HYPOTHERMIA Identifying hypoperfusion in hypothermic trauma patients InSpectra™ StO2 Tissue Oxygenation Monitor predicts hypoperfusion, even in hypothermic trauma patients1 Hypothermia (core body temperature of 35°C or less) is common in severely injured trauma patients, contributing to poor tissue perfusion and shock. In the treatment of trauma patients, hypothermia is recognized as a significant risk factor for grave complications, including multiple organ dysfunction syndrome (MODS) and mortality.1,2 Analysis of the 2004 National Trauma Bank found hypothermic trauma patients had significantly greater mortality (25.5% vs. 3.0%, P < 0.001) compared to normothermic trauma patients.2 The study also found that hypothermic patients had greater base deficits (BD), higher injury severity scores (ISS), and longer lengths of stay in the hospital.2 These findings support the need to rapidly resolve hypothermia during initial resuscitation of trauma patients. When trauma patients are hypothermic, inadequate tissue perfusion can be difficult to identify and assess. Despite significant advancements in medical technology, direct assessment of adequate oxygen delivery to body tissues can be challenging. Clinical measures traditionally used to identify, monitor and track hypoperfusion include blood pressure, BD and serum lactate.3–5 These methods are widely accepted and studies have validated their use in predicting MODS and mortality; however, they have limitations. Lactate and BD are intermittent measures, may be normal in early shock and are affected by some preexisting medical conditions.6 In addition, as indicators of global perfusion, blood pressure, BD and lactate levels may not always be sensitive to peripheral hypoperfusion.6 Better indicators of hypoperfusion, along with early identifiers of shock, are critical to initiating appropriate therapeutic interventions that may result in better clinical outcomes for the patient. artery vein Microcirculation Arterial oxygen saturation Arteriole Capillaries SaO2 SpO2 Venule Venous oxygen saturation ScvO2* SvO2* InSpectra StO2 Tissue oxygen saturation *Measures of venous oxygen saturation in central venous, heart or pulmonary artery locations. Figure 1. The InSpectra StO2 measures hemoglobin oxygen saturation in the microcirculation where oxygen is exchanged with tissue.7 Noninvasive measurement of tissue oxygen saturation in trauma patients The InSpectra™ StO2 Tissue Oxygenation Monitor uses near-infrared light to provide continuous, noninvasive measurement of tissue oxygen saturation (StO2) in the microcirculation of the thenar eminence as a surrogate for global perfusion. InSpectra StO2 is a measure of hemoglobin oxygen saturation primarily in the microcirculation where oxygen is exchanged. The InSpectra StO2 Monitor assesses tissue oxygenation and, therefore, tissue perfusion status, even when pulsatile flow is diminished during hypothermia and hypotension. The normal thenar InSpectra StO2 value in adults is 72–95%.7 Tissue oxygen saturation is as sensitive an indicator of perfusion status as BD8 and lactate.6 A study of 383 patients presenting to 7 Level I trauma centers in the United States and Canada was conducted to determine if InSpectra StO2 measurements could identify hypoperfusion, detect tissue oxygenation changes during resuscitation and predict MODS development or mortality. Monitoring with InSpectra StO2 on the thenar eminence was started within 30 minutes of arrival at the Emergency Department and continued for 24 hours. Clinicians were blinded to InSpectra StO2 results. Assessment of minimum InSpectra StO2 values obtained during the first hour of ED arrival found that InSpectra StO2 levels below 75% were a significant early predictor of MODS and mortality and may indicate serious hypoperfusion in trauma patients.8 Data revealed that 78% of patients who developed MODS and 91% of patients who died had InSpectra StO2 values below 75% during the first hour after arrival in the ED. InSpectra StO2 values above 75% indicate adequate perfusion; trauma patients who maintained InSpectra StO2 readings above 75% within the first hour of ED arrival had an 88% chance of MODS-free survival. In addition, the study showed minimum InSpectra StO2 performed similarly to BD and systolic blood pressure in predicting the likelihood of a bad outcome (MODS or death). StO2 Lactate Base Deficit Tissue Oxygen Saturation (%) 100 3.0 95 2.0 90 1.0 85 0.0 80 75 –1.0 70 –2.0 65 –3.0 60 E PR IN DU I CT O PO N ST IN DU I CT O N ST ER TO NO M Y A ST RT B CP B CP 30 M IN RE A W RM IN G O FF B CP O CL SU RE Arterial Lactate (mmoI/L) and Base Deficit (mEq/L) HYPOTHERMIA Figure 2. Variation of tissue oxygen saturation (StO2), arterial lactate and base deficit (BD) over stage of procedure.9 InSpectra StO2 Tissue Oxygenation Monitor detects subtle changes in oxygen delivery Changes in tissue perfusion may precede global indications of shock. To evaluate the ability of the InSpectra StO2 Monitor to detect subtle changes in tissue oxygenation in a controlled model of altered perfusion, InSpectra StO2 was studied in 40 patients undergoing cardiopulmonary bypass (CPB).9 Vital signs, invasive blood pressure readings and body temperature were recorded at 5-minute intervals. Blood samples were obtained at key points during surgery and every 30 minutes while on CPB. Clinicians were blinded to InSpectra StO2 readings. Study data were grouped by specific stage of the CPB procedure. Variations in InSpectra StO2, arterial lactate and BD over the course of surgery are shown in Figure 2. A decrease in InSpectra StO2 readings from 90% (7%) to 77% (17%) corresponded to a delayed lactate increase of 275.6% (221.9%) from baseline. The minimum InSpectra StO2 value preceded the maximum lactate level by mean time of 93.9 minutes (86.3 minutes). In this study, the InSpectra StO2 Monitor reliably detected subtle changes in oxygen delivery to skeletal muscle tissue. These changes were identified in real time and preceded the development of abnormal lactate levels. While a predictive relationship between InSpectra StO2 and BD was not identified, changes in InSpectra StO2 measurements temporally preceded changes in BD. In addition, study data support a previous finding7 that temperature does not influence InSpectra StO2 readings. These results suggest tissue oxygen saturation can play an important role in screening critically ill and injured patients at risk for hypoperfusion. Hypothermia has no effect on the InSpectra StO2 Monitor’s ability to assess perfusion Hypoperfusion may be difficult to identify in hypothermic trauma patients. To assess the influence of mild hypothermia and rewarming on InSpectra StO2 measurements, tissue oxygen saturation was studied in six young, healthy volunteers under general anesthesia.10 In this observational study, each volunteer’s core body temperature was cooled from approximately 36°C to a target temperature of 34°C, similar to mild hypothermia in elective cardiac surgery patients. Core temperature was maintained at approximately 34°C for 1 hour before each volunteer was rewarmed. Tissue oxygen saturation readings were obtained at 5 temperature means (SD): 36.5°C (0.5), 35.5°C (0.5), 34.5°C (0.5), 35.5°C (0.5), and 36.5°C (0.5). The means (SD) of InSpectra StO2 at each temperature were 73% (8%), 71% (11%), 67% (14%), 68% (11%), and 74% (7%). Statistically significant changes in InSpectra StO2 (P < 0.05) were found at the end of cooling and rewarming. The InSpectra StO2 Monitor detects changes in tissue oxygen saturation during mild hypothermia and rewarming. High inter-individual variability occurred during mild hypothermia, suggesting people respond differently to hypothermia. HYPOTHERMIA InSpectra StO2 identifies hypoperfusion and predicts MODS in hypothermic trauma patients The relationship of early hypothermia to MODS and mortality among severely injured trauma patients was studied in a prospective observational study at 7 Level I trauma centers in the United States and Canada.2 Severely injured patients with hypoperfusion and need for blood transfusion were monitored via the InSpectra StO2 and using traditional clinical variables. Among 359 severely injured trauma patients, hypothermia was common (43%), regardless of geographic location or month of year. Hypothermic patients were more likely than normothermic patients to develop MODS (21% vs. 9%, P = 0.003), but did not have increased mortality rates (16% vs. 12%, P = 0.28). In hypothermic patients, maximum base deficit (max BD) did not discriminate between those who did or did not develop MODS, but did predict mortality. Significant predictors of MODS included minimum InSpectra StO2 (P = 0.0002) and hypothermia (P = 0.01), but not max BD (P = 0.09). Predictors for mortality included InSpectra StO2 (P = 0.0004) and max BD (P = 0.01), but not hypothermia (P = 0.74). Hypothermia is a risk factor for multiple organ failure, but not mortality. Minimum InSpectra StO2 predicts MODS and mortality in normothermia and hypothermic patients. However, the ability of max BD to predict MODS was blunted by hypothermia. To learn more about the InSpectra StO2 Tissue Oxygenation Monitor, its unique ability to monitor hypoperfusion in hypothermic patients and studies on the use of InSpectra StO2 in trauma patients, visit www.htibiomeasurement.com. References 1.Martin RS, Kilgo PD, Miller PR, Hoth JJ, Meredith JW, Chang MC. Injury-associated hypothermia: an analysis of the 2004 National Trauma Data Bank. Shock. 2005;24:114–118. 2.Beilman GJ, Nelson T, Nathens AB, et al. Early hypothermia in severely injured trauma patients is a significant risk factor for multiple organ dysfunction syndrome but not mortality [abstract]. Crit Care. 2007;11(suppl 2):S139. Abstract P345. 3.Davis JW, Shackford SR, Holbrook TL. Base deficit as a sensitive indicator of compensated shock and tissue oxygen utilization. Surgery. 1991;173:473–476. 4.Englehart MS, Schreiber MA. Measurement of acid-base resuscitation endpoint: lactate, base deficit, bicarbonate or what? Curr Opin Crit Care. 2006;12:569–574. 5.Moore FA, McKinley BA, Moore EE. The next generation in shock resuscitation. Lancet. 2004;363(9425):1988–1996. 6.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. 7.Crookes BA, Cohn SM, Bloch S, et al. Can near-infrared spectroscopy identify the severity of shock in trauma patients? J Trauma. 2005;58:1119–1125. 8.Cohn SM, Nathens AB, Moore FA, et al. Tissue oxygen saturation predicts the development of organ dysfunction during traumatic shock resuscitation. J Trauma. 2007;62:44–55. 9.Putnam B, Bricker S, Fedorka P, et al. The correlation of nearinfrared spectroscopy with changes in oxygen delivery in a controlled model of altered perfusion. Am Surg. 2007;73:1017–1022. 10.Ali SZ, Taniguchi Y, Zmoos S, Kurz A. Influence of mild hypothermia and rewarming on near infrared spectroscopy derived tissue oxygen saturation [abstract]. Eur J Anaesthesiol. 2006;23 (suppl S37):216. Abstract A-837. HYPOTHERMIA Case Study: Continuous Tissue Oxygenation (InSpectra™ StO2) Monitoring During Resuscitation BD, HgB, Lactate InSpectra™ StO2, SpO2, SBP, DBP, HR, Temp °C • An intoxicated male in his 30s was ejected from a vehicle during a high-speed crash • Patient presented with hypothermia, Grade IV splenic laceration, grade I renal laceration, left hemopneumothorax, and left femur fracture (fx) upon arrival at the trauma center • InSpectra StO2 measurements ranged from 53% to 64% despite splenic artery embolization and active rewarming • InSpectra StO2 readings increased above 75% after additional units of packed red blood cells (PRBC), fresh frozen plasma (FFP) and cryoprecipitate were administered 160 T.C. arrival by To IR helicopter embolization 140 To ICU To CT 120 100 80 60 Bolus 2L LR 1u PRBC 40 1u PRBC FFP Cryo Normothermia Active warming starts 20 Hypothermia 20 10 0 8:00 9:00 10:00 11:00 12:00 13:00 14:00 15:00 16:00 Time InSpectra™ StO2 HgB Lac SpO2 SBP Temp °C DBP HR BD Event Markers Disclaimer This case was taken from a prospective multi-site study sponsored by Hutchinson Technology Inc. in which clinicians were blinded to InSpectra StO2 measurements.1 This case represents an example of a compromised circulation situation where the InSpectra StO2 monitor’s general indications apply. It is one of several hundred cases from a multi-site, prospective, observational clinical study and is not intended to represent the general findings of the study. Reference 1. Cohn SM, Nathens AB, Moore FA, et al. Tissue oxygen saturation predicts the development of organ dysfunction during traumatic shock resuscitation. J Trauma. 2007;62:44–55. Hutchinson Technology Inc. BioMeasurement Division – USA Authorized European Representative European Business Office – Netherlands tel: 800.419.1007 fax:320.587.1555 biom.usa@hti.htch.com www.htibiomeasurement.com tel: +31 26 365 33 71 fax:+31 26 365 33 72 biom.eu@hti.htch.com Intended Use The InSpectra™ StO2 Tissue Oxygenation Monitor is intended for use as a noninvasive monitoring system that measures an approximated value of percent hemoglobin oxygen saturation in tissue (StO2). InSpectra is a registered trademark of Hutchinson Technology Inc. in the United States of America, the European Community, Canada, China and Japan. ©2008 Hutchinson Technology Inc. 5018782 A 06/08 All Rights Reserved. Printed in the USA. RX ONLY. 0086