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SHOCK July 12, 2001. Rob Hall and Dr. John King

SHOCK July 12, 2001. Rob Hall and Dr. John King. Case. 16yo male, riding bike then swerved into traffic and was struck by a truck A: gurgling, stridor, facial trauma B: RR 35, sat 85%, subQ air on R, abrasion over sternum, dec AE on R, wheeze C: diaphoretic, HR 145, BP 70/50, +JVD

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SHOCK July 12, 2001. Rob Hall and Dr. John King

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  1. SHOCKJuly 12, 2001. Rob Hall and Dr. John King

  2. Case • 16yo male, riding bike then swerved into traffic and was struck by a truck • A: gurgling, stridor, facial trauma • B: RR 35, sat 85%, subQ air on R, abrasion over sternum, dec AE on R, wheeze • C: diaphoretic, HR 145, BP 70/50, +JVD • secondary: pelvic #, femur #, large scalp laceration, skin looks red

  3. Case • Ddx of shock in this patient • hemorrhagic: hemothorax, abdomen, pelvis #, femur #, scalp laceration • obstrucitve: tension pneumo/hemothorax • cardiogenic: cardiac tamponade • anaphylactic: the patient was stung by a bee, lost control of bike and was struck by a car

  4. “ Shock is the transition between illness and death”

  5. Definition of Shock • Shock is the clinical manifestations of the inability of the circulatory system to adequately supply tissues with nutrients and remove toxic waste

  6. Classification of Shock • Quantitative • hypovolemic, hemorrhagic, obstructive, myocardial dysfunction • Qualitative • sepsis, anaphylaxis, neurogenic, dyshemoglobinemia, cellular poisons

  7. Classification of Shock • Pre - heart • hypovolemia, venous pooling • Heart • contractility, arrythmias, mech obstruction • Post - heart • loss of vascular tone, inability to deliver to tissues, inability of tissues to utilize

  8. Etiological Classification • S - septic • S - spinal (neurogenic) • H - hypovolemic/hemorrhagic • O - obstructive (PE, pthrx, hthrx, ct) • O - other (CN, CO, HS, MetHb) • C - cardiogenic • K - anaphylaCTic

  9. Pathophysiology • FOUR unifying features of shock • intracellular calcium overload • intracellular hydrogen ion • cellular and interstitial edema • catabolic metabolism

  10. Shock Treatment Goals • FOUR goals of treatment • oxygenation • ventilation • volume replacement • vasopressor support

  11. Approach to Undifferentiated Shock • Targeted history • septic: fever, immunocompromised • hypovolemic: vomiting, diarrhea, abdo pain • hemorrhagic: trauma, bleeding (UGI, LGI, PV), abdo pain (AAA) • obstructive: chest pain, trauma • other: environmental exposures • cardiogenic: chest pain • anaphylatic: allergic reactions

  12. Approach to Undifferentiated Shock • Investigations • labs • ECG • CXR • ABG • urine

  13. Septic Shock

  14. Definitions:Consensus conference on definitions for sepsis: Critical Care Medicine 2000. Volume 28 (1): 232 - 235 • Sepsis • clinical response to infection manifested by two or more of the following as a result of infection • temp > 38 or < 36 • HR > 90 • RR > 20 or PaC02 < 32 • wbc > 12 or > 10% bands

  15. Definitions Continued • Septic Shock • sepsis induced hypotension or the requirement for vasopressors or inotropes to maintain BP despite adequate fluids in the presence of… • lactic acidosis • oliguria • acute alterations of mentation

  16. Early versus Late Septic Shock

  17. Management of Septic Shock • Fluids • boluses of NS or RL • Pressors • dopamine, norepinephrine • consider after 3 boluses of crystalloid • Antibiotics • broad spectrum empiric coverage

  18. New Approaches to Septic Shock • Vasoactive mediators • vasopressin, nitric oxide • Coagulation Cascade • protein C, protein S, antithrombin III • Inflammatory mediators • anti TNF antibodies, anti LPS, TFPI

  19. Vasopressin and Sepsis • Tsuneyoshi et al. Crit Care Medicine 2001. • Prospective study N=16 • No control • Improved hemodynamic parameters • No effect on mortality

  20. Antithrombin III and Sepsis • Human Trial control AIII Fourrier 1993 50% 28% (NS) Diaz 1994 31% 35% (NS) Baudo 1998 46% 50% (NS) Eisele 1998 41% 25% (NS)

  21. Protein C and Septic Shock • Bernard et al. NEJM 2001. • RCT 1690 patients • mortality in placebo 30.8% • mortality in tx grp 24.7% • ARR of 6.1% p=0.005 • serious bleeding 3.5% vs 2% in control (p=.06) • conclusion: decreased mortality, increased bleeding

  22. IVIG in Septic Shock • Cochrane Database of Systematic Reviews. Alejandria mm et al • 23 RCTs for total of 6991 patients • overall IVIG RR of death 0.92 (.86,.99) • anti-endotoxin monoclonal Ab RR 1.03 (.8,1.2) • polyclonal IVIG RR 0.6 (0.47,0.76) • conclusion: polyclonal IVIG promising adjunct, no evidence for monoclonal antibodies

  23. Neurogenic Shock • Spinal Shock • initial loss of spinal cord function following SCI including motor, sensory, and sympathetic function • Neurogenic Shock • loss of sympathetic autonomic function due to spinal cord injury

  24. Neurogenic Shock • Hypotension and bradycardia (relative) • Due to unopposed parasympathetic function • Arterial and venous dilation, bradycardia • Management • iv fluid • atropine • vasopressors

  25. Hemorrhagic Shock

  26. Hemorrhagic Shock Classification

  27. Hemorrhagic Shock • Management • ABCs, vascular access, crystalloid bolus X 2, blood transfusion prn • controversies • NS versus RL • crystalloid versus colloid • immediate versus delayed • small versus large volume resuscitation • Optimal endpoints of resuscitation

  28. End Points of Resuscitation • Base Deficit • used as an approximation of tissue acidosis • “an increasing base deficit in a stable appearing patient should be concerning for ongoing hemorrhage” • retrospective evidence • Rutherford EJ 1992. Retrospective review of 3791 patients. Largest study.

  29. End Points of Resuscitation • Lactate Levels • used as an indirect measure for oxygen debt, hypoperfusion, and the severity of shock • lots of animal and human data showing correlation with mortality in shock • prospective trials: correlation with mortality • “normal serum lactate levels is a suitable end point of resuscitation

  30. Colloids • Albumin, protoplasm protein fraction, hydroxyethylstarch, gelatin, dextran • Advantages • less fluid required, more volume in vascular space, potential to draw fluid in from tissues • Disadvantages • expensive, allergic reactions, coagulopathies

  31. Colloids • Cochrane Database of Systematic Reviews. BMJ 1998: 317:235-40. • Objective: effect of albumin on mortality • Study: 30 RCTs total 1419 patients • Results: RR of death 1.46 hypovolemia, 2.40 burns, 1.69 hypoalbuminemia • Pooled RR of death 1.68 (1.26,2.23) • Conclusion: albumin increases mortality

  32. Colloids • Cochrane Database 2000. Colloids versus crystalloids for fluid resuscitation. • Albumin: 18RCTs RR1.52 (1.08,2.13) • HES: 7 RCTs RR 1.16 (0.68,1.96) • Gelatin: 4 RCTs RR 0.50(.08,3.03) • Dextran: 8 RCTs RR 1.24 (.94,1.65) • Conclusion: No evidence that albumins reduce risk of death in trauma, burns, or surgery

  33. Colloids - summary • There is NO evidence that colloids decrease mortality in the resuscitation of critically ill patients. • There IS evidence that colloids increase mortality in the resuscitation of critically ill patients.

  34. Hypertonic Saline • Advantages • less volume, stays in vascular space, draws fluid • Disadvantages • hypernatremia, hyperosmolarity, seizures, coaguulopathy, anaphylactoid rxns with dextran

  35. Hypertonic Saline • Animal evidence • improved hemodynamics and mortality • Human evidence • Wade et al 1997: HS and HSD in trauma • Metanalysis of 8 RCTS of HSD and 6 HS • HS (7.5% saline): no difference in mortality • HSD (+6%dextran): decreased mortality in 7/8 trials overall 3.5%; trend only ---> Not stat sign

  36. Hypertonic Saline • Cochrane Database 2001. Alderson P. • Objective: effect on mortality • Study: metanalysis of 8 RCTs • Results: pooled RR of 0.88 (0.74, 1.95) • Conclusion: there is a trend toward reduction in mortality with HSD although not statistically significant

  37. Hypertonic Saline - Conclusions • There is evidence of TRENDS toward lower mortality in resuscitation with hypertonic saline but statistical significance has not been demonstrated ………… • More RCTs are needed………..

  38. Controlled Fluid Resuscitation • Rationale: early, aggressive fluid resuscitation with large volume dislodges soft clots and dilutes clotting factors leading to increased hemorrhage and mortality

  39. Bickell et al and Controlled Fluid Resuscitation - “here piggy,piggy”

  40. Bickell et al 1990The Detrimental Effects of Intravenous Crystalloid after Aortotomy in Swine. Surgery 110: 529-36. • Objective: does rapid volume replacement inc mortality? • Study: 16 pigs, 8 controls (no fluid), 8 tx (RL 80 ml/kg ) • Results Mortality Hemorrhage • Controls 0/8 783 ml • RL tx grp 8/8 2142ml • Bickell et al 1992. HSD vs RL after Aortotomy • HSD tx grp 5/8 1340ml

  41. Bickell et al. NEJM 1994.Immediate versus Delayed Fluid Resuscitation for Hypotensive Patients with Penetrating Torso Trauma • Study: 598 patients SBP<90, odd/even day randomization, immediate fluids vs none until OR • Immediate fluids - mortality 110/303 (38%) • Delayed fluids - mortality 86/289 (30%) • Statistically significant p = 0.04 • Conclusion: delayed fluid resuscitation reduces mortality in hypotensive patients with penetrating trauma

  42. Controlled Fluid Resuscitation • Cochrane Database 2001. Kwan I. Timing and volume of fluid administration for patients with bleeding following trauma. • 3 RCTs for early vs delayed fluids • 3 RCTs for large vs small volume • NO evidence for early or large volume fluid replacement and trends toward increased mortality

  43. Controlled Fluid Resuscitation - Conclusions • There is evidence (limited) that early, large volume aggressive fluid resuscitation increases mortality in penetrating trauma. • Further study needed on penetrating trauma without immediate access to OR and for blunt trauma

  44. Obstructive Shock

  45. Cardiogenic Shock

  46. Cardiogenic Shock • Definition • decreased cardiac output and evidence of tissue hypoxia in presence of adequate intravascular volume • Criteria • hypotension (SBP < 90), cardiac index < 2.2 L/min/m2, PCWP > 15 mmHg

  47. Cardiogenic Shock • Management • small fluid boluses • invasive monitoring • vasopressors • norepinephrine • dopamine • dobutamine

  48. Cardiogenic Shock • Dobutamine: beta adrenergic • positive B1 ionotrope; may drop BP b/c of vasodilation • SBP 70 - 100 without signs of hypoperfusion a/f fluids • Dopamine: dopaminergic, beta , alpha adrenergic • SBP 70 - 100 with signs of hypoperfusion after fluids • Norepinephrine • alpha agonist • SBP < 70 after fluids

  49. Cardiogenic Shock • Thrombolysis • GISSI (N=280) 30day mortality • streptokinase 70.1% • medical mx 69.6% • NO trial has shown reduction mortality with cardiogenic shock with thrombolysis

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