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Hemorrhagic Shock

Hemorrhagic Shock. GTCAC – AACN Fall Symposium November 8, 2013 Amy Knopke -Mooney, MD Pulmonary, Critical Care and Sleep Medicine. Discussion outline. Review basic physiology Review pathophysiology of shock Review principles of resuscitation and massive transfusion

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Hemorrhagic Shock

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  1. Hemorrhagic Shock GTCAC – AACN Fall Symposium November 8, 2013 Amy Knopke-Mooney, MD Pulmonary, Critical Care and Sleep Medicine

  2. Discussion outline • Review basic physiology • Review pathophysiology of shock • Review principles of resuscitation and massive transfusion • Complications of massive transfusion • Additional therapies for hemorrhage

  3. Basic Physiology

  4. Basic Physiology • What is shock? • Hypotension with associated organ dysfunction • Hypotension • Pressure = Flow x Resistance (P = F X R) • Flow = cardiac output • Pressure = Cardiac Output (CO) x Resistance

  5. Basic Physiology • P = CO x R • HR x SV • preload contractility afterload

  6. What is preload? • Refers to the amount of stretch/tension in cardiac myocytes prior to ventricular contraction • (Up to a point), increased tension results in increased SV

  7. Frank-Starling Relationship

  8. Physiology of Hypotension • P = CO x R • HR x SV • preload contractility afterload • 4 basic shock states • Hypovolemic • Distributive • Cardiogenic • Obstructive • Need to know your patient

  9. What about organ dysfunction?

  10. It’s the oxygen!

  11. Oxygen Delivery • DO2 = [1.39 x Hgb x SaO2 + (0.003 x PaO2)] x CO • Assuming a normal person in a resting state, DO2 is about 4x oxygen demand • Theoretically, DO2 can be maintained at a Hgb of 4 • May not necessarily be true in individuals with CVD

  12. So what’s the fix? • Give volume-- • preload SV CO DO2 • Increase Hgb --- DO2

  13. But, just because it’s simple doesn’t mean it’s easy….

  14. Resuscitation of Hemorrhagic Shock • Give volume “as fast as possible” • How fast is that? • P = F x R…… F = P / R • Rapid infusing systems, etc, increase flow by increasing driving pressure • But what about resistance….?

  15. Size matters….Poiseulle’s Law—flow = πr⁴∆P / 8ηL

  16. Poiseuille’s Law

  17. Resuscitation of Hemorrhagic Shock • Size matters, does fluid type? Not really • Crystalloid is as good as colloid (except blood) • Numerous RCTs and meta-analyses for albumin and hydroxyethyl starch • No benefit over crystalloid (even with subgroup analysis, possible increased mortality with albumin and head trauma) • Will need about 3x as much saline/LR as blood due to the volume of distribution (ISF + IVF)

  18. Resuscitation of Hemorrhagic Shock No significant benefit of LR vs NS in terms of mortality or other outcome measures although LR does reduce NAGMA (in perioperative patients) Increased risk of AKI/RRT and mortality with HES (sepsis) (RCT NEJM 2012) HES decreases VIII, vWF and platelet activity

  19. Resuscitation of Hemorrhagic Shock • Massive transfusion • > 10 U in 24 hours or > 5 U in 3-4 hours • Fairly uncommon – about 2% incidence of all trauma patients • Other populations – ruptured AAA, obstetrics, GI bleeding, peri-operative • Incidence is decreasing slightly as we are better able to control coagulopathy

  20. Complications of Massive Transfusion Coagulopathy Hypothermia Acid/Base disturbances Hypocalcemia Hyperkalemia Oxygen delivery issues TRALI/TACO

  21. Complications of Massive Transfusion • Alterations in coagulation • Dilutional coagulopathy • Blood and IVF lack platelets and coagulation factors • Each 500 cc of blood replaced can reduce clotting factor proteins by 10% • Bleeding due to dilutionalcoagulopathy occurs when coagulation factors are 25% normal – after 8-10 U PRBCs….but will be less if first resuscitated with fluids • 10 U PRBCs will decrease platelet concentration by 50% • 1U FFP will increase coagulation factor concentration by 3-10%. 1 adult dose of platelets will increase plts by 30K

  22. Complications of Massive Transfusion • Alterations in coagulation • DIC frequently complicates massive transfusion • Increased coagulation factor activation due to tissue trauma – macroscopic or microvascular • Increased coagulation factor consumption in an attempt to stop bleeding • Decreased activity of coagulation factors and platelets due to effects of shock-- hypothermia, hypoxia and acidosis

  23. Complications of Massive Transfusion • Hypothermia • Coagulation cascade is an enzymatic process • Rate of enzymatic processes are affected by temperature • Platelet activation ceases in roughly 50% of people at 30°C and is markedly reduced in the remaining 50% • Hypothermia leads to decreased platelet activation and coagulation factor activity at 34°C (93°F)

  24. Complications of Massive Transfusion • Hypothermia • 6U PRBCs (4°C) will decrease body temperature of a 70kg pt by 1°C • Open body cavity will decrease body temperature by 1°C after 40-60 min • 10U transfusion during a 1 hour operation can decrease temperature by 3°C • Consider using a blood-warmer for more than 4U transfusion

  25. Complications of Massive Transfusion • Acidosis • Tissue hypoperfusion results in lactic acid generation and acidosis • Large volume NS resuscitation (3-4L) leads to acidosis by replacing HCO3ˉ with Clˉ • Acidosis interferes with coagulation factor activity • Activity reduced by 50% at pH 7.2 • Reduced by 80% at pH 6.8

  26. Deadly triad: hypothermia, acidosis and coagulopathy

  27. Complications of Massive Transfusion • Affects of Citrate • Citrate is the preservative/anticoagulant in stored blood • Citrate metabolized by the liver to bicarbonate and (theoretically), significant metabolic ALKalosis can result • However, final acid/base status is more dependent on acid/base status of the patient, tissue perfusion and hepatic metabolism • Citrate binds ionized calcium and may lead to hypocalcemia---which results in muscle spasm and may contribute to hypotension.

  28. Complications of Massive Transfusion • Hyperkalemia • Majority of potassium is intracellular • Over time there is increased cell lysis and reduced Na+/K+-ATPase function, leading to an increased EXTRAcellular concentration of K+ but decreased INTRAcellular concentration of K+ • Each unit of blood may contain up to 7-10 meq of extracellular K+ • However, intracellular shift of K+ occurs once cells are re-warmed

  29. Complications of Massive Transfusion • Alterations of oxygen delivery • Stored RBCs have decreased concentrations of 2,3-diphosphoglycerate (2,3-DPG). • Results in INCREASED affinity for oxygen by hemoglobin and reduced tissue delivery of oxygen • Theoretical effect as red cells regenerate 2,3-DPG 6-24 hrs after transfusion.

  30. Complications of Massive Transfusion • TRALI/TACO • TRALI is the leading cause of transfusion-related mortality in the US • Incidence in critically ill around 5-8% • Mortality estimates range from 5-35% • Defined as NEW ALI/ARDS within 6 hours of transfusion • Additional ARDS risk factors must be absent (sepsis, shock, trauma, burns, aspiration, pancreatitis, bypass, etc) • “Possible TRALI”

  31. Complications of Massive Transfusion • TRALI/TACO • TRALI— • Increased risk – patient factors • Critically ill populations (high APACHE II) • Sepsis/infection and/or shock • Massive transfusions • Mechanical ventilation • Liver disease/alcohol abuse • Recent surgery • increased risk—blood component factors • Increased plasma-containing products (FFP and platelets) • Donor gender and parity • No relation to length of storage

  32. Complications of Massive Transfusion • Etiology of TRALI • “two-hit hypothesis” • Neutrophil sequestration and priming in lung microvasculature due to endothelial injury and cytokine exposure • Low rate of TRALI even in cases of presence of HLA antibodies and corresponding antigen present • Neutrophil activation by donor antibodies (HLA/HNA) or antigens (bioactive lipids or other proteins) resulting in release of inflammatory cytokines, protease and reactive oxygen species leading to further injury of pulmonary capillary bed and leak

  33. Complications of Massive Transfusion • TACO • Transfusion-associated circulatory overload • Increased risk • Elderly patients • Compromised cardiac function • Positive fluid balance • Rapidity of product administration (relative to fluid balance)

  34. TRALI vs TACO • Possible fever • Possible hypotension • PCWP < 18 mmHg • Fluid balance negative to equal • Normal BNP (or unchanged) • Normothermic • Possible hypertension • PCWP > 18 mmHg • Positive fluid balance • Elevated BNP

  35. Complications of Massive Transfusion • TRALI/TACO • Treatment • Supportive care – maintain oxygenation and consider PPV • 50-80% of TRALI patients will require mechanical ventilation • Use of diuretics in patients with TACO and hemodynamically stable TRALI • No indication for steroids • Also, for TRALI, should notify the blood bank – will review all donated units, notify the blood supplier--may perform HL/NA testing on remaining units and may exclude an identified donor from future donations. (1 donor, 290 units, 40% TRALI – single HLA Ab variant)

  36. Transfusion—what to give? • Ideally would like to transfuse to a target, presuming pressure can be maintained through IVF • Common transfusion parameters • Hgb >7 • INR </= 1.2-1.5 • Platelets >50-100K • Fibrinogen > 100

  37. Transfusion Triggers • Hemoglobin thresholds • Cochrane analysis 19 RCTs transfusion triggers of 7 vs 10 • 46 vs 84% risk of transfusion • Trend toward lower mortality • No difference in ICU or hospital LOS • No increased risk of MI • TRICC (1999) – RCT comparing same triggers • Trend toward decreased mortality for a restrictive strategy • EXCEPT in patients with ischemic heart disease • Suggestion to transfuse >10 g/dl with active ischemia and goal of 8-10 g/dl in patients with ischemic heart disease

  38. Transfusion Triggers • Cardiac surgery • 2 RCTs comparing restrictive (<8) vs liberal (<9-10) strategies • No difference in mortality, shock, ARDS or renal failure • Restrictive strategy used less blood • NEJM 2013 – RCT • Patients with acute GI bleed (may be hypotensive, but NOT in shock) • Transfused at either Hgb<7 (restrictive) or Hgb <9 (liberal) • 51% (restrictive) vs 14% (liberal) did NOT receive blood (p<0.001) • 95% (restrictive) vs 91% (liberal) survival difference (p=0.02) • 40% (restrictive) vs 48% (liberal) adverse outcomes (p=0.02) – ALL related to TACO.

  39. Massive Transfusion—what to give? • Various studies suggesting a “high-transfusion ratio” may be beneficial (RCTs lacking so far) • 1:1:1 ratio – PRBCs : FFP : plts (6:6:1 if apheresis) • Rationale – pre-existing coagulopathy due to DIC, crystalloid use and relative dilute nature of stored blood products • This ratio provides Hct 29, plts 90, coagulation factor activity 65% (INR<1.5)

  40. Massive Transfusion • 1:1:1 High-transfusion ratio • Retrospective study of combat trauma • 81% vs 66% vs 35% survival in patients receiving PRBC:FFP ratios of 1:1.4 vs 1:2 vs 1:8 respectively • 2 retrospective trauma series • Decreased 30-day mortality in patients who EITHER received >1:2 ratio of PRBC:FFP OR PRBC:plts

  41. Other therapies for hemorrhage

  42. Coagulation Cascade

  43. Other therapies for hemorrhage • Recombinant activated Factor VII (rVIIa) • Approved for treatment of bleeding in hemophilia • All other uses are off-label • Trauma • Surgical hemorrhage • Liver disease • Intracranial hemorrhage • Warfarin and new anticoagulants • Accounts for >90% of use of rVIIa • Cost is about $4000 per dose

  44. Other therapies for hemorrhage -- rVIIa • 2008 meta-analysis—22 RCTs • Results • Significant reduction in transfusions • Did not decrease mortality or increase rate of thrombosis • 2011 meta-analysis of 16 RCTs • No improvement in survival • Increased risk of thrombosis for patients with ICH or cardiac surgery

  45. Other therapies for hemorrhage -- rVIIa • Criticisms • Meta-analyses have included a very wide-group of patients and there is not enough evidence to weigh in for or against it’s use in a particular sub-group of patients • 2009 RCT in cardiac surgery patients • Two doses – 40 mcg/kg vs 80 mcg/kg • Significantly reduced need for re-operation in both groups • Trend toward increased adverse events (death or thrombosis) – 7% vs 14% vs 12%

  46. Other therapies for hemorrhage - rVIIa • 2006 RCT of trauma patients undergoing massive transfusion • 200, 100 and 100 mcg/kg • Significant reduction in transfusion needs • No difference in mortality or adverse events • May be most beneficial in coagulopathic patients and/or hypothermia • unlike other clotting factors, the activity of rVIIa is not reduced at 33°C • Activity IS reduced by acidosis

  47. Other therapies for hemorrhage - rVIIa • Adverse events • Reports range from 2-10% • Both venous and arterial thromboses • Meta-analysis of 35 RCTs • Increased risk of arterial thrombosis 5.5% vs 3% • Particularly among >75 yo (11% vs 4%) • Increased risk with increasing doses of rVIIa • Increased risk with underlying atherosclerotic vascular disease

  48. Hemorrhagic Shock Physiology is important – know your patient Give volume quickly in the shortest, widest thing you have Consider higher transfusion ratios of massive hemorrhage Watch out for the deadly triad – hypothermia, acidosis, coagulopathy TRALI vs TACO Remember the risks of rVIIa as well as potential benefits

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