Anemia in critically ill patients. Intensive Care Training Program Radboud University Medical Centre Nijmegen

Size: px

Start display at page:

Download "Anemia in critically ill patients. Intensive Care Training Program Radboud University Medical Centre Nijmegen"

Constance Newton
7 years ago
Views:

1 Anemia in critically ill patients Intensive Care Training Program Radboud University Medical Centre Nijmegen

2 Anemia during ICU stay 60-80% of all patients become anemic during the course of their ICU stay (50-70% < 6 mmol/l) Aetiology includes inflammation, erythropoietin production, blunting of erythropoietin response, blood loss, nutritional deficiencies, renal failure Both anemia and transfusion (20-50%) are associated with increased morbidity/ mortality

3 30-60 ml/d Hb mmol/l/d

7 Treatment of shock Macrocirculation Microcirculation Mitochondria Cardiac output Hemoglobin SaO2 Serious defects Serious defects Preload - volume therapy Contractility - inotropic agents Afterload - vasodilators Transfusion Oxygenation No treatment Vasodilators? No treatment

8 Transfusion Trigger TRICC Trial Inclusion criteria Expected IC stay > 24 h Hb < 5.6 mmol/l within 72 h Euvolemia Exclusion criteria Age < 16 y Active blood loss Chronic anemia (Hb < 5.6) Power of study based on N = 2300 Pregnancy Brain death or imminent death Admission after cardiac surgery versus mmol/l Hébert PC. N Engl J Med 1999;340:

9 Results TRICC trial N = 838 Restrictive Liberal 30 NS NS NS 0.05 Mortality (%) D mortality 60 D mortality ICU mortality Hospital mortality Decreased 30 D mortality if APACHE II < 20 or age < 55 years Hébert PC. N Engl J Med 1999;340:

10 Mechanical ventilation N = 713 Restrictive Liberal Duration MV (D) 8.3 ± ± 8.7 Mortality 30 D (%) 21,3 26,4 Mortality 60 D (%) ICU mortality (%) Hospital mortality (%) Hébert PC. Chest 2001;119:

11 Safety with cardiovascular disease N = 357 Restrictive Liberal 30 NS NS NS NS Mortality (%) D mortality 60 D mortality ICU mortality Hospital mortality Hébert PC. Crit Care Med 2001;29:

12 Safety with ischemic heart disease N = 257 Restrictive Liberal 30 NS NS NS NS Mortality (%) D mortality 60 D mortality ICU mortality Hospital mortality Hébert PC. Crit Care Med 2001;29:

14 Transfusion after trauma N = 203 Restrictive Liberal 10 NS NS NS NS Mortality (%) D mortality 60 D mortality ICU mortality Hospital mortality McIntyre L. J Trauma 2004;57:

15 Transfusion after TBI N = Restrictive NS Liberal (%) No differences in LOS D mortality McIntyre L. J Neurocrit Care 2006;5:4-9

16 TRACS trial N = 502 (single centre) Adult patients after cardiac surgery with CPB Hematocrit 0.24 versus 0.30 Composite end-point 30 day mortality and cardiogenic shock/ards/aki Hajjar LA. JAMA 2010;304:

17 TRACS trial P < % receiving transfucion % primary end-point Restrictive Liberal 0 Restrictive Liberal Hajjar LA. JAMA 2010;304:

19 Neurocritical care Prevention of secondary cerebral insults Hypotension Hypoxia Hypocapnia Fever ICP increase

20 Cerebral blood flow DO2 (ml O2/min) = CO (l/min) [{Hb (mmol/l) SaO2 (%) 2.24 (ml O2/mmol Hb)} + (0.003 PO2)] Cerebral DO2 (ml O2/min) = CBF (l/min) [{Hb (mmol/l) SaO2 (%) 2.24 (ml O2/mmol Hb)} + (0.003 PO2)] Hagen - Poiseuille equation Flow = πr4 CPP 8 L η

21 Determinants of CBF Cerebral Blood Flow Cerebral Blood Flow Cerebral Perfusion Pressure Cerebral Metabolic Rate of Oxygen Autoregulatie + Autoregulatie - Cerebral Blood Flow Cerebral Blood Flow Partial Pressure of Carbon Dioxide Cerebral oxygenation CaO2 PaO2

22 General cardiovascular response to anemia Increase heart rate and contractility Reduction in blood viscosity decreases afterload and enhances venous return Isovolemic anemia increases cardiac output and blood pressure - if cardiac function is normal Increases in oxygen extraction ration protects against tissue hypoxia

23 Diringer MN. Curr Opin Crit Care 2007;13:

24 Cerebrovascular response to anemia Higher CPP and lower viscocity increase CBF Anemia induces cerebral vasodilation by pervascular neuron NO synthesis and sympathetic β2-stimulation

25 The effect of anemia Cerebral Oxygen Delivery More severe if combined with hypotension CBF CaO2 Normal Mild hemodilution Moderate anemia Severe anemia

26 Risk of RBC transfusion

27 Minimising blood loss

29 TRALI New ALI within 6h of blood transfusion Neutrophilic aggregates in pulmonary vasculature + pulmonary edema Recipient and transfusion related factors Mortality up to 20% Sachs UJ. Curr Opin Hemat 2011;18:

30 TRALI threshold model Sachs UJ. Curr Opin Hemat 2011;18:

31 Individual risk factors Sachs UJ. Curr Opin Hemat 2011;18:

32 Transfusion related risk factors - Plasma Antibodies in plasma directed against HLA (mostly class II) and HNA (mostly 3a) Usually female donors with history of pregnancy Sachs UJ. Curr Opin Hemat 2011;18:

33 Mechanisms Direct activation of neutrophils by antibodies (HLA class I) Binding of antibodies to endothelial antigens with neutrophil activation through Fc-segment (HLA-I) Antibodies bind to monocytes releasing IL-8 and activating neutrophils (HLA class II) Substances accumulating during storage activate neutrophils (CD40L) (soluble mediators) Sachs UJ. Curr Opin Hemat 2011;18:

34 Transfusion related risk factors - RBC s Lowest risk per component Soluble mediator (??) responsible for TRALI Relation with storage time unclear Sachs UJ. Curr Opin Hemat 2011;18:

35 Transfusion related risk factors - platelets Intermediate risk Either by antibodies in plasma (storage), soluble mediators accumulating during storage or changes in platelet during storage Sachs UJ. Curr Opin Hemat 2011;18:

36 Sachs UJ. Curr Opin Hemat 2011;18:

The Sepsis Puzzle: Identification, Monitoring and Early Goal Directed Therapy

The Sepsis Puzzle: Identification, Monitoring and Early Goal Directed Therapy Cindy Goodrich RN, MS, CCRN Content Description Sepsis is caused by widespread tissue injury and systemic inflammation resulting