Trauma resuscitation

1. Trauma Resuscitation
…and stuff…
Dr Christopher Moseley
CME Teaching 8th October 2015

2. Objectives
• Not going to cover ATLS protocol
• A quick case
• Damage control Resuscitation
• Permissive hypotension
• Haemostatic resuscitation
• Useful clinical markers for prognosis and
monitoring

3. Case 1: Pedestrian versus car

4. Case 1: Pedestrian versus Car
• 60 yo, hit and run.
• Brought in by SJA, you’re in T1…he’s
thrashing around
• GCS 14, HR 120, SBP 80, RR 24, T 35.5.
• O/E flail chest right, left chest sounds OK,
abdomen nontender (…but GCS
is 14), unstable pelvis.

5. Case 1: Pedestrian versus Car
• Chest drain R: 300 mls blood + air
• Intubated
• Vitals after this: HR 120, SBP 95
• FAST negative
• Pelvis bound
• CXR: R CT good position, L lung OK.
• What fluids do you want? Do you want bld? How much?
How will you monitor your resusitation efforts?
• Where will you go with this pt next?
• What are the common pitfalls in this situation?

6. Recognize your in it!

8. Preventing death from hemorrhage is
a team sport – (ish)
If you’re going to die from injury, statistically speaking it
will be due to a severe traumatic brain injury; close
behind that is death from exsanguination.
• Get to us early
• Good airway management
• Good resuscitation
• SURGICAL INTERVENTION

9. Damage Control Resusitation
Systematic approach from street to ICU
DCR aims to maintain circulating volume, control
haemorrhage and correct the ‘lethal triad’ of
coagulopathy, acidosis and hypothermia
1) Permissive Hypotension (aka minimal normotension)
(this is controversial)
2) Early haemostatic resuscitation
3) Damage control surgery

11. Permissive Hypotension
“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

13. • PIG model: rip a hole in the pigs aorta and then
resuscitate them.
• Resuscitate to to normal (MAP=80) – 78% mortality
• No fluid (MAP 40) 11% mortality
• Moderate (MAP 60) 22% mortality
• *stern et al Annals Emerg. Med 22 155-163 1993

15. • RATS: model of uncontrolled hemorrhage with pre-
hospital and hospital phases.
• Randomized to different arms: No resus, No
prehospital resus, prehospital resus to MAP 40,
preshospital to MAP 80.
• Results – no resusitation 100% fatal, no initial fluid
100% mortality. MAP 40 60% survial, MAP 80 100%
fatal – greatest blood loss

17. • SHEEP: non fatal model – pulmonary vein
haemorrage.
• Hole in pulmonary vein and chest tube inserted see
what comes out.
• Fluid vs No fluid
• blood loss 3.5 lt vs 1.5 lt.
• Time of bleeding 48min vs 29min.
*sackles et al Annals Emer med 29 392-399
????Who died of this injury???

19. Houston Trial

20. • non- blinded semi-randomized prospective study
• n = 598 adults with penetrating torso injury and SBP
<90mmHg an immediate resuscitation group (even
days) and a delayed resuscitation group (odd days)
(resuscitation started in OR, not ED)
• Outcome: mortality benefit favoring delayed
resuscitation: 70% vs 62% (p= 0.04)

21. • RCT with n=110
• titrating the initial fluid therapy to SBP 70 mmHg
versus 100 mmHg during active hemorrhage
• no difference in mortality
• small study. Patients BP was again similar in both
groups regardless of the BP target (e.g. 100 ± 17
mmHg in the 70-mmHg group) suggesting
physiological adaptation
Dutton et al

22. 1)Excessive crystalloid administration is associated with
hypothermia, coagulopathy and death in bleeding
patients.
2)A strategy of permissive hypotension is likely
beneficial in the early stages of resuscitation,
particularly for penetrating trauma
3)if you think your patient is bleeding and you have
ready access to blood products, you can skip
crystalloid all together and go straight for the good
stuff.
Permissive hypotension

23. Caveats:
1)Patients with a severe head (GCS < 8) and spinal
injury are probably an exception to the permissive
hypotension strategy; in such cases, a mean arterial
pressure of > 80 mmHg has been recommended to
promote cerebral perfusion
2) Hypertonic saline solutions are a safe and reasonable
option for the hypotensive, head injured patient,
although there is no conclusive evidence of their
benefit
Permissive hypotension - summary

24. AIM: (minimal normotension)
In most circumstance a MAP of 65 should be our aim,
no benefit going above this.
MAP<65 – give fluids/products
MAP>65 – check perfusion (radial pulse and pulseox
waveform) – if bad perfusion can give fentanl BP
should drop and then give products
Permissive hypotension - summary

25. HAEMOSTATIC RESUSITATION
In the bleeding trauma patient if it
doesn’t carry oxygen or it doesn’t clot
then use with caution

26. 1 in 4 trauma patients bleed abnormally
The phenomenon of an early coagulopathy in trauma
– which goes by many names, including the Acute
Coagulopathy of Trauma-Shock (ACoTS) – can occur
soon after injury, and is physiologically distinct from
the DIC-like phenomenon associated with the “lethal
triad”
Trauma patients bleed abnormally

28. Hypothermia
Decreases platelet responsiveness, increases platelet
sequestration in liver and spleen, reduces Factor
function eg Factors XI and XII. Alters fibrinolysis
Acidosis
pH strongly effects activity of Factors V, VIIa and X.
Acidosis inhibits thrombin generation. Cardiovascular
effects of acidosis (pH <7.2) – decreased contractility
and CO, vasodilatation and hypotension, bradycardia
and increased dysrhythmias
Lethal Triad

29. Hypothermia
Decreases platelet responsiveness, increases platelet
sequestration in liver and spleen, reduces Factor
function eg Factors XI and XIIAlters fibrinolysis
Acidosis
pH strongly effects activity of Factors V, VIIa and X.
Acidosis inhibits thrombin generation. Cardiovascular
effects of acidosis (pH <7.2) – decreased contractility
and CO, vasodilatation and hypotension, bradycardia
and increased dysrhythmias
Lethal Triad

30. Early
hyperfibrinolysis

31. • Give blood products instead of isotonic crystalloid
fluid aiming for limited volume replacement.
• Large volume crystalloids can lead to dilutional
coagulopathy and exacerbate bleeding.
• Crystalloids have no O2 carrying capacity and do
little to correct the anaerobic metabolism and O2
debt associated with shock.
• Oedema, compartment syndrome, resp distress
Blood Vs Crystalloid

32. Provides resuscitation with blood components
resembling whole blood with the aims of:
• maintain circulating volume
• limit ongoing bleeding
• prevent the lethal trial of hypothermia, acidosis and
acute coagulopathy of trauma
Typical triggers are:
• expected or actual haemorrhagic shock
• 4 PRBCs administered and instability persists
Haemostatic Resusitation

33. • Involves blood component ratios of 1 or 2 RBCs : 1
FFP : 1 platelets
• Rick Dutton freely admits that he made up the ratio
of 1:1:1 based in the rationale that it mimics the
composition of whole blood
• Australian National Guidelines advocates 2:1:1 ratio
HOW?

34. • There is no RCT evidence for RBC:FFP:platelet ratios
of 1-2:1:1 versus other ratios/ fluids
• The PROPPR trial (2015) found no statistically
significant mortality difference on the primary
outcome of mortality between massive transfusion
protocols based on 1:1:1 and 2:1:1 ratios. There was
an absolute difference in mortality of about 4%
favouring the 1:1:1 ratio
Evidence

35. • Other agents may be given based on blood tests:
• INR >1.5 - FFP
• PHb <100 in an actively bleeding -> PRBCs
• Calcium <0.8 - calclium gluconate
• Platelets <80 - platelets
• platelet dysfunction (e.g. drugs) - platelets
Adjuncts

36. Thromboelastogram
• Point of care test (30mins)
• Measures clot strength
• it shows the interaction of platelets with the
coagulation cascade (aggregation, clot strengthening,
fibrin cross linking and fibrinolysis)
• does not necessarily correlate with blood tests such
as INR, APTT and platelet count (which are often
poorer predictors of bleeding and thrombosis)
• WHY? – to guide fluid/blood resusitation

37. TEG Interpretation
R (Reaction Time) – Time to first clot formation. Determine by clotting
factors. Corrected by FFP
K (K time) – Time to reach fixed strength (20mm). Determine by fibrinogen.
Correct with Cryoprecipitate
Alpha Angle – Speed of fibrin cross linking. Correct with cryoprecipitate
MA (Maximum Amplitude) – overall stability, determine by platlets. Correct
with platlests
LY30 - amplitude at 30 minutes; percentage decrease in amplitude at 30
minutes post-MA and gives measure of degree of fibrinolysis. Correct with
antifibrinolytics such a TXA

38. Tranexamic Acid
Tranexamic acid (TXA) is an anti-fibrinolytic agent
that can/should be used early in the resuscitation of
bleeding trauma patients
The effect of TXA on mortality in bleeding trauma
patients is very time-dependent, conferring a huge
survival advantage if given early

39. Tranexaminc Acid
Tranexamic acid (TXA) use is supported by the
CRASH2 trial:
• a multicenter international RCT
• Mortality benefit if given to major trauma patients
within 3 hours of injury.

40. Cryoprecipitate
• Fibrinogen is the primary substrate for clot
formation (along with platelets)
• There is a consistent link between falling fibrinogen
and mortality in trauma
• The key is to measure and follow serum fibrinogen in
bleeding patients – a fibrinogen less than 1.0 g/L
identifies a hypofibrinogenemic state, the antidote
for which is cryoprecipitate.

41. Clinical judgment
If you resuscitate based on vital signs alone,
you will under-resuscitate about 50% of
trauma patients

42. Clinical judgment
Clinical judjment is probably not so great for
predicting the need for massive transfusion
and calculated parameters like Shock index
don’t seam to help.

43. Clinical judgment
• a good sense of situation awareness
• ability to rapidly assess response to your initial
resuscitative efforts.
So clinical trigger for DCR:
• expected or actual haemorrhagic shock
• 4 PRBCs administered and instability persists

44. How are you doing?
Single best predictor of
out come????

45. . . . . INR
WHY?
It encompasses the two reasons these patients die
1) in brain injury you release tissue thromboplastin
you therefore use all your factor seven and your INR
goes up.
2)Haemorrage causing coagulopathy.

46. How do we monitor progress????

47. LACTATE and Base Excess
• Both closely related to shock and volume loss
• Reflect metabolic derangements and tissue level

48. Don’t forget urine output!
• If your patient if making >50mls and hour your
probably doing ok

51. Trauma Resuscitation
…and stuff…
This Is the sum total of my
knowledge on the subject so
questions to the boss!