|
| SPECIAL ARTICLE |
|
| Year : 2007 | Volume
: 51
| Issue : 6 | Page : 479-485 |
 |
|
End points in trauma management
N Ganapathy
M.D., D.A., F.C.C.P., D.C.C.M., (Cardio) M.C.A.M., Secretary, National Board for Trauma Courses, ITACCS (Indian Chapter), India
| Date of Acceptance | 26-Sep-2007 |
| Date of Web Publication | 20-Mar-2010 |
Correspondence Address:
N Ganapathy
Director, Dhanvantri Critical Care Center, 27, 28, Poonkundranar Street, Karungalpalayam, Erode - 638 003, Tamilnadu
India
 Source of Support: None, Conflict of Interest: None  | Check |
Fluid resuscitation following traumatic haemorrhage has historically been instituted as soon after injury as possible. Patients suffering from haemorrhagic shock may receive several liters of crystalloid, in addition to colloid solutions, in order to normalize blood pressure, heart rate, urine output and mental status, which are the traditional endpoints of resuscitation. Current theory and recent investigations have questioned this dogma. Resuscitation goals may be different when the patient is actively haemorrhaging and once bleeding has been controlled. Newer markers of tissue and organ system perfusion may allow a more precise determination of adequate resuscitation Keywords: Trauma; Resuscitation; Tissue hypoxia; Occult hypoperfusion; Perfusion
How to cite this article:
Ganapathy N. End points in trauma management. Indian J Anaesth 2007;51:479-85 |
 Introduction | |  |
Severely injured trauma victims are at high risk of development of the multiple organ dysfunction syndrome (MODS) or death. To maximize chances for survival, treatment priorities must focus on resuscitation from shock (defined as inadequate tissue oxygenation to meet tissue O 2 requirements), including appropriate fluid resuscitation and rapid hemostasis. Inadequate tissue oxygenation leads to anaerobic metabolism and resultant tissue acidosis. The depth and duration of shock leads to a cumulative oxygen debt. [1] Resuscitation is complete when oxygen debt has been repaid, tissue acidosis is eliminated and normal aerobic metabolism is restored in all tissue beds. Use of the endpoints may allow early detection and reversal of this state.
No fluid resuscitation may lead to death from exsanguinations,whereasaggressivefluidresuscitationmay "pop the clot" and lead to more bleeding. "limited", "hypotensive", and/or "delayed" fluid resuscitation may be beneficial.
The traditional markers of "successful" resuscitation, including restoration of normal blood pressure, heart rate, and urine output, remain the standard of care as per the Advanced Trauma Life Support Course. [2] When these parameters remain abnormal, i.e., uncompensated shock, the need for additional resuscitation is clear. After normalizing these parameters, up to 85% of severely injured trauma victims still have evidence of inadequate tissue oxygenation based on findings of an ongoing metabolic acidosis or evidence of gastric mucosal ischaemia. [3],[4] This condition has been described as compensated shock. Recognition of this state and its rapid reversal are critical to minimize risk of MODS or death.
| Goals of resuscitation | | |
- Management of resuscitation prior to control of haemorrhage
- Management of resuscitation following control of haemorrhage
| Management of resuscitation prior to control of haemorrhage | | |
The first priority or sine qua non of any hypotensive trauma patient is recognition and control of haemorrhage.
Life threatening haemorrhage occurs into one or more of five compartments.
Possible sites for exsanguinating haemorrhage are shown in [Table 1].
Using computerised tomography (CT) or operative explorationfor occultbleedingmaytake significantamount oftime, duringwhichthepatient will stillbe activelybleeding.
| Fluids for control of haemorrhage | | |
Fluids must be administered to stave (to stop somethingbad fromhappening) off exsanguination. Howmuch fluid to give? What kind of fluid? These questions are at the core of modern resuscitation research. Given the analogy of fluid into a bucket with a hole in the bottom, what level of resuscitation produces the best clinical results?
The degree of ischaemia sustained by the body and the duration over which the ischaemia occurs determines the development of multiple organ dysfunction syndrome (MODS) or death. Fluid therapy is directed towards reestablishment and maintenance of a normal blood pressure.
| Clinical problems associated with early fluid administration | | |
- Is often colder than body temperature producing a thermal stress
- Reduces blood viscosity which enhances bleeding from injured vessels
- Lowers the hematocrit and dilutes clotting factors and red cell mass
- When rapidly infused may impair immune system function [5].
| Choice of resuscitation fluid | | |
Research continues to define the ideal fluid for resuscitation of trauma patients. Isotonic crystalloid solutions like 0.9% normal saline and Ringer's lactate rapidly distribute throughout the extra cellular space and only 10-20% or less of the infused volume remains in the circulation. [6] Isotonic colloids like, albumin, hetastarch and dextran, expands plasma volume either slightly less, equal or more than the infused volume respectively. [7]
| The roleof 7.5% hypertonic saline (HS) in trauma resuscitation | | |
There has been substantial interest and extensive pre-clinical experience in evaluating the use of hypertonic saline solution for volume support. [8] Hypertonic solutions mobilize an amount of cellular water proportional to osmotic load (2,400 mOsm.L -1 ), and increases the plasma volume three to four times the infused volume. This not only tend to reduce overall volume requirement in trauma and perioperative patients but also shows a beneficial effect by shrinking the cell volume, which is a feature of shock and surgical stress. The main source of volume expansion by hypertonic solution is from red blood and endothelial cells and this result in improved microcirculation. The main advantages of hypertonic saline resuscitation includes, haemodynamic effects through combination of volume expansion and decreased vascular resistance which increases regional blood flow to coronary, renal, intestinal and skeletal muscle circulation, its effects on lowering intra cranial pressure (ICP) in brain injured patients, [9] especially children, [10] and most recently, multiple studies have suggested its beneficial role in immunomodulation. [11],[12],[13] Based on these evidences it has been suggested that resuscitation with hypertonic saline (HS) present significant potential as an immunomodulatory agent for trauma victims. The increase in plasma volume by HS infusions occurs immediately but this response is short lived. The addition of dextran to hypertonic saline (HSD) not only provides slightly better volume expansion; but more importantly, it provide sustained volume expansion. [14],[15]
In summary, HS/HSD can be used safely for rapid and sustained resuscitation of trauma patient particularly for penetrating trauma requiring surgery and for those sustaining head trauma, as this may also reduce cerebral oedema in patients with severe head injuries. Caution should be exercised when treating moribund patient or those with chronic debilitating diseases.
| To summarise | | |
- The hypotensive trauma patients at the time of medical intervention has usually stopped bleeding and has formed a soft clot at the point of injury. This clot is maintained in place by systemic vasoconstriction and low blood pressure both of which can be easily overcome by a crystalloid bolus intend to raise the blood pressure.
- Attempting to achieve normal blood pressure in the actively bleeding patients is associated with disruption of native hemostatic mechanisms, dilution of clotting factors and red cell mass, greatly increased blood loss and decreased survival. [16],[17],[18]
Benefits and risks of early aggressive prehospital fluid resuscitation in trauma [19] are shown in [Table 2].
| Goals of early resuscitation | | |
The physician treating patient with early shock should sail a narrow course between tolerating a low blood pressure, particularly early in the patient's clinical course, while keeping a watchful eye on the indicators which will suggest that ischaemia is advancing too far.
The recommendations for resuscitation in patients who are still actively haemorrhaging are:
Blood pressure 80 systolic, 50-60 mean
Heart rate Less than 120
Oxygenation Oximeter should be working, saturation > 96%
Urine output > 20 cc.hr -1
Mentation Patients should follow commands accurately
Lactate level < 4mg.dl -1
Base deficit < - 5
Hematocrit 30%
| Clinical practice guideline | | |
Resuscitation endpoints Global
1. Oxygen delivery
- Supranormal oxygen
- Mixed venous oxygen saturation (SvO 2 )
2. Haemodynamic profiles
- Central venous pressure (CVP)
- Pulmonary capillary wedge pressure (PCWP)
- Right ventricular end diastolic volume index (RVEDVI)
3. Acid-base status
- Bicarbonate concentrations
- Arterial lactate
- End-tidal carbon dioxide levels
Regional
1. Tissue oxygenation and partial pressure of carbon dioxide (PCO 2 )
- Tissue oxygen and carbon dioxide electrodes
- Near infrared spectroscopy
2. Gastric mucosal ischaemia
- Gastric tonometry
- Sublingual monitoring of the partial pressure of carbon dioxide
- Physical examination
Major outcomes considered
- Survival without organ system dysfunction
- Risk for multiple organ dysfunction syndrome or death
- Physiologic derangement
| Oxygen delivery | | |
In high risk trauma patients the survivors had significantly higher O 2 delivery and cardiac index (CI) values than the non survivors. [20],[21] The parameters are: CI (>4.5 L.min -1 .m -2 ), O 2 delivery (DO 2 ³ 600 mL.min -1 .m -2 ) and O 2 consumption (VO 2 ³ 170 ml.min -1 .m -2 ). Using these parameter as goals of resuscitation resulted in decreased compliance, length of stay and hospital costs. [22] Adding to "ABCs" of resuscitation "D" for delivery of O 2 and "E" for ensuring exraction and utilization of O 2 by tissues was included. [23] Attaining supranormal haemodynamic parameters improved survival and decreased the frequency of organ failure. [24] Oxygen delivery was augmented by volume overloading, followed by obutamine infusion if necessary and finally blood transfusion upto haemoglobin of 14 gm.dL -1 .
| Mixed venous oxygen saturation | | |
Use of mixed venous O 2 saturation (SvO 2 ) levels should reflect the adequacy of O 2 delivery to tissue in relation to global tissue O 2 demands. Resuscitated patients to a normal CI (2.5 - 3.5 L.min -1 .m -2 ), supernormal CI (>4.5 L.min -1 .m -2 ), or normal SvO 2 (>70%) do not result in MODS or death.
| Additional invasive haemodynamic parameters | | |
Occult cardiac dysfunction is seen in many trauma patients. Early invasive haemodynamic monitoring ofhigh risk trauma victims identified occult shock early and may have helped to prevent MODS and death. [25] Fluid resuscitation is the primary treatment for trauma patients in haemorrhagic shock and the indicator of adequate volume status is optimized preload. CVP and PCWP have limitations in critically ill patients due to changes in ventricular compliance (edema, ischaemia or contusion) and intrathoracic pressure (mechanical ventilation). In these situations RVEDVI may more accurately reflect left ventricular preload than CVP or PCWP. CI correlates better with RVEDVI than PCWP up to very high levels of positive end-expiratory pressure.
The haemodynamic variables left ventricular stroke work index (LVSWI = stroke index x mean arterial pressure x 0.0144) and left ventricular power output (LVP = cardiac index x [mean arterial pressure - central venous pressure]), that encompass blood pressure and flow with purely flow-derived haemodynamic and O 2 transport variables are predictors of outcome in critically ill trauma patients. [26] The only variables that significantly correlated with lactate clearance and survival were heart rate, LVSWI and LVP. The desired value of LVP (>320 mm Hg x L.min -1 .m -2 ).
| Arterial base deficit | | |
Inadequate tissue O 2 delivery leads to anaerobic metabolism. The degree of anaerobiosis is produced to the depth and severity of haemorrhagic shock. This should be reflected in the base deficit and lactate level.Arterial pH is not as useful as it will be "defended" by the body's compensatory mechanisms. [27] Higher base deficit was associated with lower blood pressure on admission and greater fluid requirements. Base deficit is classified as mild (base deficit 2-5 mmol.L -1 ) moderate, (base deficit 6-14 mmol.L -1 ), or severe (base deficit > 14 mmol.L -1 ). Patients with an increasingbase deficit had ongoing blood loss. [28] Trauma patients who normalized their lactate levels; persistently high base deficit had greater risk of MODS and death. These patients demonstrated impaired O 2 utilization, as evidenced by lower O 2 consumption and O 2 utilization coefficient. [29] Using base deficit, core temperature and ISS (Injury Severity Score), could predict outcome. Severe hypothermia (<33degree C), severe metabolic acidosis (base deficit > 12 mmol.L -1 ), and a combination (temperature <35.5 degree C and base deficit >5 mmol.L -1 ) were strong predictors of death. [30] Elevated base deficit is not only predictive of mortality, but of complications, such as the need for blood transfusions and organ failure, particularly the acute respiratory distress syndrome (ARDS). [31] Base deficit levels may be confounded by a number of factors.Alcohol intoxication can worsen base deficit for similar levels of injury severity and haemodynamics after trauma. Development of a hyperchloremic metabolic acidosis from resuscitation with normal saline or lactated Ringer's solution can increase base deficit for the same degree of injury severity. [32] Administration of sodiumbicarbonate will at least transiently improve base deficit and bicarbonate levels and confound their use as endpoints for resuscitation. There is little role for sodium bicarbonate in the treatment of haemorrhagic shock.
| Arterial lactate | | |
In patients with noncardiogenic circulatory shock not only were initial lactate levels important, but the response of the lactate level to an intervention, such as fluid resuscitation, would add predictive value. [33] The time needed to normalize serum lactate levels was an important prognostic factor for survival. [34] The patients were resuscitated to supranormal values of O 2 transport. [35] All patients who had normalized lactate levels at 24 hours survived. Those patients who normalized their levels between 24 and 48 hours had a 25% mortality rate. Patients who did not normalize by 48 hours had an 86% mortality rate. The initial and peak lactate levels, as well as the duration of hyperlactatemia, correlates with development of MODS after trauma. [36] The desired value of lactate is less than 2.5 mmol.L -1 . Serial measurement of lactate is recommended. It can be easily measured. Lactate clearance may be decreased with liver dysfunction or sepsis.
| End-tidal carbon dioxide levels | | |
Reduced cardiac output and/or abnormal distribution of pulmonary blood flow can lead to increased pulmonary dead space. This can then lead to an increase in the difference between arterial and alveolar CO 2 , as measured by end-tidal CO 2 . Survivors had higher end-tidal CO2, lower arterial-end tidal CO 2 differences, and decrease alveolar dead space ratio (estimated as the arterial-end tidal CO 2 difference/arterial PCO 2 ) compared to nonsurvivors. [37]
| Gastric tonometry | | |
On the regional level, compensated shock disproportionately decreases blood flow to the splanchnic bed to maintain cerebral and coronary blood flow. Examination of the gut-related parameters may be useful as a marker of the severity of shock and also to demonstrate the pathophysiologic connection between gut ischaemia and later MODS. Gastric ischaemia is monitored using gastric tonometry.
Hypercabia is a universal indicator of critically reduced tissue perfusion. Management of gastric PCO 2 (PgmCO 2 ) and intramucosal pH (pHi) through gastric tonometry is used in trauma patients as an indicator of restoration of blood flow. pHi correlated with sepsis score. Lower pHi correlated with development of MODS and increased mortality in critically ill patients, particularly if the low pHi persisted for >12 hours. Gastric pHi is 7.4. pHi <7.32 is a good predictor of MODS and mortality. [38]
The esophageal wall is also an important site for tissue PCO 2 measurement in haemorrhagic shock. The most proximal area of the gastrointestinal tract, the sublingual mucosa has become a useful site for measurement of PCO 2 (PSLCO 2 ) recently. The normal value of PSLCO2 is 45 mm Hg.
| Tissue oxygen and carbon dioxide electrodes | | |
Skeletal muscle blood flow decreases early in the course of shock and is restored late during resuscitation, making skeletal partial pressure of oxygen a sensitive indicator for low flow. A fibreoptic probe with pH, PCO 2 and PO 2 sensors are placed directly into the muscle. The probe is inserted through a 20 gauge radial artery cannula sutured to the skin and extends 1cm beyond the cannula tip with the sensors in the interstitium of the skeletal muscle. Continuous monitoring of pHm, PmCO 2 . PmO 2 should reflect the gradient of these variables between intravascular and intracellular and not between arterial and mixed venous blood. The desired values are pHm = 7.2; PmCO 2 = 50 mm Hg; PmO 2 = 40 mm Hg; The critical PmO2 = 15 mm Hg is threshold for anaerobic metabolism.
| Near infrared spectroscopy (NIRS) | | |
Measurement of skeletal muscle oxyhaemoglobin levels by NIRS offers a non-invasive method for monitoring adequacy of resuscitation in terms of normalizing tissue oxygenation. In human volunteers donating 470ml of whole blood, cerebral cortex and calf muscle O 2 saturation measured by NIRS decreased in proportion to blood loss. The oxygenation index ([oxygenated haemoglobin] - [deoxygenated haemoglobin]) also decreased proportionally. [39] In addition to monitoring tissue oxygenation, NIRS can provide information regardingmitochondrial function. Normally, tissue oxyhaemoglobin levels, reflecting local O 2 supply, are tightly coupled to cytochrome a, a 3 redox, reflecting mitochondrial O 2 consumption. [40]
| Physical examination | | |
Despite all the interest in laboratory values, as well as data from invasive and non-invasive monitoring devices, used to determine the adequacy of resuscitation, one should not discount the value of a good physical examination. Kalpan, et al, examined the ability of 2 intensivists to diagnose hypoperfusion by physical examination of patients' extremities. [41] The intensivists described the patients' extremities as either warm or cool. Compared with patients with warm extremities, those with cool extremities had lower CI, pH, bicarbonate levels, and SvO2; and higher lactate levels.
| Future investigation | | |
Prevention of organ ischaemia or damage may be possible in the next millenium through the administration of agents which regulate cellular function. Future possibilities in traumatic shock management include manipulation of shock-related pathophysiological alterations such as complement and granulocyte activation, endothelial activation, leukostasis and edema formation with resultant organ injury. These may be possible through the use of oxygen carriers (fluorocarbons and modified haemoglobins), antioxidants, nitric oxide scavengers and anti-endotoxin compounds.
The search for the "holy grail", i.e., a single endpoint that works for all trauma patients, may be unrealistic. For example, acid-base parameters may not work in patients with acid-base disturbances that are acute (alcohol intoxication) or chronic (renal failure). For older patients, beta-blockade and heart rate control may be valuable and use of inotropes that increase myocardial work along with massive volume loading may be detrimental.
| Conclusion | | |
Fluid resuscitation is an integral, mandatory component of the management of the patient in shock from traumatic haemorrhage. The classic theory of instituting resuscitative fluids early following injury is now being disputed.Adequacy of resuscitation is no longer judged by the presence of normal vital signs, but by the achievement of normalization of organ and tissue specific measured values. The role of the anaesthesiologist and intensivist is to recognize the presence of shock following traumatic haemorrhage and to resuscitate the patient with the appropriate fluid, in the appropriate amount, at the appropriate time.
| References | | |
| 1. | Shoemaker WC, Appel PL, Kram HB. Tissue oxygen debt as a determinant of lethal and nonlethal postoperative organ failure. Crit Care Med 1988; 16:1117-20.  [PUBMED] |
| 2. | Bickell WH, Wall Jr MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994; 331:1105-1109. |
| 3. | Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation during active haemorrhage: impact on in-hospital mortality. J Trauma 2002; 52:1141-1146. [PUBMED] [FULLTEXT] |
| 4. | American College ofSurgeons Committee on Trauma:Advanced Trauma Life Support Course for Doctors, 1997.American College of Surgeons, Chicago, IL, USA. |
| 5. | Knoferl MW, Angele MK, Ayala A, Cioffi WG, Bland K, Chaudry IH. Do different rates of fluid resuscitation adversely or beneficially influence immune reponses after trauma hemorrhage? J Trauma 1999;46:23-30. |
| 6. | Hambly PR, Dutton RP. Excess mortality associated with the use of rapid infusion system at a level 1 trauma center. Resuscitation 1996;31:127-133. |
| 7. | Heckbert SR, Vedder NB, Hoffman W, et al. Outcome after hemorrhagic shock in trauma patients. J Trauma 1998;45:545-554. [PUBMED] [FULLTEXT] |
| 8. | Soucy DM, Rude M, Hisa WC, et al. The effects of varying fluid volume and rate of resuscitation during uncontrolled haemorrhage. J Trauma 1999;46:209-215. |
| 9. | Chang M, Mondy S, Meredith JW, Holcroft JW. Redefining cardiovascular performance during resuscitation: ventricular stroke work, power and the pressure - volume diagram. J Trauma 1998; 45:470-478. |
| 10. | McKinely BA, Parmely CL, Butler BD. Skeletal muscle PO2,PCO 2 and pH in hemorrhage, shock and resuscitation in dogs.J Trauma 1998; 44:119-127. |
| 11. | McKinley BA, Ware DN, Marvin RG, Moore FA. Skeletal muscle pH, PCO2 and PO2 during resuscitation of severe hemorrhagic shock. J Trauma 1998; 45:633-636. [PUBMED] [FULLTEXT] |
| 12. | Waxman K,Annas C, Daughters K, Tominaaga GT, Scannell G. A method to determine the adequacy of resuscitation using tissue oxygen monitoring. J Trauma 1994; 36:852-856. |
| 13. | Puyana JC, Soller BR, Zhang SB, Heard SO. Continuous measurement of gut pH with near-infrared spectroscopy during hemorrhagic shock. J Trauma 1999; 46:914. |
| 14. | SatoY, Weil MH, Tang W, et al. Esophageal PCO2 as a monitor of perfusion failure during hemorrhagic shock. J Appl Physiol 1997; 82:558-562. |
| 15. | Weil MH, Nadagawa Y, Tang W, et al. Sublingual capnometry: a new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock. Crit Care Med 1999; 27:1225-1229. |
| 16. | Burris D, Rhee P, Kaufman C, et al. Controlled resuscitation for uncontrolled hemorrhagic shock. J Trauma 1999; 46:216-222. |
| 17. | Stern A, Dronen SC, Birrer P, Wang X. Effect of blood pressure on haemorrhagic volume in a near - fatal haemorrhage model incorporating a vascular injury. Ann Emerg Med 1993;22:155-63. |
| 18. | Capone A, Safar P, Stezoski SW, Peitzman A, Tisherman S. Uncontrolled hemorrhagic shock outcome model in rats. Resuscitation 1995;29:143-152. |
| 19. | From Haljamal H, Mc Cunn M. Fluid resuscitation and circulatory support In: International Textbook on Prehospital Trauma Care. Edited byE.Soreeicle and C. Grande. Publication pending. |
| 20. | Shoemaker WC, Montgomery ES, Kaplan E, Elwyn DH. Physiologic patterns in surviving and nonsurviving shock patients: Use of sequential cardiorespiratory variables in defining criteria for therapeutic goals and early warning of death. Arch Surg 1973; 106:630-636. [PUBMED] |
| 21. | Shoemaker WC,Appel P, Bland R. Use of physiologic monitoring to predict outcome and to assist in clinical decisions in critically ill postoperative patients. Am J Surg 1983; 146:43-38. [PUBMED] [FULLTEXT] |
| 22. | Shoemaker WC, Appel PL, Kram HB, Waxman K, Lee T-S. Prospective trial of supranormal values of survivors as therapeutic goals in high risk surgical patients. Chest 1988; 94:1176-86. |
| 23. | Fiddian-Green RG, Hagland U, Gutierrez G, Shoemaker WC. Goals for the resuscitation of shock. Crit Care Med 1993; 21:S25-S31. |
| 24. | Bishop MH, Shoemaker WC, Appel PL, et al. Relationship between supranormal circulatory values, time delays, and outcome in severely traumatized patients. Crit Care Med 1993; 21:56-63. [PUBMED] |
| 25. | Cheatham ML, Nelson LD, Chang MC, Safcsak K. Right ventricular end-diastolic volume index as a predictor of preload status in patients on positive end-expiratory pressure. Crit Care Med 1998; 26:1801-1806. [PUBMED] [FULLTEXT] |
| 26. | Chang MC, Meredith JW. Cardiac preload, splanchnic perfusion, and their relationship during resuscitation in trauma patients. J Trauma 1997; 42:577-82. [PUBMED] [FULLTEXT] |
| 27. | Chang MC, Cheatham ML, Nelson LD, Rutherford EJ, Morris JA. Gastric tonometry supplements information provided by systemic indicators of oxygen transport. J Trauma 1994; 37:488-94. |
| 28. | Kincaid EH, Meredith JW, Chang MC. Determining optimal cardiac preload during resuscitation using measurements of ventricular compliance. J Trauma 2001; 50:665-669. [PUBMED] [FULLTEXT] |
| 29. | 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; 187:384-392. [PUBMED] [FULLTEXT] |
| 30. | Krishna G, Sleigh JW, Rahman H. Physiological predictors of death in exsanguinating trauma patients undergoing conventional trauma surgery. Aust NZ J Surgery1998; 68:826-829. |
| 31. | 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. [PUBMED] [FULLTEXT] |
| 32. | Brill SA, Schreiber MA, Stewart TR, Brundage SI. Base deficit does not predict mortality when secondary to hyperchloremic acidosis. Shock 2002; 17:459-462. |
| 33. | Vincent J-L, Dufaye P, Berre J, Leeman M, Degaute J-P, Kahn RJ. Serial lactate determinations during circulatory shock. Crit Care Med 1983; 11:449-451. |
| 34. | Abramson D, Scalea TM, Hitchcock R, et al. Lactate clearance and survival following injury. J Trauma 1993; 35:584-589. [PUBMED] |
| 35. | Shoemaker WC, Appel P, Bland R. Use of physiologic monitoring to predict outcome and to assist in clinical decisions in critically ill postoperative patients. Am J Surg 1983; 146:43-38. [PUBMED] [FULLTEXT] |
| 36. | Manikis P, Jankowski S, Zhang H, Kahn RJ, Vincent J-L. Correlation of serial blood lactate levels to organ failure and mortality after trauma. Am J Emerg Med 1995; 13:619-622. |
| 37. | Tyburski JG, Collinge JD, Wilson RF, et al. End-tidal CO2derived values during emergency trauma surgery correlated with outcome: A prospective study. J Trauma 2002; 53:738-743. [PUBMED] [FULLTEXT] |
| 38. | Chang MC, Cheatham ML, Nelson LD, Rutherford EJ, Morris JA. Gastric tonometry supplements information provided by systemic indicators of oxygen transport. J Trauma 1994; 37:488-94. |
| 39. | Torella F, Cowley RD, Thorniley MS, McCollum CN. Regional tissue oxygenation during haemorrhage: can near infrared spectroscopy be used to monitor blood loss? Shock 2002; 18:440-444. [PUBMED] [FULLTEXT] |
| 40. | Cairns CB, Moore FA, Haenel JB, et al. Evidence for early supply independent mitochondrial dysfunction in patients developing multiple organ failure after trauma. J Trauma 1997; 42:532-6. [PUBMED] [FULLTEXT] |
| 41. | Kaplan LJ, McPartland K, Santora TA, Trooskin SZ. Start with a subjective assessment of skin temperature to identity hypoperfusion in intensive care unit patients. J Trauma 2001; 50:620-628. [PUBMED] [FULLTEXT] |
[Table 1], [Table 2]
|
