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Trauma resuscitation
1) The document discusses a case of a pedestrian hit by a car with injuries including a flail chest, unstable pelvis, and internal bleeding. The goals of treatment are to prevent death from hemorrhage through early intervention, good airway management, resuscitation, and surgical intervention. 2) It introduces the principles of damage control resuscitation (DCR) including permissive hypotension to limit blood loss, early use of blood products to replace lost volume and clotting factors, and damage control surgery to control bleeding. DCR aims to address the "lethal triad" of coagulopathy, acidosis, and hypothermia. 3) Clinical markers like thromboelastography
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Trauma resuscitation
- 1. Trauma Resuscitation …and stuff… DrChristopher Moseley CME Teaching 8th October 2015
- 2. Objectives • Not goingto cover ATLS protocol • A quick case • Damage control Resuscitation • Permissive hypotension • Haemostatic resuscitation • Useful clinical markers for prognosis and monitoring
- 3. Case 1: Pedestrianversus car
- 4. Case 1: Pedestrianversus 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: Pedestrianversus 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.
- 8. Preventing death fromhemorrhage 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 Systematicapproach 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 ofa 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: modelof 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: nonfatal 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.
- 20. • non- blindedsemi-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 withn=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 administrationis 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 asevere 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) Inmost 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 thebleeding trauma patient if it doesn’t carry oxygen or it doesn’t clot then use with caution
- 26. 1 in 4trauma 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.
- 31. • Give bloodproducts 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 withblood 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 bloodcomponent 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 isno 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 agentsmay 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 ofcare 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 (ReactionTime) – 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 isthe 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 youresuscitate based on vital signs alone, you will under-resuscitate about 50% of trauma patients
- 42. Clinical judgment Clinical judjmentis 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 • agood 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 youdoing? 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 wemonitor progress????
- 47. LACTATE and BaseExcess • Both closely related to shock and volume loss • Reflect metabolic derangements and tissue level
- 48. Don’t forget urineoutput! • If your patient if making >50mls and hour your probably doing ok
- 51. Trauma Resuscitation …and stuff… ThisIs the sum total of my knowledge on the subject so questions to the boss!
Editor's Notes
- #6 Unfortunately, the classic stages of hemorrhagic shock (a la ATLS) are of limited clinical relevance in the real world, because of:Differences in compensation for different types of injuries (e.g. blunt versus penetrating trauma)Age (e.g. blunted physiological responses in the elderly)ComorbiditiesMedications (e.g. beta-blockade may conceal shock by preventing tachycardia)Also, bradycardia (rather than tachycardia) is often seen in major haemorrhage:One theory is that there are 2 phases of response to bleeding:— inital catacholamine surge with tachycardia, followed by— subsequent bradycardia of uncertain mechanism (parasympathetically mediated?)But there also seems to be a group of patients who have relative bradycardia — they fail to mount the initial tachycardia. Some have also noted that bradycardia is more common in acute rapid blood loss (Thomas and Dixon, 2004).Some have explained the bradycardia as being due to vagal stimulation from peritoneal stimulation in intra-abdominal hemorrhage, but bradycardia has been seen in penetrating extremity trauma too (Thompson et al, 1990).
- #7 FIRST THING – recognize it’s a trauma code and not a medical code so don’t start ALS as its bullshit. one person on AIRWAY 2) two people in fingure thorocstomy – bilateral, fingure in and sweep around. Why – massive pneumothorax and its treated, haemothorax and its drained. USS - ? pericardial tamponade – If 2 and 3 show nothing then stop!!! Adenaline may get the heart pumping but you aint getting the brain back – you don’t want that!
- #9 And while much of the damage from head injury is spoken for at the time of accident, the initial resuscitation of a bleeding trauma patient can have a tremendous impact on survival. To be clear, the most important step in managing these patients is surgical source control – most patients with massive hemorrhage need an operation to stay the hemorrhage. The state in which a patient arrives to the operating room or the intensive care unit – alive or near death, cold and coagulopathic or warm and well perfused – is up to you.
- #10 DAMAGE CONTROL RESUSCITATION Damage control resuscitation (DCR) is a systematic approach to the management of the trauma patient with severe injuries that starts in the emergency room and continues through the operating room and the intensive care unit (ICU)DCR involves haemostatic resuscitation, permissive hypotension (where appropriate) and damage control surgeryDCR aims to maintain circulating volume, control haemorrhage and correct the ‘lethal triad’ of coagulopathy, acidosis and hypothermia until definitive intervention is appropriate
- #12 Walter Cannon – during WW1 in the early days of IVI it was noted that patients given fluids bleed more. This is the basis of permissive hypotension.
- #13 Since Then there have been Many Many Animal studies looking at the effect of IV fluid resusitation on bleeding and mortality in major haemorrage
- #19 * who died of this injury – pulmonary haemorrage?? – Princess dianna – she stayed at the scene bleeding out from pulmonary haemorrage for more than an hour. Its very treatable in an emergence department – its reasons like this stay and play is out and pre-hospital ambulance should scoup and run.
- #20 First major trial to look at fluid resusitation in humans in major trauma.
- #21 patients were generally generally young fit patients with penetrating trauma. took place in a high-volume trauma centre in Houston with very short door-to-theatre times.good baseline balance: demographics, mortality before reaching OR, time to OR good separation: 1608 and 283 mL fluid given in ER in the two groupshigh potential for bias: not blinded, not randomisedBP was actually the same in both groups regardless of whether resuscitation was immediate or delayed. crystalloid was used, not a modern haemostatic resuscitation lacks external validity to settings where delayed presentations or blunt trauma predominates, or to traumatic brain injury
- #23 it is reasonable to restrict fluid boluses to patients who lose their radial pulse or are demonstrating signs of abnormal end-organ perfusion. Even ye olde 9th edition of ATLS is hip to this, changing its initial fluid challenge recommendations from 2L crystalloid to 1L, giving consideration to the early use of blood products. I would further editorialize to suggest that 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 blood
- #25 give fentanyl 20-25 mcg (decreases catacholamine release resulting in vasodilation, if MAP drops <65 mmHg then give fluids/ blood products as above)
- #26 Haemostatic resuscitation is a key component of damage control resuscitation and forms the basis of most massive transfusion protocols. It involves resuscitation with blood components resembling whole blood aims to avoid or ameliorate acute coagulopathy of trauma and the complications of aggressive crystalloid fluid resuscitation while maintaining circulating volume. damage control resuscitation is an approach to major trauma that integrates permissive hypotension, haemostatic resuscitation and damage control surgery
- #28 Bleeding causes acidosis, hypothermia, and coagulopathy. Then the cycle begins as they all beget each other. If this continues for too long, it is irreversible.
- #33 Now we know why we do it, whats the aim and hom?
- #34 500mls – HC 38-50 plt 150-400 Add 150ml anticoagulant Patient recieves 650 mls back – Hct 29plt 88, clotting 60
- #35 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, but the study was not powered to detect this. A post-hoc secondary outcome of death by exsanguination in the first 24 hours also favoured the 1:1:1 ratio. The trial was a pragmatic unblinded outcome and neither arm of the trial managed to achieve the intended blood product ratios, though there was clear separation between the 2 groups.
- #37 Thromboelastography (TEG) is a simple way of assessing many parts of the coagulation cascade from primary and secondary hemostasis to fibrinolysis. Thrombus formation typically requires four components: platelets which form the initial hemostatic plug, clotting factors which reinforce the platelets, fibrin which serves as a hemostatic glue, and other clot-supporting cells.TEG examines each phase of the clotting process by introducing citrated blood into a sample cup. The cup oscillates slowly (to simulate sluggish venous flow) around a submerged torsion pin. As coagulation occurs, the pin adheres to the clot and moves with it. The magnitude of pin motion is directly related to the clot’s strength. Amplitude decreases as fibrinolysis begins, and the pin begins to slip.
- #41 In a massively bleeding patient, fibrinogen can drop to clinically important levels faster than other blood components, and its breakdown and synthesis are affected by hypothermia and acidosis — leading to a vicious cycle of abnormal clot formation and excessive bleeding (Figure 10).
- #42 A pitfall of trauma
- #48 Also good link between lactate clearance in first two hour and reduced mortality