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Paediatric septic-shock


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Paediatric septic-shock

  1. 1. Paediatric Septic Shock Dr.Sajid Nomani MEM (GWU)
  2. 2. 8 year old female arrives at ED with HR 180, RR 35, looks toxic. Has had URTI symptoms for past couple of days. Paeds Reg called by ED doctor saying can you come and have a look. You make your first assessment  HR 180  T 39.9f  RR-32br/min  BP 70/50mmhg  SPO2 90% on RA  Quiet, tired, opens eyes  Cap refill 4 seconds Worry??????
  3. 3. Why are we worried about it? Still remains significant cause of morbidity and mortality 19 milln. Cases worldwide / year( adhikari et al) 30% of paediatric patients with sepsis will develop septic shock. Mortality rates in septic shock are 20-30% (up to 50% in some countries).
  4. 4. Risk factors for Sepsis in Children < 1 year of age Very low birthweight infants Prematurity Presence of underlying illness Co-morbidities Boys Genetic factors
  5. 5. So What is SEPSIS ….. ..???????????? Sepsis is a life threatening response to infection. It represents a continuum through SIRS, sepsis, and septic shock
  6. 6. How do we define it Systemic Inflammatory Response Syndrome Infection Sepsis Severe Sepsis Septic Shock
  7. 7. SIRS…in peds Core Temp >38.5 or < 36 degrees Mean HR > 2SD for age or persitant elevation over 0.5-4hrs If < 1yr old: bradycardia HR < 10th centile for age Mean RR > 2 SD above normal for age Leucocyte abnormality. ≥2 criteria should be present ≥ 2 SIRS criteria but no infection : SIRS ≥ 2 SIRS criteria + sign of acute organ failure : severe SIRS
  8. 8. Sepsis SIRS + suspected or proven infection Severe Sepsis Sepsis + sepsis induced organ dysfunction, / tissue hypo perfusion Septic Shock Sepsis + Hypotnsn /CV organ dysfunction
  9. 9. Cardiovascular dysfunction Despite >40ml/kg Isotonic fluid bolus in 1 hour: Decrease in BP <5th centile for age Need for vasoactive drug to maintain BP 2 of the following: Unexplained metabolic acidosis  Increase lactate  Oliguria  Prolonged cap refill > 5 seconds  Core-peripheral temp gap >3 degrees 
  10. 10. What makes you suspect shock??
  11. 11. Clinical Manifestations Variable….depends upon loads/site/pathogens/comorbidites Fever Increased HR Increased RR Altered mental state Skin: Hypoperfusion Increased capillary refill Petechiae, purpura Cool vs warm.
  12. 12. Cold Shock Warm Shock HR Tachycardia Tachycardia Peripheries Cool Warm Pulses Difficult to palpate Bounding Skin Mottled, pale Flushed Capillary refill Prolonged Blushing Mental state Altered Altered Urine Oliguria Oliguria
  13. 13. Blood Pressure in Children This is main difference with adults. Blood pressure does not fall in septic shock until very late. CO= HR x SV HR in children much higher therefore BP falling is late. Hypotension formula : 70+(age× 2)
  14. 14. Etio+ pathophysiology Pneumonia < Intraabdominal < UTI Cultures are positive in only 1/3rd cases Staph aureus and Streptococcus pneumoniae(gr +) E coli, klebsiella species,Pseudomonas aeruginosa(gr -)
  15. 15. PATHOPHYSIOLOGY Infectious organism/ endotoxin  activates immune system Their interaction c infectioning organism stimulates  Cytokines Cytokines  produce vasodilation & damage endothelium of vessles  ↑cap.permiablity→cap.leakage  Inhibits + ↑ Antifibrinolysis → microvascular thrombosis →MOD & DIC Specific inflam.mediator→ impaired cardiac contractility & myocard. d/f Adrenal gland are prone to microvascular thrombosis & hemorrhage in septic shock ↓ ↓ SVR & myocardial d/f
  16. 16. Management…. Recognise early Resuscitation must be done in a proactive time-sensitive manner. Every minute counts – “golden hour” Every hour without appropriate resuscitation increases mortality risk by 40%
  17. 17. Coming back to our patient…. HR 180 Initial management T 39.9f BP 70/50mmhg SPO2 90% on RA Quiet, tired, opens eyes Mod respiratory distress Cap refill 4 seconds + Symptoms of URTI WHAT NEXT???? EGDT ??????????? Blood & Imaging Source control Disposition ?????????
  18. 18. IV /IO-2 max.bore Monitor O2 ABC resuscitation.
  19. 19. EGDT
  20. 20. GOAL: SEPSIS INDUCED HYPOPERFUSION IN FIRST 6 HOURS  Central venous pressure 8-12 mm Hg  Mean arterial pressure (MAP) ≥ 65 mm Hg  Urine output ≥ 0.5 ml/kg/hr  Scvo2 or Smvo2 ≥ 70% or ≥ 65%, respectively   Decreased lactate Source control   Better perfusion  Improvement in Mental status
  21. 21. 0-5min:  Recognise Sign of poor perfusion  Maintain airway and establish IV/IOaccess 5-15 min:  20mls/kg isotonic saline boluses up to and over 60mls/kg  Correct hypoglycemia  0.5-1gm/kg  Dx25:-2-4ml/kg  Dx10:-5-10ml/kg Our pt.  BP- 76/50  HR-170  CRT -≥4sec. Repeat bolus upto 60ml/kg or Sign of overload
  22. 22. Fluid Refractory Shock Inotrops /vasopressor to maintain  Map->65  Cvp- 8-12  Svo2->70% Central line Arterial line First dose of Antibiotic Catecholamine Resistant shock  Stress dose of Hydrocort 15-60 min….
  23. 23. O -5min 5-15m Recognise Sign of poor perfusion Maintain airway and establish access Push 20mls/kg isotonic saline or colloid boluses up to and over 60mls/kg Correct hypoglycemia Antimicrobials, Correct hypoglycemia 15 -60m fluid Responsiveness Observe in PICU Fluid Refractory shock
  24. 24. 15min Fluid Refractory Shock Begin dopamine / Norad/ Epineph. Establish central venous access Establish arterial access Titrate Adrenaline for cold shock and noradrenaline for warm shock to normal MAP-CVP and SVC sats>70% 60 min Catecholamine resistant shock
  25. 25. Catecholamine Resistant Shock At Risk of adrenal insufficency – give hydrocortisone-draw a baseline cortisole Evaluate Scvo2 >70% Normal BP ,poor perfusion SVC < 70% Transfuse PRBC Hb>10 Add Dopamine/NPS Milrinone Low BP,poor perfusion Cold Shock SVC < 70% Transfuse PRBC,Hb>10 Adrenaline Dobutamine+Norad. ECMO Low BP Scvo2 >70 Warm Shock Additional volume & Noradrenaline ± Vasopressin
  26. 26. Therapeutic endpoints Clinical  Heart Rate normalized for age  Capillary refill < 2sec  Normal pulse quality  No difference in central and peripheral pulses  Warm extremities  Blood pressure normal for age  Urine output >1 mL/kg/h  Normal mental status  CVP >8 mmHg
  27. 27. During the first 6 hrs, if the venous O2 saturation target not achieved with fluid resuscitation:  Packed RBC transfusion to achieve a hematocrit of ≥ 30% Active source control
  28. 28. SOURCE CONTROL  Specific anatomic site of infection should be established as rapidly as possible and within the first 6 hours of presentation  Formally evaluate patient for a focus of infection amenable to source control measures (eg: abscess drainage, tissue debridement)  Implement source control measures as soon as possible following successful initial resuscitation (Exception: infected pancreatic necrosis, where surgical intervention best delayed.)  Choose source control measure with maximum efficacy and minimal physiologic upset.  Remove intravascular access devices /cathetor if potentially infected.
  29. 29. Investigations Sepsis Work up  Lactate , ABG , CBC  PCT , CRP  Metabolic Panel /Electrolyte  Coagulation Profile  Urine, blood, sputum ,stool, throat swab cultures  Viral cultures  Never do CSF in shocked patient. Imaging:  CXR, CT, MRI, PET scan, ECHO, Ultrasound
  30. 30. Other treatment Maintain Glucose control Nutrition Maintain Hb > 10g/dL No stress ulcer protection /no DVT protection before puberty age Early CVVH
  31. 31. Drug Dose Comments Dopamine 2-20mcg/kg/min Historically 1st choice in kids Alpha, beta and dopamine receptor activation Can be given peripherally Dobutamine 5-10mcg/kg/min Chronotropic as well as inotropic Afterload reduction Adrenaline 0.05- 1mcg/kg/min Initially increases contractility/heart rate High doses increase PVR Noradrenaline 0.05 – 1 mcg/kg/min Vasopressor Increases PVR Milrinone 0.25-0.75mcg/kg/min Phosphodiesterase inhibitor Afterload reduction
  32. 32. Take home points…. Early Recognition Early goal directed therapy Remember golden hour Early and Emperic antimicrobials Early source control and aggressive therapy
  33. 33. qUESTIONS????????????????