The Bleeding Trauma Patient

The Bleeding Trauma Patient
by Dr Pete Sherren
By popular request, Here are the slides from a presentation given by HEMS critical care physician Dr Pete Sherren.

These notes accompany the slides:
Hypothermia, acidaemia and coagulopathy or the ‘lethal triad’, is a well described entity in the trauma population and is associated with significant mortality [1]. Traditionally the aetiology of a trauma induced coagulopathy was thought to be multifactorial and involve hypothermia, acidaemia, dilutional coagulopathy, pre-existing bleeding diathesis and disseminated intravascular coagulation (Figure 1).

Figure 1. A diagram showing some of the mechanisms leading to coagulopathy in the injured.

In 2003 Brohi et al showed that around 25% of severely injured trauma patients present to hospital with a significant coagulopathy which was unrelated to fluid administration [2]. This early coagulopathy has become known as the Acute Traumatic coagulopathy (ATC) or Acute Coagulopathy of Trauma Shock (ACoTS). It is associated with an increase in transfusion requirements, injury severity scores, organ dysfunction and mortality rates [2-5].
ATC is an impairment of haemostasis involving a dynamic interaction between endogenous anticoagulants and fibrinolysis that is initiated immediately after an injury [5]. ATC is driven by an endothelial injury and hypoperfusion, which results in in increased thrombomodulin expression and activation of protein C (Figure 3). The inhibitory effect of activated protein C on clotting factors V/VIII and plasminogen activator inhibitor-1 (PAI-1), would appear key in the development of ATC [5,6].

Figure 2. Expression of thrombomodulin following a traumatic injury results in increased activation of protein C with resulting impairment of clotting factors V/VIII and reduction in thrombin generation. Activated Protein C also has an inhibitory effect on PAI-1 which results in unregulated tPA activity and fibrinolysis.

Damage control resuscitation (DCR) describes a package of care for the haemorrhaging trauma patient. It involves early damage control surgery, haemostatic resuscitation and permissive hypotension. DCR aims to control haemorrhage early while aggressively targeting the ATC and lethal triad. DCR has emerged as the accepted standard of care and some observational studies have suggested a survival benefit [6].

  • Damage Control Surgery – The priority for any haemorrhaging trauma patient is good haemostasis. Unstable patients with major trauma do not tolerate prolonged definitive surgery and hence the emergence of damage control surgery. The aim of damage control surgery is to normalise physiology at the expense of anatomy.
  • Haemostatic resuscitation – Describes the aggressive early use of packed red blood cells, clotting products and coagulation adjuncts in an attempt to mitigate the effects of the ATC and lethal triad in major trauma patients. The exact PRBC:FFP ratio remains unclear, but should ideally be less than 2:1 [7]. In massive transfusions along with appropriate FFP, platelet and fibrinogen supplementation, consideration should be given to early adjunctive therapies such as tranexamic acid [8] while maintaining ionised calcium levels greater than 1.0 mmol/L [9].
  • Permissive hypotension – Involves titrated volume resuscitation, which targets a subnormal end point that maintains organ viability until haemorrhage is controlled. By avoiding overzealous fluid resuscitation which targets normotension, the hope is to preserve the first and often best clot. Although permissive hypotension is frequently employed in traumatic haemorrhage, there is really only robust evidence that it is advantageous in penetrating trauma [10]. In blunt trauma there is a relative paucity of good evidence to guide practice, while strong evidence exists for maintaining cerebral perfusion pressures when there are associated head injuries. The end points for resuscitation will depend on age, premorbid autoregulatory state and acute pathology.

DCR is an ever evolving concept and potential emerging management strategies include –

  • Thromboelastometry (TEG/ROTEM) to guide haemostatic resuscitation instead of ratio based transfusions.
  • Prothrombin complex concentrate (FII, VII, IX and X) in non-warfarin patients
  • Fibrinogen complex concentrate (fibrinogen and FXIII) over cryoprecipitate.
  • Alkalising agents such as Tris-hydroxymethyl aminomethane (THAM) in massive transfusion with severe acidaemia
  • Novel hybrid resuscitation strategies.
  • High flow/low pressure resuscitation – endothelial resuscitation and microvascular washout.
  • Suspended Animation
  • Platelet function analysis in trauma with platelet mapping and aggregometry vs traditional PF-100

Learning points

  • Early coagulation dysfunction is common in trauma patients with haemorrhagic shock.
  • Tailored management of the ‘lethal triad’ and ATC is essential.
  • DCR is an emerging standard of care; however, some of its components are pushing the boundaries of what is good evidence based medicine.

1. Moore EE. Staged laparotomy for the hypothermia, acidosis, and coagulopathy. Am J Surg 1996;172:405-410.
2. Brohi K, Singh J, Heron M, Coats T. Acute Traumatic coagulopathy. J Trauma. 2003;54:1127-1130.
3. Davenport R, Manson J, De’Arth H, Platton S, Coates A, Allard S, Hart D, Pearse RM, Pasi J, MacCullum P, Stanworth S, Brohi K. Functional definition and characterization of acute traumatic coagulopathy. Crit Care Med. 2011;39(12):2652-2658.
4. Maegele M, Lefering R, Yucei N, Tjardes T, Rixen D,Paffrath T, Simanski C, Neugebauer E, Bouillon B; AG Polytrauma of the German Trauma Society (DGU). Early coagulopathy in multiple injury: an analysis from the German Trauma Registry on 8724 patients. Injury. 2007 Mar;38(3):298-304.
5. Firth D, Davenport R, Brohi K. Acute traumatic coagulopathy. Curr Opin Anaesthesiol. 2012 Apr;25(2):229-34.
6. Cotton BA, Reddy N, Hatch QM, LeFebvre E, Wade CE, Kozar RA, Gill BS, Albarado R, McNutt MK, Holcomb JB. Damage control resuscitation is associated with a reduction in resuscitation volumes and improvement in survival in 390 damage control laparotomy patients. Ann Surg. 2011 Oct;254(4):598-605.
7. Davenport R, Curry N, Manson J, De’Ath H, Coates A, Rourke C, Pearse R, Stanworth S, Brohi K. Hemostatic effects of fresh frozen plasma may be maximal at red cell ratios of 1:2. J Trauma. 2011 Jan;70(1):90-5; discussion 95-6.
8. CRASH-2 collaborators, Roberts I, Shakur H, Afolabi A, Brohi K, Coats T, Dewan Y, Gando S, Guyatt G, Hunt BJ, Morales C, Perel P, Prieto-Merino D, Woolley T. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet. 2011 Mar 26;377(9771):1096-101, 1101.e1-2.
9. Dawes R, Thomas GO. Battlefield resuscitation. Curr Opin Crit Care. 2009 Dec;15(6):527-35
10. Bickell WH, Wall MJ Jr, Pepe PE, Martin RR, Ginger VF, Allen MK, Mattox KL. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994 Oct 27;331(17):1105-9.
11. Schöchl H, Maegele M, Solomon C, Görlinger K, Voelckel W. Early and individualized goal-directed therapy for trauma-induced coagulopathy. Scand J Trauma Resusc Emerg Med. 2012 Feb 24;20:15.

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