Severe trauma patient transfusion management is challenging; the identification of both occult and inadequately resuscitated shock is a major clinical problem with traditional markers. Additionally, occult shock can present with normal global haemodynamics . Severe polytrauma patient triage is crucial for good decision making regarding massive transfusion protocol (MTP) activation, which improves trauma haemorrhage outcomes . Transfusion recommendations in trauma management attempt to maintain haemoglobin levels at 70-90 g/l . Transfusions can be life saving but may also cause serious complications (i.e., TRALI, DIC, etc.) [12, 13]; inadequate transfusion and over-transfusion (Hb ≥ 110 g/l) are also harmful . Fewer transfusions can lead to low DO2 with global or local (i.e., different local DO2 in tissues and organs according to local perfusion) ischemia development with regard to oxygen consumption. Many articles have discussed the benefits of the restriction transfusion strategy compared with liberal transfusions . Haemoglobin could not be evaluated separately in traumatic haemorrhagic shock treatments; however, other markers may account for patient comorbidities (i.e., coronary disease), age and clinical status. Hb targets could differ according to the treatment period; Hb values of approximately 70 g/l could be low during initial treatments, particularly with a low CI or with severe comorbidities. This value could be sufficient in the next period of critical care, which starts after the initial shock and bleeding are resolved. Higher haemoglobin levels in the initial treatment period could reduce haemodilutions and decrease any potential ischemia if re-bleeding occurs; thus, mortality could be reduced . Additional transfusion benefits could include restored blood viscosity and enhanced rheological properties of the blood. Transfusion of PRBC, which are the most frequent transfusion media, compared to fresh blood transfusions, may not provide immediate increase of oxygen delivery to tissues primarily due to transfusion storage length. A decrease in LPR could delay an increase in haemoglobin levels for 7-10 hours, and tissue ischemia could be eliminated over long time intervals . Similarly, this phenomenon could be observed with LPR and ScvO2 trends, whereby a decrease in LPR could delay an increase in ScvO2 for 10 hours . The average observed haemoglobin in the first 24 hours of this study, which included the suspected haemoconcentration period, were 97.70 ± 18.67 g/l; therefore, it could be speculated that if this value was approximately 70 g/l, then tissue ischemia could be eliminated at a much later period, and organ dysfunction could be worsened.
Additionally, fluid administration, which is a core treatment for shock and hypovolemia for preserving effective haemodynamic functions and tissue perfusion, has limits and adverse effects. Excessive fluid amounts lead to diluted coagulation factors, hypothermia  and endothelial glycocalyx damage . Hypervolemia and fluid overload also lead to interstitium expansion. These influence the transcapillary gas and substrate exchange and decrease oxygen transport to tissues . Hypovolemia leads to vasoconstriction and microvasculatory blood flow restriction, which cause ischemia due to low oxygen and substrate delivery . Tissue perfusion could be altered with the administration of vasoactive agents, and knowledge of metabolic tissue conditions (i.e., LPR) during haemostatic resuscitation could help guide treatment.
Lactataemia evaluation in shock is typically difficult in practice; elevated arterial lactate levels are associated with increased mortality and morbidity , and lactate normalisation is one of most frequent resuscitation targets. Arterial lactate could be elevated without clinical signs of shock but could also be an indication of on-going ischemia . In contrast, during a shock state, lactate could accumulate in low or non-perfused tissues, and serum levels could be falsely determined to be low. After tissue perfusion is restored, lactate levels increase as a sign of reperfusion, and high lactate levels could be connected with normal aerobic metabolism. The normalisation of lactate values depends on the hepatic clearance of lactate or its consumption in tissues, which could also decrease during shock. It is expected that lactate levels will follow the oxygen debt, but in some clinical conditions, lactate levels may normalise without the resolution of tissue oxygen debt . There are also a number of non-ischemic factors that elevate lactate levels (e.g., stress and catecholamines) . Arterial lactate levels should, therefore, be critically evaluated because assessment of the lactate levels alone fails to discriminate between ischemia and aerobiosis .
The measurement of LPR could be more useful than that of arterial lactate levels alone when discriminating between occult shock with ischemic tissue conditions and aerobic metabolism. LPR may be used as an early indicator of emerging ischemia during shock [24, 25] and could also help to discriminate between elevated ischemic or non-ischemic lactate levels and to distinguish between the anaerobic aspects of hyperlactataemia . Hyperlactataemia with elevated LPR levels is associated with higher mortality than hyperlactataemia with normal LPR levels . LPR levels over 25 indicate anaerobic metabolism onset  and are a more precise marker of ischemia than lactate levels alone .
ScvO2 is a frequently used marker that is useful in guiding fluid, catecholamine and transfusion therapy . It is a global parameter of the oxygen extraction sum from the blood, and therefore, normal values do not exclude severe local tissue damage or regional tissue ischemia. It is expected that low ScvO2 could reflect low DO2. The most respected target value for shock resuscitation is an ScvO2 value above 70% ; however, emerging ischemia originates at the cellular level, and changes in the LPR value could precede that in the ScvO2 value by 10 or 11 hours . A low ScvO2 could lead to DO2 manipulation, but a normal or high ScvO2 could lead to false satisfaction due to treatment, allowing background cell dysfunction to occur.
Haemodynamic monitoring of CO is typically the next most frequent measurement in the evaluation of traumatic haemorrhagic shock. Trauma patients may have a low CI in the first hours after trauma (i.e., the ebb phase of shock). Tachycardia could then occur to preserve CI during hypovolemia, and later, CI rises to supranormal values to act as a physiologic reserve marker and as a compensatory reaction to overcoming distress (i.e., the flow phase of shock). In contrast, a normal CI value may not ensure adequate tissue perfusion . Many authors have examined the evaluation of the VO2/DO2 relationship. A normalised VO2 seems to be essential for organism recovery, and oxygen supply independency is a key strategy for haemodynamic optimisation . Increasing DO2 to supranormal values, however, was found to be beneficial in some studies , but not in others . Additionally, excessive oxygen supply may be deleterious due to ineffective metabolic costs; however, it may be reasonable to increase the DO2 to 20% above the critical DO2 value (i.e., the limit of DO2/VO2 dependency) . Velmahos GC demonstrated that patients who achieved supranormal haemodynamic parameters (i.e., CI > 4.5 l/min/m2, DO2I > 600 ml/min/m2 and VO2I > 170 ml/min/m2) after severe trauma had better outcomes than patients who did not achieve those limits . A spontaneously high DO2 could be used as a simple physiologic reserve marker and a predictor of outcomes. An excessive artificial increase in DO2 without a functional organism reserve could be detrimental . Resuscitation efforts should be limited to what is only necessary with respect to human variability .
In this study, Hb < 70 g/l (i.e., without a CI distinction, whereby different CI are included) was associated with pathologic lactate, ScvO2 and LPR values; therefore, treatment interventions or more intensive monitoring were inevitable (Table 2.). Pathologic blood lactate levels in all Hb intervals were also observed and certainly influenced the reduced lactate clearance during the first 24 hours after trauma.
To eliminate tissue ischemia (i.e., normalise LPR), it is rational to increase the DO2, but only in patients with Hb values of 70-90 g/l and a low CI; with a normal CI and Hb < 70 g/l; or, most likely, with a low CI and Hb < 70 g/l (Table 3.). An artificial CI increase to supranormal values could be beneficial, but only if it is accomplished when Hb < 70 g/l to avoid an ischemic LPR; however, potential adverse vasoactive medication effects may occur. It may be beneficial to transfuse to Hb 70-90 g/l and a normal CI, which will also lead to a normal LPR. An ischemic LPR with supranormal CI values was not observed, supporting the benefits of the physiologic reaction to trauma discussed above. Increasing a low CI to normal is rational in patients with Hb levels at 70-90 g/l and most likely <70 g/l. In cases where Hb > 90 g/l, the increase of a low CI to normal levels leads to a decrease in LPR; however, the LPR in both of these situations is under the ischemic threshold. A low CI should be avoided.
To avoid tissue ischemia, transfusions are applicable in patients with Hb < 70 g/l and a normal CI and most likely in low CI cases as well. An Hb increase to over 90 g/l could only be warranted when patients have a low CI; however, it is preferable to increase a low CI. With regard to LPR, it was shown that supranormal CI levels could be used to treat tissue ischemia, but the artificial elevation of CI could be dangerous . Another requirement is to adequately correct the blood oxygen content using not only Hb but also SaO2 and PaO2.
This study has several limitations. Tissue monitoring in the early phase of management of severe trauma patients is typically difficult. In this timeframe, physicians employ several necessary interventions, including diagnostic and therapeutic methods. The observations of this study were performed in addition to and did not influence the standard care of the examined critically ill patients; tissue monitoring was begun within 6 hours after admission. The study was performed in full working Trauma centre. The authors enrolled only 48 patients, and each patient was enrolled by a physician associated with this study. The authors also had limited human and economic resources. The study was financial supported partially by a grant, and certain technical problems with encountered with equipment during testing.