Damage control resuscitation

1. PRINCIPLES OF DAMAGE
CONTROL RESUSCITATION
Dr Kav Senasinghe
CME March 2016, SCGH ED

2. 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

3. 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

4. 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.

5. 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

6. 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

7. 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

8. 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%

11. 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

12. 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

13. 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

14. PERMISSIVE
HYPOTENSION
• Keep the blood pressure low enough to avoid
exsanguination whilst maintaining end-organ
perfusion
• Prevent “clot busting”/dislodgement
• Avoid excessive fluid administration

15. PERMISSIVE
HYPOTENSION: THE
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.

16. PERMISSIVE
HYPOTENSION: THE
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

17. PERMISSIVE
HYPOTENSION: THE
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)

18. PERMISSIVE
HYPOTENSION: THE
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

19. PERMISSIVE
HYPOTENSION: THE
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

20. PERMISSIVE
HYPOTENSION
• Keep the blood pressure low enough to avoid
exsanguination whilst maintaining end-organ
perfusion
• Prevent “clot busting”/dislodgement
• Avoid excessive fluid administration

21. 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)

22. 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

23. 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+

24. 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+

25. 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 -
haemodilution
The Bottom Line:
May be appropriate/not harmful in many trauma patients but aggressive
use is associated with increased mortality in haemorrhagic shock

26. 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+

27. 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

28. 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

30. 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

31. 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

32. 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

33. 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

34. 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

35. 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.

36. 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

37. DAMAGE CONTROL
SURGERY
• Initial operation with
haemostasis and packing
• Transport to ICU to
correct hypothermia,
acidosis, coagulopathy
• Return to theatre for
definitive repair

38. 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+

39. 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.

41. 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