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 Table of Contents    
REVIEW ARTICLE  
Year : 2018  |  Volume : 11  |  Issue : 2  |  Page : 80-87
Guiding management in severe trauma: Reviewing factors predicting outcome in vastly injured patients


1 Department of Anesthesiology, University Hospital of Crete, Heraklion, Greece
2 Department of General Surgery, University Hospital of Crete, Heraklion, Greece

Click here for correspondence address and email

Date of Submission24-Jul-2017
Date of Acceptance16-Nov-2017
Date of Web Publication29-May-2018
 

   Abstract 


Trauma is one of the leading causes of death worldwide, with road traffic collisions, suicides, and homicides accounting for the majority of injury-related deaths. Since trauma mainly affects young age groups, it is recognized as a serious social and economic threat, as annually, almost 16,000 posttrauma individuals are expected to lose their lives and many more to end up disabled. The purpose of this research is to summarize current knowledge on factors predicting outcome – specifically mortality risk – in severely injured patients. Development of this review was mainly based on the systematic search of PubMed medical library, Cochrane database, and advanced trauma life support Guiding Manuals. The research was based on publications between 1994 and 2016. Although hypovolemic, obstructive, cardiogenic, and septic shock can all be seen in multi-trauma patients, hemorrhage-induced shock is by far the most common cause of shock. In this review, we summarize current knowledge on factors predicting outcome – more specifically mortality risk – in severely injured patients. The main mortality-predicting factors in trauma patients are those associated with basic human physiology and tissue perfusion status, coagulation adequacy, and resuscitation requirements. On the contrary, advanced age and the presence of comorbidities predispose patients to a poor outcome because of the loss of physiological reserves. Trauma resuscitation teams considering mortality prediction factors can not only guide resuscitation but also identify patients with high mortality risk who were previously considered less severely injured.

Keywords: Injury, mortality, predicting factors, trauma

How to cite this article:
Lilitsis E, Xenaki S, Athanasakis E, Papadakis E, Syrogianni P, Chalkiadakis G, Chrysos E. Guiding management in severe trauma: Reviewing factors predicting outcome in vastly injured patients. J Emerg Trauma Shock 2018;11:80-7

How to cite this URL:
Lilitsis E, Xenaki S, Athanasakis E, Papadakis E, Syrogianni P, Chalkiadakis G, Chrysos E. Guiding management in severe trauma: Reviewing factors predicting outcome in vastly injured patients. J Emerg Trauma Shock [serial online] 2018 [cited 2018 Jun 25];11:80-7. Available from: http://www.onlinejets.org/text.asp?2018/11/2/80/233412





   Introduction Top


According to the World Health Organization (WHO), trauma is one of the leading causes of death worldwide, with road traffic collisions, suicides, and homicides counting for the majority of injury-related deaths.[1] Because trauma mainly affects young and productive age groups, it has been recognized as a serious social and economic threat, as annually, almost 16,000 posttrauma individuals are expected to lose their lives and many more to end up disabled. In the United States alone 50 million patients are hospitalized for trauma every year, and trauma-related injuries are responsible for 30% of admissions in the Intensive Care Units (ICUs).[1] As expected, traumatic brain injury (TBI) is the main cause of the majority of trauma-related deaths, followed by hemorrhage-induced hypovolemic shock and multiple organ failure syndrome (MOFS).[2],[3]

It has been proposed that there is a specific risk distribution pattern for injury-related deaths in patients sustaining severe trauma. Immediate deaths at the incident scene are usually the result of great vessel rupture or severe TBI. Deaths seen within 4 h after trauma are mainly due to intra-abdominal and/or intra-thoracic hemorrhage and pneumothorax. Finally, MOFS and other trauma-related complications such as sepsis are responsible for trauma patient's demise throughout their hospital stay.[4] It is important to stress that statistically, patients surviving the first 6 h after severe trauma are less likely to die. In those patients, life-threatening injuries and other risk factors have been correctly identified and successfully managed.[5]

Although hypovolemic, obstructive, cardiogenic, and distributive shock can all be seen in multi-trauma patients, hemorrhage-induced circulatory failure is by far the most common cause of shock.[4],[6] Excluding all other causes that may lead a trauma patient to die at the scene of the incident, excessive blood loss that causes hypovolemic shock is of major concern during initial assessment and resuscitation, as it greatly influences the patient's vital signs, tissue perfusion, body temperature, and the adequacy of clotting. Fortunately, early diagnosis of hemorrhage, along with the development of management guidelines based on massive transfusion protocols, have reduced mortality rates.[7],[8],[9] The objectives of this collective review are to summarize current knowledge on factors predicting outcome – specifically mortality risk – in severely injured patients.


   Methods Top


This systematic review utilized a search of PubMed medical library, Cochrane database, and advanced trauma life support (ATLS) Guiding Manuals. ≤Mortality,≥ ≤trauma outcome,≥ ≤predicting factors,≥ ≤coagulopathy,≥ ≤trauma scores,≥ ≤trauma and shock,≥ ≤fibrinogen and mortality,≥ ≤base deficit and lactate,≥ ≤vital signs,≥ ≤hemorrhagic shock,≥ ≤electrolytes in trauma,≥ ≤hematocrit and platelets,≥ ≤blood transfusions,≥ ≤biochemistry in trauma,≥ ≤patient factors and mortality,≥ ≤age and gender in trauma,≥ ≤arterial blood gases,≥ ≤guidelines and trauma,≥ ≤ATLS,≥ were all used as key words. The research was based on publications between 1994 and 2016. Summarizing, most (but not all) of the predicting factors describe patient's status of physiology, coagulation, vital signs, and trauma scores.

Vital signs

Conventionally, vital signs assessment has been described as a useful index of the intravascular volume status. Indeed heart rate (HR) is considered to be a sensitive marker of blood loss, in patients not taking bradycardia-inducing medication. Trauma patients are expected to primarily present with tachycardia, and eventually, hypotension as the process of blood loss continues.[4] A review of 30 studies (19 of which reported on traumatic hemorrhage) assessed the relationship between blood loss and vital signs. No specific relation between a given vital sign and expected amount of blood loss was proved. A HR-specific area under curve (AUC) ranging from 0.56 to 0.74 was actually shown to be the factor with the lowest sensitivity.[10] The Los Angeles County Trauma System database [11] presented a retrospective evaluation of 130,906 adult trauma patients, 3727 of whom were hypotensive (systolic blood pressure [BP] <90 mmHg) on admission and almost half of them (44%) had relative bradycardia (HR <90 bpm). Besides, patients with bradycardia had increased mortality risk when compared to tachycardic patients, with low HR to be an independent risk factor for mortality with an odds ratio of 1.60.[11] Similar studies support that tachycardia is independently associated with hypotension.[12] Accordingly, injured patients with normal HR (<80 bpm) are expected to have poor prognosis independently of trauma severity, especially when lactate level and base deficit (BD) are increased. The greater mortality odds ratio (4.11) was found when a discrepancy between HR and lactate levels existed.[13] A retrospective study of 70 trauma patients failed to prove any difference between vital signs and in-hospital survival, with the latter being correlated with lactate levels as a sensitive marker of tissue perfusion.[14] It has also been postulated that elevated lactate levels and BD, when combined with normal BP in blunt trauma patients, predict a poor outcome suggesting that tissue blood flow and occult hypoperfusion is far more important than systolic BP per se.[15] Moreover, low baseline (preinjury) BP seems to have a negative impact on elderly trauma patient's survival resulting in a 3-fold increase in mortality.[16]

The relative lack of sensitivity of vital signs to predict outcome can be explained under basic physiology principles. Delivery of oxygen to tissues depends on cardiac output (CO), hemoglobin levels, and oxygen saturation. BP is the product of CO multiplied by Systemic Vascular Resistance (SVR) and given by the equation BP = CO × SVR. BP can be maintained at the expense of elevated SVR when CO and consequently tissue oxygen delivery are critically low.[4] The shock index (SI) (HR divided by systolic BP – HR/BP) or the modified SI (MSI) (HR divided by mean artery pressure – HR/MAP) are by far the most sensitive markers of hypoperfusion and strong predictors of outcome. The results from several studies indicate that patients with SI >0.9–1 are more likely to die within 28 days after trauma or need massive transfusions to keep an adequate perfusion pressure.[17],[18],[19] SI can be safely used for the identification of patients who will require massive transfusion or exploratory laparotomy or suffer complications and increased mortality. Admission in level I trauma facilities is therefore advised for trauma patients with SI >1.[20] Kristensen et al.[21] reported on the association between mortality and SI in 111,019 patients of their cohort study. They found a positive correlation between SI >1 and 30-day mortality, although age, preexisting hypertension, and calcium or b-blockers intake, were found to modify that relationship.[21] The results of a recent large prospective study of 9860 adult trauma patients showed that an MSI higher than 1.3 or lower than 0.7 strongly predicted increased mortality and hospital stay. SI had lower mortality predicting value than MSI, implying that mean and not systolic BP ensures tissue perfusion.[22]

Hypothermia (namely, body core temperature below 35°C [95°F]) is a well-known predictor of poor outcome in trauma patients. As part of the so called ≤lethal triad≥ along with acidosis and coagulopathy, may potentially exert harmful effects on the patient's physiological response to trauma, leading even to death.[4] Hypothermia is considered to be rather an epiphenomenon during physiological alterations induced by severe trauma and as such, often eludes clinical attention. The incidence of hypothermia among trauma patients may be found as high as 65%.[23] Severe injury can indeed make trauma patients almost 6 times more susceptible to heat loss, increasing thus the risk of hypothermia.[24] On the other hand, low environmental temperature, resuscitation using cold fluids, and the anesthesia per se are all predisposing factors for the development of hypothermia. The detrimental physiologic effects of hypothermia on organic function are well known and include arrhythmogenesis, depression of cardiac muscular activity, impairment of platelet (PLT) function, fibrinogen and other clotting factors depletion, decrease in liver drug metabolism and up to 50% decrease in glomerular filtration rate. Central nervous system function is also influenced by core temperature, making neurologic assessment of hypothermic trauma patients, unreliable.[25] In a retrospective study of 701491 trauma patients with recorded temperature on admission, Martin et al.[26] reported a 1.57% incidence of hypothermia (core temperature below 35°C) with hypothermic patients to exhibit significantly increase in mortality risk (25.5% vs. 3.0% in normothermic patients). Hypothermia not only proved to be an independent risk factor for increased mortality but also had a negative impact in ICU and ventilator days.[26] Interestingly, the harmful side effects of hypothermia seem to persist longer that hypothermia itself. Balvers et al.[27] concluded that the presence of hypothermia during ICU admission in a level I trauma center is associated with increased 1-day, as well as 1-month, mortality risk (odds ratio 2.72 and 2.82, respectively).[27]

Despite the previous wide use of mild hypothermia (32°C–35°C) for its ≤neuroprotective≥ effects in TBI patients, recent human studies not only failed to demonstrate any advantage of hypothermia but also proved an association between low body core temperature and increased risk of death, both in TBI and non-TBI patients.[28] Indeed, in a large multi-center randomized trial (Eurotherm 3235 trial), worse neurologic outcome, increased complication rates, and higher mortality risk were observed in TBI patients who were offered therapeutic hypothermia.[29] Consequently, hypothermia should no longer included in modern guidelines for the management of severe TBI.[30]

Lactate levels and base deficit

By definition, hemorrhage-induced hypovolemic shock is closely related either to tissue hypoxia because of a decrease in levels of saturated hemoglobin or to tissue hypoperfusion due to elimination of CO. Cellular metabolism shifts toward anaerobic pathways to maintain homeostasis with lactate acid being its major byproduct. BD represents a numerical value that can be modified by oxygen tension into the blood stream, minute ventilation, administration of medications, and resuscitation with fluids and blood products. Since arterial lactate acid level is closely related to tissue perfusion, it represents a valuable marker of the outcome in severe trauma patients.[4]

Gale et al.[31] reported on 1829 blunt trauma patients with elevated lactate on admission, in a large multi-centre prospective cohort study. Both, lactate levels and BD were higher in nonsurvivors. A 1 mmol/l increase in lactate levels was related to a 17% increase in mortality risk, while a 1 meq/l increase in BD caused the mortality risk to increase up to approximately 4%. After adjustment for Injury Severity Scores (ISSs), GCS, age and vital signs, Odom et al.[32] in a large retrospective trial of 4472 trauma patients at a level I trauma center found a proportional relationship between lactate blood levels and mortality risk. Trauma patients with normal lactate levels (that is below 2.5 mmol/L) had an odds ratio of 1 for mortality risk, whereas patients with moderately elevated (2.5–3.9 mmol/L) and high (>4 mmol/L) lactate levels had an odds ratio of 1.5 and 3.8, respectively, for death probability. After analyzing the subgroup of trauma patients with high lactate levels and profound shock, the authors concluded that lactate clearance during the first 6 h greatly predicts mortality.[32] That means that failure to reverse tissue hypoxia and consequent cellular derangement during the first 6 h following severe trauma is an indisputable marker of poor outcome. Interestingly, normotensive patients with elevated lactate blood levels are at high risk of dying because of their injury, thus questioning the true value of ≤normal≥ vital signs.[32] In 2014, Heinonen et al. conducted a retrospective study of 615 patients, 493 of which had complete lactate data. The survival rate of the patients with lactate values <2.5 mmol/L was 88%. Of the patients with high lactate levels that cleared within 24 and 48 h the survival rate were 81% and 71%, respectively. The survival rate among patients not achieving a normal lactate within 48 h was 46% but was higher in those with penetrating as opposed to blunt injury (67% versus 38%). The overall survival was 81%. The authors concluded that prolonged lactate clearance predicts increased mortality in severely injured trauma patients.[33] Lactate clearance has been proposed as a guide to resuscitation protocols in several studies.[34],[35],[36]

Furthermore, inotropic agents may play a role in increasing the lactate levels. Aerobic glucose metabolism to lactate may be a preferred way to rapidly produce significant energy amounts. Therefore, stimulating increased aerobic glucose metabolism has been shown to increase lactate levels in the absence of tissue hypoxia. Most notably, the administration of epinephrine has long been shown to result in a dose-dependent increase in lactate levels.[37]

There are conflicting reports about the effect of alcohol intoxication on lactate levels measurement and interpretation. It is well known that in patients abusing alcohol, found in almost one third of trauma cases, may cause metabolic acidosis.[38],[39] According to a large retrospective study by Gustafson et al.,[40] excessive ethanol consumption is related to lower mortality in patients with elevated lactate blood levels and lactic acidosis, presumably because of the ethanol-induced increase in lactate blood levels that produces false-positive laboratory results. The authors suggest a readjustment of low lactate threshold values used for the diagnosis of lactic acidosis in alcohol abused trauma patients.[40]

Coagulopathy

Clotting deficiency exerts a profound effect on trauma patient's outcome.[4] Coagulopathy is erroneously equated with hypocoagulopathy and bleeding diathesis which is partially true. Mechanisms of hemostasis are built on a sensitive balance between coagulation (hypocoagulation vs. hypercoagulation) and fibrinolysis (hyperfibrinolysis vs. early shutdown), which can be dissociated by trauma-induced metabolic effects. Trauma-induced coagulopathy (TIC) is a well-known mortality predicting factor.[41],[42]

In their study of over 20000 injured patients from a trauma cohort registry, MacLeod et al.[43] reported a substantial prevalence of coagulopathy, with 28% of trauma patients having abnormal prothrombin time (PT >14 s) and 8% abnormal partial thromboplastin time (APTT >34 s) before transfusion or fluid resuscitation. After adjustment for other risk factors as age, ISS, BP, hematocrit, and BD, patients with an abnormal PT had 35%, while those with elevated APTT, 326% increased risk of death.[43] On the other hand, in a study of 65 posttrauma ICU patients, Schreiber et al.[44] found, using thrombelastograph analysis (TEG), that 62% of patients exhibited hypercoagulation by the 1st day of ICU admission, although clotting times and PLT count were within normal range. Similarly, subclinical deep vein thrombosis was detected in 58% of asymptomatic trauma patients through contrast venography.[45]

Polymerization of fibrinogen into fibrin, along with PLT adhesion constitutes the final step for clot formation. Following bleeding control, and during fibrinolysis, a plasmin-mediated degradation of fibrin, secures vascular patency and prevents uncontrolled diffuse intravascular coagulation. Trauma interferes in both, formation and degradation of fibrinogen, causing major imbalance of clotting mechanism.[41] According to European guidelines on the management of major bleeding and coagulopathy following trauma, fibrinogen levels should always be assessed. The presence of fibrinogen levels below 1.5–2 g/L justifies administration of supplemental fibrinogen,[8] as low fibrinogen levels on admission, associated with hypotension (<90 mmHg) and increased lactate blood levels on hospital arrival, cause mortality risk to increase both at 24 h and 28 days.[46] Severe trauma patients may present with hyperfibrinolysis in up to 11%, are usually hypotensive during admission, have prolonged PT and APTT, are candidates for massive transfusion (odds ratio [OR], 19.1), and more prone to die during hospital stay (OR: 55.5).[47]

The CRASH-2 study, reported on more than 20,000 trauma patients and assessed the effect of administration of tranexamic acid (TXA) on the risk of bleeding, as well as the probability of hemorrhage-induced mortality.[48] Early administration of TXA resulted in significant reduction in bleeding risk, especially when applied within the 1st h after injury. Importantly, the authors found that administration of TXA three or more hours following trauma, did not reduce the mortality risk, but instead, led to increase in probability of death.[48] Failure of TXA administration to reduce mortality in trauma patients presented with coagulopathy-related hemorrhage has also been reported in several recent studies.[49],[50] Understanding the spectra of TIC, Moore et al.[51] categorized 2540 trauma patients according to fibrinolysis phenotype on TEG. Fibrinolysis shut down (inhibited fibrinolysis and inadequate fibrin degradation) was the most common phenotype (46%) followed by physiologic fibrinolysis (36%) and hyperfibrinolysis (18%). Hyperfibrinolysis was the phenotype with the higher mortality risk (OR: 3.3) versus fibrinolysis shut down (OR: 1.6).[51] Viscoelastometric assays (Thromboelastography and Rotational Thromboelastography), may prove useful in diagnosing specific derangements of coagulation in trauma patients, guide blood transfusion and predict mortality.[52]

PLT aggregation plays a critical role in coagulation cascade and the formation of clot. Keeping PLT count above 100,000/μL in trauma patients presenting with ongoing bleeding or TBI and above 50,000/μL in those without hemorrhage helps to reduce blood loss and improve survival.[8] It has been proved that a 50,000/μL increase in PLT absolute number results in approximately 12% drop in hemorrhage-related death risk, whereas the need for red blood cells (RBCs) transfusion lowers by 0.7 units at the same time.[53] On the other hand, trauma patients presented with PLT counts of more than 300,000/μL had 24-h mortality risk of 14%, compared with those with PLT counts of <100,000/μL, who carried a 24-h death risk of 33%.[53] According to Definitive Surgical Trauma Care Guidelines, PLT levels must be kept 50K for bleeding patients and 20K for those not actively bleeding patients.[54] Efforts should thus be made to keep PLT counts as higher as indicated for the higher the PTL count the better the survival.[53],[55]

Blood transfusion

Indisputably, blood transfusion can be proved a lifesaving procedure in severely bleeding trauma patients, although carrying several life-threatening complications, such as transfusion-related acute lung injury and transfusion-related immunomodulation, which may in turn increase morbidity and mortality.[56],[57],[58] Indeed, it has been shown that blood transfusion within the first 24 h following admission is correlated with a 6-fold increase in systemic inflammatory response syndrome (SIRS), making thus blood transfusion an independent predictor for either ICU admission (OR: 4.62) or mortality (OR: 4.23).[59] Blood transfusion was also proved to be a strong dose-dependent risk factor for the development of postinjury MOF.[60] It has also been recognized as a strong predictor of the length of hospitalization and mortality, with the latter increased by 16% for each unit of transfused RBC.[61] After Perel et al.[62] classified trauma patients according to their mortality risk based on Glasgow Coma Scale (GCS), age, HR, systolic BP, time since injury, and type of injury, they found that blood transfusion increased the risk of death in low-risk patients (<20% mortality risk), while carried significant benefits in high risk patients, that is, those who had mortality risk above 50%.[62]

Age, gender, and comorbidities

Excluding patients who die at the trauma scene or soon after admission from severe TBI or heavy bleeding, development of cardiovascular and respiratory complications, along with sepsis, ARDS, and MOF is strongly related to in-hospital mortality.[4],[7],[63],[64] As respiratory and cardiovascular impairment inevitably follows aging, trauma patients older than 65 years of age exhibit a 5-fold increase in mortality risk even following minor trauma (ISS <16).[65] Two recent meta-analyses on mortality in geriatric trauma patients concluded that age, along with the presence of comorbidities and other injury-related factors, is one of the strongest predictors of mortality. Indeed, trauma patients older than 75 years of age had 50%–67% higher possibility of dying compared to younger ones.[66],[67]

Morbidly obese patients with body mass index exceeding 35–40 kgXm −2 are known to be more susceptible to cardiovascular and respiratory comorbidities. Obesity and morbid obesity have been found to be independent risk factors for longer hospitalization and increased mortality in trauma patients.[68],[69] Moreover, physical status per se seems to greatly predict inpatient morbidity and in-hospital mortality in severe trauma patients,[70],[71] as mortality odds ratio significantly differs between ASA II and ASA I patients.[71]

As shown in a recent meta-analysis by Liu et al.,[72] males are more prone to porttrauma complications, have longer hospital stay and exhibit higher mortality rates than females. Female trauma patients are also at lower risk for sepsis and MOF, according to a recent analysis on a large number of injured patients registered in Trauma Register DGU.[73]

Scores and scales

As brain injury is the leading cause of death in trauma patients,[3] assessment of severity and potential neurologic outcome is of utmost importance. The GCS has been designed to globally evaluate the individual's neurological status,[30],[74] by assessing motor, verbal, and eyes responses. Although a low-GCS score on admission does not necessarily predict poor neurological outcome, GCS assessment 15 days after injury is a strong predictor of outcome and mortality risk.[75] Indeed, several studies showed that a low initial GCS (3/15) is related to an almost 50% survival rates and a 13.2% good neurological outcome. Pupil size and response proved to be stronger predicting factors of mortality than motor response, since almost 80% of patients with bilaterally fixed dilated pupils, eventually died.[76],[77],[78]

Currently, there are multiple trauma scoring systems, aiming at the classification of injuries according to their severity and the health status of the injured patients. Scoring systems such as Revised Trauma Score, Acute Physiology and Chronic Health Evaluation score, Sequential Organ Failure Assessment, and SIRS score, are all used to assess homeostasis, physiology, and organ function in trauma patients, whereas scoring systems such as ISS, new ISS, and ICD-based ISS are targeting mainly at the severity of the injury itself.[79],[80] Currently, there are numerous studies comparing scoring systems. Yet, their clinical application in everyday practice has been questioned, as more data are needed to be published to extract powerful and safe results.[81],[82],[83],[84]

SIRS criteria (temperature >38°C or <36°C, HR >90 bpm, respiratory rate >20 breaths per minute, and number of neutrophils >12,000/ml or <4000 ml) are usually used to assess critical illness. Combining SIRS criteria with other trauma severity markers allows for more accurate prognosis, regarding both morbidity and mortality in trauma patients.[85],[86],[87] As shown in a large series of trauma patients, Physiologic Trauma Score that combines the assessment of SIRS, evaluation of GCS and patient's age, is easy to calculate, superior to ISS, and efficient to predict mortality with an AUC of 0.95.[88]

Other markers

Calcium is a key element for coagulation cascade and vessel contraction process, and as such, is expected to have significant impact on resuscitation and outcome in injured patients. Magnotti et al.[89] showed that the presence of low (<1 mmol/L) ionized calcium levels on admission cause mortality rates to double (from 8.7% up to 15.5%). These results were confirmed by other studies, that showed that ionized calcium levels are also associated with hypotension,[90] as well as, severe calcium depletion is closely related to an up to 30% increase in mortality rates.[90],[91]

Acute gastrointestinal injury is considered the gastrointestinal onset of MOF due to critical illness independently of cause. Indeed, in severely ill patients, blood circulation shifts away from the gut, thus preserving functional integrity of the heart, kidneys, and brain. Ischemia follows allowing MOF process to commence.[92] Consequently, even in the absence of overt pancreatic or bowel trauma, serum amylase levels may be found elevated in trauma patients with massive bleeding. Hyperamylasemia (serum amylase levels above 250 U/L) has been shown to associate with higher risk of developing MOFS and increased mortality rates.[93],[94] Amylase-induced autodigestion process seems to be one of the main predisposing factors for increase mortality in hypovolemic trauma patients presenting with hyperamylasemia.[94]

Accordingly, serum S 100B protein, which is a brain-specific protein, has been found to correlate with inflammation processes and tissue hypoperfusion, even in non-TBI patients. Elevated serum S 100B protein levels serve as a marker of poor survival.[95],[96] Peripheral tissue oxygenation monitoring is a novel method for the early detection of tissue hypoperfusion and identify the patients who are susceptible to develop MOF.[97],[98]

Finally, trauma is well known to cause metabolic and hormonal alterations. Growth hormone and glucagon-like peptide 2 levels were found to be higher in nonsurviving trauma patients in a small observational study.[99]


   Conclusions Top


Most of the studies assessing mortality predicting factors in severely injured patients were retrospective or observational, and as such, they produced low levels of evidence. Although most contributing factors were excluded during regression and multivariate analysis of mortality risk, the risk of bias was still present, emphasizing thus the need for randomized trials. Currently, the main mortality-predicting factors in trauma patients are those associated with basic human physiology and tissue perfusion status (lactate levels, temperature), coagulation adequacy (clot formation and fibrinolysis), and resuscitation requirements (massive transfusions). On the other hand, advanced age and the presence of comorbidities predispose patients to a poor outcome because of the loss of physiological reserves. The clinician should pay great attention in identifying those factors, so to accordingly apply resuscitation and final treatment.

Compliance with Ethical Standards
"The authors (Emmanuel Lilitsis, Sofia Xenaki, Elias Athanasakis, Eleftherios Papadakis, Pavlina Syrogianni, George Chalkiadakis, Emmanuel Chrysos) declare that they have no competing interests."

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Krug EG, Sharma GK, Lozano R. The global burden of injuries. Am J Public Health 2000;90:523-6.  Back to cited text no. 1
    
2.
Mackenzie EJ, Rivara FP, Jurkovich GJ, Nathens AB, Frey KP, Egleston BL, et al. The national study on costs and outcomes of trauma. J Trauma 2007;63:S54-67.  Back to cited text no. 2
    
3.
K. Soreide. Epidemiology of major trauma. Br J Surg 2009;96:697-8.  Back to cited text no. 3
    
4.
International ATLS Committee, ACS, ATLS subcommittee. American College of Surgeons Committee on Trauma. Advance Life Support for doctors, Student course Manual 9th edition. J Trauma Acute Care Surg 2013;74:1363-6.  Back to cited text no. 4
    
5.
Demetriades D, Kimbrell B, Salim A, Velmahos G, Rhee P, Preston C, et al. Trauma deaths in a mature Urban trauma system: Is ≤trimodal≥ distribution a valid concept? J Am Coll Surg 2005;201:343-8.  Back to cited text no. 5
    
6.
Bouglé A, Harrois A, Duranteau J. Resuscitative strategies in traumatic hemorrhagic shock. Ann Intensive Care 2013;3:1.  Back to cited text no. 6
    
7.
Pfeifer R, Tarkin IS, Rocos B, Pape HC. Patterns of mortality and causes of death in polytrauma patients – Has anything changed? Injury 2009;40:907-11.  Back to cited text no. 7
    
8.
Rossaint R, Bouillon B, Cerny V, Coats TJ, Duranteau J, Fernández-Mondéjar E, et al. The European guideline on management of major bleeding and coagulopathy following trauma: Fourth edition. Crit Care 2016;20:100.  Back to cited text no. 8
    
9.
Stephens CT, Gumbert S, Holcomb JB. Trauma-associated bleeding: Management of massive transfusion. Curr Opin Anaesthesiol 2016;29:250-5.  Back to cited text no. 9
    
10.
Pacagnella RC, Souza JP, Durocher J, Perel P, Blum J, Winikoff B, et al. Asystematic review of the relationship between blood loss and clinical signs. PLoS One 2013;8:e57594.  Back to cited text no. 10
    
11.
Ley EJ, Salim A, Kohanzadeh S, Mirocha J, Margulies DR. Relative bradycardia in hypotensive trauma patients: A reappraisal. J Trauma 2009;67:1051-4.  Back to cited text no. 11
    
12.
Mizushima Y, Ueno M, Watanabe H, Ishikawa K, Matsuoka T. Discrepancy between heart rate and makers of hypoperfusion is a predictor of mortality in trauma patients. J Trauma 2011;71:789-92.  Back to cited text no. 12
    
13.
Callaway DW, Shapiro NI, Donnino MW, Baker C, Rosen CL. Serum lactate and base deficit as predictors of mortality in normotensive elderly blunt trauma patients. J Trauma 2009;66:1040-4.  Back to cited text no. 13
    
14.
Bohnen JD, Chang DC, Ramly EP, Olufajo OA, Le RT, Kaafarani HM, et al. Low baseline (pre-injury) blood pressure predicts inpatient mortality in elderly trauma patients: A bi-institutional study. J Trauma Acute Care Surg 2016;81:1142-9.  Back to cited text no. 14
    
15.
Victorino GP, Battistella FD, Wisner DH. Does tachycardia correlate with hypotension after trauma? J Am Coll Surg 2003;196:679-84.  Back to cited text no. 15
    
16.
Strnad M, Lesjak VB, Vujanović V, Pelcl T, Križmarić M. Predictors of mortality and prehospital monitoring limitations in blunt trauma patients. Biomed Res Int 2015;2015:983409.  Back to cited text no. 16
    
17.
Sloan EP, Koenigsberg M, Clark JM, Weir WB, Philbin N. Shock index and prediction of traumatic hemorrhagic shock 28-day mortality: Data from the DCLHb resuscitation clinical trials. West J Emerg Med 2014;15:795-802.  Back to cited text no. 17
    
18.
Rau CS, Wu SC, Kuo SC, Pao-Jen K, Shiun-Yuan H, Chen YC, et al. Prediction of Massive Transfusion in Trauma Patients with Shock Index, Modified Shock Index, and Age Shock Index. Int J Environ Res Public Health 2016;13:E683.  Back to cited text no. 18
    
19.
Olaussen A, Blackburn T, Mitra B, Fitzgerald M. Review article: Shock index for prediction of critical bleeding post-trauma: A systematic review. Emerg Med Australas 2014;26:223-8.  Back to cited text no. 19
    
20.
Pandit V, Rhee P, Hashmi A, Kulvatunyou N, Tang A, Khalil M, et al. Shock index predicts mortality in geriatric trauma patients: An analysis of the National Trauma Data Bank. J Trauma Acute Care Surg 2014;76:1111-5.  Back to cited text no. 20
    
21.
Kristensen AK, Holler JG, Hallas J, Lassen A, Shapiro NI. Is shock index a valid predictor of mortality in emergency department patients with hypertension, diabetes, high age, or receipt of β-or calcium channel blockers? Ann Emerg Med 2016;67:106-113.  Back to cited text no. 21
    
22.
Singh A, Ali S, Agarwal A, Srivastava RN. Correlation of shock index and modified shock index with the outcome of adult trauma patients: A prospective study of 9860 patients. N Am J Med Sci 2014;6:450-2.  Back to cited text no. 22
    
23.
Luna GK, Maier RV, Pavlin EG, Anardi D, Copass MK, Oreskovich MR, et al. Incidence and effect of hypothermia in seriously injured patients. J Trauma 1987;27:1014-8.  Back to cited text no. 23
    
24.
Peng RY, Bongard FS. Hypothermia in trauma patients. J Am Coll Surg 1999;188:685-96.  Back to cited text no. 24
    
25.
Perlman R, Callum J, Laflamme C, Tien H, Nascimento B, Beckett A, et al. Arecommended early goal-directed management guideline for the prevention of hypothermia-related transfusion, morbidity, and mortality in severely injured trauma patients. Crit Care 2016;20:107.  Back to cited text no. 25
    
26.
Martin RS, Kilgo PD, Miller PR, Hoth JJ, Meredith JW, Chang MC, et al. Injury-associated hypothermia: An analysis of the 2004 National Trauma Data Bank. Shock 2005;24:114-8.  Back to cited text no. 26
    
27.
Balvers K, Van der Horst M, Graumans M, Boer C, Binnekade JM, Goslings JC, et al. Hypothermia as a predictor for mortality in trauma patients at admittance to the Intensive Care Unit. J Emerg Trauma Shock 2016;9:97-102.  Back to cited text no. 27
[PUBMED]  [Full text]  
28.
Wang HE, Callaway CW, Peitzman AB, Tisherman SA. Admission hypothermia and outcome after major trauma. Crit Care Med 2005;33:1296-301.  Back to cited text no. 28
    
29.
Andrews PJ, Sinclair HL, Rodriguez A, Harris BA, Battison CG, Rhodes JK, et al. Hypothermia for intracranial hypertension after traumatic brain injury. N Engl J Med 2015;373:2403-12.  Back to cited text no. 29
    
30.
Carney N, Totten AM, O'Reilly C, Ullman JS, Hawryluk GW, Bell MJ, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery 2017;80:6-15.  Back to cited text no. 30
    
31.
Gale SC, Kocik JF, Creath R, Crystal JS, Dombrovskiy VY. A comparison of initial lactate and initial base deficit as predictors of mortality after severe blunt trauma. J Surg Res 2016;205:446-55.  Back to cited text no. 31
    
32.
Odom SR, Howell MD, Silva GS, Nielsen VM, Gupta A, Shapiro NI, et al. Lactate clearance as a predictor of mortality in trauma patients. J Trauma Acute Care Surg 2013;74:999-1004.  Back to cited text no. 32
    
33.
Heinonen E, Hardcastle TC, Barle H, Muckart JDJ. Lactate clearance predicts outcome after major trauma. Afr J Emerg Med 2014:61-5.  Back to cited text no. 33
    
34.
Régnier MA, Raux M, Le Manach Y, Asencio Y, Gaillard J, Devilliers C, et al. Prognostic significance of blood lactate and lactate clearance in trauma patients. Anesthesiology 2012;117:1276-88.  Back to cited text no. 34
    
35.
Vincent JL, Quintairos E Silva A, Couto L Jr., Taccone FS. The value of blood lactate kinetics in critically ill patients: A systematic review. Crit Care 2016;20:257.  Back to cited text no. 35
    
36.
Cheddie S, Muckart DJ, Hardcastle TC. Base deficit as an early marker of coagulopathy in trauma. S Afr J Surg 2013;51:88-90.  Back to cited text no. 36
    
37.
Griffith FR Jr., Lockwood JE, Emery FE. Adrenalin lactacidemia: Proportionality with dose. Am J Physiol 1939;3:415-21.  Back to cited text no. 37
    
38.
Dunne JR, Tracy JK, Scalea TM, Napolitano LM. Lactate and base deficit in trauma: Does alcohol or drug use impair their predictive accuracy? J Trauma 2005;58:959-66.  Back to cited text no. 38
    
39.
Herbert HK, Dechert TA, Wolfe L, Aboutanos MB, Malhotra AK, Ivatury RR, et al. Lactate in trauma: A poor predictor of mortality in the setting of alcohol ingestion. Am Surg 2011;77:1576-9.  Back to cited text no. 39
    
40.
Gustafson ML, Hollosi S, Chumbe JT, Samanta D, Modak A, Bethea A, et al. The effect of ethanol on lactate and base deficit as predictors of morbidity and mortality in trauma. Am J Emerg Med 2015;33:607-13.  Back to cited text no. 40
    
41.
Schreiber MA. Coagulopathy in the trauma patient. Curr Opin Crit Care 2005;11:590-7.  Back to cited text no. 41
    
42.
Chang R, Cardenas JC, Wade CE, Holcomb JB. Advances in the understanding of trauma-induced coagulopathy. Blood 2016;128:1043-9.  Back to cited text no. 42
    
43.
MacLeod JB, Lynn M, McKenney MG, Cohn SM, Murtha M. Early coagulopathy predicts mortality in trauma. J Trauma 2003;55:39-44.  Back to cited text no. 43
    
44.
Schreiber MA, Differding J, Thorborg P, Mayberry JC, Mullins RJ. Hypercoagulability is most prevalent early after injury and in female patients. J Trauma 2005;58:475-80.  Back to cited text no. 44
    
45.
Geerts WH, Code KI, Jay RM, Chen E, Szalai JP. A prospective study of venous thromboembolism after major trauma. N Engl J Med 1994;331:1601-6.  Back to cited text no. 45
    
46.
Rourke C, Curry N, Khan S, Taylor R, Raza I, Davenport R, et al. Fibrinogen levels during trauma hemorrhage, response to replacement therapy, and association with patient outcomes. J Thromb Haemost 2012;10:1342-51.  Back to cited text no. 46
    
47.
Ives C, Inaba K, Branco BC, Okoye O, Schochl H, Talving P, et al. Hyperfibrinolysis elicited via thromboelastography predicts mortality in trauma. J Am Coll Surg 2012;215:496-502.  Back to cited text no. 47
    
48.
Roberts I, Shakur H, Coats T, Hunt B, Balogun E, Barnetson L, et al. The CRASH-2 trial: A randomised controlled trial and economic evaluation of the effects of tranexamic acid on death, vascular occlusive events and transfusion requirement in bleeding trauma patients. Health Technol Assess 2013;17:1-79.  Back to cited text no. 48
    
49.
Harvin JA, Peirce CA, Mims MM, Hudson JA, Podbielski JM, Wade CE, et al. The impact of tranexamic acid on mortality in injured patients with hyperfibrinolysis. J Trauma Acute Care Surg 2015;78:905-9.  Back to cited text no. 49
    
50.
Valle EJ, Allen CJ, Van Haren RM, Jouria JM, Li H, Livingstone AS, et al. Do all trauma patients benefit from tranexamic acid? J Trauma Acute Care Surg 2014;76:1373-8.  Back to cited text no. 50
    
51.
Moore HB, Moore EE, Liras IN, Gonzalez E, Harvin JA, Holcomb JB, et al. Acute fibrinolysis shutdown after injury occurs frequently and increases mortality: A Multicenter evaluation of 2,540 severely injured patients. J Am Coll Surg 2016;222:347-55.  Back to cited text no. 51
    
52.
Veigas PV, Callum J, Rizoli S, Nascimento B, da Luz LT. A systematic review on the rotational thrombelastometry (ROTEM®) values for the diagnosis of coagulopathy, prediction and guidance of blood transfusion and prediction of mortality in trauma patients. Scand J Trauma Resusc Emerg Med 2016;24:114.  Back to cited text no. 52
    
53.
Brown LM, Call MS, Margaret Knudson M, Cohen MJ, Trauma Outcomes Group, Holcomb JB, et al. Anormal platelet count may not be enough: The impact of admission platelet count on mortality and transfusion in severely injured trauma patients. J Trauma 2011;71:S337-42.  Back to cited text no. 53
    
54.
International Association for Trauma Surgery and Intensive Care (IATSIC). Definitive Surgical Trauma Care (DSTC) – World Congress Surgery. Consensus Meeting. Basel: International Association for Trauma Surgery and Intensive Care (IATSIC); 2017.  Back to cited text no. 54
    
55.
Hallet J, Lauzier F, Mailloux O, Trottier V, Archambault P, Zarychanski R, et al. The use of higher platelet: RBC transfusion ratio in the acute phase of trauma resuscitation: A systematic review. Crit Care Med 2013;41:2800-11.  Back to cited text no. 55
    
56.
Toy P, Popovsky MA, Abraham E, Ambruso DR, Holness LG, Kopko PM, et al. Transfusion-related acute lung injury: Definition and review. Crit Care Med 2005;33:721-6.  Back to cited text no. 56
    
57.
Blajchman MA. Transfusion immunomodulation or TRIM: What does it mean clinically? Hematology 2005;10 Suppl 1:208-14.  Back to cited text no. 57
    
58.
Malone DL, Dunne J, Tracy JK, Putnam AT, Scalea TM, Napolitano LM, et al. Blood transfusion, independent of shock severity, is associated with worse outcome in trauma. J Trauma 2003;54:898-905.  Back to cited text no. 58
    
59.
Dunne JR, Malone DL, Tracy JK, Napolitano LM. Allogenic blood transfusion in the first 24 hours after trauma is associated with increased systemic inflammatory response syndrome (SIRS) and death. Surg Infect (Larchmt) 2004;5:395-404.  Back to cited text no. 59
    
60.
Moore FA, Moore EE, Sauaia A. Blood transfusion. An independent risk factor for postinjury multiple organ failure. Arch Surg 1997;132:620-4.  Back to cited text no. 60
    
61.
Robinson WP 3rd, Ahn J, Stiffler A, Rutherford EJ, Hurd H, Zarzaur BL, et al. Blood transfusion is an independent predictor of increased mortality in nonoperatively managed blunt hepatic and splenic injuries. J Trauma 2005;58:437-44.  Back to cited text no. 61
    
62.
Perel P, Clayton T, Altman DG, Croft P, Douglas I, Hemingway H, et al. Red blood cell transfusion and mortality in trauma patients: Risk-stratified analysis of an observational study. PLoS Med 2014;11:e1001664.  Back to cited text no. 62
    
63.
Probst C, Zelle BA, Sittaro NA, Lohse R, Krettek C, Pape HC, et al. Late death after multiple severe trauma: When does it occur and what are the causes? J Trauma 2009;66:1212-7.  Back to cited text no. 63
    
64.
Thompson HJ, Rivara FP, Nathens A, Wang J, Jurkovich GJ, Mackenzie EJ, et al. Development and validation of the mortality risk for trauma comorbidity index. Ann Surg 2010;252:370-5.  Back to cited text no. 64
    
65.
Clement ND, Tennant C, Muwanga C. Polytrauma in the elderly: Predictors of the cause and time of death. Scand J Trauma Resusc Emerg Med 2010;18:26.  Back to cited text no. 65
    
66.
Hashmi A, Ibrahim-Zada I, Rhee P, Aziz H, Fain MJ, Friese RS, et al. Predictors of mortality in geriatric trauma patients: A systematic review and meta-analysis. J Trauma Acute Care Surg 2014;76:894-901.  Back to cited text no. 66
    
67.
Sammy I, Lecky F, Sutton A, Leaviss J, O'Cathain A. Factors affecting mortality in older trauma patients-A systematic review and meta-analysis. Injury 2016;47:1170-83.  Back to cited text no. 67
    
68.
Liu T, Chen JJ, Bai XJ, Zheng GS, Gao W. The effect of obesity on outcomes in trauma patients: A meta-analysis. Injury 2013;44:1145-52.  Back to cited text no. 68
    
69.
Ditillo M, Pandit V, Rhee P, Aziz H, Hadeed S, Bhattacharya B, et al. Morbid obesity predisposes trauma patients to worse outcomes: A National Trauma Data Bank analysis. J Trauma Acute Care Surg 2014;76:176-9.  Back to cited text no. 69
    
70.
Ringdal KG, Skaga NO, Steen PA, Hestnes M, Laake P, Jones JM, et al. Classification of comorbidity in trauma: The reliability of pre-injury ASA physical status classification. Injury 2013;44:29-35.  Back to cited text no. 70
    
71.
Skaga NO, Eken T, Søvik S, Jones JM, Steen PA. Pre-injury ASA physical status classification is an independent predictor of mortality after trauma. J Trauma 2007;63:972-8.  Back to cited text no. 71
    
72.
Liu T, Xie J, Yang F, Chen JJ, Li ZF, Yi CL, et al. The influence of sex on outcomes in trauma patients: A meta-analysis. Am J Surg 2015;210:911-21.  Back to cited text no. 72
    
73.
Trentzsch H, Lefering R, Nienaber U, Kraft R, Faist E, Piltz S, et al. The role of biological sex in severely traumatized patients on outcomes: A matched-pair analysis. Ann Surg 2015;261:774-80.  Back to cited text no. 73
    
74.
Dinsmore J. Traumatic brain injury: An evidence-based review of management. Continuing education in anaesthesia, critical care & pain advance access. BJA Continuing Education in Anesthesia Crtitical Care and Pain 2013;33:189-95.  Back to cited text no. 74
    
75.
Kouloulas EJ, Papadeas AG, Michail X, Sakas DE, Boviatsis EJ. Prognostic value of time-related glasgow coma scale components in severe traumatic brain injury: A prospective evaluation with respect to 1-year survival and functional outcome. Int J Rehabil Res 2013;36:260-7.  Back to cited text no. 75
    
76.
Chamoun RB, Robertson CS, Gopinath SP. Outcome in patients with blunt head trauma and a glasgow coma scale score of 3 at presentation. J Neurosurg 2009;111:683-7.  Back to cited text no. 76
    
77.
Hoffmann M, Lefering R, Rueger JM, Kolb JP, Izbicki JR, Ruecker AH, et al. Pupil evaluation in addition to glasgow coma scale components in prediction of traumatic brain injury and mortality. Br J Surg 2012;99 Suppl 1:122-30.  Back to cited text no. 77
    
78.
Emami P, Czorlich P, Fritzsche FS, Westphal M, Rueger JM, Lefering R, et al. Impact of Glasgow Coma Scale score and pupil parameters on mortality rate and outcome in pediatric and adult severe traumatic brain injury: A retrospective, multicenter cohort study. J Neurosurg 2017;126:760-7.  Back to cited text no. 78
    
79.
Orhon R, Eren SH, Karadayı S, Korkmaz I, Coşkun A, Eren M, et al. Comparison of trauma scores for predicting mortality and morbidity on trauma patients. Ulus Travma Acil Cerrahi Derg 2014;20:258-64.  Back to cited text no. 79
    
80.
Lecky F, Woodford M, Edwards A, Bouamra O, Coats T. Trauma scoring systems and databases. Br J Anaesth 2014;113:286-94.  Back to cited text no. 80
    
81.
Tohira H, Jacobs I, Mountain D, Gibson N, Yeo A. Systematic review of predictive performance of injury severity scoring tools. Scand J Trauma Resusc Emerg Med 2012;20:63.  Back to cited text no. 81
    
82.
Cook A, Weddle J, Baker S, Hosmer D, Glance L, Friedman L, et al. Acomparison of the injury severity score and the trauma mortality prediction model. J Trauma Acute Care Surg 2014;76:47-52.  Back to cited text no. 82
    
83.
Deng Q, Tang B, Xue C, Liu Y, Liu X, Lv Y, et al. Comparison of the ability to predict mortality between the injury severity score and the new injury severity score: A Meta-analysis. Int J Environ Res Public Health 2016;13:825.  Back to cited text no. 83
    
84.
Hwang SY, Lee JH, Lee YH, Hong CK, Sung AJ, Choi YC, et al. Comparison of the sequential organ failure assessment, acute physiology and chronic health evaluation II scoring system, and trauma and injury severity score method for predicting the outcomes of Intensive Care Unit trauma patients. Am J Emerg Med 2012;30:749-53.  Back to cited text no. 84
    
85.
Malone DL, Kuhls D, Napolitano LM, McCarter R, Scalea T. Back to basics: Validation of the admission systemic inflammatory response syndrome score in predicting outcome in trauma. J Trauma 2001;51:458-63.  Back to cited text no. 85
    
86.
Bochicchio GV, Napolitano LM, Joshi M, McCarter RJ Jr., Scalea TM. Systemic inflammatory response syndrome score at admission independently predicts infection in blunt trauma patients. J Trauma 2001;50:817-20.  Back to cited text no. 86
    
87.
Hoover L, Bochicchio GV, Napolitano LM, Joshi M, Bochicchio K, Meyer W, et al. Systemic inflammatory response syndrome and nosocomial infection in trauma. J Trauma 2006;61:310-6.  Back to cited text no. 87
    
88.
Kuhls DA, Malone DL, McCarter RJ, Napolitano LM. Predictors of mortality in adult trauma patients: The physiologic trauma score is equivalent to the trauma and injury severity score. J Am Coll Surg 2002;194:695-704.  Back to cited text no. 88
    
89.
Magnotti LJ, Bradburn EH, Webb DL, Berry SD, Fischer PE, Zarzaur BL, et al. Admission ionized calcium levels predict the need for multiple transfusions: A prospective study of 591 critically ill trauma patients. J Trauma 2011;70:391-5.  Back to cited text no. 89
    
90.
Cherry RA, Bradburn E, Carney DE, Shaffer ML, Gabbay RA, Cooney RN, et al. Do early ionized calcium levels really matter in trauma patients? J Trauma 2006;61:774-9.  Back to cited text no. 90
    
91.
Choi YC, Hwang SY. The value of initial ionized calcium as a predictor of mortality and triage tool in adult trauma patients. J Korean Med Sci 2008;23:700-5.  Back to cited text no. 91
    
92.
Chen H, Zhang H, Li W, Wu S, Wang W. Acute gastrointestinal injury in the Intensive Care Unit: A retrospective study. Ther Clin Risk Manag 2015;11:1523-9.  Back to cited text no. 92
    
93.
Malinoski DJ, Hadjizacharia P, Salim A, Kim H, Dolich MO, Cinat M, et al. Elevated serum pancreatic enzyme levels after hemorrhagic shock predict organ failure and death. J Trauma 2009;67:445-9.  Back to cited text no. 93
    
94.
Schmid-Schönbein GW, Hugli TE. A new hypothesis for microvascular inflammation in shock and multiorgan failure: Self-digestion by pancreatic enzymes. Microcirculation 2005;12:71-82.  Back to cited text no. 94
    
95.
Zhao P, Gao S, Lin B. Elevated levels of serum S100B is associated with the presence and outcome of haemorrhagic shock. Clin Lab 2012;58:1051-5.  Back to cited text no. 95
    
96.
Stamataki E, Stathopoulos A, Garini E, Kokkoris S, Glynos C, Psachoulia C, et al. Serum S100B protein is increased and correlates with interleukin 6, hypoperfusion indices, and outcome in patients admitted for surgical control of hemorrhage. Shock 2013;40:274-80.  Back to cited text no. 96
    
97.
Ikossi DG, Knudson MM, Morabito DJ, Cohen MJ, Wan JJ, Khaw L, et al. Continuous muscle tissue oxygenation in critically injured patients: A prospective observational study. J Trauma 2006;61:780-8.  Back to cited text no. 97
    
98.
Cohn SM, Nathens AB, Moore FA, Rhee P, Puyana JC, Moore EE, et al. Tissue oxygen saturation predicts the development of organ dysfunction during traumatic shock resuscitation. J Trauma 2007;62:44-54.  Back to cited text no. 98
    
99.
Rowan MP, Beckman DJ, Rizzo JA, Isbell CL, White CE, Cohn SM, et al. Elevations in growth hormone and glucagon-like peptide-2 levels on admission are associated with increased mortality in trauma patients. Scand J Trauma Resusc Emerg Med 2016;24:119.  Back to cited text no. 99
    

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Correspondence Address:
Prof. Emmanuel Chrysos
Department of General Surgery, University Hospital of Crete, GR-71110, Heraklion Crete
Greece
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JETS.JETS_74_17

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