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Septic shock management
- 1. Management of septicshock By Dr. C. Kannan 1st year post graduate Department of pediatrics MGMCRI
- 2. OBJECTIVES What is septicshock? Basic pathophysiology Recognition of septic shock Fluid resuscitation and therapeutic goals Choosing antibiotics
- 3. SHOCK Shock is asyndrome 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 • Formof distributive shock • Invasion of microorganisms • Exaggerated by Immune response to infection Release and activation of immune mediators • Typical changes are Vasodilation Capillary permeability
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- 6. PATTERN-RECOGNITION RECEPTORS Four mainclasses • Toll-like receptors • C-type lectin receptors • Retinoic acid inducible gene 1–like receptors • Nucleotide-binding oligomerization domain–like receptor
- 7. SEPTIC SHOCK • SIRS Systemicinflammatory 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 • Severesepsis 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 < 5th 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 Extremes ofage Immunocompromised Malnutrition Asplenia Chronic antibiotics use Any insult (shock, trauma, burns and pancreatitis)
- 11. CULPRITS OF SEPSIS VincentJ-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 • Septicshock 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 • Initialassessment 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 • Usedin 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 • Most successful in children younger than age six- may be employed in older children • Fluids, inotropes, antibiotics, transfusions
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- 16. IN FIRST 3& 6 HOURS
- 17. FLUID RESUCITATION • Compensatedshock 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 concernsin 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 theamount of bolus is 20 ml/kg? • Magic number??
- 20. FLUID INTOLERANCE • Featuresof 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 Capillaryleak Uncorrected hypovolemia Loss of crystalloids and colloids • Management Slow down the fluid rate Consider colloids Consider inotrope/pressor depending upon BP Positive pressure ventilation( CPAP/Invasive ventilation)
- 22. THERAPEUTIC GOALS • HRfor 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 • Preoxygenationwith 100% oxygen with NRM • Avoid sedative drugs in moribund patients • Select appropriate ET tube/cuffed tube • To 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 • Head end elevation to 30-45 degree (aspiration / VAP)
- 25. BLOOD TRANSFUSIONS Indications forRBC 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 therapyin 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/hyperglycaemiaboth 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 shockpersists 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 SEVEREDISEASE • 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 actson 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
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- 35. Question • Write Dopamineorders for a 10 kg child with fluid refractory septic shock
- 37. TAKE HOME MESSAGE Septicshock is a clinical diagnosis, needs high suspicion Early recognition and resuscitation of septic shock Early fluid resuscitation Early initiation/Choosing/Narrowing of antibiotics Timely initiation of inotropes/vasopressors, if needed Therapeutic goals in 3 & 6 hours
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- 39. CASE DEFINITION SUSPECTED CASE Acutefebrile 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 • Resides in a pandemic community.
- 40. Contd., PROBABLE CASE Acute febrilerespiratory illness who is • Positive for influenza A But unsubtypable for H1 and H3 by influenza RT-PCT or • Positive for influenza A Influenza rapid test or IFA + suspected case or • Who died of an unexplained acute respiratory Illness is epidemiologically linked to a probable or confirmed case.
- 41. Contd., CONFIRMED CASE Acute febrilerespiratory 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
- 42. • Give examplesof distributive shock Anaphylactic/Neurogenic/Septic shock
- 43. Important receptors ofimmune cells implicated in pathophysiology of septic shock • Toll-like receptors • C-type lectin receptors • Retinoic acid inducible gene 1–like receptors and • Nucleotide-binding oligomerization domain–like receptors.
- 44. 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
- 45. • Most commonorganisms involved in sepsis ? • Pseudomonas • Klebsiella • Acenetobacter • E coli • Staph aureus
- 46. Most common siteof Intraosseous route ? Successful upto which ? • Lower 1/3rd of femur • Upper 1/3rd of tibia • Lower 1/3rd of tibia • Age upto 6
- 47. Clinical features offluid 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
- 48. Therapeutic goals ofseptic 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
- 49. Role of alpha1 and beta 2 receptors in blood vessels ? • Alpha -1 (vasoconstriction) • Beta-2 (vasodilation)
- 50. What is mixedvenous oxygen saturation (called SvO2) ? Clinical role ? • Percentage 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%.
- 51. Parameters catecholamines MAP increasedby Dopamine/Adrenaline Both CO & SVR are increased by Dopamine Both increasing CO & decreasing SVR by Dobutamine Most potent vasopressor Noradrenaline DBP increased by Adre/Noradre http://www.who.int/childgrowth/standards/weight_for_age/en/