Damage control resuscitation

Damage Control

Resuscitation

Dr James Wheeler

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)

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

Causes of Shock in Trauma

• Hypovolaemic• Haemorrhage

• Obstructive• Tension PTX• Cardiac tamponade

• Distributive• Neurogenic / Spinal

• Cardiogenic• Direct cardiac contusion

Cause of Haemorrhagic Shock

• Direct Tissue Damage• Dysruption of blood vessels with associated blood loss enough to

cause tissue hypoperfusion

• CoagulopathyIntrinsic 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

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

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

Recognising patients at risk 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

Prehospital Goals(Where trauma centre 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

Initial Mx in Trauma 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)….

Haemorrhage Mx

• Localise source/s • Clinical / imaging

• Initial control / minimise bleeding • Pressure / Splinting / Traction /

Tourniquet….• DCR

• Plan for early definitive Mx of haemorrhage

DCR Evidence

• What we 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

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

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

Haemostatic ResuscitationCauses of coagulopathy 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

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

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+

Mx of Haemorrhagic Shock - 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!

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

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 / bagABO & 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

Haemostatic Resuscitation

Whole Blood Component 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)

Damage Control Resuscitation(in a 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

Damage Control Resuscitation(in a 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

SCGH Massive transfusion protocol

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+

The Future

• CryoStat

• Consensus on blood product use:• Accurate bedside monitoring of Coagulation

parameters to guide blood product use• Thromboelastography - ROTEM

Summary

• Identify those with / 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

Difficulties

• Alcohol / drug affected patients

• Head injured patient

• Delayed transfer to definitive care

• Complications of massive transfusion

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