Open Access

The optimal endpoint of resuscitation in trauma patients

Critical Care20027:19

https://doi.org/10.1186/cc1862

Published: 20 December 2002

Abstract

Although it has never been prospectively validated, the base excess (BE) is regarded as the standard end-point of resuscitation in trauma patients. In a rat hemorrhage model, in this edition of Critical Care, Totapally and colleagues demonstrate that the BE is an insensitive and slowly responsive indicator of changes in intravascular volume. This contrasts with changes in the esophageal-arterial carbon dioxide gap which more closely followed changes in blood volume. Esophageal or sublingual capnometry may prove to be a useful tool for monitoring the adequacy of resuscitation in trauma victims.

Keywords

base excess carbon dioxide esophageal capnometry hemorrhage resuscitation sublingual capnometry tissue hypoxia trauma

The assessment of intravascular volume and the adequacy of volume resuscitation are among the most difficult clinical challenges. Systolic blood pressure, heart rate and urine output change minimally in early hemorrhagic shock. Hypotension, tachycardia, cold extremities, decreased urine output and poor capillary refill are only present in patients who have lost in excess of 30% of their blood volume (classIII hemorrhage) [1]. Furthermore, both the central venous pressure and the changes in the central venous pressure in response to volume loading are poor indicators of intravascular volume and recruitable cardiac index [2]. While flow to the brain and the myocardium is preserved in patients with 'compensated shock', splanchnic and renal perfusion may be seriously compromised [3]. Splanchnic hypoperfusion leads to both functional and structural changes in the gut mucosa, with increased permeability and translocation of bacteria and bacterial products [4]. Increased mucosal permeability has been strongly associated with the development of the multiorgan dysfunction syndrome [4,5].

The expedient detection and correction of tissue hypoperfusion associated with 'compensated shock' may limit organ dysfunction, may reduce complications and may improve patient outcome. It is probable that the earlier tissue hypoperfusion is detected and corrected, the greater the likelihood that outcome will be improved [6]. Indeed, Rivers and colleagues reported a 32% relative reduction in the 28 day, all cause mortality of patients with severe sepsis who received early aggressive volume resuscitation in the emergency department [7]. Rivers et al. used the central venous oxygen saturation as the endpoint of resuscitation in the intervention group, while treatment in the control group was guided by standard clinical endpoints including the central venous pressure. While their study clearly demonstrates the value of early aggressive volume resuscitation, the use of central venous oxygen saturation to guide early resuscitation is not practical and has important limitations [8].

The base excess (BE) has become the standard endpoint of resuscitation in trauma patients. Remarkably, while the BE has been demonstrated to be of prognostic value, it has never been assessed prospectively in trauma patients [9,10,11,12,13,14,15]. The use of the BE is based on the principle that tissue hypoxia associated with poor perfusion will result in the generation of hydrogen ions and a metabolic acidosis. However, it is probable that tissue hypoperfusion may occur in the absence of a significant change in the BE. Furthermore, as significant time is required for the liver and kidney to regenerate bicarbonate [16], it can be expected that there will be a long lag phase between the correction of intravascular volume and normalization of the BE.

Both of these assumptions are elegantly demonstrated in the study by Totapally and colleagues reported in the present issue of Critical Care [17]. In a rat hemorrhage model these authors demonstrated that the BE responded slowly to changes in intravascular volume and that there was a significant increase in the BE only when the mean arterial blood pressure fell by greater than 50%. However, Totapally etal. demonstrated that changes in the esophageal carbon dioxide gap closely mirrored changes in the intravascular volume. Similar findings have been reported by other investigators. In patients with penetrating trauma, Baron and colleagues demonstrated that sublingual carbon dioxide measurements correlated well with the degree of blood loss [18]. Both Ivatury and colleagues and Kirton and coworkers have demonstrated that gastric intramucosal pH correlates well with the degree of injury and that optimizing the gastric intramucosal pH in the first 24 hours following trauma is associated with a reduction in the incidence of organ failure and death [19,20,21].

The study by Totapally and colleagues suggests that the BE is an insensitive indicator of the degree of the intravascular volume deficit following hemorrhage and that it responds slowly to volume resuscitation. Esophageal and sublingual capnometry, however, appear to provide near instantaneous information regarding the degree of the volume deficit and the adequacy of volume resuscitation [22,23,24,25]. This technology is simple and noninvasive, and is ideally suited for use in the emergency room and the trauma bay. The esophageal or sublingual pCO2 gap may prove to be a useful endpoint for the resuscitation of trauma victims.

Conflict of interest

The author has no financial interest in any product mentioned in this paper. The author has received a research grant from Optical Sensors Inc, Minneapolis, MN, USA, the manufacturer of the Nellcor N-80 CapnoProbe SL device.

Abbreviations

BE: 

= base excess.

Authors’ Affiliations

(1)
Professor of Medicine and Critical Care, Department of Critical Care Medicine, University of Pittsburgh

References

  1. American College of Surgery: Shock. In Advanced Trauma Life Support for Doctors; Student Course Manual 6 Edition Chicago: American College of Surgery 1997, 87-112.Google Scholar
  2. Michard F, Teboul JL: Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence. Chest 2002, 121: 2000-2008. 10.1378/chest.121.6.2000View ArticlePubMedGoogle Scholar
  3. Ba ZF, Wang P, Koo DJ, Cioffi WG, Bland KI, Chaudry IH: Alterations in tissue oxygen consumption and extraction after trauma and hemorrhagic shock. Crit Care Med 2000, 28: 2837-2842. 10.1097/00003246-200008000-00026View ArticlePubMedGoogle Scholar
  4. Pastores SM, Katz DP, Kvetan V: Splanchnic ischemia and gut mucosal injury in sepsis and the multiple organ dysfunction syndrome. Am J Gastroenterol 1996, 91: 1697-1710.PubMedGoogle Scholar
  5. Doig CJ, Sutherland LR, Sandham JS, Fick GH, Verhoef M, Meddings JB: Increased intestinal permeability is associated with the development of multiple organ dysfunction syndrome in critically ill ICU patients. Am J Respir Crit Care Med 1998, 158: 444-451.View ArticlePubMedGoogle Scholar
  6. Carlet J, Artigas A, Bihari D, Burchardi H, Gajdos P, Hemmer M, Langer M, Richard C, Wolff M: Third European Consensus Conference in Intensive Care Medicine. Tissue hypoxia: how to detect, how to correct, how to prevent? Am J Respir Crit Care Med 1996, 154: 1573-1578.View ArticleGoogle Scholar
  7. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001, 345: 1368-1377. 10.1056/NEJMoa010307View ArticlePubMedGoogle Scholar
  8. Marik PE, Varon J: Goal-directed therapy in sepsis [letter]. N Engl J Med 2002, 346: 1025. 10.1056/NEJM200203283461314View ArticlePubMedGoogle Scholar
  9. Siegel JH, Rivkind AI, Dalal S, Goodarzi S: Early physiologic predictors of injury severity and death in blunt multiple trauma. Arch Surg 1990, 125: 498-508.View ArticlePubMedGoogle Scholar
  10. Davis JW, Parks SN, Kaups KL, Gladen HE, O'Donnell-Nicol S: Admission base deficit predicts transfusion requirements and risk of complications. J Trauma 1996, 41: 769-774.View ArticlePubMedGoogle Scholar
  11. Rutherford EJ, Morris JA Jr, Reed GW, Hall KS: Base deficit stratifies mortality and determines therapy. J Trauma 1992, 33: 417-423.View ArticlePubMedGoogle Scholar
  12. Kincaid EH, Chang MC, Letton RW, Chen JG, Meredith JW: Admission base deficit in pediatric trauma: a study using the National Trauma Data Bank. J Trauma 2001, 51: 332-335.View ArticlePubMedGoogle Scholar
  13. Porter JM, Ivatury RR: In search of the optimal end points of resuscitation in trauma patients: a review. J Trauma 1998, 44: 908-914.View ArticlePubMedGoogle Scholar
  14. Ivatury RR, Sugerman H: In quest of optimal resuscitation: tissue specific, on to the microcirculation. Crit Care Med 2000, 28: 3102-3103. 10.1097/00003246-200008000-00082View ArticlePubMedGoogle Scholar
  15. Rixen D, Raum M, Bouillon B, Lefering R, Neugebauer E, of the Deutsche Gesellschaft fur Unfallchirurgie: Base deficit development and its prognostic significance in posttrauma critical illness: an analysis by the trauma registry of the Deutsche Gesellschaft fur unfallchirurgie. Shock 2001, 15: 83-89.View ArticlePubMedGoogle Scholar
  16. Stacpoole PW: Lactic acidosis. Endocrinol Metab Clin North Am 1993, 22: 221-245.PubMedGoogle Scholar
  17. Totapally BR, Fakioglu H, Torbati D, Wolfsdorf J: Esophageal capnometry during hemorrhagic shock and after resuscitation in rats. Crit Care 2003, in press.Google Scholar
  18. Baron BJ, Inerrt R, Zehtabchi S, Stavile KL, Scalea TM: Diagnostic utility of sublingual for detecting hemorrhage in pCO 2 patients with penetrating trauma [abstract]. Acad Emerg Med 2002, 9: 492. 10.1197/aemj.9.5.492View ArticleGoogle Scholar
  19. Ivatury RR, Simon RJ, Havriliak D, Garcia C, Greenbarg J, Stahl WM: Gastric mucosal pH and oxygen delivery and oxygen consumption indices in the assessment of adequacy of resuscitation after trauma: a prospective, randomized study. J Trauma 1995, 39: 128-134.View ArticlePubMedGoogle Scholar
  20. Ivatury RR, Simon RJ, Islam S, Fueg A, Rohman M, Stahl WM: A prospective randomized study of end points of resuscitation after major trauma: global oxygen transport indices versus organ-specific gastric mucosal pH. J Am Coll Surg 1996, 183: 145-154.PubMedGoogle Scholar
  21. Barquist E, Kirton O, Windsor J, Civetta-Hudson J, Lynn M, Herman M, Civetta J: The impact of antioxidant and splanchnic-directed therapy on persistent uncorrected gastric mucosal pH in the critically injured trauma patient. J Trauma 1998, 44: 355-360.View ArticlePubMedGoogle Scholar
  22. Marik PE: Sublingual capnograpahy: a clinical validation study. Chest 2001, 120: 923-927. 10.1378/chest.120.3.923View ArticlePubMedGoogle Scholar
  23. Weil MH, Nakagawa Y, Tang W, Sato Y, Ercoli F, Finegan R, Grayman G, Bisera J: Sublingual capnometry: a new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock. Crit Care Med 1999, 27: 1225-1229. 10.1097/00003246-199907000-00001View ArticlePubMedGoogle Scholar
  24. Jin X, Weil MH, Sun S, Tang W, Bisera J, Mason EJ: Decreases in organ blood flows associated with increases in sublingual pCO 2 during hemorrhagic shock. J Appl Physiol 1998, 85: 2360-2364.PubMedGoogle Scholar
  25. Povoas HP, Weil MH, Tang W, Moran B, Kamohara T, Bisera J: Comparisons between sublingual and gastric tonometry during hemorrhagic shock. Chest 2000, 118: 1127-1132. 10.1378/chest.118.4.1127View ArticlePubMedGoogle Scholar

Copyright

© BioMed Central Ltd 2003

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