- Email: [email protected]
Measuring the Physiologic Response to Traumatic Injury
TRAUMA NOTEBOOK
MEASURING
PHYSIOLOGIC RESPONSE TRAUMATIC INJURY
THE
TO
Author: Kathryn Moore, DNP, RN, FCCM, CCRN, CEN, ACNP-BC, ANP-BC, GNP-BC, Atlanta, GA Section Editor: Kathryn Moore, DNP, RN, FCCM, CCRN, CEN, ACNP-BC, ANP-BC, GNP-BC
Earn Up to 8.5 CE Hours. See page 92. n the November 2014 issue of JEN, issue, the physiology of trauma was described in this column. This article will address the issues related to problems surrounding the identification of specific and optimal criteria on which to base effective triage decisions for trauma patients based on the physiology of the injury. The trauma community has not yet clearly identified the factors that predict which patients should be transported to a trauma center. 1 There have been no prospective randomized controlled trials upon which to base criteria necessary for appropriate early triage in either phase. The prospective and retrospective data analyses available demonstrate a combination of physiologic and anatomic parameters that provided the most accurate trauma triage information. 1 The current instruments used to triage trauma patients include the Revised Trauma Score, the Abbreviated Injury Score, the Injury Severity Score, and the Trauma Score-Injury Severity Score. These scores include both physiologic and anatomic criteria. Trauma patients often have multiple, complex injuries that may not fully manifest until later in the course of treatment. Hemorrhage due to trauma injuries may be obvious; however, more insidious internal hemorrhage may be masked by compensatory mechanisms, making triage difficult. The existing instrument scores do not provide the information needed to make decisions early in the management of patients with multiple trauma injuries. This discussion will examine potential triage markers from among anatomic, physiologic, and mechanism of injury information available at the time of admission to the emergency department. Based on existing literature and on the physiology of compensated hemorrhagic
I
Kathryn Moore is Associate Professor, Clinical, Nell Hodgson Woodruff School of Nursing, Emory University, Atlanta, GA. For correspondence, write: Kathryn Moore, DNP, RN, FCCM, CCRN, CEN, ACNP-BC, ANP-BC, GNP-BC, Nell Hodgson Woodruff School of Nursing, Emory University, Office 348, 1520 Clifton Road NE, Atlanta, GA 30322; E-mail: [email protected]. J Emerg Nurs 2015;41:86-8. Available online 11 November 2014 0099-1767 Copyright © 2015 Emergency Nurses Association. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jen.2014.10.002
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shock, the following parameters have the potential to provide additional information in the triage process: (1) the Shock Index; (2) age in years; (3) blood glucose level; (4) arterial base deficit; (5) serum lactate level; (6) need for mechanical ventilation; (7) fraction of inspired oxygen (FIO2); (8) endtidal carbon dioxide (ETCO2); and (9) need for blood administration. Most of the additional parameters to be explored are physiologic measures because the physiologic measures are the indicators of individual differences in patients. 2 The flaw of the existing triage models is the lack of reliance on all the available physiologic parameters. The model most used in the field is the Revised Trauma Score, which relies only on respiratory rate, systolic blood pressure (SBP), and the Glasgow Coma Score. 3 The physiologic response to trauma is complex and includes a neuro-endocrine response and an inflammatory mediator response. In the assessment of the multi-trauma patient, it is important to consider that many physiologic mediator systems have been activated and can modify both the character and magnitude of the physiologic response. 2 The Shock Index will be examined because it is an indicator of hemodynamic instability. Allgower and Burri (1967) first explored a mathematical quotient derived from the heart rate (HR) divided by the SBP as a more sensitive indicator of hemodynamic instability, or the Shock Index; this Dutch study was described in English by Rady and colleagues in 1992. 4 The Shock Index is a calculation of HR divided by SBP and is normally 0.5 to 0.7. The Shock Index has been shown to be elevated in the setting of acute hypovolemia and left ventricular dysfunction, both of which are elements of shock. 4–6 The Shock Index has been documented as being useful as an early predictor of shock in persons with uncontrolled hemorrhage, ruptured ectopic pregnancy, gastrointestinal bleeding, sepsis, and trauma. 4,7–9 A 2004 study using healthy volunteers found the Shock Index to be more useful in the recognition of hemodynamic response to early acute blood loss of less than 450 mL than either HR or SBP alone. 10 The Shock Index also provides insight into occult tissue hypoperfusion. Occult hypoperfusion is defined as hypoperfusion in the face of normal vital signs and is associated with increased hospital length of stay and increased
VOLUME 41 • ISSUE 1
January 2015
Moore/TRAUMA NOTEBOOK
mortality in trauma patients. 11 Trauma outcomes are improved with early rapid stabilization and correction of hypoperfusion. Occult hypoperfusion is difficult to detect immediately after severe trauma and is responsible for inadequate organ perfusion, leading to ischemic injury and tissue hypoxia. 12 Occult hypoperfusion is often masked by normal vital signs, most notably the SBP and pulse rate. 13 The error of solely relying on pulse rate and blood pressure in persons with occult hypoperfusion results in under-resuscitation, increased length of hospital stay, and increased morbidity and mortality in the trauma patient. 12–14 Hypoperfusion is related to hypovolemic shock, the hallmark of which is the loss of intravascular volume. 15 This loss of intravascular volume leads to decreased venous return and decreased preload, which decreases stroke volume and cardiac output. The compensatory mechanisms for maintaining adequate perfusion are tachycardia and elevated systemic vascular resistance. 15 Occult hypoperfusion is detected by measures of lactic acidosis, including serum lactate, serum bicarbonate, and arterial base deficit. 12,14,16 This state of lactic acidosis is commonly measured in trauma care with the laboratory values of serum lactate and arterial base deficit. 17,18 The literature has evaluated the utility of base deficit and serum lactate as markers of early tissue hypoperfusion in trauma patients evaluated within the first 48 hours after traumatic injuries and found it to be useful, 19 but it still is not used regularly in practice because of the use of more traditional approaches such as mean arterial pressure, SBP, central venous pressure, and serum bicarbonate by the trauma community. In a sentinel work performed by Rutherford and colleagues 17 at Vanderbilt University in 1992, base deficit was found to be “an expedient and sensitive measure of both the degree and duration of inadequate tissue perfusion.” This work has been cited in many of the follow-up studies that have been performed to examine base deficit as a marker of hypoperfusion and shock. A 1998 study evaluated arterial base deficit in trauma patients and found a persistently high arterial base deficit to be associated with altered oxygen utilization. 20 Base deficit has continued to perform well in the literature as a marker of hypoperfusion and shock and as a predictor of mortality and morbidity in trauma patients. It has been shown to be a useful guide in the resuscitation of trauma patients and in diagnosing significant abdominal injury, tissue oxygen use, and compensated shock. 18,19,21,22 Glucose can be considered a parameter because early hyperglycemia is independently associated with significantly higher infection and mortality rates in trauma patients. 23,24 The presence of hyperglycemia at the time of admission
January 2015
VOLUME 41 • ISSUE 1
appears to correlate with higher mortality and greater morbidity in trauma patients. 24,25 In addition to predicting poor outcomes in trauma patients, elevation of serum glucose levels at admission may be an indicator of inadequate resuscitation in trauma patients. 26 ETCO2 or capnography provides information about respiratory status, presence of hypoxia, CO2 production, and pulmonary perfusion and is an indirect measure of cardiac output. 27,28 ETCO2 is included as a physiologic variable in the 2010 American Heart Association resuscitation guidelines. 29 Blood administration in trauma is an indicator of injury severity. Patients presenting with massive hemorrhage may require the initiation of a massive transfusion protocol. Patients receiving transfusion of blood products generally have better outcomes than those not receiving a transfusion. 30 By examining these additional parameters that are not generally relied on in the early phase of trauma care in the emergency department, we may well be able to add to the opportunities to more quickly identify injury severity and the potential for morbidity and mortality in the trauma population. Additional information will provide a more complete picture of the severity of the trauma patient earlier in the process of patient care with a hope of improving patient outcomes.
REFERENCES 1. The EAST Practice Management Guidelines Work Group. Triage of the trauma patient. http://www.east.org/resources/treatmentguidelines/triage-of-the-trauma-patient. Published 2010. Accessed October 15, 2014. 2. Peitzman AB, Billiar TR, Harbrecht BG, Kelly E, Udekwu AO, Simmons RL. Hemorrhagic shock. Curr Probl Surg. 1995;32(11): 925-1002. 3. Moore L, Lavoie A, LeSage N, et al. Statistical validation of the Revised Trauma Score. J Trauma. 2006;60(2):305-311. 4. Rady MY, Nightingale P, Little RA, Edwards JD. Shock index: a reevaluation in acute circulatory failure. Resuscitation. 1992;23(3):227-234. 5. Rady MY. The role of central venous oximetry, lactic acid concentration and shock index in the evaluation of clinical shock: a review. Resuscitation. 1992;24(1):55-60. 6. Keller AS, Kirkland LL, Rajasekaran SY, Cha S, Rady MY, Huddleston JM. Unplanned transfers to the intensive care unit: the role of the shock index. J Hosp Med. 2010;5(8):460-465. 7. Hillman KM, Bristow PJ, Chey T, et al. Antecedents to hospital deaths. Intern Med J. 2001;31(6):343-348. 8. Cao H, Eshelman L, Chbat N, Nielsen L, Gross B, Saeed M. Predicting ICU hemodynamic instability using continuous multiparameter trends. Conf Proc IEEE Eng Med Biol Soc. 2008;2008:3803-3806.
WWW.JENONLINE.ORG
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9. Jaramillo S, Barnhart K, Takacs P. Use of the shock index to predict ruptured ectopic pregnancies. Int J Gynaecol Obstet. 2011;112(1):68.
21. Davis JW, Shackford SR, Mackersie RC, Hoyt DB. Base deficit as a guide to volume resuscitation. J Trauma. 1988;28(10):1464-1467.
10. Birkhahn RH, Gaeta TJ, Terry D, Bove JJ, Tloczkowski J. Shock index in diagnosing early acute hypovolemia. Am J Emerg Med. 2005;23(3): 323-326.
22. Chang MC, Rutherford EJ, Morris JAJr.. Base deficit as a guide to injury severity and volume resuscitation. J Tenn Med Assoc. 1993;86(2):59-61.
11. Thom O, Taylor DM, Wolfe RE, Myles P, Krum H, Wolfe R. Pilot study of the prevalence, outcomes and detection of occult hypoperfusion in trauma patients. Emerg Med J. 2010;27(6):470-472. 12. Blow O, Magliore L, Claridge JA, Butler K, Young JS. The golden hour and the silver day: detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma. J Trauma. 1999;47(5):964-969. 13. Meregalli A, Oliveira RP, Friedman G. Occult hypoperfusion is associated with increased mortality in hemodynamically stable, highrisk, surgical patients. Crit Care. 2004;8(2):R60-R65. 14. Claridge JA, Crabtree TD, Pelletier SJ, Butler K, Sawyer RG, Young JS. Persistent occult hypoperfusion is associated with a significant increase in infection rate and mortality in major trauma patients. J Trauma. 2000;48(1):8-14. discussion 14–15. 15. Guyton AC, Hall JE. Textbook of Medical Physiology. 11th ed., Philadelphia, PA: Elsevier Saunders; 2006. 16. Howell MD, Donnino M, Clardy P, Talmor D, Shapiro NI. Occult hypoperfusion and mortality in patients with suspected infection. Intensive Care Med. 2007;33(11):1892-1899.
23. Laird AM, Miller PR, Kilgo PD, Meredith JW, Chang MC. Relationship of early hyperglycemia to mortality in trauma patients. J Trauma. 2004;56(5):1058-1062. 24. Bochicchio GV, Salzano L, Joshi M, Bochicchio K, Scalea TM. Admission preoperative glucose is predictive of morbidity and mortality in trauma patients who require immediate operative intervention. Am Surg. 2005;71(2):171-174. 25. Shin S, Britt RC, Reed SF, Collins J, Weireter LJ, Britt LD. Early glucose normalization does not improve outcome in the critically ill trauma population. Am Surg. 2007;73(8):769-772. 26. Duane TM, Dechert T, Dalesio N, et al. Is blood sugar the next lactate?. Am Surg. 2006;72(7):613-617. discussion 617–618. 27. Monnet X, Teboul JL. End-tidal carbon dioxide and arterial pressure for predicting volume responsiveness by the passive leg raising test: reply to Piagnerelli and Biston. Intensive Care Med. 2013;39(6):1165. 28. Monnet X, Julien F, Ait-Hamou N, et al. Lactate and venoarterial carbon dioxide difference/arterial-venous oxygen difference ratio, but not central venous oxygen saturation, predict increase in oxygen consumption in fluid responders. Crit Care Med. 2013;41(6):1412-1420.
17. Rutherford EJ, Morris JAJr., Reed GW, Hall KS. Base deficit stratifies mortality and determines therapy. J Trauma. 1992;33(3):417-423.
29. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S729-S767.
18. Davis JW, Shackford SR, Holbrook TL. Base deficit as a sensitive indicator of compensated shock and tissue oxygen utilization. Surg Gynecol Obstet. 1991;173(6):473-476.
30. Nunez TC, Young PP, Holcomb JB, Cotton BA. Creation, implementation, and maturation of a massive transfusion protocol for the exsanguinating trauma patient. J Trauma. 2010;68(6):1498-1505.
19. Davis JW, Mackersie RC, Holbrook TL, Hoyt DB. Base deficit as an indicator of significant abdominal injury. Ann Emerg Med. 1991;20(8):842-844. 20. Kincaid EH, Miller PR, Meredith JW, Rahman N, Chang MC. Elevated arterial base deficit in trauma patients: a marker of impaired oxygen utilization. J Am Coll Surg. 1998;187(4):384-392.
88
JOURNAL OF EMERGENCY NURSING
Submissions to this column are encouraged and may be sent to Kathryn Moore, DNP, RN, FCCM, CCRN, CEN, ACNP-BC, ANP-BC, GNP-BC [email protected]
VOLUME 41 • ISSUE 1
January 2015
MEASURING
PHYSIOLOGIC RESPONSE TRAUMATIC INJURY
THE
TO
Author: Kathryn Moore, DNP, RN, FCCM, CCRN, CEN, ACNP-BC, ANP-BC, GNP-BC, Atlanta, GA Section Editor: Kathryn Moore, DNP, RN, FCCM, CCRN, CEN, ACNP-BC, ANP-BC, GNP-BC
Earn Up to 8.5 CE Hours. See page 92. n the November 2014 issue of JEN, issue, the physiology of trauma was described in this column. This article will address the issues related to problems surrounding the identification of specific and optimal criteria on which to base effective triage decisions for trauma patients based on the physiology of the injury. The trauma community has not yet clearly identified the factors that predict which patients should be transported to a trauma center. 1 There have been no prospective randomized controlled trials upon which to base criteria necessary for appropriate early triage in either phase. The prospective and retrospective data analyses available demonstrate a combination of physiologic and anatomic parameters that provided the most accurate trauma triage information. 1 The current instruments used to triage trauma patients include the Revised Trauma Score, the Abbreviated Injury Score, the Injury Severity Score, and the Trauma Score-Injury Severity Score. These scores include both physiologic and anatomic criteria. Trauma patients often have multiple, complex injuries that may not fully manifest until later in the course of treatment. Hemorrhage due to trauma injuries may be obvious; however, more insidious internal hemorrhage may be masked by compensatory mechanisms, making triage difficult. The existing instrument scores do not provide the information needed to make decisions early in the management of patients with multiple trauma injuries. This discussion will examine potential triage markers from among anatomic, physiologic, and mechanism of injury information available at the time of admission to the emergency department. Based on existing literature and on the physiology of compensated hemorrhagic
I
Kathryn Moore is Associate Professor, Clinical, Nell Hodgson Woodruff School of Nursing, Emory University, Atlanta, GA. For correspondence, write: Kathryn Moore, DNP, RN, FCCM, CCRN, CEN, ACNP-BC, ANP-BC, GNP-BC, Nell Hodgson Woodruff School of Nursing, Emory University, Office 348, 1520 Clifton Road NE, Atlanta, GA 30322; E-mail: [email protected]. J Emerg Nurs 2015;41:86-8. Available online 11 November 2014 0099-1767 Copyright © 2015 Emergency Nurses Association. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jen.2014.10.002
86
JOURNAL OF EMERGENCY NURSING
shock, the following parameters have the potential to provide additional information in the triage process: (1) the Shock Index; (2) age in years; (3) blood glucose level; (4) arterial base deficit; (5) serum lactate level; (6) need for mechanical ventilation; (7) fraction of inspired oxygen (FIO2); (8) endtidal carbon dioxide (ETCO2); and (9) need for blood administration. Most of the additional parameters to be explored are physiologic measures because the physiologic measures are the indicators of individual differences in patients. 2 The flaw of the existing triage models is the lack of reliance on all the available physiologic parameters. The model most used in the field is the Revised Trauma Score, which relies only on respiratory rate, systolic blood pressure (SBP), and the Glasgow Coma Score. 3 The physiologic response to trauma is complex and includes a neuro-endocrine response and an inflammatory mediator response. In the assessment of the multi-trauma patient, it is important to consider that many physiologic mediator systems have been activated and can modify both the character and magnitude of the physiologic response. 2 The Shock Index will be examined because it is an indicator of hemodynamic instability. Allgower and Burri (1967) first explored a mathematical quotient derived from the heart rate (HR) divided by the SBP as a more sensitive indicator of hemodynamic instability, or the Shock Index; this Dutch study was described in English by Rady and colleagues in 1992. 4 The Shock Index is a calculation of HR divided by SBP and is normally 0.5 to 0.7. The Shock Index has been shown to be elevated in the setting of acute hypovolemia and left ventricular dysfunction, both of which are elements of shock. 4–6 The Shock Index has been documented as being useful as an early predictor of shock in persons with uncontrolled hemorrhage, ruptured ectopic pregnancy, gastrointestinal bleeding, sepsis, and trauma. 4,7–9 A 2004 study using healthy volunteers found the Shock Index to be more useful in the recognition of hemodynamic response to early acute blood loss of less than 450 mL than either HR or SBP alone. 10 The Shock Index also provides insight into occult tissue hypoperfusion. Occult hypoperfusion is defined as hypoperfusion in the face of normal vital signs and is associated with increased hospital length of stay and increased
VOLUME 41 • ISSUE 1
January 2015
Moore/TRAUMA NOTEBOOK
mortality in trauma patients. 11 Trauma outcomes are improved with early rapid stabilization and correction of hypoperfusion. Occult hypoperfusion is difficult to detect immediately after severe trauma and is responsible for inadequate organ perfusion, leading to ischemic injury and tissue hypoxia. 12 Occult hypoperfusion is often masked by normal vital signs, most notably the SBP and pulse rate. 13 The error of solely relying on pulse rate and blood pressure in persons with occult hypoperfusion results in under-resuscitation, increased length of hospital stay, and increased morbidity and mortality in the trauma patient. 12–14 Hypoperfusion is related to hypovolemic shock, the hallmark of which is the loss of intravascular volume. 15 This loss of intravascular volume leads to decreased venous return and decreased preload, which decreases stroke volume and cardiac output. The compensatory mechanisms for maintaining adequate perfusion are tachycardia and elevated systemic vascular resistance. 15 Occult hypoperfusion is detected by measures of lactic acidosis, including serum lactate, serum bicarbonate, and arterial base deficit. 12,14,16 This state of lactic acidosis is commonly measured in trauma care with the laboratory values of serum lactate and arterial base deficit. 17,18 The literature has evaluated the utility of base deficit and serum lactate as markers of early tissue hypoperfusion in trauma patients evaluated within the first 48 hours after traumatic injuries and found it to be useful, 19 but it still is not used regularly in practice because of the use of more traditional approaches such as mean arterial pressure, SBP, central venous pressure, and serum bicarbonate by the trauma community. In a sentinel work performed by Rutherford and colleagues 17 at Vanderbilt University in 1992, base deficit was found to be “an expedient and sensitive measure of both the degree and duration of inadequate tissue perfusion.” This work has been cited in many of the follow-up studies that have been performed to examine base deficit as a marker of hypoperfusion and shock. A 1998 study evaluated arterial base deficit in trauma patients and found a persistently high arterial base deficit to be associated with altered oxygen utilization. 20 Base deficit has continued to perform well in the literature as a marker of hypoperfusion and shock and as a predictor of mortality and morbidity in trauma patients. It has been shown to be a useful guide in the resuscitation of trauma patients and in diagnosing significant abdominal injury, tissue oxygen use, and compensated shock. 18,19,21,22 Glucose can be considered a parameter because early hyperglycemia is independently associated with significantly higher infection and mortality rates in trauma patients. 23,24 The presence of hyperglycemia at the time of admission
January 2015
VOLUME 41 • ISSUE 1
appears to correlate with higher mortality and greater morbidity in trauma patients. 24,25 In addition to predicting poor outcomes in trauma patients, elevation of serum glucose levels at admission may be an indicator of inadequate resuscitation in trauma patients. 26 ETCO2 or capnography provides information about respiratory status, presence of hypoxia, CO2 production, and pulmonary perfusion and is an indirect measure of cardiac output. 27,28 ETCO2 is included as a physiologic variable in the 2010 American Heart Association resuscitation guidelines. 29 Blood administration in trauma is an indicator of injury severity. Patients presenting with massive hemorrhage may require the initiation of a massive transfusion protocol. Patients receiving transfusion of blood products generally have better outcomes than those not receiving a transfusion. 30 By examining these additional parameters that are not generally relied on in the early phase of trauma care in the emergency department, we may well be able to add to the opportunities to more quickly identify injury severity and the potential for morbidity and mortality in the trauma population. Additional information will provide a more complete picture of the severity of the trauma patient earlier in the process of patient care with a hope of improving patient outcomes.
REFERENCES 1. The EAST Practice Management Guidelines Work Group. Triage of the trauma patient. http://www.east.org/resources/treatmentguidelines/triage-of-the-trauma-patient. Published 2010. Accessed October 15, 2014. 2. Peitzman AB, Billiar TR, Harbrecht BG, Kelly E, Udekwu AO, Simmons RL. Hemorrhagic shock. Curr Probl Surg. 1995;32(11): 925-1002. 3. Moore L, Lavoie A, LeSage N, et al. Statistical validation of the Revised Trauma Score. J Trauma. 2006;60(2):305-311. 4. Rady MY, Nightingale P, Little RA, Edwards JD. Shock index: a reevaluation in acute circulatory failure. Resuscitation. 1992;23(3):227-234. 5. Rady MY. The role of central venous oximetry, lactic acid concentration and shock index in the evaluation of clinical shock: a review. Resuscitation. 1992;24(1):55-60. 6. Keller AS, Kirkland LL, Rajasekaran SY, Cha S, Rady MY, Huddleston JM. Unplanned transfers to the intensive care unit: the role of the shock index. J Hosp Med. 2010;5(8):460-465. 7. Hillman KM, Bristow PJ, Chey T, et al. Antecedents to hospital deaths. Intern Med J. 2001;31(6):343-348. 8. Cao H, Eshelman L, Chbat N, Nielsen L, Gross B, Saeed M. Predicting ICU hemodynamic instability using continuous multiparameter trends. Conf Proc IEEE Eng Med Biol Soc. 2008;2008:3803-3806.
WWW.JENONLINE.ORG
87
TRAUMA NOTEBOOK/Moore
9. Jaramillo S, Barnhart K, Takacs P. Use of the shock index to predict ruptured ectopic pregnancies. Int J Gynaecol Obstet. 2011;112(1):68.
21. Davis JW, Shackford SR, Mackersie RC, Hoyt DB. Base deficit as a guide to volume resuscitation. J Trauma. 1988;28(10):1464-1467.
10. Birkhahn RH, Gaeta TJ, Terry D, Bove JJ, Tloczkowski J. Shock index in diagnosing early acute hypovolemia. Am J Emerg Med. 2005;23(3): 323-326.
22. Chang MC, Rutherford EJ, Morris JAJr.. Base deficit as a guide to injury severity and volume resuscitation. J Tenn Med Assoc. 1993;86(2):59-61.
11. Thom O, Taylor DM, Wolfe RE, Myles P, Krum H, Wolfe R. Pilot study of the prevalence, outcomes and detection of occult hypoperfusion in trauma patients. Emerg Med J. 2010;27(6):470-472. 12. Blow O, Magliore L, Claridge JA, Butler K, Young JS. The golden hour and the silver day: detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma. J Trauma. 1999;47(5):964-969. 13. Meregalli A, Oliveira RP, Friedman G. Occult hypoperfusion is associated with increased mortality in hemodynamically stable, highrisk, surgical patients. Crit Care. 2004;8(2):R60-R65. 14. Claridge JA, Crabtree TD, Pelletier SJ, Butler K, Sawyer RG, Young JS. Persistent occult hypoperfusion is associated with a significant increase in infection rate and mortality in major trauma patients. J Trauma. 2000;48(1):8-14. discussion 14–15. 15. Guyton AC, Hall JE. Textbook of Medical Physiology. 11th ed., Philadelphia, PA: Elsevier Saunders; 2006. 16. Howell MD, Donnino M, Clardy P, Talmor D, Shapiro NI. Occult hypoperfusion and mortality in patients with suspected infection. Intensive Care Med. 2007;33(11):1892-1899.
23. Laird AM, Miller PR, Kilgo PD, Meredith JW, Chang MC. Relationship of early hyperglycemia to mortality in trauma patients. J Trauma. 2004;56(5):1058-1062. 24. Bochicchio GV, Salzano L, Joshi M, Bochicchio K, Scalea TM. Admission preoperative glucose is predictive of morbidity and mortality in trauma patients who require immediate operative intervention. Am Surg. 2005;71(2):171-174. 25. Shin S, Britt RC, Reed SF, Collins J, Weireter LJ, Britt LD. Early glucose normalization does not improve outcome in the critically ill trauma population. Am Surg. 2007;73(8):769-772. 26. Duane TM, Dechert T, Dalesio N, et al. Is blood sugar the next lactate?. Am Surg. 2006;72(7):613-617. discussion 617–618. 27. Monnet X, Teboul JL. End-tidal carbon dioxide and arterial pressure for predicting volume responsiveness by the passive leg raising test: reply to Piagnerelli and Biston. Intensive Care Med. 2013;39(6):1165. 28. Monnet X, Julien F, Ait-Hamou N, et al. Lactate and venoarterial carbon dioxide difference/arterial-venous oxygen difference ratio, but not central venous oxygen saturation, predict increase in oxygen consumption in fluid responders. Crit Care Med. 2013;41(6):1412-1420.
17. Rutherford EJ, Morris JAJr., Reed GW, Hall KS. Base deficit stratifies mortality and determines therapy. J Trauma. 1992;33(3):417-423.
29. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S729-S767.
18. Davis JW, Shackford SR, Holbrook TL. Base deficit as a sensitive indicator of compensated shock and tissue oxygen utilization. Surg Gynecol Obstet. 1991;173(6):473-476.
30. Nunez TC, Young PP, Holcomb JB, Cotton BA. Creation, implementation, and maturation of a massive transfusion protocol for the exsanguinating trauma patient. J Trauma. 2010;68(6):1498-1505.
19. Davis JW, Mackersie RC, Holbrook TL, Hoyt DB. Base deficit as an indicator of significant abdominal injury. Ann Emerg Med. 1991;20(8):842-844. 20. Kincaid EH, Miller PR, Meredith JW, Rahman N, Chang MC. Elevated arterial base deficit in trauma patients: a marker of impaired oxygen utilization. J Am Coll Surg. 1998;187(4):384-392.
88
JOURNAL OF EMERGENCY NURSING
Submissions to this column are encouraged and may be sent to Kathryn Moore, DNP, RN, FCCM, CCRN, CEN, ACNP-BC, ANP-BC, GNP-BC [email protected]
VOLUME 41 • ISSUE 1
January 2015