SEVERE SEPSIS&SEPTIC SHOCK IN PEDIATRICS.

1. Abdel Razzaq Abu Mayaleh, MD PRCS _ New Hospital - Hebron Based partially onwww.picucourse.org SEVERE SEPSIS&SEPTIC SHOCK IN PEDIATRICS.

2. INTRODUCTION • SEPSIS:- it’s an infection plus systemic manifestation of • infection. • SEVERE SEPSIS :- Sepsis plus sepsis-induced organ • dysfunction or tissue hypo perfusion. • SEPTIC SHOCK:- sepsis-induced hypotension persisting • despite adequate fluid resuscitation and elevated lactate. • HYPOTENTION:- S.BP < 70 + 2 ×wt. • (80 + 2 × wt) • SHOCK:-DO2 < VO2 . . .

3. A clinician, armed with the sepsis bundles, attacks the three heads of severe sepsis: hypotension, hypoperfusion and organ dysfunction. Crit Care Med 2004; 320(Suppl):S595-S597

4. Septic Shock Epidemiology • During the last 2 decades the incidence of sepsis & septic shock has increased across all age groups. This is thought to be due to: • ↑ use of invasive procedures • ↑ use of immunosuppressive drugs • ↑ microbacterial ressistance • Child mortality improved dramatically from 97% → 9% due to the advance in critical care technology.

5. Septic Shock: “Warm Shock” • Early, compensated, hyperdynamic state • Clinical signs • Warm extremities with bounding pulses, tachycardia, tachypnea, confusion. • Physiologic parameters • widened pulse pressure, increased cardiac ouptut and mixed venous saturation, decreased systemic vascular resistance. • Biochemical evidence: • Hypocarbia, elevated lactate, hyperglycemia

6. Septic Shock: “Cold Shock” • Late, uncompensated stage with drop in cardiac output. • Clinical signs • Cyanosis, cold and clammy skin, rapid, thready pulses, shallow respirations. • Physiologic parameters • Decreased mixed venous sats, cardiac output and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leak • Biochemical abnormalities • Metabolic acidosis, hypoxia, coagulopathy, hypoglycemia.

7. MANAGEMENT-GENERAL • Goal: increase oxygen delivery and decrease oxygen demand: • Oxygen • Fluid • Temperature control • Antibiotics • Correct metabolic abnormalities • Spare WOB ? • Inotropes DO2 = C.O. x CaO2 Hg X SatO2 X 1.34 . VO2 (O2 Extraction) septic . . normal . DO2

8. Fluid Resuscitation • Aggressive fluid resuscitation with boluses of 20 ml/kg over 5-10 min • Blood pressure by itself is not a reliable endpoint for resuscitation • Initial resuscitation usually requires 40-60 ml/kg, but more may be required

9. Therapeutic Endpoints • Capillary refill < 2 sec • Warm extremities • Urine output > 1 ml/kg/hr • Normal mental status • Decreased lactate • Central venous O2 saturation > 70%

10. Hemodynamic Support • Hemodynamic profile may be variable • Dopamine for hypotension • Epinephrine or norepinephrine for dopamine-refractory shock • Dobutamine for low cardiac output state • Inhaled NO useful in neonates with post-partum pulmonary hypertension and sepsis

11. Other Therapies • Steroids: recommended for children with catecholamine resistance and suspected or proven adrenal insufficiency. • Activated protein C not studied adequately in children yet. • GM-CSF shown to be of benefit in neonates with sepsis and neutropenia. • Extracorporeal membrane oxygenation (ECMO) may be considered in children with refractory shock or respiratory failure.

12. 2005 Shock ABC FLUID BOLUS-20-60cc/kg Dopamine/ dobutamine Cold shock Warm shock NE NE EPI steroids Milrinone

13. 0 min 5 min Recognize decreased mental status and perfusion.Maintain airway and establish access according to PALS guidelines. Push 20 cc/kg isotonic saline or colloid boluses up and over 60 cc/kg. Correct hypoglycemia and hypocalcaemia. Administer antibiotics. 15 min Fluid refractory shock * * Establish central Venous access, begin dopamine or dobutamine therapy and establish arterial monitoring . Fluid responsive * Fluid refractory – dopamine/ dobutamine resistant shock Titrate epinephrine for cold shock, norepinephrine for warm shock to normal clinical endpoints and ScvO2 saturation ≥70% . Observe in PICU

14. Catecholamine-resistant shock Begin hydrocortisone if at risk for absolute adrenal insufficiency 60 min Normal Blood Pressure Cold Shock ScvO2 Sat <70% Low Blood Pressure Cold Shock ScvO2 Sat < 70% Low Blood pressure Warm Shock ScvO2 Sat ≥ 70% Add Vasodilator or type III phosphodiesgerase inhibitor with volume loading Titrate volume and epinephrine Titrate volume and norepinephrine Persistent Catecholamine- resistant shock Start Cardiac output measurement and direct fluid, inotrope, vasopressor, vasodilator, and hormonal therapies to attain CL>3.3 and <6.0 L/min/m² Refractory shock Consider ECMO

15. VENTILATOR MANAGEMENT • Assist control mode-volume ventilation • Reduce tidal volume to 6ml/kg predicted body wt. • Keep Pplat <30cm H2O • Maintain SaO2 / pO2 88-95% • Anticipated PEEP setting at various FiO2 requirements • FiO2 0.3 0.4 0.5 0.5 0.6 0.7 0.8 0.9 1.0 • PEEP 5 5 8 10 12 14 16 18 20

16. Sedation and Analgesia in Sepsis • Sedation protocol for mechanically ventilated patients with standardized subjective sedation scale target. • Intermittent bolus • Continuous infusion with daily awakening/retitration Grade B Kollef, et al. Chest 1998; 114:541-548 Brook, et al. CCM 1999; 27:2609-2615 Kress, et al. NEJM 2000; 342:1471-1477

17. Neuromuscular Blockers • Avoid if possible • Used longer than 2-3 hrs • PRN bolus • Continuous infusion with twitch monitor Grade E

18. 100 96 Intensive treatment 92 P=0.01 In-hospital survival (%) 88 Conventional treatment 84 80 0 0 50 100 150 200 250 Days after admission The Role of IntensiveInsulin Therapy in the Critically Ill • At 12 months, intensive insulin therapy reduced mortality by 3.4% (P<0.04) Adapted from Figure 1B, page 1363, with permission from van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med 2001;345:1359-67

19. Glucose Control • After initial stabilization • Glucose < 150 mg/dL • Continuous infusion insulin and glucose or feeding (enteral preferred) • Monitoring • Initially q30–60 mins • After stabilization q4h Grade D

20. Bicarbonate Therapy • Bicarbonate therapy not recommended to improve hemodynamics in patients with lactate induced pH >7.15 • Grade C • Cooper, et al. Ann Intern Med 1990; 112:492-498 • Mathieu, et al. CCM 1991; 19:1352-1356

21. Primary Stress Ulcer Risk Factors Frequently Present in Severe Sepsis • Mechanical ventilation • Coagulopathy • Hypotension

22. Choice of Agents forStress Ulcer Prophylaxis • H2 receptor blockers • Role of proton pump inhibitors Grade C Cook DJ, et al. Am J Med 1991; 91:519-527

23. Blood Product AdministrationRed Blood Cells Tissue hypoperfusion resolved No extenuating circumstances • Coronary artery disease • Acute hemorrhage • Lactic acidosis Transfuse < 7.0 g/dl to maintain 7.0-9.0 g/dL Grade B

24. Blood Product Administration • Do not use erythropoietin to treat sepsis-related anemia. Erythropoietin may be used for other accepted reasons. Grade B

25. Blood Product Administration • Fresh frozen plasma • Bleeding • Planned invasive procedures. • Grade E

26. Blood Product Administration • Do not use antithrombin therapy. • Grade B Warren et al. JAMA 2001; 1869-1878

27. Blood Product Administration • Platelet administration • Transfuse for < 5000/mm3 - • Transfuse for 5000/mm3 – 30,000/mm3 with significant bleeding risk • Transfuse < 50,000/mm3 for invasive procedures or bleeding Grade E