led James to hypothesize that
“. . . continued attempts at resuscitation based on elevated lactate levels may lead to unnecessary use of blood transfusion and inotropic agents . . .”
after other indicators of perfusion have returned to normal.4
Relationship of InSpectra StO2 and lactate
InSpectra StO2 and lactate have been compared in several studies.
· Beilman found in a porcine model of hemorrhagic shock that InSpectra StO2 returned to baseline within the first 15 minutes of resuscitation, while lactate remained elevated at 45 minutes after resuscitation.6
· McKinley studied eight severely injured trauma patients and found a statistically significant correlation (r=0.82 and p =<0.05) between the means of InSpectra StO2 and lactate during the 24 hours of resuscitation and for the 12 hours following resuscitation.7
· In a follow-up analysis of the InSpectra StO2 Trauma Study, Moore found StO2 < 75% and lactate > 4 mmol/L in the first hour of hospital arrival were equally predictive of Multiple Organ Dysfunction Syndrome (MODS) and mortality.8
· Putnam and colleagues studied the relationship of InSpectra StO2 and lactate in patients undergoing cardiac bypass and found that “StO2 normalized before the clearance of lactate, further suggesting that tissue oxygen saturation provides more timely information regarding a return to normal levels of tissue perfusion.”9
In summary, InSpectra StO2 and lactate compare favorably as clinically significant markers of the onset of hypoperfusion. The primary differences are evident during and upon completion of resuscitation. InSpectra StO2 is a direct measure of tissue oxygenation and therefore tissue perfusion status. InSpectra StO2 responds in real-time to interventions targeted to improve perfusion, while lactate clearance lags behind, potentially resulting in unnecessary interventions.
References
1. DeBacker D. Lactic acidosis. Minerva Anestesiologica.2003;69(4):281-284.
2. Mizock B, Falk J. Lactic acidosis in critical illness. Crit Care Med.1992;20(1):80-93.
3. Luchette F, Jenkins A, Friend LA, Su C, Fischer J, James H. Hypoxia is not the sole cause of lactate production during shock. J Trauma. 2002;52(3):415-419.
4. James JH, Luchette F, McCarter F, Fischer J. Lactate is an unreliable indicator of tissue hypoxia in injury or sepsis. The Lancet.1999;354:505-508.
5. Abramson D, Scalea T, Hitchcock R, Trooskin S, Henry S, Greenspan J. Lactate clearance and survival following injury. J Trauma.1993;35(4):584-589.
6. Beilman G, Groehler K, Lazaron V, Ortner J. Near-Infrared Spectroscopy Measurement of Regional Tissue Oxyhemoglobin Saturation During Hemorrhagic Shock. Shock. 1999;12(3):196-200.
7. McKinley B, Marvin R, Cocanour C, Moore F. Tissue hemoglobin O2 saturation during resuscitation of traumatic shock monitored using near infrared spectroscopy. J Trauma. 2000;48(4):647-642.
8. Moore FA. Tissue oxygen saturation predicts the development of organ failure during traumatic shock resuscitation. In: Faist, E, ed. International Proceedings of the 7th World Congress on Trauma, Shock, Inflammation and Sepsis; Munich, Germany, 13-17 March 2007. Bologna, Italy: Medimond; 2007:111–114.
9. Putnam B, Bricker S, Fedorka P, Zelada J, Shebrain S, Omari B, Bongard F. The correlation of near-infrared spectroscopy with changes in oxygen delivery in a controlled model of altered perfusion. Am Surg. 2007;73(10):1017-22.