Research progress of acute coagulopathy of trauma-shock

Acute coagulopathy of trauma-shock (ACoTS) occurs in 25% of patients with severe trauma in the early phase, and the mortality of those patients is four-fold higher than patients without coagulopathy. The pathophysiology of this complicated phenomenon has been focused on in recent years. Tissue injury and hypoperfusion, activated protein C and Complements play important roles in the early phase after trauma. While the use of blood products, hypothermia, acidosis and inflammation are the main mechanism in late phase. Supplementing coagulation factors and platelets to improve ACoTS are inefficient. Only positive resuscitation from shock and improving tissue hypoperfusion have expected benefits.     

Management of major blood loss: An update

Haemorrhage remains a major cause of potentially preventable deaths. Trauma and massive transfusion are associated with coagulopathy secondary to tissue injury, hypoperfusion, dilution and consumption of clotting factors and platelets. Concepts of damage control surgery have evolved, prioritizing the early control of the cause of bleeding by non‐definitive means, while haemostatic control resuscitation seeks early control of coagulopathy. Haemostatic resuscitation provides transfusions with plasma and platelets in addition to red blood cells (RBCs) in an immediate and sustained manner as part of the transfusion protocol for massively bleeding patients. Transfusion of RBCs, plasma and platelets in a similar proportion as in whole blood prevents both hypovolaemia and coagulopathy. Although an early and effective reversal of coagulopathy is documented, the most effective means of preventing coagulopathy of massive transfusion remains debated and randomized controlled studies are lacking. Results from recent before‐and‐after studies in massively bleeding patients indicate that trauma exsanguination protocols involving the early administration of plasma and platelets are associated with improved survival. Furthermore, viscoelastic whole blood assays, such as thrombelastography (TEG)/rotation thromboelastometry (ROTEM), appear advantageous for identifying coagulopathy in patients with severe haemorrhage, as opposed to conventional coagulation assays. In our view, patients with uncontrolled bleeding, regardless of its cause, should be treated with goal‐directed haemostatic control resuscitation involving the early administration of plasma and platelets and based on the results of the TEG/ROTEM analysis. The aim of the goal‐directed therapy should be to maintain a normal haemostatic competence until surgical haemostasis is achieved, as this appears to be associated with reduced mortality.     

Le concept de damage control resuscitation

Objective

Damage control is a strategy of care for bleeding trauma patients, involving minimal rescue surgery associated to perioperative resuscitation. The purpose of this review is to draw up a statement on current knowledge available on damage control.

Data sources

References were obtained from recent review articles, personal files, and Medline database research of English and French publications. All categories of articles on this topic have been selected.

Data synthesis

Historical damage control surgery, that consist of abbreviated laparotomy with second-look after resuscitation, is now included in a wider concept called “damage control resuscitation”, addressing the lethal triad (coagulopathy, hypothermia and acidosis) at an early phase. Care is focused on coagulopathy prevention. Early resuscitation, or damage control ground zero, has been improved: aggressive management of hypothermia, bleeding control techniques, permissive hypotension concept and early use of vasopressors. Transfusion practices also have evolved: early platelets and coagulation factors administration, use of hemostatic agents like recombinant FVIIa, whole blood transfusion, denote the damage control hematology. Progress in surgical practices and development of arteriographic techniques lead to wider indications of damage control strategy.     

Gerinnungsmanagement bei Polytrauma mit Hilfe viskoelastischer Tests

Exsanguination represents the most common and potentially preventable cause of death in major trauma patients. Rapid surgical intervention coupled with an early and aggressive hemostatic therapy not only results in survival benefits of coagulopathic trauma patients, but also reduces the incidence of complications and costs. Standard coagulation tests are not suitable to adequately characterize the complexity of trauma-induced coagulopathy (TIC). This fact has led to a renaissance of viscoelastic tests, such as rotational thromboelastometry (ROTEM®) and thrombelastography (TEG®), which can be used as point-of-care monitors. In some trauma centers treatment algorithms have been developed, where hemostatic therapy is based on viscoelastic test results. Shock and tissue trauma activate profibrinolytic pathways which in turn result in premature dissolution of formed clots. Tranexamic acid rapidly and inexpensively blocks hyperfibrinolysis. ROTEM®/TEG® measurements revealed that diminished clot strength is associated with an increased bleeding tendency. Depending on the underlying cause, administration of fibrinogen concentrate and/or platelet concentrate administration improves clot firmness. Thrombin generation is initially less compromised and can be improved by the administration of plasma, prothrombin complex concentrate, or with restrictiveness by recombinant activated factor VII.     

Blood component therapy in trauma guided with the utilization of the perfusionist and thromboelastography

25-35% of all seriously injured multiple trauma patients are coagulopathic upon arrival to the emergency department, and therefore early diagnosis and intervention on this subset of patients is important. In addition to standard plasma based tests of coagulation, the thromboelastogram (TEG) has resurfaced as an ideal test in the trauma population to help guide the clinician in the administration of blood components in a goal directed fashion. We describe how thromboelastographic analysis is used to assist in the management of trauma patients with coagulopathies presenting to the emergency department, in surgery, and in the postoperative period. Indications for the utilization of the TEG and platelet mapping as point of care testing that can guide blood component therapy in a goal directed fashion in the trauma population are presented with emphasis on the more common reasons such as massive transfusion protocol, the management of traumatic brain injury with bleeding, the diagnosis and management of trauma in patients on platelet antagonists, the utilization of recombinant FVIIa, and the management of coagulopathy in terminal trauma patients in preparation for organ donation. The TEG allows for judicious and protocol assisted utilization of blood components in a setting that has recently gained acceptance. In our program, the inclusion of the perfusionist with expertise in performing and interpreting TEG analysis allows the multidisciplinary trauma team to more effectively manage blood products and resuscitation in this population.     

The acute coagulopathy of trauma shock: Clinical relevance

Recent observational studies have identified an acute coagulopathy in trauma victims that is present on arrival in the emergency room. It has been associated with a four-fold increase in mortality and increased incidence of organ failure. Conventional trauma resuscitation and transfusion protocols are designed for dilutional coagulopathy and appear inadequate in the management of acute traumatic coagulopathy and massive transfusion.Acute Coagulopathy of Trauma Shock (ACoTS) is caused by a combination of tissue injury and shock, and may occur without significant fluid administration, clotting factor depletion or hypothermia. The mechanism through which acute coagulopathy develops is unclear but activation of the protein C pathway has been implicated.Standard coagulation tests do not identify cases in a timely fashion and ACoTS should be suspected in any trauma patient with a significant magnitude of injury and shock, as evidenced by an abnormal admission base deficit on blood gas. Development of point of care coagulometers and whole blood coagulation analysers, such as rotational thromboelastometry, may enable earlier laboratory identification of this group. Retrospective studies performed by the American military indicate that resuscitation of severely injured patients with higher ratios of plasma given early may improve outcome and reduce overall blood product use. The place of adjunctive pharmaceutical agents within this strategy remains unclear.There is an acute coagulopathy associated with trauma and shock that is an independent predictor of outcomes. Delineation of this entity, with directed management protocols should lead to a reduction in avoidable deaths from haemorrhage after trauma.     

Fresh frozen plasma should be given earlier to patients requiring massive transfusion

BACKGROUND: Acidosis, hypothermia, and coagulopathy were identified more than 20 years ago as a deadly triad for patients presenting with exsanguinating hemorrhage. This led to fundamental changes in initial management of severely injured patients. Despite major advances, hemorrhage remains a leading cause of early death in trauma patients. Recent studies report most severely injured patients to be coagulopathic at admission, before resuscitation interventions, and that traditional massive transfusion practice grossly underestimates needs. The hypothesis for this study is that our pre-intensive care unit (ICU) massive transfusion (MT) protocol does not adequately correct coagulopathy, and that early uncorrected coagulopathy is predictive of mortality. METHODS: Data maintained in our Trauma Research Database were reviewed. Univariate logistic regression analysis was used to analyze the association of early ICU international normalized ratio (INR) and outcomes, including survival. RESULTS: Ninety-seven of 200 patients admitted during 51 months (ending January 2003) and resuscitated using our standardized ICU shock resuscitation protocol received MT (> or =10 units packed red blood cells [PRBC]) during hospital day 1 (age, 39 +/- 2; ISS, 29 +/- 1; survival, 70%.) All patients required emergency operating room and/or interventional radiology procedures and arrived in the ICU 6.8 +/- 0.3 hours after admission. Coagulopathy, present at hospital admission (pre-ICU INR, 1.8 +/- 0.2), persisted at ICU admission (initial ICU INR, 1.6 +/- 0.1). Pre-ICU resuscitation, 9 +/- 1 L crystalloid fluid, 12 +/- 1 units PRBC, 5 +/- 0.4 units fresh frozen plasma (FFP), was consistent with our MT protocol by which FFP was not given until after 6 units PRBC. ICU resuscitation involved 11 +/- 1 L lactated Ringer's solution (LR) and 10 +/- 1 units PRBC. Mean pH was normal within 8 hours. Mean temperature increased from approximately 35 degrees C to >37 degrees C within 4 hours. In the ICU during resuscitation, patients received 10 +/- 1 units FFP for coagulopathy; the ratio of FFP:PRBC was 1:1. Mean INR decreased to 1.4 +/- 0.03 within 8 hours and remained nearly constant for the remaining 16 hours of ICU resuscitation, indicating moderate coagulopathy. Statistical analysis found severity of coagulopathy (INR) at ICU admission associated with survival outcome (p = 0.02; area under receiver operator curve [ROC] = 0.71.) CONCLUSION: These data indicate acidosis and hypothermia to be well managed. Coagulopathy was not corrected in the ICU despite adherence to pre-ICU MT and ICU protocols, likely because of inadequate pre-ICU intervention. More aggressive pre-ICU intervention to correct coagulopathy may be effective in decreasing PRBC requirement during ICU resuscitation, and, because of the association with increased mortality, could improve outcome. We have revised our pre-ICU MT protocol to emphasize early FFP in a FFP:PRBC ratio of 1:1. We think that treatment of coagulopathy can be improved with the development of standardized protocols, both empiric and data driven.     

Fibrin patch in a pig model with blunt liver injury under severe hypothermia

Background

Rapid control of hemorrhage is one of the key aspects in trauma handling. To cope with bleeding, local hemostatic approaches are useful, along with surgical and systemic homostatic therapy. In this experimental study, we investigated the efficacy of a fibrinogen/thrombin containing collagen patch (TachoSil) in a coagulopathic pig model with blunt liver trauma under severe hypothermia.

Methods

Eighteen anesthetized pigs underwent hemodilution by exchanging 70% of the blood volume with Ringer Lactate solution and hydroxyethyl starch 130/0.4 (1:1). Ten minutes after induction of a grade III blunt liver trauma, the animals randomly received treatment with TachoSil (FT-patch, n = 9) or a collagen patch (Tachotop, control group, n = 9). Blood loss, hemodynamics, and coagulation parameters were observed for 2 h. To confirm the consistency of liver trauma, pathologic examination of the liver tissue was performed.

Results

Hypothermia (33.5°C ± 0.5°C) and hemodilution led to severe coagulopathy as measured by thromboelastometry and coagulation parameters. After trauma and patch application, thromboelastometry and coagulation parameters in the control group showed further deterioration compared with the stable parameters in the FT-patch group. The total blood loss was significantly reduced in the FT-patch group (FT-patch: 1195 mL; control group: 2495 mL; P < 0.001). Concordantly, the control animals were hemodynamically jeopardized to a higher degree. Microscopy confirmed a similar degree of liver injury.

Conclusions

Despite severe hypothermia and coagulopathy, TachoSil provided effective hemorrhage control in pigs with blunt liver injury. Therefore, TachoSil demonstrated usefulness as an additional early therapy in cases of uncontrolled bleeding following severe trauma.     

Coagulation management in trauma patients

Hemorrhage after traumatic injury results in coagulopathy which only worsens the situation. This coagulopathy is caused by depletion and dilution of clotting factors and platelets, increased fibrinolytic activity, hypothermia, metabolic changes and anemia. The effect of synthetic colloids in compensating the blood loss further aggravates the situation. Bedside coagulation monitoring permits relevant impairment of the coagulation system to be detected very early and the efficacy of the hemostatic therapy to be controlled directly. Administration of fresh frozen plasma, platelet concentrations, clotting factors and probably antifibrinolytic agents is essential in restoring the impaired coagulation system in trauma patients.     

Factor VIIa for correction of traumatic coagulopathy

INTRODUCTION: Activated factor VIIa (FVIIa) was developed to treat hemophiliacs with high-titer antibodies to factor VIII. FVIIa initiates thrombin formation by binding with exposed tissue factor. Anecdotal reports have described the utility of FVIIa in correcting coagulopathy from trauma, but no large series exists. We present our experience with 81 coagulopathic trauma patients treated using FVIIa in years 2001-2003, compared with "control" patients matched from the trauma registry from the same time period. METHODS: Use of FVIIa was restricted to active hemorrhage with clinical coagulopathy. We recorded the cause of coagulopathy, dose of FVIIa administered, effect on clinical coagulation, pertinent laboratory values, length of stay, number and type of blood products administered, and patient outcome. For the same time period we also examined outcomes in coagulopathic patients who did not receive FVIIa. RESULTS: Causes of coagulopathy were diverse, and included acute traumatic hemorrhage (46 patients), traumatic brain injury (20), warfarin use (9), congenital Factor VII deficiency (2), and other acquired hematologic defects (4). Coagulopathy was reversed in 61/81 cases (75%), with an associated reduction in PT from 19.6 to 10.8 (p=0.000018). 34 patients (42%) survived to hospital discharge (20/46 traumatic hemorrhage, 5/20 TBI, 4/9 on warfarin, 2/2 factor deficient, 3/4 other). Patients died from irreversible shock, multiple organ system failure, or traumatic brain injury. FVIIa patients had a higher mortality than coagulopathic controls matched by specific anatomic injuries, admission lactate value, and predicted probability of survival. Only a group identified by all three characteristics had a similar mortality to the FVIIa cohort, but the number of patients that could be matched this way was too small to be meaningful. CONCLUSION: FVIIa therapy lead to an immediate reduction in coagulopathic hemorrhage in most cases, accompanied by a significant improvement in laboratory measures. Application of FVIIa as a therapy of last resort makes the identification of equivalent control patients difficult. Use of FVIIa should be considered for any patient with coagulopathic hemorrhage in which surgically-accessible bleeding has been controlled. Prospective trials of FVIIa in patients with traumatic coagulopathy are strongly indicated, and should focus on appropriate patient selection and the dose and timing of therapy.     

Recombinant activated factor VII for the rapid correction of coagulopathy in nonhemophilic neurosurgical patients

OBJECTIVE: Coagulopathy is a significant contraindication for neurosurgery. Unfortunately, many coagulopathic patients require urgent neurosurgical intervention. Standard use of blood products, including fresh-frozen plasma or prothrombin complexes, to correct the coagulopathy often leads to significant delays in treatment. Recombinant activated factor VII (rFVIIa) is a medication originally designed to treat bleeding in hemophiliacs but also seems to correct a wide variety of coagulopathies rapidly and safely in nonhemophilic patients. METHODS: The medical records of nine patients with coagulopathy requiring urgent neurosurgical intervention were reviewed retrospectively. Each patient was given a dose ranging from 40 to 90 microg/kg of rFVIIa before undergoing surgery. Pre-rFVIIa coagulation and post-rFVIIa coagulation parameters were obtained. Once correction of the coagulopathy was verified, each patient underwent the appropriate neurosurgical procedure. RESULTS: The average age of the patients was 40.9 years; six were women. The causes of the coagulopathy included anticoagulant medication, liver dysfunction, and dilutional coagulopathy after traumatic hemorrhage. Neurosurgical indications included intraparenchymal/intraventricular hemorrhage, hydrocephalus, diffuse cerebral edema, and epidural hematoma. Post-rFVIIa coagulation parameters obtained as early as 20 minutes after infusion of the medication showed normalization of values. There were no procedural or operative complications and no postoperative hemorrhagic complications. No associated thromboembolic or other complications with the use of rFVIIa were observed. CONCLUSION: The use of rFVIIa for the urgent surgical treatment of coagulopathic patients is quite promising. Further studies, including randomized, prospective trials using rFVIIa to address issues such as optimal dosing, efficacy, surgical indications, cost-effectiveness, morbidity, and mortality are needed.     

Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway?

OBJECTIVES: Coagulopathy following major trauma is conventionally attributed to activation and consumption of coagulation factors. Recent studies have identified an acute coagulopathy present on admission that is independent of injury severity. We hypothesized that early coagulopathy is due to tissue hypoperfusion, and investigated derangements in coagulation associated with this. METHODS: This was a prospective cohort study of major trauma patients admitted to a single trauma center. Blood was drawn within 10 minutes of arrival for analysis of partial thromboplastin and prothrombin times, prothrombin fragments 1+2, fibrinogen, thrombomodulin, protein C, plasminogen activator inhibitor-1, and D-dimers. Base deficit (BD) was used as a measure of tissue hypoperfusion. RESULTS: A total of 208 patients were enrolled. Patients without tissue hypoperfusion were not coagulopathic, irrespective of the amount of thrombin generated. Prolongation of the partial thromboplastin and prothrombin times was only observed with an increased BD. An increasing BD was associated with high soluble thrombomodulin and low protein C levels. Low protein C levels were associated with prolongation of the partial thromboplastin and prothrombin times and hyperfibrinolysis with low levels of plasminogen activator inhibitor-1 and high D-dimer levels. High thrombomodulin and low protein C levels were significantly associated with increased mortality, blood transfusion requirements, acute renal injury, and reduced ventilator-free days. CONCLUSIONS: Early traumatic coagulopathy occurs only in the presence of tissue hypoperfusion and appears to occur without significant consumption of coagulation factors. Alterations in the thrombomodulin-protein C pathway are consistent with activated protein C activation and systemic anticoagulation. Admission plasma thrombomodulin and protein C levels are predictive of clinical outcomes following major trauma.     

Gerinnungsmanagement beim Polytrauma

Hemorrhage after traumatic injury results in coagulopathy which only worsens the situation. This coagulopathy is caused by depletion and dilution of clotting factors and platelets, increased fibrinolytic activity, hypothermia, metabolic changes and anemia. The effect of synthetic colloids used for compensating the blood loss, further aggravates the situation through their specific action on the hemostatic system. Bedside coagulation monitoring permits relevant impairment of the coagulation system to be detected very early and the efficacy of the hemostatic therapy to be controlled directly. Administration of fresh frozen plasma (FFP), platelet concentrates and antifibrinolytic agents is essential for restoring the impaired coagulation system in trauma patients. Clotting factor concentrates should be administered if coagulopathy is based on diagnosed depletion of clotting factors, if FFP is not available and if transfusion of FFP is insufficient to treat the coagulopathy. Recombined FVIIa is frequently employed during severe bleeding which could not be treated by conventional methods but the results of on-going clinical trials are not yet available.     

The coagulopathy of trauma

Trauma is a leading cause of death, with uncontrolled hemorrhage and exsanguination being the primary causes of preventable deaths during the first 24 h following trauma. Death usually occurs quickly, typically within the first 6 h after injury. One out of four patients arriving at the Emergency Department after trauma is already in hemodynamic and hemostatic depletion. This early manifestation of hemostatic depletion is referred to as the coagulopathy of trauma, which may distinguished as: (i) acute traumatic coagulopathy (ATC) and (ii) iatrogenic coagulopathy (IC). The principle drivers of ATC have been characterized by tissue trauma, inflammation, hypoperfusion/shock, and the acute activation of the neurohumoral system. Hypoperfusion leads to an activation of protein C with cleavage of activated factors V and VIII and the inhibition of plasminogen activator inhibitor-1 (PAI-1), with subsequent fibrinolysis. Endothelial damage and activation results in Weibel–Palade body degradation and glycocalyx shedding associated with autoheparinization. In contrast, there is an IC which occurs secondary to uncritical volume therapy, leading to acidosis, hypothermia, and hemodilution. This coagulopathy may, then, be an integral part of the “vicious cycle” when combined with acidosis and hypothermia. The awareness of the specific pathophysiology and of the principle drivers underlying the coagulopathy of trauma by the treating physician is paramount. It has been shown that early recognition prompted by appropriate and aggressive management can correct coagulopathy, control bleeding, reduce blood product use, and improve outcome in severely injured patients. This paper summarizes: (i) the current concepts of the pathogenesis of the coagulopathy of trauma, including ATC and IC, (ii) the current strategies available for the early identification of patients at risk for coagulopathy and ongoing life-threatening hemorrhage after trauma, and (iii) the current and updated European guidelines for the management of bleeding and coagulopathy following major trauma.     

急性创伤性凝血病与创伤复苏治疗

由创伤引起的急性剖伤性凝血病可发生于创伤早期,通常仅见于休克患者。凝血病产生不可控制的失血是严重创伤的主要死亡原因。关键在患者入院当初,早期发现创伤性凝血病。创伤性凝血病的启动因素可能是组织低灌注引发蛋岛C——凝血酶调节蛋白系统过度活化,产生全身性抗凝和原发性纤溶亢进,从而加大失血量,加重出血性休克。最后导致器官功能衰竭和高病死率。因此,急性创伤性凝血病治疗的焦点在于缩短休克期和低灌注状态。要纠正严重创伤伴发的“致命性三联征”。特别对于微血管出血尚未被制止的严重创伤患者,宜积极输入新鲜血浆、浓缩血小板及冷沉淀物。防止不恰当地应用大量输晶体液,或库存血,或蕊缩红细胞液。在大量失血情况下,输注新鲜全血比成分输血更有优越性。重组活化FVII是促进凝血酶生成的强效药物,需要避一步明确其适应证及局限性。     

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创伤性凝血病的发病机制十分复杂,具有多源性,涉及凝血系统的多个方面,其具体发生机制尚未完全明确。已知的发病机制主要有:稀释性凝血病、低温性凝血病、酸中毒性凝血病和消耗性凝血病等。对发病机制的新认识为临床创伤后凝血功能障碍的检测及治疗带来了新的改变。除常规实施"小容量复苏"和"允许性低血压"复苏的损伤控制性复苏策略外,近年来研究发现:对创伤低凝病人给予1:1的新鲜冰冻血浆(FFP)与红细胞(RBC)大比例血浆输注,可大幅度降低出血病死率和总病死率;抗纤溶治疗是近年来创伤止血治疗的重要进展。     

Exsanguination in trauma: A review of diagnostics and treatment options

Trauma patients with haemorrhagic shock who only transiently respond or do not respond to fluid therapy and/or the administration of blood products have exsanguinating injuries. Recognising shock due to (exsanguinating) haemorrhage in trauma is about constructing a synthesis of trauma mechanism, injuries, vital signs and the therapeutic response of the patient. The aim of prehospital care of bleeding trauma patients is to deliver the patient to a facility for definitive care within the shortest amount of time by rapid transport and minimise therapy to what is necessary to maintain adequate vital signs. Rapid decisions have to be made using regional trauma triage protocols that have incorporated patient condition, transport times and the level of care than can be performed by the prehospital care providers and the receiving hospitals. The treatment of bleeding patients is aimed at two major goals: stopping the bleeding and restoration of the blood volume. Fluid resuscitation should allow for preservation of vital functions without increasing the risk for further (re)bleeding. To prevent further deterioration and subsequent exsanguinations ‘permissive hypotension’ may be the goal to achieve. Within the hospital, a sound trauma team activation system, including the logistic procedure as well as activation criteria, is essential for a fast and adequate response. After determination of haemorrhagic shock, all efforts have to be directed to stop the bleeding in order to prevent exsanguinations. A simultaneous effort is made to restore blood volume and correct coagulation. Reversal of coagulopathy with pharmacotherapeutic interventions may be a promising concept to limit blood loss after trauma. Abdominal ultrasound has replaced diagnostic peritoneal lavage for detection of haemoperitoneum. With the development of sliding-gantry based computer tomography diagnostic systems, rapid evaluation by CT-scanning of the trauma patient is possible during resuscitation. The concept of damage control surgery, the staged approach in treatment of severe trauma, has proven to be of vital importance in the treatment of exsanguinating trauma patients and is adopted worldwide. When performing ‘blind’ transfusion or ‘damage control resuscitation’, a predetermined fixed ratio of blood components may result in the administration of higher plasma and platelets doses and may improve outcome. The role of thromboelastography and thromboelastometry as point-of-care tests for coagulation in massive blood loss is emerging, providing information about actual clot formation and clot stability, shortly (10 min) after the blood sample is taken. Thus, therapy guided by the test results will allow for administration of specific coagulation factors that will be depleted despite administration with fresh frozen plasma during massive transfusion of blood components.     

Blood transfusion in trauma patients: unresolved questions

Massive transfusion is an essential part of resuscitation efforts in acute trauma patients. The goal is to quickly correct trauma-induced coagulopathy and replace red blood cell (RBC) mass with the minimal number as well as the appropriate choice of blood components to minimize the possible adverse effects of transfusions. Early trauma induced coagulopathy (ETIC) is present in about 20% of patients upon hospital admission and predicts for decreased survival. The mechanism of ETIC is still being elucidated; however, most theories of ETIC's pathophysiology justify the early use of plasma. Most massive transfusion protocol (MTP) ratios deliver blood products in a ratio of 1:1:1 for RBCs:plasma:platelets, which is supported by the majority of the literature demonstrating improved patient survival with higher ratios (>1 plasma and platelet for every 2 RBCs transfused). Indeed, formula-driven MTPs allow trauma services to react quickly to ETIC and provide coagulation factors and platelets in these ratios without having to wait for the results of coagulation assays while the patient's coagulopathy worsens. New MTPs are being created which are adjusted according to an individual's coagulation laboratory values based on point-of-care laboratory tests, such as thromboelastography. When creating an MTP, product wastage due to inappropriate activation and improper product storage should be considered and closely monitored. Another area of discussion regarding transfusion in trauma includes the potential association of prolonged storage of RBCs and adverse outcomes, which has yet to be confirmed. Significant progress has been made in the transfusion management of trauma patients, but further studies are required to optimize patient care and outcomes.     

Diagnosis of postoperative coagulopathic hemorrhage in oncology patients

The condition of the hemostatic system during operation and in the early postoperative period was studied in 288 oncological patients in blood loss of different volumes. A relation of changes in hemostasis to the amount of blood lost was found. The increase in the volume of blood loss was caused first of all by the traumatic character of the operation itself, i.e. surgical hemorrhages, while the coagulopathic hemorrhages were of a secondary character. They evolve as acute and subacute syndrome with generalized, hypercompensated or moderate fibrinolysis in the form of hemodilution coagulopathy with predominant reduction of the number of platelets and their dysfunctions, or are mixed in character. A complex of rapid methods for the diagnosis of coagulopathic hemorrhages is recommended.