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Damage control resuscitation
Damage Control Resuscitation (DCR) is a systematic approach for managing major trauma patients at risk of exsanguinating hemorrhage. It incorporates permissive hypotension to minimize blood loss while hemorrhage is uncontrolled, haemostatic resuscitation using blood products instead of crystalloids to prevent coagulopathy, and early hemorrhage control through surgery. DCR aims to decrease mortality and morbidity by recognizing patients at risk of hemorrhagic shock, providing adequate tissue oxygenation through hypotensive resuscitation while limiting further blood loss and clot disruption, and preventing the triad of hypothermia, acidosis and coagulopathy through haemostatic resuscitation and blood product administration according to a
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Introduction to Damage Control Resuscitation by Dr. James Wheeler.
Definition and strategies of DCR include permissive hypotension, haemostatic resuscitation, and haemorrhage control.
Head injuries are the leading cause of death in trauma; haemorrhagic shock is preventable and crucial.
Different types of shock: hypovolaemic, obstructive, distributive, and cardiogenic causes.
Causes of haemorrhagic shock include tissue damage, coagulopathy, and critical intrinsic and extrinsic factors.
Intrinsic dysregulation and risk factors for trauma-induced coagulopathy are detailed.
Key principles include rapid haemorrhage control and management of coagulopathy and related disorders.
Determining at-risk patients for uncontrolled haemorrhage using specific scoring systems.
Goals include haemorrhage control and rapid transport to trauma centers; delays increase mortality.
Activation of trauma team and simultaneous management including haemorrhage control and resuscitation.
Focus on locating hemorrhage sources and initial control approaches prior to definitive management.
The detrimental impact of shock on patient outcomes; ongoing research into optimal resuscitative practices.
Animal and human studies on permissive hypotension indicate decreased mortality without raising risk.
Guidelines on when and how to implement permissive hypotension while preventing complications.
Describes haemo-dilution, acidosis, hypothermia, and other factors affecting coagulopathy.
Studies demonstrate better outcomes with massive transfusion protocols and the use of Tranexamic Acid.
Strategies for early intervention to prevent coagulopathy include fixed ratios of blood components.
Historical reliance on crystalloids for trauma resuscitation, highlighting their advantages.
Disadvantages of aggressive crystalloid use include increased bleeding and worse outcomes.
Details on various blood product types, storage, and their respective components.
Comparative analysis of blood components and their role in resuscitation.
Permissive and haemostatic resuscitation protocols for patients in uncontrolled shock.
Protocol for initiating treatment during haemorrhagic shock before definitive control is established.
Introduction to SCGH's protocols for managing massive transfusions in trauma patients.
Essential physiological and haematological parameters to monitor during treatment.
Discussion on improving blood product use through advanced coagulation monitoring techniques.
Emphasizes early identification, individualized resuscitation, and the need for monitoring and protocols.
Identifies challenges in managing trauma care including patient conditions and massive transfusion complications.
List of studies and articles cited throughout the presentation for further exploration of topics discussed.
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Damage control resuscitation
- 1. Damage Control Resuscitation DrJames Wheeler
- 2. Damage Control Resuscitation •Definition: • A systematic approach to major exsanguinating trauma incorporating several strategies to decrease mortality and morbidity: 1. Permissive hypotension (Minimal Normotension) 2. Haemostatic resuscitation (Massive Transfusion Protocol) 3. Haemorrhage Control (Damage control surgery)
- 3. Trauma Patient Mortality •Head injury = leading cause of death (largely determined at the time of Injury) • Haemorrhagic Shock = leading preventable cause of death in trauma
- 4. Causes of Shockin Trauma • Hypovolaemic • Haemorrhage • Obstructive • Tension PTX • Cardiac tamponade • Distributive • Neurogenic / Spinal • Cardiogenic • Direct cardiac contusion
- 5. Cause of HaemorrhagicShock • Direct Tissue Damage • Dysruption of blood vessels with associated blood loss enough to cause tissue hypoperfusion • Coagulopathy Intrinsic Factors • Trauma Induced Coagulopathy (TIC) / Acute Coagulopathy of Trauma (ACT) • 10-40% of trauma patients • Presence associated with 4-5 x increased mortality Extrinsic Factors • Hypothermia • Dilution (crystalloids, blood components) • Acidosis / Tissue Hypoperfusion
- 6. Trauma Induced Coagulopathy (TIC): •Definition: • Intrinsic dysregulation of the blood coagulation in the setting of trauma • Pre-requisistes: • Tissue Hypoperfusion • Physical Tissue Damage • Factors released by the tissue and endothelium in response to injury and hypoxia cause coagulopathy by several mechanisms: • Anticoagulation • Thrombin-thrombomodulin Protein C system dysfn • Platelet dysfunction • Hyperfibrinolysis
- 7. Principles of DCR •Rapid Physical Control of Haemorrhage • Provide adequate tissue oxygenation while reducing the likelihood of UNCONTROLLED HAEMORRHAGE • Recognise patients at risk of uncontrolled haemorrhage • Introduce practices to reduce likelihood of: • Clot rupture & Excessive blood loss • Avoid “Excessive” intravascular pressures but maintaining adequate tissue perfusion = PERMISSIVE HYPOTENSION / Minimal Normotension • Coagulopathy • Haemodilution • Hypothermia • Acidosis = HAEMOSTATIC RESUS / Massive Transfusion Protocol
- 8. Recognising patients atrisk of Uncontrolled Haemorrhage • Clinically obvious / gestalt • Scoring Systems: • Trauma Associated Severe Haemorrhage (TASH) Score: • SBP < 100 mmHg • HR > 120 bpm • HB < 70 g/l • Positive EFAST with haemodynamic instability • Pelvic / long bone fracture • BE <-10 mmol/L • INR >1.5 • Assessment of Blood Consumption (ABC) Score • SBP < 90 mmHg • HR >120 bpm • Penetrating Mechanism • Positive FAST Score 2 = 38%, 3 = 45%, 4 = 100% chance of massive transfusion • Thromboelastography / Coagulation testing
- 9. Prehospital Goals (Where traumacentre available) 1. Control Haemorrhage 2. Rapid transport to trauma centre (definitive control) 3. Initiate resuscitation guided by: • Mental status • Peripheral pulses • Consider delayed resuscitation (= nil resus fluids) Studies in patients with penetrating trauma needing thoracotomy have shown a 2.63x increased risk of death with each prehospital procedure performed
- 10. Initial Mx inTrauma Centre • Activation of trauma team • on or prior to arrival • Gen Surg / Anaes / ICU / Ortho / Blood Bank / Radiology • Primary survey (ABC’s) • Exclude early life threats (tamponade, tension PTX…)& establish presence or risk of HAEMORRHAGIC SHOCK • Manage Haemorrhage (immediate & plan definitive) • Resuscitate patient (DCR) • Usually all happen concurrently • Secondary Survey (may not get to this)….
- 11. Haemorrhage Mx • Localisesource/s • Clinical / imaging • Initial control / minimise bleeding • Pressure / Splinting / Traction / Tourniquet…. • DCR • Plan for early definitive Mx of haemorrhage
- 12. DCR Evidence • Whatwe know! • Shock = BAD • Longer the period of Shock = Worse • Haemorrhaging trauma patients develop coagulopathy • What we are still trying to work out?! • How do we BEST maximise tissue perfusion without exacerbating haemorrhage and coagulopathy • Evidence = limited but developing • anecdotal / animal studies / human retrospective & RCT’s
- 13. The Evidence: Permissive Hypotension •Multiple animal studies • Reliable rebleeding point in pigs at SBP 94mmHg • Hypotensive pigs aggressively resucitated (80ml/kg crystalloids) • 3 x blood loss & greatly increased mortality compared with nil resucitation • Review of fluid resus in animals (Mapstone) – Permissive Hypotension vs Normotension • RR death 0.37 in permissive hypotension group • Anecdotal / Retrospective • WWI / WWII / Vietnam War • Resuscitation in absence of bleeding control can be harmful • Human Studies • Penetrating torso with BP<80 mmHg RCT (Houston): Delayed vs Immediate resus • Delayed: lower mortality (30% vs 38%), less crystalloids (375ml vs 2.5L, nil diff in MAP) • Hypotensive trauma patients RCT : SBP target 70mmHg vs 100mmHg • No change in mortality (ie. No increased mortality) • Note no sig diff in SBP in the 2 groups • Evidence suggests effect the same for Blunt & Penetrating
- 14. Permissive Hypotension Goals •When to implement: • While there is, or the potential for, uncontrolled haemorrhage • Not when there is controlled haemorrhage (goal is normotension) • How: • Titrate small bolus (250ml) fluid administration to a hypotensive goal: • SBP of 70-90mmHg OR • normal mentation and palpable peripheral pulse (~radial >80mmHg, ~brachial >60mmHg) • Consider fentanyl bolus to prevent hypertensive episodes • Aim is to prevent clot dislodgement / decrease rate of blood loss in the immediate period after trauma, while maintaining “adequate” end organ perfusion • Use in head injury is controversial • Some groups aim for normotension • Some advocate increased BP goals >100 mmHg • Some suggest nil change to other cases of haemorrhagic shock pt’s
- 15. Haemostatic Resuscitation Causes ofcoagulopathy in trauma • Haemodilution: • Iatrogenic Dilutional • excessive / any crystalloid use • Physiologic Dilutional (extracellular fluid shifts) • Acidosis • pH<7.1-7.2 impairs thrombin prodn • Hypothermia • Impairs thrombin prodn & platelet fn • <33°C causes ~20%loos of coag fn • Hypocalcaemia – citrate poisoning due to massive transfusion • Acute Traumatic Coagulopathy (ATC) • Occurs if extensive tissue damage & hypoperfusion • ?increased Activated Protein C • Inactivates factors Va & VIIIa • Promotes fibrinolysis • Functionally decreases thrombin
- 16. Haemostatic Resuscitation: The Evidence •Massive transfusion protocol • Multiple studies show increased survival • Higher crystalloid use >mortatlity • Higher ratio of FFP : RBC increased survival • More recent wars (Afghanistan) • Tranexamic Acid (TXA) • CRASH 2 (2010, 20000 patients, RCT) • Antifibrinolytic • TXA increased survival, no increase in thrombotic episodes • Recombinant Factor VIIa • Recent Cochrane review found no improvement in mortality
- 17. Haemostatic Resuscitation: Prevent /reduce coagulopathy • Identify at risk group & act before coagulopathy develops: • Massive transfusion protocol • Early use of blood components as the primary resuscitation fluid • Use in the same ratio as they are lost through haemorrhage (exact ratio’s controversial) • PRBC : FFP 1:1 • PRBC : Platelet (adult dose) 4:1 • Fibrinogen • Give TRANEXAMIC ACID • Prevent hypothermia / significant acidosis • Monitor and give maintain iCa2+
- 18. Mx of HaemorrhagicShock - Crystalloids • Historically resuscitation of trauma patients involved: • RAPID restoration of circulating blood volume with CRYSTALLOID SOLUTIONS to maintain normotension / perfusion • Advantages of crystalloids: • Cheap • Readily available / easy storage • No risk of transfusion reactions / infectious agents / hyperkalaemia / hypocalcaemia… • The above Mx may be appropriate / not harmful in most trauma patients • But aggressive fluid resuscitation with crystalloids has disadvantages!
- 19. Disadvantages of Crystalloids •Increased Haemorrhage • Coagulopathy (Haemodilution / hypothermia / acidosis) • Clot rupture with restoration of normal blood pressure • Compartment syndromes • abdo, limbs • Larger volumes needed when compared to blood products (3:1 rule) • Lowers plasma osmotic pressures – more extravasation in damaged areas (Hartmann’s worse than N Saline) • Increased inflammatory repsonse • Hartmann’s • Acidosis • N Saline • Hartmann’s in those with impaired lactate metabolism (DKA, liver failure) Aggressive use associated with increased mortality in haemorrhagic shock
- 20. Haemostatic Resuscitation: Blood Products Volume(ml) Contents Grouping Storage PRBC 200 50-70% HCT ABO & Rh 42 days FFP 250-330 All coag factors ~1/2 unit WB ABO 12 months Platelets 100-400 200 x 109 Platelets / bag ABO & Rh 5 days Cryo 30-40 Firinogen / VIII / XIII / VWF ~2 x unit WB ABO 12 months Whole Blood 24 hours Remember: •temperature •citrate (hypoCa2+ after 4-6U PRBC in an hour) •potassium
- 21. Haemostatic Resuscitation Whole BloodComponent Therapy (1 PRBC / 1 FFP / 1 PLAT / 1 CRYO) RBC (HCT) 38-50% 20% COAGS 100% 50-60% PLATELETS 150-400 X 103 / ul 280 x 103 / ul FIBRINOGEN 1500mg 750 - 3000mg Volume 450ml ~700ml (more with flush)
- 22. Damage Control Resuscitation (ina patient with haemorrhagic shock that cannot be controlled in the ED) • Permissive Hypotension • No head injury • Goal = SBP 70-90 mmHg (MAP 50-65) OR normal mentation & peripheral pulses • Head injury • Controversial • Some suggest permissive hypotension is contraindicated • Goal = normotension (depends on patient) • Others use standard permissive hypotension • Others adjust goal to SBP >100 mmHg
- 23. Damage Control Resuscitation (ina patient with haemorrhagic shock that cannot be controlled in the ED) • Haemostatic Resuscitation • If blood available: • Initiate massive transfusion protocol • Fixed product ratio’s • Blood / FFP / Platelets / cryoprecipitate / calcium • Monitoring of coagulation • If blood not immediately available: • Give 250-500ml boluses of crystalloids until blood available or resus goals met • Warm Fluids / Cover Patient • TXA • give early (best <3/24) once risk of haemorrhagic shock determined • 1g Stat and 1g over 8/24 • Relative contraindications: thrombophilic disorder • Early definitive control of bleeding • Consider rVIIa? • If fibrinogen and platelets in sufficient numbers
- 24.
- 25. Things to monitor •Physiological parameters: • Mental status • Urine output (>0.5ml/kg/hr) • Peripheral pulses / MAP • CVP • Temp (>35C) • Haematological parameters • Hb (>90g/l) • Platelets (>50-80 x 109) • Coag’s: INR (<1.5), Fibrinogen(>1g/l) • CV SaO2 (>70%) / lactate (<4mmol/l) / pH (>7.2) • iCa2+ (>1.1mmol/l) • K+
- 26. The Future • CryoStat •Consensus on blood product use: • Accurate bedside monitoring of Coagulation parameters to guide blood product use • Thromboelastography - ROTEM
- 27. Summary • Identify thosewith / at risk of haemorrhagic shock on arrival • Fluid resuscitation individualised for each patient • Permissive hypotension in patients without head injury • Early use of blood products as resus fluids • Massive transfusion protocol – with fixed product ratios • Monitor coagulation • Use TXA in all patients requiring transfusion for uncontrolled haemorrhage • Early definitive Mx of haemorrhage • Once haemorrhage controlled – then aim for normal CV parameters • monitor lactate / BE
- 28. Difficulties • Alcohol /drug affected patients • Head injured patient • Delayed transfer to definitive care • Complications of massive transfusion
- 29. References • Bickell WH,Wall MJ Jr, Pepe PE, et al.: Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994, 331:1105-1109. • Kaweski SM, Sise MJ, Virgilio RW, et al.: The effect of prehospital fluids on survival in trauma patients. J Trauma 1990, 30:1215-1218. • Kowalenko T, Stern SA, Dronen SC, Wang x: Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma 1992, 33:349- 353 • Alberto S. Santibanez-Gallerani, M.D., Annabel E. Barber, M.D., Shelley J. Williams, M.S., Yan Zhao, B.S., G. Tom Shires, M.D. Improved Survival with Early Fluid Resuscitation Following Hemorrhagic Shock. World J. Surg. 25, 592–597, 2001 • Pek Ghe Tan, Marion Cincotta, Ornella Clavisi, Peter Bragge, Jason Wasiak, Loyal Pattuwage and Russell L Gruen. Review article: Prehospital fluid management in traumatic brain injury. Emergency Medicine Australasia (2011) 23, 665–676 • Philip F Stahel, Wade R Smith, Ernest E Moore. Current trends in resuscitation strategy for the multiply injured patient. Injury, Int. J. Care Injured (2009) 40S4, S27–S35