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Dealing with Coagulopathy in Trauma

Dealing with Coagulopathy in Trauma. Dr . K. Subramani MD DA FRCA CST FANZCA EDIC FICCM Professor and Head Division of Critical Care & Surgical ICU Christian Medical College Vellore. Coagulopathy in trauma. Incidence of Lab detectable coagulopathy in trauma 25-35%. Lethal triad

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Dealing with Coagulopathy in Trauma

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  1. Dealing with Coagulopathy in Trauma Dr. K. Subramani MD DA FRCA CST FANZCA EDIC FICCM Professor and Head Division of Critical Care & Surgical ICU Christian Medical College Vellore

  2. Coagulopathy in trauma • Incidence of Lab detectable coagulopathy in trauma 25-35%. • Lethal triad • Coagulopathy independent of this is called ATC • Biochemical response to Trauma and Injury • Can develop in Traumatic Brain injury too. • Complicated if patient is on anticoagulant / antiplatelet medication

  3. Why Worry? • Bleeding is a leading cause of death in the initial hours • More transfusions • Longer duration of mechanical ventilation • Longer stay • More multi-organ dysfunction • Mortality compared with no coagulopathy • 3 to 4 fold • Likely death within 24 hours is 8 times

  4. Aetiology • Coagulation is a balance • Clotting vs Fibrinolysis • Multifactorial aetiology • Nature of injury • Severity of Injury • Associated Shock • Resuscitative measures

  5. Trauma induced coagulopathy

  6. The Lethal TriadAcidosis • Acidosis • Hypoperfusion– Metabolic acidosis • Lactic Acidosis • Worse if one develops ischaemic hepatitis • Chloride induced • Reduced activity of prothrombinase complex < pH 7.2

  7. The Lethal TriadHypothermia • Hypothermia • Temperature • < 36 C 65% • < 33 C 9% • Exposure and fluid resuscitation • Hypothermia + Acidosis predicts high mortality.

  8. The Lethal TriadCoagulopathy • Resuscitation related iatrogenic coagulopathy • Pre-hospital resuscitation • Red cells alone • Crystalloid or artificial colloid • “Storage Lesion”

  9. Diffuse Intravascular coagulation • Tissue Thromboplastinrelease • Bone marrow, amniotic fluid, brain phospholipids • DIC • Consumptive coagulopathy • Microvascular thrombosis – organ failure

  10. Acute Traumatic Coagulopathy • Hypo-coagulation • Fibrinolysis • Hyper-coagulation • Predictors • Shock • Severity of Injury • Head injury • worsening base deficit

  11. Acute Traumatic CoagulopathyThe story of Protein C • Mechanism • Activation of Protein C • Short period of hypoperfusion • Depletion of Factors V, VIII and plasminogen inhibitors • Prevents clotting to maintain flow • Sustained hypoperfusion • Increased Thrombin-thrombomodulin • Paradoxically, thrombin leads to Hypocoagulable state.

  12. Acute Traumatic CoagulopathyThe story of Protein C • Widespread activation of Protein C • Impairs thrombin generation and a hypocoagulable state • Consumption of Plasminogen activator inhibitor • Reduced activation of Thrombin activable Fibrinolysis Inhibitor • Enhanced fibrinolysis • Protein C Depletion • Associated with increased morbidity and mortality • Lung injury, VAP, Multi-organ failure • Increased risk of thromboembolic complicatioms

  13. Fibrin related issues • Hyperfibrinolysis • Related to degree of shock • 30 minute lysis time at 3% • Massive transfusion (91 vs 30%) • Death due to haemorrhage (46 vs 5%) • Fibrinolysis shutdown • 30 minute lysis time at <0.8% 64% • Death due to multiple organ failure

  14. Other factors • Release of Thrombin rich microparticles. • Platelet Dysfunction • Quantitative • Qualitative • Transfusion related • Hypocalcemia • Citrate toxicity – Worse with Ischaemic hepatitis

  15. Diagnosis • Standard coagulation tests • Prothrombin time and INR • Activated Partial Thromboplastin time • Fibrinogen and D Dimer levels (FDP) • Advantages • Available in most places • Disadvantages • Delay in getting reports • Not real time as more bleeding and product transfusion would have occurred • Point of Care testing • TEG and ROTEM

  16. DiagnosisPT, INR and APTT • Greater than 1.5 times lab reference value • Mortality (Odds ratio 1.35 for PT and 4.26 for APTT) • In ATC, standard coagulation tests may be normal • Tested at Temperature of 37 Degrees! • Do not test platelet function • Platelet function tests • Platelet function analyser • Electrical impedence whole blood aggregometer

  17. Viscoelastic dynamic tests • TEG and ROTEM • Clotting • Assesses all aspects of coagulation • Clot initiation, Strength • Factors and platelets • Demonstrated hypo and hypercoagulability in the face of normal PT / APTT • Fibrinolysis

  18. ROTEM

  19. Thromboelastogram

  20. Diagnosis • Factor levels • Fibrinogen • Factors V and VIII • Above with thrombin, Factors IX and X, aPC levels predict coagulopathy. • Scoring systems • TASH – Trauma Associated Severe Haemorrhage • McLaughlin Score • ABC – Assessment of blood consumption score

  21. Treatment • ATLS • Damage Control Resuscitation • Antifibrinolytic (Crash 2 and MATTERs) • Massive Transfusion protocol activation • Transfusion strategies • Limit Crystalloids and avoid artificial colloids • 1:1:1 red cell:FFP:Platelets • PROMMTT • Reduced death during the first 6 hours • Reduction in mortality if more plasma was transfused early • PROPPR • Reduced death rate in the first three hours • 1:2 Plasma:Blood (European) • Fresh Whole blood

  22. TreatmentTransfusion Strategies • Viscoelastic test based transfusion • No strong evidence as yet • Confounders - alcohol

  23. TreatmentFibrinolysis related issues • Tranexemic Acid • CRASH 2 Trial (Clinical Randomisation of Txa in Significant haemorrhage) • Absolute RR 1.5%; NNT 67 : 1 • Incidence of Thrombosis was not significant • MATTERs (Military application of Txa in traumatic emergency resuscitation) • Absolute RR 14% NNT 15 : 1 in MTP 7 : 1 • Incidence of thrombosis was higher in Txa, but not significant

  24. Treatment • Recombinant Factor VII • Prothrombin Complex Concentrate • Desmopressin • Patients on anticoagulants / antiplatelet medications • Reverse appropriately

  25. Monitoring • Standard Monitoring • ECG • Pulse oximetry, • Core temperature • Invasive arterial pressure • Urine output • Major Venous access

  26. Monitoring • General • Bloods • Full Blood Count • Blood Gas Analysis • Lactate, Base Excess, Ionised Calcium • Oxygenation and ventilation indices • Electrolytes • Sodium, Potassium, Calcium • Coagulation • TEG or ROTEM • Standard Coagulation tests • Fibrinogen • Platelet count • D Dimers / FDP

  27. Platelet margination

  28. Newer Concepts

  29. Newer ConceptsEndothelial Glycocalyx

  30. Endothelial Glycocalyx

  31. Endothelial Glycocalyx

  32. Endothelial Glycocalyx in Inflammation

  33. Glycocalyx • Starling’s equation • Endothelial permeability • Activation and propagation of coagulation • Role of albumin other than “maintaining oncotic pressure”

  34. New Concepts Blood Products

  35. Whole Blood vs Component Therapy

  36. Whole blood • Military experience

  37. Cold stored Platelets • Current practice • Room Temperature storage • Agitation

  38. For your practice • Do not preciptate or worsen the existing coagulopathy • Follow principles of damage control resuscitation • Change your practice as new evidence emerges • Practice good general acute care or critical care

  39. Thank You

  40. TEG Based transfusion

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