Damage control resuscitation

PRINCIPLES OF DAMAGE CONTROL RESUSCITATION

Dr Kav SenasingheCME March 2016, SCGH ED

IS IT IMPORTANT TO OUR PRACTICE?• Traumatic injury is the

leading cause of death in under 45s

• Most victims are young males

• Most preventable deaths are due to haemorrhage - leading preventable cause of death in trauma

CAUSES OF SHOCK IN TRAUMA

• Hypovolaemic Shock - haemorrhage (accounts for ~40% of all trauma-associated deaths)

• Obstructive Shock - Cardiac Tamponade, Tension Pneumothorax

• Distributive shock - Neurogenic/Spinal

• Cardiogenic - direct cardiac contusion

HAEMORRHAGIC SHOCK• Hemorrhagic shock is a condition of

reduced tissue perfusion, resulting in the inadequate delivery of oxygen and nutrients that are necessary for cellular function. Whenever cellular oxygen demand outweighs supply, both the cell and the organism are in a state of shock.

WHAT CAUSES HAEMORRHAGIC SHOCK?

• Direct Tissue Damage

• Disruption of blood vessels with associated blood loss can be enough to cause tissue hypoperfusion

• Coagulopathy

• Intrinsic - Trauma-Induced Coagulopathy (TIC)/Acute Coagulopathy of Trauma (ACT)

• Extrinsic

• Hypothermia

• Dilutional (administration of crystalloids/blood products)

• Acidosis/Tissue Hypo-perfusion

WHAT IS DAMAGE CONTROL

RESUSCITATION?• A treatment strategy that targets conditions that exacerbate haemorrhage in trauma patients

1. Find the bleeding, Stop the bleeding

1. Recognise the risk of an uncontrolled haemorrhage +/- activation of Massive Transfusion Protocols

2. Restore blood volume rapidly and effectively (Permissive Hypotension) - maximise tissue perfusion whilst minimising clot rupture and excessive blood loss

3. Maintain bloods function by maintaining the blood composition (Haemostatic Resus) - haemostasis, oxygen-carrying capacity, oncotic pressure, biochemistry







SCORING SYSTEMS• Trauma-Associated Haemorrhage Score

• M or F• Hb (<70g/L +8, >120g/L 0)• Base Excess (< -10mmol/L = +4, >-2mmol/L = 0)• SBP ( <100mmHg = +4, >120mmHg = 0)• HR (>120bpm = +2, <120bpm = 0)• Positive FAST scan for intraabdominal fluid = +3• Clinically Unstable Pelvic Fracture = +6• Open or Dislocated Femoral Fracture = +3

• Assesment of Blood Consumption (ABC) Score• SBP <90mmHg• HR >120bpm• Penetrating Mechanism• Positive Fluid on FAST Exam• Score of 4 predicts 100% need for massive transfusion, Score of 3 predicts 45%

• McLaughlin Score• HR >105bpm• SBP <110mmHg• pH <7.25• Hct <32%













PERMISSIVE HYPOTENSION: THE

EVIDENCE• “Injection of a fluid that will increase blood pressure has dangers in itself. … If the pressure is raised before the surgeon is ready to check any bleeding that might take place, blood that is sorely needed may be lost.”

• — Walter Cannon, 1918

Walter Bradford Cannon

PERMISSIVE HYPOTENSION

• Keep the blood pressure low enough to avoid exsanguination whilst maintaining end-organ perfusion

• Prevent “clot busting”/dislodgement

• Avoid excessive fluid administration


EVIDENCE• Mapstone J, Roberts I, Evans P. Fluid resuscitation strategies: a systematic review of animal trials. J Trauma. 2003 Sep;55(3):571-89. Review. PubMed PMID: 14501908.• Meta-analysis of animal trials• 44 trials comparing fluid vs no fluid resus• Fluid resuscitation appears to reduce the risk of death in

animal models of severe haemorrhage, but increases the risk of death in those with less severe haemorrhage.

• Excessive fluid resuscitation could therefore be harmful in some situations.

• Hypotensive resuscitation reduced the risk of death in all the trials investigating it.


EVIDENCE• 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. PubMed PMID: 7935634. [Free Full Text]• non-blinded, semi-randomised prospective study• n=598 adults with penetrating torso injury and SBP <90mmHg• immediate resuscitation group (even days), delayed resuscitation group (odd days) - resus.

started in OR, not ED• immediate resus (average 870ml) - isotonic crystalloid as per local paramedical protocol and

ongoing isotonic crystalloid infusion in ED• delayed resus (average 92ml) - delayed any fluids/blood products until theatre.• Outcome: mortality benefit favouring delayed resuscitation: 70% vs 62% (p=0.04) • Comments:

• high-volume trauma centre in Houston - short door-to-theatre times• patients were usually young and fit• high potential for bias - not blinded, not randomised• Crystalloid was used - not haemostatic resuscitation• lacks external validity to settings where delayed presentation or blunt trauma predominates• did not include TBI


EVIDENCE• Dutton RP, Mackenzie CF, Scalea TM. Hypotensive

resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma. 2002 Jun;52(6):1141-6. PubMed PMID: 12045644.• RCT with n=110• titrating intial fluid therapy to SBP 70mmHg vs 100mmHg during active haemorrhage

until haemostasis• no difference in mortality• comments:

• small study with heterogenous patients - mostly young males, 51% penetrating trauma

• BP was similar in both groups regardless of the BP targets (suggests physiological adaptation was occurring)


EVIDENCE• Bjoern Hussmann, Matthias Heuer, Rolf Lefering, Alexander Touma, Carsten Schoeneberg, Judith Keitel, and Sven Lendemans. Prehospital Volume Therapy as an Independent Risk Factor after Trauma. BioMed Research International Volume 2015, Article ID 354367, 9 pages http://dx.doi.org/10.1155/2015/354367• Trauma Register of German Trauma Society - anonymous and

standardised multicenter database of severely injured patients. Since 1993.

• Restrospective analysis• Patients between 2002 - 2010 with following criteria

• Primary admission to hospital (no transfers)• Injury Severity Score (ISS) >/=16• Age >/= 16 years• Data available for prehospital and hospital volume therapy, PRBC

administration, GCS, Hb conc, base excess, one coagulation parameter, BP at accident site, blunt trauma, therapeutic measures (resus, intubation, chest tube insertion) and prehospital time

http://dx.doi.org/10.1155/2015/354367


EVIDENCE• Prehospital Volume Therapy as an Independent Risk Factor after Trauma.• 7,641 cases met the criteria and assigned to 1 of 5 groups -

0 - 500mL, 501 - 1000ml…>2001mL• increasing volume groups correlated with male, car/MBA,

prehospital intubation, adrenaline, chest tube insertion• Mortality: group 1: 18.3%, group 5 24.0%; p<0.01• Conclusions: Prehospital volume therapy in patients without

severe TBI represents an independent risk factor for mortality

• Limitations:• Anonymized data - could not access patient files for

further analysis• Retrospective analysis - only associations and not

causalities can be ascribed

PERMISSIVE HYPOTENSION

• Keep the blood pressure low enough to avoid exsanguination whilst maintaining end-organ perfusion

• Prevent “clot busting”/dislodgement

• Avoid excessive fluid administration

PERMISSIVE HYPOTENSION:

TREATMENT PRINCIPLES• When to use it• Uncontrolled Haemorrhage (or potential for it)• Not in controlled haemorrhage (Where goal is

normotension)• Controversial in Head injury - Cerebral hypoperfusion

• some suggest aim for normotension• some suggest SBP>100mmHg

• How to apply it• Small boluses (250ml) of fluid to a hypotensive goal

(SBP 85 - 100mmHg or MAP>65mmHg) + good radial pulse + pulse-oximetry

• If the BP is too high, use titrated aliquots of Fentanyl (e.g 25mcg IV)







HAEMOSTATIC RESUSCITATION:PRINCIPLES OF MANAGEMENT

• Identify at risk group as early as possible - Massive Transfusion Protocol

• Early use of blood components as the primary resuscitation fluid instead of crystalloid/colloids

• Use in the same ratio as they are lost through haemorrhage (Exact ratios are controversial)• PRBC:FFP:Platelets 1or2:1:1

• Give Tranexamic Acid• Prevent hypothermia• Prevent acidosis• Monitor and maintain Ca2+






CRYSTALLOIDS• The Good• Cheap• Readily available• Easily stored• No risk of transfusion

reactions/BBV

• The Bad• Increased haemorrhage -

increased clot rupture with restoration of normal BP

• Dilutional coagulopathy• Dilutional anaemia - impaired

oxygen delivery• Hypothermia• Metabolic Acidosis (N. Saline)• Lowers plasma oncotic

pressures - haemodilutionThe Bottom Line:

May be appropriate/not harmful in many trauma patients but aggressive use is associated with increased mortality in

haemorrhagic shock






HAEMOSTATIC RESUS: THE PROPPR TRIAL

• PROPPR Study Group*, JAMA. 2015;313(5):471-482 Transfusion of Plasma, Platelets, and Red Blood Cells in a 1:1:1vs a 1:1:2 Ratio and Mortality in Patients With Severe Trauma• 1:1:1 (intervention) vs 2:1:1(control) ratio in pt with

severe trauma and predicted to require MTP• RCT. Treating clinicians were non-blinded. • 12 North American Level 1 trauma centre sites• Sample size 680 pts

PROPPR OUTCOMES• Primary outcome - no significant difference in mortality at 24hours or at 30 days• Authors Conclusions - Among patients with severe trauma and major bleeding,

early administration of plasma, platelets, and red blood cells in a 1:1:1 ratio compared with a 1:1:2 ratio did not result in significant differences in mortality at 24 hours or at 30 days.

• Strengths:• Randomised, multi center• Minimal loss to follow-up

• Weaknesses:• unblinded• 30 day max follow-up time• study was powered to detect an absolute difference of 10% mortality - unable to

detect a smaller effect - 2968 patients would have been required to detect the observed difference of 4.2% (24 hour mortality) with 90% power

• Bottom line:• no difference in 1:1:1 vs 2:1:1 ratio - although study was underpowered for the

observed difference• 1:1:1 resulted in reduced mortality from exsanguination within the 1st 24 hours

WHAT CAUSES HAEMORRHAGIC SHOCK?

• Direct Tissue Damage

• Disruption of blood vessels with associated blood loss can be enough to cause tissue hypoperfusion

• Coagulopathy

• Intrinsic - Trauma-Induced Coagulopathy (TIC)/Acute Coagulopathy of Trauma (ACT)

• Extrinsic

• Hypothermia

• Dilutional (administration of crystalloids/blood products)

• Acidosis/Tissue Hypo-perfusion

TRAUMA-INDUCED COAGULOPATHY• Trauma-induced coagulapathy (TIC) and Acute Traumatic

Coagulopathy (ATC)• “not simply a dilution coagulopathy or consumptive

coagulopathy”

• Characterized by• Isolated factor V inhibition - functionally decreases thrombin• Dysfibrinogenaemia• Systemic Anticoagulation• Impaired platelet function• Hyperfibrinolysis

• Exacerbated by• hypothermia• acidosis• resuscitation by hypocoagulable fluid

HYPOTHERMIA• Severe hypothermia is associated with a

high mortality• <35 deg - platelet dysfunction• <33 deg - clotting enzyme

synthesis/kinetics, plasminogen activator • Progressive delay in the initiation of

thrombus formation• Causes

• Pre-hospital• ED - resuscitation period• Theatre - exposure of peritoneum, resus fluids

• Treat• Warmed fluids• Bair Hugger/warm blankets• Minimise exposure• Increase ambient temp.• Continuous Temp. Monitoring

ACIDOSIS AND BASE EXCESS

• Both are independent predictive factors of mortality and identify anaerobic metabolism (tissue hypoperfusion)

• pH strongly affects activity of Factors V, VIIa and X

• Acidosis inhibits Thrombin generation

• pH<7.2 - decreased contractility and CO, vasodilation, hypotension, bradycardia, dysrhythmias

• Lactate is demonstrated to have the best association with hypovolaemic shock and death - useful marker as an endpoint of resuscitation

TRAUMA TRIAD OF DEATH• Hypothermia

• Decreased cardiac output

• Arrhythmias• Decreased function of

coagulation factors and platelets

• Acidosis• reduced contractility,

bradycardia, dysrhythmias, vasodilation, hypotension

• Decreased function of coagulation factors and platelets

TRANEXAMIC ACID• TXA is an anti-fibrinolytic agent• The effect of TXA on mortality in a

bleeding patient is time dependant - survival advantage if given early

• CRASH2 Trial - Placebo vs (1g/10min + 1g/8hrs)

• Hospital Mortality within 4 weeks of injury reduced with TXA (14.5% vs. 16%, p=0.0035)

• Death due to haemorrhage reduced with TXA (4.9% vs. 5.7%, p=0.0077)

• No significant increase in clots (MI, CVA, PE) (1.7% vs. 2.0%, p0.084)

• TXA = good.

CRYOPRECIPITATE• Fibrinogen (plus platelets) is

the primary substrate for clot formation

• Reduced fibrinogen levels correlate with increased mortality

• If fibrinogen is <1.0g/L give Cryoprecipitate• Contains: Fibrinogen, Factor

VIII, vWF, Factor XIII• There is research into factors

predicting hypofibrinogenaemia on admission of trauma patients - triage revised trauma scores(T-RTS)/ISS - watch this space

DAMAGE CONTROL SURGERY

• Initial operation with haemostasis and packing

• Transport to ICU to correct hypothermia, acidosis, coagulopathy

• Return to theatre for definitive repair

MONITORING PROGRESS• Physiology

• Mental status• MAP/Pulses• Temp• Urine Output

(>0.5ml/kg/hr)• Blood tests

• Hb, Plt, Coags, INR, Fibrinogen, (?ROTEM)

• Lactate/Base Excess• Calcium• K+

THROMBOELASTOMETRY (ROTEM)• Viscoelastic method for testing

haemostasis in whole blood - point of care test

• Displays a reaction curve showing elasticity over time when a clot forms and dissolves

• Jury is still out. It has applications in liver and cardiac surgery. At the moment, limited evidence in it’s role during Trauma. Some studies show reasonable sensitivity and specificity in diagnosing Acute Traumatic Coagulopathy (72.7%, 77.5%)

• Crit Care. 2015 Mar 23;19:97. doi: 10.1186/s13054-015-0823-y. Detection of acute traumatic coagulopathy and massive transfusion requirements by means of rotational thromboelastometry: an international prospective validation study. Hagemo JS1,2, Christiaans SC3,4, Stanworth SJ5, Brohi K6, Johansson PI7,8, Goslings JC9, Naess PA10, Gaarder C11.

TAKE HOME MESSAGES• Identify those with/at risk of

haemorrhagic shock• Stop the bleeding• Permissive Hypotension (in patients

without head injury)• Haemostatic Resuscitation - early use

of blood products - Massive Transfusion Protocol

• Use TXA in all patients with uncontrolled haemorrhage

• Correct the correctible - hypothermia, electrolyte derangements

• Monitor• Don’t delay definitive treatment -

Damage Control Surgery

Date post:	08-Jan-2017
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Damage control resuscitation

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