Septic shock management

Dr. C. Kannan, Post Graduate, MGMCRI, Pudhucherry, India

1. Management of septic shock By Dr. C. Kannan 1 st year post graduate Department of pediatrics MGMCRI

2. OBJECTIVES

3. SHOCK Shock is a syndrome that results from Inadequate oxygen delivery to meet metabolic demands Oxygen supply is less than Oxygen demand If untreated this leads to Metabolic acidosis Organ dysfunction Death

4. SEPTIC SHOCK Form of distributive shock Invasion of microorganisms Exaggerated by Immune response to infection Release and activation of immune mediators Typical changes are Vasodilation Capillary permeability

5. PATHOPHYSIOLOGY OF SEPTIC SHOCK

6. PATTERN-RECOGNITION RECEPTORS Four main classes Toll-like receptors C-type lectin receptors R etinoic acid inducible gene 1–like receptors N ucleotide-binding oligomerization domain–like receptor

7. SEPTIC SHOCK SIRS Systemic inflammatory Response Syndrome Seen in early stages of septic shock Criteria Temperature changes (>38°C or <36°C) Tachycardia (>160/min in infants, >150/min in children) Tachypnea (>60/min in infants, >50/min in children) Leucocytosis/ leucopenia Sepsis SIRS with suspected or proven sepsis

8. SEPTIC SHOCK Severe sepsis Sepsis + CVS dysfunction/ARDS or Sepsis with 2 or more organ failures Septic shock Sepsis + CVS dysfunction despite >40ml/ hr isotonic fluid in 1 hour CVS dysfunction SBP < 5 th centile/required vasoactive medication CFT > 5 sec Oliguria < 0.5 ml/kg/ hr Base deficit > 5 Lactate twice the normal

9. SEPTIC SHOCK Warm shock Early compensated Warm peripheries Bounding pulses Increased CO Decreased SVR Widened pulse pressure Hypocarbia Hyperglycaemia Metabolic acidosis Cold shock Late hypotensive Cold and clammy Weak thready pulses Decreased CO Increased SVR Narrow pulse pressure Hypoxia Hypoglycaemia Metabolic acidosis Capillary leak & Oliguria

10. RISK FACTORS

11. CULPRITS OF SEPSIS Vincent J-L,   Rello  J,  Marshall J,  et al. EPIC II G roup of Investigators. International study of the prevalence and outcomes of infection in intensive care units. JAMA 2009 ; 302 : 2323 - 9 . doi : 10 . 1001 / jama.2009.1754 .  pmid:19952319

12. EARLY RECOGNITION Septic shock is a clinical diagnosis High index of suspicion is warranted Altered mental status with fever Altered alertness Lethargy Poor eye contact Somnolence Inconsolable cry Clinical triad of impending septic shock Hyper/hypothermia Altered mental status Peripheral vasodilation Any fever + irritability/ lethargy + decreased urine output- look for tachycardia out of proportion with fever- Septic shock

13. PRIMARY RESUSCITATION Initial assessment of ABC 100% oxygen via NRM Early administration of broad spectrum antibiotics Securing minimum 2 IV lines/ intraosseous line Collect briefly the past history to R/O underlying cause Initial investigations ABG Blood sugar RFT and Electrolytes CBC PT/PTT Type and cross match Cultures

14. INTRAOSSEOUS TECHNIQUE Used in poor peripheral vascular access- 2 IV line attempts unsuccessful- choose IO Sites: Tibial tuberosity, lower end of femur and lower end of tibia Intraosseous needle / bone marrow aspiration needle Position: Fluid should infuse easily without evidence of soft-tissue swelling M ost successful in children younger than age six- may be employed in older children Fluids, inotropes, antibiotics, transfusions

15. ANTIMICROBIALS

16. IN FIRST 3 & 6 HOURS

17. FLUID RESUCITATION Compensated shock NS/RL 20 ml/kg over 1 hour Assess the vitals and titrate the fluids accordingly Hypotensive shock (uncompensated shock) Rapid boluses of NS/RL - 20 ml/kg Until SBP/MAP normal for age Can reach upto 60 ml/kg in 1 hour

18. FLUID RESUCITATION General concerns in fluid therapy in any kind of shock Assess the vitals and CCF features At the end of each boluses/aliquots In cardiac patients start at 10-20 ml/kg over 1 hour Once shock is revived wean the fluid and Maintain according to the requirement

19. QUESTION Why the amount of bolus is 20 ml/kg? Magic number??

20. FLUID INTOLERANCE Features of overload or pulmonary edema New onset/worsening of rales Hepatomegaly Increased oxygen requirement (WOB) Causes Capillary leak into lungs Cardiogenic pulmonary edema ARDS Fluid overload

21. FLUID INTOLERANCE Pathophysiology C apillary leak Uncorrected hypovolemia Loss of crystalloids and colloids Management Slow down the fluid rate Consider colloids Consider inotrope/ p ressor depending upon BP Positive pressure ventilation( CPAP/Invasive ventilation)

22. THERAPEUTIC GOALS HR for age SBP/MAP for age Urine O/P > 1 ml/kg/ hr Warm peripheries with CFT <3 sec Normal mental status Improving metabolic acidosis/reducing lactate

23. INTUBATION AND VENTILATION Indications Increased work of breathing Pulmonary edema Hypoventilation Altered mental status(GCS <8) Refractory shock Severe hypoxemia +/- hypercapnia and Moribund state

24. INTUBATION & VENTILATION Preoxygenation with 100% oxygen with NRM Avoid sedative drugs in moribund patients Select appropriate ET tube/cuffed tube T o prevent peritubal air leaks Target tidal volume of 6 mL/kg Plateau pressure in ARDS must be ≤30 cm H2O PEEP on little higher side in mod/severe ARDS H ead end elevation to 30-45 degree (aspiration / VAP)

25. BLOOD TRANSFUSIONS Indications for RBC transfusions are Hb <7.0 (Target Haemoglobin is 7 to 9) Metabolic acidosis with base deficit > 5 Elevated lactate Other blood components are indicated depending upon the needs Platelets transfusion if counts < 100,000 Bleeding due to DIC, consider FFP or cryoprecipitate

26. STEROIDS Timely hydrocortisone therapy in children with Fluid refractory Catecholamine resistant shock and Suspected or proven absolute (classic) adrenal insufficiency 1-2 mg/kg of hydrocortisone bolus followed by 1mg/kg Q6-8H.

27. ACID BASE/SUGAR/ELECTROLYTES Hypo/hyperglycaemia both are common in SS Periodic monitoring is warranted In persistent hypoglycaemia consider early steroids and 10%D Insulin infusion in persistent hyperglycaemia Electrolytes and RFT should be monitored Wide anion gap acidosis common in SS due to lactate Bicarbonate correction is not required Adequate fluid correction is enough

28. REFRACTORY SHOCK If shock persists despite of Adequate filling Inotrope/ vasopressor Initiation of steroids Haematocrit >30% Suspect PHTN Pericardial effusion Tension pneumothorax Hypoadrenalism Hypothyroidism On going blood loss Intraabdominal catastrophe and HTN

29. INDICATORS OF SEVERE DISEASE Low or falling WBC count Low or falling platelet count High requirement of fluid Short history(<12 hours) Rapid progression of multiorgan failure

30. SYMPATHETIC RECEPTORS ALPHA Alpha -1 (vasoconstriction) 1-a prostatic urethra 1-b blood vessels Alpha -2 Presynaptic Brake to sym system Post synaptic Blood vessels & brain BETA Beta-1 Heart & GJ cells Beta-2 (vasodilation) Bronchus, GIT, Bladder Uterus, Liver, Skeletal muscle Blood vessels Beta-3 Adipose tissue Coronary vessels

31. CATECHOLAMINES Adrenaline acts on Alpha – 1 & 2 Increases SBP & HR Beta – 1 & 2 Noradrenaline Alpha – 1 & 2 Increases SBP & DBP Beta – 1 Decreases HR

32. CATECHOLAMINES Dopamine D-1 @ 1-2 mics/kg/min (Renal vasodilation) Beta-1 @ 2-10 mics/kg/min (Increases contractility) Alpha-1 @ >10 mics/kg/min (Vasoconstriction) Dobutamine Selective beta-1 agonist increases contractility and vasodilation

33. DOSES

34. RULE OF “6”

35. Question Write Dopamine orders for a 10 kg child with fluid refractory septic shock

36. TAKE HOME MESSAGE

37. THANK YOU !!

38. CASE DEFINITION SUSPECTED CASE Acute febrile respiratory illness (fever ≥ 38 C) Within 7 days of close contact with a confirmed case or Within 7 days of travel to pandemic areas or R esides in a pandemic community.

39. Contd., PROBABLE CASE A cute febrile respiratory illness who is P ositive for influenza A But unsubtypable for H1 and H3 by influenza RT-PCT or P ositive for influenza A Influenza rapid test or IFA + suspected case or W ho died of an unexplained acute respiratory Illness is epidemiologically linked to a probable or confirmed case.

40. Contd., CONFIRMED CASE Acute febrile respiratory illness Found to be positive in any of following method Real Time PCR Viral culture Four-fold rise in H1N1 virus specific neutralizing antibodies Through any of WHO approved laboratory

41. Give examples of distributive shock Anaphylactic/Neurogenic/Septic shock

42. Important receptors of immune cells implicated in pathophysiology of septic shock Toll-like receptors C-type lectin receptors R etinoic acid inducible gene 1–like receptors and N ucleotide-binding oligomerization domain–like receptors.

43. What is SIRS ? Criteria for SIRS ? Systemic inflammatory Response Syndrome Seen in early stages of septic shock Criteria Temperature changes (>38°C or <36°C) Tachycardia (>160/min in infants, >150/min in children) Tachypnea (>60/min in infants, >50/min in children) Leucocytosis/ leucopenia

44. Most common organisms involved in sepsis ? Pseudomonas Klebsiella Acenetobacter E coli Staph aureus

45. Most common site of Intraosseous route ? Successful upto which ? Lower 1/3 rd of femur Upper 1/3 rd of tibia Lower 1/3 rd of tibia Age upto 6

46. Clinical features of fluid overload ? Causes ? Features of overload or pulmonary edema New onset/worsening of rales Hepatomegaly Increased oxygen requirement (WOB) Causes Capillary leak into lungs Cardiogenic pulmonary edema ARDS Fluid overload

47. Therapeutic goals of septic shock ? Should achieved within ? All must be achieved within first 6 hours HR for age SBP/MAP for age Urine O/P > 1 ml/kg/ hr Warm peripheries with CFT >3 sec Normal mental status Improving metabolic acidosis/reducing lactate

48. Role of alpha 1 and beta 2 receptors in blood vessels ? Alpha -1 (vasoconstriction) Beta-2 (vasodilation)

49. What is mixed venous oxygen saturation (called SvO2) ? Clinical role ? P ercentage of oxygen bound to haemoglobin in blood returning to the right side of the heart. Reflects The amount of oxygen "left over" after the tissues usage Amount of oxygen extracted by tissues Helps to determine whether the cardiac output and oxygen delivery is high enough to meet a patient's needs A true mixed venous sample is drawn from the tip of the pulmonary artery catheter Normal SvO2 60-80%. 

50. Parameters catecholamines MAP increased by Dopamine/Adrenaline Both CO & SVR are increased by Dopamine Both increasing CO & decreasing SVR by Dobutamine M ost potent vasopressor N oradrenaline DBP increased by Adre / Noradre http:// www.who.int/childgrowth/standards/weight_for_age/en /