Damage control resuscitation from major haemorrhage in polytrauma
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1 Eur J Orthop Surg Traumatol (2014) 24: DOI /s GENERAL REVIEW Damage control resuscitation from major haemorrhage in polytrauma William Carlino Received: 27 November 2012 / Accepted: 11 January 2013 / Published online: 31 January 2013 Ó Springer-Verlag France 2013 Abstract Trauma is a global disease that affects patients across the socio-economic spectrum. Uncontrolled major haemorrhage occurs from both blunt and penetrating trauma which may lead to hypovolaemic shock and ultimately death. In polytrauma patients that require urgent resuscitation secondary to major haemorrhage, high volume fluid infusions followed by definitive surgical care have been superseded by damage control resuscitation. DCR is a systematic approach to major trauma that integrates the principles of haemostatic resuscitation, permissive hypotension and damage control surgery (DCS). The aim of DCR is to aggressively minimise hypovolaemic shock and limit the development of coagulopathy, hypothermia and acidosis known as the lethal triad. Besides increased volumes of scientific knowledge to underpin modern trauma resuscitation techniques upon, patient survival is also dependent upon effective teamwork and leadership. In conclusion, successful resuscitation from major haemorrhage depends upon a variety of factors distilled into a trauma team with effective leadership, excellent technical and non-technical team skills as well as the early initiation of DCR. Keywords Damage control resuscitation Major haemorrhage Haemostatic resuscitation Permissive hypotension Coagulopathy Early triage decisions, the rapid implementation of damage control resuscitation (DCR) and a dedicated trauma team W. Carlino (&) Department of Trauma and Orthopaedics, Weston General Hospital, Weston Super Mare, UK wcarlino@doctors.org.uk are all integral to successful resuscitation from major haemorrhage. All hospitals that receive major trauma should currently have a multidisciplinary team to receive, evaluate and initiate DCR. Evidence suggests that trauma teams reduce the time between arrival in hospital and initiation of definitive treatment as well as improve outcome [1]. Effective leadership and management skills are also central to improving outcome in survivable major trauma [2]. Trauma is a global disease that affects patients across the socio-economic spectrum. Everyday approximately 300,000 people sustain severe injuries, of which nearly 10,000 result in a fatality [3]. The two leading causes of death in trauma are secondary to neurological injury and haemorrhage [4]. Uncontrolled major haemorrhage occurs from both blunt and penetrating trauma which may lead to hypovolaemic shock and ultimately death. A consensus definition of major haemorrhage in the acute trauma setting remains contentious, but has been described as a blood transfusion requirement of over 4 units within 2 4 h [5]. In polytrauma patients that require urgent resuscitation secondary to major haemorrhage, high volume fluid infusions followed by definitive surgical care have been superseded by DCR [5]. The concept of DCR was established by military trauma experience during the Iraq and Afghanistan conflicts before being transcribed for use in civilian trauma management [6]. DCR is a systematic approach to major trauma that integrates the principles of haemostatic resuscitation, permissive hypotension and damage control surgery (DCS) [7]. DCR utilises the CABC (catastrophic bleeding, airway, breathing, circulation) to aggressively minimise hypovolaemic shock and limit the development of coagulopathy, hypothermia and acidosis known as the lethal triad [6]. It
2 138 Eur J Orthop Surg Traumatol (2014) 24: has been stated that when the lethal triad is present, death is imminent [8]. The lethal triad is a self-perpetuating vicious cycle precipitated by hypoperfusion secondary to haemorrhagic shock. This causes reduced oxygen delivery to tissues at a cellular level, and the ensuing anaerobic metabolism produces lactate and consequently a metabolic acidosis. Anaerobic metabolism limits endogenous heat production which can result in or exacerbate pre-existing hypothermia from the field (Fig. 1). The acute coagulopathy of trauma is more complex than the original perception of it as fluid dilution and consumption of clotting agents. Current knowledge suggests that it is directly triggered by tissue injury and the subsequent activation of inflammatory pathways resulting in hyperfibrinolysis and anticoagulation [9]. Up to 1/3 of polytrauma patients are hypocoagulable on arrival in hospital ([10]), which has been associated with a fourfold increased risk in mortality [9]. Fig. 1 Adapted from damage control resuscitation for patients with major trauma. BMJ [7] Damage Control Resuscitation Algorithm Major Trauma Haemorrhage Hypoperfusion Exposure Coagulopathy Acidosis Lethal Triad Hypothermia Damage Control Resuscitation Permissive hypotension Haemostatic resuscitation Damage control surgery
3 Eur J Orthop Surg Traumatol (2014) 24: Haemostatic resuscitation is the aggressive restoration of circulating volume using haemostatic agents in patients with haemorrhagic shock. This targets both the hypoperfusion and the acute coagulopathy of trauma. The decision to initiate haemostatic resuscitation is based upon the mechanism of injury and the clinical condition of the patient. Laboratory tests of clotting such as prothrombin time and activated partial thromboplastin time are inherently poor guides to the presence of coagulopathy or as a measure of physiological response to treatment [7]. The haemostatic agents currently recommended for use are derived from military experience in which red blood cells (RBC), fresh frozen plasma (FFP) and platelets have been used in a 1:1:1 ratio as part of a massive transfusion protocol [11]. Massive transfusion protocols within civilian hospitals vary between departments. However, all relate to the immediate release of haematological products from blood bank reserves in pre-defined ratios for instances of uncontrolled haemorrhage [12]. Despite the widespread existence of massive transfusion protocols, it takes time to thaw FFP before it is warmed and available for transfusion. Patients who die from major haemorrhage in hospital can do so rapidly and may well do so before FFP is available despite having received RBC transfusion early in their management. However, one military study reported an absolute reduction in mortality of 46 % when using RBC:FFP in 1:1 rather than a conventional ratio of 1:8 [13]. Military data are derived typically from young, fit, healthy males which have to be taken into account before application across a broader civilian population. Nevertheless, some evidence has also emerged from civilian trauma practice that illustrates a survival benefit in patients undergoing massive transfusion that receive RBC:FFP ratios of 1:1 too [14]. Although there is limited evidence to support the use of 1:1 blood products, the strategy appears to be effective in some populations, and importantly, it is logical to combat coagulopathy pre-emptively. The use of platelets to combat the acute coagulopathy of trauma is based on even less evidence. A recent European update on haemostatic resuscitation recommended aiming for a platelet count of greater than /L and a maintenance level of platelets of greater than /L [15]. The rationale behind the recommendation was based upon preexisting knowledge relating to medical conditions causing thrombocytopaenia. Spontaneous bleeding from these conditions seldom occurs at platelet levels above /L which has consequently been extrapolated for use in trauma. This is a safe vantage point to begin considering the usage of platelets in trauma, but trauma is intrinsically different and less predictable than chronic medical conditions. The use of tranexamic acid in trauma is derived from usage in obstetrics and gynaecology to control menorrhagia and post-partum haemorrhage. The CRASH 2 trial demonstrated that the risk of death from bleeding was significantly reduced in all polytrauma patients administered with a loading dose of 1 g over 10 min and subsequently an infusion of 1 g over 8 h of tranexamic acid [16]. Although the results showed outcomes were better in the penetrating compared with blunt trauma group, all cause mortality was also reduced. As such, tranexamic acid should be considered in all severely injured patients [16]. Hypothermia should be prevented where possible rather than reversed. Although no consensus definition exists [17], it has been defined as a condition in which the normal metabolic and physiologic function of the body is impaired due to a drop in core temperature below 35 C. It can be stratified to mild hypothermia (34 36 C) or severe hypothermia (\34 C) [18]. The avoidance and treatment of hypothermia are critical in relation to coagulopathy. Hypothermia is frequently the result of post-traumatic environmental exposure in the field, during transfer and in hospital. It can also be a consequence of using large volumes of unwarmed fluids as well as hypovolaemia itself. Patients should therefore be managed from the outset with avoidance of hypothermia a foremost priority. The transfer vehicle, resuscitation area and theatre should all be appropriately warmed, and the patient insulated as much as possible. All fluids infused into the patient should be warmed. Coagulation function is critically dependent on core temperature which mediates enzyme and platelet function as well as fibrinolytic activity [19]. Although normal clotting factors are present at temperatures as low as 33 C, hypothermia produces a coagulopathy equal to half the clotting activity seen at normothermia. Hypothermia is also a harbinger of injury severity and mortality. Two small-scale studies reported increased mortality and Injury Severity Score in patients with severe (\34 C) hypothermia compared with normothermic patients. [18], [20]. In the first paper, patients with a temperature of \32 C had 100 % risk of mortality [20]. Hypothermia should therefore be proactively prevented although the exact temperature at which hypothermia begins to adversely affect survival is yet to be defined. In polytrauma, metabolic acidosis is a byproduct of cellular hypoperfusion secondary to haemorrhagic shock. Acidosis is also intrinsically linked to the coagulation cascade with most stages inhibited by acidosis. The causal factor postulated in one animal study is that acidosis augments fibrinogen breakdown by nearly double, compared with control values [21]. In addition to depleted fibrinogen levels, acidosis also causes impaired enzyme activity, a reduction in platelet levels, a prolonged clotting time and an increased bleeding time [22]. The usual caution should be exercised when interpreting this animal data and using it as model for understanding the human pathophysiology of acidosis in trauma.
4 140 Eur J Orthop Surg Traumatol (2014) 24: The principle of permissive hypotension challenges the accepted practices of aggressive intravenous fluid replacement in bleeding polytrauma patients. Historically colloid and more recently crystalloid have been utilised to replace lost circulating volume with the intention of restoring a normal blood pressure [23]. Shock has been defined as a life threatening condition in which the vital organs receive inadequate oxygen delivery to meet metabolic demand [24]. It therefore seems rational to replenish lost circulating volume as rapidly as possible to augment delivery of fluid volume to vital organs. Unfortunately, neither crystalloid nor colloid can deliver oxygen to metabolically compromised cells. Both can, however, exacerbate the coagulopathy of trauma with a dilutional coagulopathy and blow clots through increased blood pressure [5], [7]. It is also well recognised that infusing cold fluids in polytrauma patients exacerbates hypothermia [5]. Permissive hypotension restricts early fluid resuscitation to maintaining a systolic blood pressure to approximately 90 mmhg. Although this provides sub-optimal end organ perfusion, it is thought to facilitate haematological control and therefore increase the likelihood of survival. There is little quality data from human studies to inform fluid management in haemorrhagic shock, though considerable animal work has contributed to our preliminary understanding. One systematic review conducted from animal studies concluded that the effect of fluid resuscitation was related to the severity of haemorrhage. In cases of severe haemorrhage, fluid resuscitation was effective in reducing the risk of death. Conversely, when haemorrhage was less severe, fluid resuscitation increased the risk of death [25]. The effect of hypotensive resuscitation was to reduce mortality across both severe and less severe forms of haemorrhagic shock [25]. To what extent can this data be extrapolated across into the human population with polytrauma and multiple medical co-morbidities? This question was to a certain extent the focus of a landmark paper which reported outcomes from two groups of hypotensive patients that had sustained penetrating torso injuries. Patients were randomised in the field to receive intravenous fluids or not until transfer out of the emergency department. The group managed with fluid resuscitation had an increased risk of mortality. Patients from the delayed resuscitation group had a significantly higher chance of survival, shorter overall hospital stay as well as a trend towards less intra-operative blood loss [26]. Caution should be exercised when interpreting this paper as the study population was predominantly composed of young males and did not address hypotension in blunt trauma. A more recent study found no difference in outcome for trauma patients managed using permissive hypotension versus conventional blood pressure parameters [27]. It was, however, acknowledged that maintaining lower blood pressures in trauma patients who have sustained haemorrhagic injuries to anatomical sites which are difficult to access was logical [27]. The principle of hypotensive management to exercise control over haemorrhage and protect clot formation appears rational, though it may be that a dogmatic approach to encompass blunt and penetrating trauma may not be appropriate. In addition to mechanism, the heterogeneity of injury patterns as well as patient factors likely influences outcome. Damage control surgery is now an integrated rather than independent component of DCR management. It consists of a staged surgical approach to management with an initial time restricted (theoretically less than 1 h) surgical intervention to preserve life by addressing the source of haemorrhage [6]. After initial surgery, the patient should be physiologically optimised on the intensive care unit before returning for definitive surgical intervention [6]. DCS acknowledges that successful trauma outcomes are based on restoring physiological parameters rather than immediate full anatomical restoration [28]. Identifying patients who require DCR can be challenging as there is no clear cut diagnostic algorithm. Patients who present with hypotension, tachycardia and readily identifiable blood loss are straightforward to diagnose and initiate DCR upon. Frequently, trauma patients are young with a large physiological reserve and therefore do not exhibit all of the altered physiological parameters classically associated with hypovolaemic shock. As such, recognising potential patterns of injury from the mechanism, in addition to physiological parameters, metabolic assessment and clinician judgment can help identify patients who require DCR. Trauma resuscitation is rapidly evolving and taken new direction from recent armed conflict in Iraq and Afghanistan. A large body of experiential evidence is being accumulated relating to outcomes from personnel exposed to major trauma. Large-scale randomised clinical trauma trials are ethically and organisationally challenging to undertake and fund. Consequently, much of our acquired knowledge will relate to trauma sustained by fit, young healthy men and experimental data from animal models. The ever changing demographic landscape of civilian trauma encompasses all age groups with varying levels of physiological reserve and complex medical co-morbidities. This makes it difficult to directly transcribe military experience and animal data into the civilian trauma environment. The advent of United Kingdom trauma centres with affiliated trauma units has signalled a change in attitude towards trauma management. This partly acknowledges trauma resuscitation is a specialist endeavour which is not successfully undertaken by clinicians with a part time interest in trauma. Unfortunately, this represents slow
5 Eur J Orthop Surg Traumatol (2014) 24: uptake of recommendations published regarding specialist trauma management 24 years ago [29]. Besides increased volumes of scientific knowledge to underpin modern trauma resuscitation techniques upon, patient survival is dependent upon effective teamwork and leadership. Non-technical skills training has increasingly been recognised in medical practice to play a significant role in successful outcomes and maximise the input of all those involved [30]. This is not to detract from the importance of surgical and clinical expertise required to manage complex trauma. Indeed, effective teams optimise both technical and non-technical contributions from every individual member. Other factors will also continue to influence trauma outcomes including political willpower both nationally and within hospitals, working relationships between specialties, seniority of the attending trauma team (particularly at night) and evolving attitudes towards trauma management itself. The future of trauma management continues to herald complex challenges, but an increasing knowledge and experience base should catalyse a move towards improved outcomes. In conclusion, successful resuscitation from major haemorrhage depends upon a variety of factors distilled into a trauma team with effective leadership, excellent technical and non-technical team skills, the early initiation of DCR and immediate access to ITU and operating facilities. Conflict of interest References None. 1. West JG, Trunkey DD, Lim RC (1995) Systems of trauma care: a study of two counties. Clin Orthop Relat Res 318:4 2. Cotton BA et al. (2006) The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock 296(6632): Roberts I et al (2005) Trauma care research and the war on uncertainty. BMJ 331(7525): Chesnut RMR et al (1993) The role of secondary brain injury in determining outcome from severe head injury. J Trauma 34(2): Harris T, Thomas GOR, Brohi K (2012) Early fluid resuscitation in severe trauma. BMJ 345(2):e5752 e Hodgetts TJ, Mahoney PF (2007) Damage control resuscitation. J Royal 34(2): Jansen JO et al (2009) Damage control resuscitation for patients with major trauma. BMJ(Abstr) 338:b Moore EE (1996) Staged laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg (2): Brohi K et al (2003) Acute traumatic coagulopathy. J Trauma 54(6): Holcomb JB et al (2007) Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma 62(2): Dawes R, Thomas GOR (2009) Battlefield resuscitation. Curr Opin in Crit Care 15(6): Cotton BA et al (2008) Damage control hematology: the impact of a trauma exsanguination protocol on survival and blood product utilization. J Trauma 64(5): Borgman MA, Spinella PC, Perkins JG (2007) The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma 105(2): Duchesne JC et al (2008) Review of current blood transfusions strategies in a mature level I trauma center: were we wrong for the last 60 years? J Trauma 65(2): (discussion ) 15. Ozier Y et al. (2007) Management of bleeding following major trauma: a European guideline. Crit Care 153(4): Williams-Johnson JA et al (2010) Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2) A randomised, placebo-controlled trial. West Indian Med J 59(6): Alam HB et al (2012) Hypothermia and hemostasis in severe trauma: a new crossroads workshop report. J Trauma Acute Care Surg 73(4): Luna GK et al (1987) Incidence and effect of hypothermia in seriously injured patients. J Trauma 27(9): Doufas AG (2003) Consequences of inadvertent perioperative hypothermia. Best Prac Res Clin Anaesthesiol 17(4): Jurkovich GJ, Greiser WB, Luterman A (1987) Hypothermia in trauma victims: an ominous predictor of survival. J Trauma 28(Suppl 2):S241 S Fries D, Martini WZ (2010) Role of fibrinogen in trauma-induced coagulopathy. Br J Anaesth 105(2): Lynn M et al (2002) Updates in the management of severe coagulopathy in trauma patients. Intensive Care Med 28(Suppl 2): S241 S Regel G et al (1995) Treatment results of patients with multiple trauma: an analysis of 3406 cases treated between 1972 and 1991 at a German level I trauma Center. J Trauma 38(1): Strehlow MC (2010) Early identification of shock in critically ill patients. Emerg Med Clin N Am 38(1): Mapstone J, Roberts I, Evans P (2003) Fluid resuscitation strategies: a systematic review of animal trials. J Trauma 55(3): Bickell WH et al (1994) Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Eng J Med 331(17): Dutton RP, Mackenzie CF, Scalea TM (2002) Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma Acute Care Surg 52(6): Bowley DM, Barker P, Boffard KD (2000) Damage control surgery concepts and practice. Central, J R Army Medical Corps 29. Anderson ID et al (1988) Retrospective study of 1000 deaths from injury in England and Wales. BMJ Clin Res Ed 296 (6632): McCulloch P et al (2009) The effects of aviation-style nontechnical skills training on technical performance and outcome in the operating theatre. Qual Saf Health Care 18(2):
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