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Shock

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  • 1. Recent Advances in the Treatment of Shock Jon Meliones MD, MS, FCCM Professor of Pediatrics & Anesthesia Duke University Medical Center
  • 2. Shock • Definition –Diagnosis –Effects of Shock • Types of Shock • Treatment for Shock
  • 3. Shock • Definition – Acute disruption of both the micro- and macro-circulation – Inadequate DO2 (Do2 = C.O. x Oxygen content), VO2 and cellular oxygen deficiency • Limitation or maldistribution of blood flow
  • 4. Stages of Shock • Compensated – Vital organ function maintained – BP remains normal • Uncompensated – Microvascular perfusion becomes marginal – Organ and cellular function deteriorate – Hypotension develops • Irreversible – MOSF with end organ injury
  • 5. Hypotension: MAP < 5th percentile for age lowest acceptable SBP = 70 + [2 x age (in yrs)] Age of child Lowest acceptable SBP Term neonates 60 Infants 1-12mo 70 Children 1-10yr 70 + [2 x age (in years)] Children >10yr 90
  • 6. Shock Quick Look • The lowest acceptable SBP for a 6 year old child is – 76 – 80 FORMULA = 70 + [2 x age (in years)] – 82 70 + [2 x 6] – 93 70 + 12 82
  • 7. Early Reversal of Septic Shock • Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome (Han et al, Pediatrics 2003) Controlling for severity of illness, with each hour of persistent shock, risk of mortality doubled
  • 8. LFTs, ileus ARDS MS SHOCK BP UO
  • 9. How do we Treat Shock? • American College of Critical Care Medicine – Guidelines for management of pediatric septic shock • Guidelines are not hard – BUT: they’re demanding – Time-sensitive • Requires some hustle to get it right – Cannot be followed if you’re working alone • You will need help
  • 10. Stepwise management of hemodynamic support with goals of normal perfusion and perfusion pressure (MAP-CVP) in infants and children with septic shock. Proceed to next step if shock persists. 0 min Recognize decreased mental status and perfusion. Maintain airway and establish access according to PALS guidelines. 5 min Push 20cc/kg isotonic saline or colloid boluses up to and over 60 cc/kg Correct hypoglycemia and hypocalcemia NO Fluid refractory shock? YES 15 min Observe in hospital or Establish central venous access, begin PICU as appropriate dopamine therapy and establish arterial monitoring NO Fluid refractory-dopamine resistant YES shock? Observe in PICU Titrate epinephrine for cold shock, norepinephrine for warm shock to normal MAP-CVP and SVC O2 saturation > 70% 60 min At Risk of Adrenal Catecholamine-resistant Not at Insufficiency? shock? Risk? Give hydrocortisone Do not give hydrocortisone Normal Blood Pressure Low Blood Pressure Low Blood Cold Shock Cold Shock Pressure SVC O2 sat < 70% SVC O2 sat < 70% Warm Shock Titrate Volume and Norepinephrine Add vasodilator or Type III PDE Titrate Volume and (? vasopressin or angiotensin) inhibitor Epinephrine with volume loading Persistent catecholamine-resistant shock ? Place pulmonary artery catheter and direct fluid, inotrope,vasopressor,vasodilator, and hormonal therapies to attain normal MAP-CVP and CI > 3.3 and < 6.0 L/min/m2 and consider ECMO
  • 11. Stepwise management of hemodynamic support with goals of normal perfusion and perfusion pressure (MAP-CVP) in infants and children with septic shock. Proceed to next step if shock persists. Recognize decreased mental status and perfusion. Maintain airway and establish access according to 0 min PALS guidelines. Push 20cc/kg isotonic saline or colloid boluses up 5 min to and over 60 cc/kg Correct hypoglycemia and hypocalcemia
  • 12. Recognize Shock Cold “High SVR” Shock • Tachycardic • Maybe  BP • Skin and extremities: – cool – pale – mottled – cyanotic – poor cap refill
  • 13. Recognize Shock Warm “Low SVR” Shock • Tachycardic • Maybe  BP – Diastolic hypotension • Skin and extremities: – warm – flushed – flash capillary refill
  • 14. Recognize Shock Poor capillary refill • Anything longer than 2 seconds is delayed – If you get as far as 5 sec, you’d better be calling for help
  • 15. Recognize Shock • Neurological – Poor muscle tone – Uncooperative – Depressed or fluctuating mental status are late signs • Renal – Scant, concentrated urine
  • 16. Shock: Diagnosis Noninvasive • Impaired perfusion – Capillary refill – Peripheral Vs core temp • Vital signs –  HR, B.P. nl- ,  RR • End organ function-  UOP – Mental status changes
  • 17. Shock: Diagnosis Invasive • Laboratory evaluation – Metabolic acidosis • Lactic acidosis • pH < 7.2 – Mixed venous saturations • Depressed = inadequate DO2 • Elevated = maldistribution, impaired utilization
  • 18. Monitoring C.O. in Shock • Optimize DO2 and Enhance VO2 • Echocardiography - Differentiate Systolic/Diastolic Function • SvO2 to Monitor DO2 – High SvO2 • No benefit in driving delivery – Low SvO2 • Enhance Delivery
  • 19. Secondary Effects Organ Dysfunction • Renal insufficiency • Respiratory insufficiency – Primary pump failure – Secondary to shock • Coagulation abnormalities – DIC
  • 20. Secondary Effects Organ Dysfunction • Hepatic dysfunction – Closely linked to outcome • GI – Related to ischemia • Endocrine disturbances – Ca++, hypoadrenalism • Neuro – Hypoperfusion syndromes
  • 21. Shock • Hypovolemic Shock • Cardiogenic Shock • Septic Shock • Distributive • Endocrine
  • 22. Hypovolemic Shock Physiology Diagnosis Management
  • 23. Hypovolemic Shock • # 1 Cause of Death World Wide – Hemorrhagic - Trauma, GI Bleeding – Gastroenteritis • Children: Frequently extreme – Late Dx - Previously Healthy – Inability to compensate for rapid changes in volume
  • 24. Physiology of Hypovolemic Shock •  Intravascular volume- –  Preload-  stroke volume (SV) -  C.O.-  DO2.  SvO2 • Compensation-  Endogenous catechols –  HR-  C.O-  DO2 –  SVR-  B.P. • Compensation for <15%
  • 25. Hypovolemic Shock (Puppies) 140 30%  in SVR 120 40%  100 in Blood Vol 80 % 50%  Control 60 in C.O. 40 Vascular Resistance Blood Pressure 20 Cardiac Output 0 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 % Blood Volume Deficit
  • 26. Delaying Resuscitation in Hypovolemic Shock Effects Outcome Loss (% Control) 10 0 BP 5 0 Blood Late Resuscitation - Death 0 2 4 6 8 10 12 Time (hrs)
  • 27. Diagnosis of Hypovolemic Shock • Early –  HR,  Perfusion ( SVR) –  Pulse width (low SV) • Late –  HR,  Perfusion, BP – End organ dysfunction
  • 28. Treatment of Hypovolemic Shock • Volume infusion – Goal = reverse signs of  DO2 – Replace what is lost – Crystalloid 20 ml/kg x 2 – No response - invasive monitor • If CVP>10, &  DO2, need re-eval
  • 29. Hypovolemic Shock Summary • Primary goal – Volume replacement • Secondary goal – Prevent ischemia – Minimize inflammatory mediator release • Use of Albumin increases mortality
  • 30. Septic Shock Definition Molecular Basis Diagnosis Treatment
  • 31. Terminology in Sepsis • Infection= response to micro-org • Bacteremia= bug in blood • Systemic Inflammatory Response Syndrome (SIRS) – T>38, <36 – HR – RR, PaCO2 <32 – WBC>12,000, <4,000, >10% bands
  • 32. Terminology in Sepsis • Sepsis = SIRS as response to a known infection • Severe Sepsis = Sepsis + organ dysfunction • Septic shock = Sepsis + inadequate tissue DO2 • Multiple Organ Dysfunction Syndrome (MODS) – Organ dysfunction that requires intervention
  • 33. Molecular Basis of Shock NFkB - nuclear transcription factor TNF TNF TNF R2 R1 Fas Acute Acute Apoptosis Inflammatory Inflammatory Response Response iNO Tissue Factor NFkB Complement Cytokines Endonuclease Adhesion Molecules
  • 34. Sepsis bacteremia trauma fungemia pancreatitis Sepsis SIRS Infection viremia burns other other Adapted from Bone, 1996
  • 35. Cascade Host Microbes Endotoxin/ Exotoxin Host response Death Multiorgan Pathophysiologic dysfunction Changes
  • 36. Infection Microbial Products (endotoxin/Peptidoglycans) Cellular Responses Thromboanes Oxidases Kinins Cytokines Leukotrienes/PAF sPLA2 Complement TNF, IL1, IL6, IL8 Inflammation/Vascular Injury
  • 37. Inflammation/Vascular Injury Mediators (e.g. TNF) Tissue Factors Endothelial Injury Coagulation Sys. Activation Consume Protein C Apoptosis Impaired Fibrinolysis Uncontrolled Inflammation Coagulation / DIC MOSF Shock Death
  • 38. Therapeutic Interventions Antibiotics Eliminate endotoxin Host Microbes Endotoxin/ Exotoxin Antagonize mediators Anti-inflammatory intervention Host response Reverse coagulopathy Death Multiorgan Pathophysiologic dysfunction Changes Supportive Measures
  • 39. Infection Treatment Microbial Products Block Endotoxin (Endotoxin/Peptidoglycans) Cellular Responses Mediators (e.g. TNF) Block Mediators Coagulation activation Block Coagulation Coagulopathy Cytoprotectives
  • 40. Adverse Systemic Effects of Cytokines and Endotoxin • Hypotension- Fluid refractory – Upregulation of Inducible NO (iNO) – NO + O2, superoxide - free radicals • Cardiac dysfunction -systolic & diastolic – TNFa (Hagmolen: Euro. J of Peds 2000) • Coagulopathy: Microvascular thrombosis and inflammation – Protein C pathway – TNFa
  • 41. Diagnosis of Septic Shock • Establish presence of infection  HR, NL -  BP,  -  Perfusion • • Uncoupling of HR & BP (Toweill CCM 2000) • Metabolic acidosis / lactic acidosis • Elevated SVO2 • Organ dysfunction – Renal – Respiratory
  • 42. Early vs Late Septic Shock Early hyperdynamic shock Late septic shock Intact O2 utilization Disrupted O2 utilization Capillary leak Myocardial dysfunction Poor prognostic indicators: •decreased VO2 •decreased avDO2 •decreased O2 extraction
  • 43. Meta Analysis - Corticosteroids Favors Steroids Favors Control Luce (1988) 1.07 (0.72-1.60) * VASSCg (1987) 0.95 (0.57-1.58) * Bone (1987) 1.35 (0.98-1.84) * Sprung(1984) 1.11 (0.74-1.67) * Thompson(1978) 1.01 (0.77-1.31) * Lucas(1984) 1.09 (0.36-3.27) * Schumer(1976) 0.30 (0.13-0.72) Klastersky(1971) 0.97 (0.65-1.45) * CS Group (1963) 1.72 (1.23-2.41) * Common Relative Risk 1.13 (0.99-1.29) * * Cronin CCM 1995 0 0.5 1 1.5 2 2.5 3 3.5
  • 44. Summary of Clinical Trials in Sepsis Mortality % # studies # pts con exp p value High dose steroids 39 <.05 >9 1300 35 Anti-bradykinin 2 755 36 39 Anti-PAF 2 870 50 45 Anti-PG (ibuprofen) 3 508 40 38 IL-1Ra 3 1898 35 31 Anti-TNF mAb 8 4139 36 35 TNF soluble receptor p75-SR 45 <.05 1 141 30 p75 SR phaseI/II 1 444 29 34 p75-SR phase III 1 1340 28 27 NO synthase inhibitor 2 1059 50 56
  • 45. New Selective Therapy • Recombinant Human Activated Protein C – Protein C pathway • Antithrombotic/ profibrinolytic agent • Maintains vascular patency – Loss of protein C: • Loss of modulation • Vascular dysfunction – Selective replacement (Bernard: NEJM 2001) • 1690 pts • Mortality: CTL = 31%: Tx = 25% • Serious bleeding = CTL = 2%: Tx = 3.5%
  • 46. Controversy in Manipulating Inflammatory Response • Target Therapy - No Benefit – Too Little? Too Late? Timing? • Early Global Therapy - No Benefit – Timing, Dose, Disease? – Poor Understanding of Pathophysiology? – Clinical Trials? • Cocktail Therapy -What, When, Dose?
  • 47. Treatment in Septic Shock • Control Infection • Reverse cardiovascular dysfunction – Early aggressive restoration of preload – 0.9% NS may  base deficit (Skellett: Arch Dis Child 2000) – Inotropic agents in fluid refractory shock (Ceneviva: Ped 1998) • Prevent secondary end organ injury – Renal- Maintain BP – Respiratory- monitor • Steroids (steroid deficient shock) (Annane: CCM 2000)
  • 48. Distributive Shock • Anaphylaxis, spinal shock • Maldistribution of blood flow • NL or  CO, Inadequate tissue DO2 • Treatment – Fluid – Reversal of etiology
  • 49. Differential Dx in Shock State CO SVR BP CVP PCWP    NL /    Hypovolemic   NL /   Cardiac Sys     Cardiac Dias NL NL    NL /    Sepsis Early     Sepsis Late 
  • 50. Differential Dx in Shock State CO SVR BP CVP PCWP    NL /    Hypovolemic   NL /   Cardiac Sys     Cardiac Dias NL NL  / NL /    Sepsis Early      Sepsis Late
  • 51. Conclusion • Hypovolemic Shock - – Early Intervention to Prevent Ischemia/Reperfusion • Cardiogenic Shock - – Targeted Treatment • Septic Shock - ???
  • 52. Global or Selective Modification of the Inflammatory Response • Steroids - No Benefit, ? • Anti TNFa No Benefit • Adhesion Molecules – Selectin Inhibitors No Benefit • Interleukin 1, 6 No Benefit • Complement Current Trials

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