Leanna R. Miller, RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP Education Specialist LRM Consulting Nashville, TN

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1 Leanna R. Miller, RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP Education Specialist LRM Consulting Nashville, TN Learning Outcomes Identify triggers to the IIR. Describe the pathophysiologic changes that occur in patients with sepsis. Explain strategies that will improve outcomes in patients with heightened IIR. 1

Consulting Nashville, TN Learning Outcomes Identify triggers to the IIR.

2 Etiology ARDS Sepsis DIC ATN Shock SIRS Criteria (2 or more) Temperature > 38 C or < 36 C Heart rate > 90 beats RR > 20 or paco 2 < 32 WBC > 12,000 or < 4,000 or > 10% bands 2

3 Incidence of Severe Sepsis > 750,000 new cases each year 28 50% mortality leading cause of death in noncardiac ICUs 9 th leading cause of death Endothelium COAGULATION CASCADE Tissue Factor Monocyte IL-6 IL-1 TNF- Factor VIIIa Factor Va PAI-1 Suppressed fibrinolysis THROMBIN TAFI Neutrophil Fibrin Tissue Factor IL-6 Fibrin clot Inflammatory Response to Infection Thrombotic Response to Infection Fibrinolytic Response to Infection 4/30/12 Pathophysiology role of initial insult immunosuppression injury stress response 3

fibrinolysis THROMBIN TAFI Neutrophil Fibrin Tissue Factor IL-6 Fibrin clot Inflammatory Response to Infection Thrombotic Response

4 Pathophysiology Transluminal migration SIRS nosocomial pneumonia Pathophysiology Flow dependent O 2 consumption DO 2 > 600 VO 2 > 150 Pathophysiology tissue ischemia and reperfusion xanthine oxidase O 2 free radicals (ROS) tissue injury 4

2 > 600 VO 2 > 150 Pathophysiology tissue ischemia and

5 Pathophysiology gut ischemia/reperfusion injury gut PLA 2 - prime PMNs - sequester in lungs - lung microvascular permeability Assessing Acute Immune Inflammatory Response Procalcitonin (PCT) ng/ml C reactive protein (CRP) 0 5 mg/l IL pg/ml 5

permeability Assessing Acute Immune Inflammatory Response

6 1 st Six Hours idelays in management of sepsis result in higher mortality rates and increased utilization of hospital resources Transition from Sepsis to Severe Sepsis ioccurs most often during the 1 st 24 hours of hospitalization iincrease in mortality of 20 46% 6

Transition from Sepsis to Severe Sepsis ioccurs most often during

7 Transition i tissue O 2 delivery & CV insufficiency accompanies transition iusually not detected by VS nor SIRS criteria O 2 Transport & Utilization iglobal tissue hypoxia resulting from IIR ihypoxia stimulates further inflammation O 2 Transport & Utilization io 2 delivery is insufficient to meet O 2 cell level iresults in increased lactate levels 7

resulting from IIR ihypoxia stimulates further inflammation O 2 Transport & Utilization io

8 O 2 Transport & Utilization isvo 2 < 65% or ScvO 2 < 70% result in increased lactate and suggest the presence of global tissue hypoxia greater extraction by tissues O 2 Transport & Utilization inormal SvO 2, ScvO 2 & lactate suggest O 2 supply meets demand 8

hypoxia greater extraction by tissues O 2 Transport &

9 O 2 Transport & Utilization i high SvO 2, ScvO 2 & lactate indicates that despite adequate global systemic O 2 delivery, the tissues are unable to extract the O 2 O 2 Transport & Utilization icytopathic tissue hypoxia microvascular shunting microcirculatory failure mitochondrial dysfunction O 2 Transport & Utilization i Tissue hypoxia further activates endothelial mediators loss of vascular integrity inflammatory cytokines procoagulants reduced fibrinolysis 9

microvascular shunting microcirculatory failure mitochondrial dysfunction O 2 Transport & Utilization i Tissue

10 Sepsis Pathophysiology Identification of High Risk Patient i SIRS Infection Trauma Ischemic or reperfusion injury Sterile inflammation Identification of High Risk Patient i Single lactate > 4.0 or more at initial presentation i Failure to clear lactate levels during the 1 st 6 hours is associated with increased morbidity and mortality 10

11 Identification of High Risk Patient i C reactive protein i Endotoxin i Brain natriuretic peptide i Procalcitonin i IL 6 i Protein C Identification of High Risk Patient iterminal illness itachypnea ihypoxia iseptic shock ithrombocytopenia Identification of High Risk Patient iband count > 5% iinfection of lower respiratory tract iresidence in nursing home ialtered mental status 11

illness itachypnea ihypoxia iseptic shock ithrombocytopenia Identification of High Risk Patient

12 Management of IIR Initial Resuscitation serum lactate identifies tissue hypoperfusion in patients who are not hypotensive Management of IIR Initial Resuscitation Endpoints CVP 8 to 12 mm Hg MAP > 65 mm Hg UP > 0.5 ml/kg/hr SvO 2 > 70% Management of IIR Early antimicrobial therapy empiric antibiotics within 4 and 8 hours of hospital presentation Surviving Sepsis Campaign recommends antibiotics within 1 hour 12

13 Management of IIR source of infection & local hospital sensitivity & resistance patterns surgical consultation resistant organisms when patients live in nursing homes or are IV drug users Early Hemodynamic Optimization isupranormal physiologic endpoints in ICU patients up to 72 hours have led to negative & deleterious results Hemodynamic Variables SBP < 90 mm Hg MAP < 70 mm Hg SvO 2 > 70% CI > 3.5 L/min/m 2 13

Hemodynamic Optimization isupranormal physiologic endpoints in ICU patients up to 72 hours have led to

14 Volume Therapy irepletion of intravascular volume irapid, repeated 500 ml boluses of either crystalloid or colloid icvp 8 12 mm Hg Volume Therapy i4% albumin or NS ifound no significant difference in mortality between the group Vasoactive Agents idopamine 5 20 g/kg/min inorepinephrine 2 20 g/min iphenylephrine g/min ivasopressin units/min (VASST study) 14

difference in mortality between the group Vasoactive Agents idopamine 5 20 g/kg/min

15 Vasoactive Agents iin patients with pre-existing tachycardia or coronary disease it may be preferable to administer norepinephrine and phenylephrine Vasoactive Agents iadverse consequences splanchnic hypoperfusion excess tachycardia coronary ischemia RBC Replacement iif ScvO 2 remains < 70% after optimization of preload, afterload and arterial O 2 saturation increase Hct to 30% optimal erythrocyte transfusion fresh vs. stored blood 15

excess tachycardia coronary ischemia RBC Replacement iif ScvO 2 remains < 70% after optimization of preload,

16 Inotropic Therapy isepsis may be accompanied by myocardial suppression in 10 15% of patients dobutamine titrated at 2.5 g/kg/min every minutes to ScvO 2 of 70% milrinone (long half life and accumulates in renal failure) Decreasing O 2 consumption iintubation, sedation, analgesia icontrol fever Steroid Therapy iinflammatory cascade leads to: inadequate release or response to ACTH peripheral steroid receptor level 16

5 g/kg/min every 20 30 minutes to ScvO 2 of 70% milrinone (long half life and accumulates in renal failure)

17 Steroid Therapy i Low doses of hydrocortisone decreased requirement for vasopressors and lowered mortality Hydrocortisone 50 mg IV every 6 hours Fludrocortisone 50 g PO every day Steroid Therapy i Dexamethasone does not interfere with adrenocorticotropin test results, so immediate empiric treatment with 2 mg of this steroid may be given and the test performed at a more convenient time. Activated Protein C iendogenous anticoagulant profibrinolytic anti inflammatory anti apoptotoic effect improves microcirculatory flow 17

results, so immediate empiric treatment with 2 mg of this steroid may be given and the test performed at a more convenient time.

18 Endothelium COAGULATION CASCADE Activated Protein C Activated Protein C Tissue Factor Monocyte IL-6 IL-1 TNF- Factor VIIIa Inactivation Factor Va Inactivation Prevention of activation Inactivation PAI-1 Suppressed fibrinolysis THROMBIN TAFI Neutrophil Fibrin Tissue Factor IL-6 Fibrin clot Inflammatory Response to Infection Thrombotic Response to Infection Fibrinolytic Response to Infection 4/30/12 O 2 demand 55% peripheral shunting & delivery-limited VO 2 sudden in VO 2 = early warning VO 2 remains low = poor outcome CI > 5.5 DO VO

IL-6 Fibrin clot Inflammatory Response to Infection Thrombotic Response to Infection Fibrinolytic Response to Infection 4/30/12 O 2 demand

19 82 - year old female admitted with perforated diverticular abscess HR 123 BP 110/60/77 RAP / PAOP 8 / 10 PAP 24 / 10 CI 3.1 SvO 2.78 SaO 2.96 Hemoglobin 10.2 DO 2 I = C1 ( 1.38 x Hgb x SaO 2 ) X 1.38 X 10.2 X 0.96 x ml/min/m 2 (normal = ml/min/m 2 ) 19

78 SaO 2.96 Hemoglobin 10.2 DO 2 I = C1 ( 1.38 x Hgb x SaO 2 ) 10 3.

20 VO 2 I = CI X 1.38 X Hgb X (SaO 2 - SvO 2 ) X x 1.38 x 10.2 x ( ) x ml/min/m 2 (Normal ml/min/m 2 ) 20

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