Septic Shock by Dr Ruth M Divinagracia - Philippine College of ...

What To Do Before TheSubspecialist Arrives: SepticShockRuth M. Divinagracia, M.D.Clinical Associate ProfessorCollege of Medicine and Philippine General HospitalUniversity of the PhilippinesAttending PhysicianMakati Medical CenterSaint Luke’s Medical Center Global CityRD 5/12

Septic Shock• Acute organ dysfunction secondary to infection(sepsis) associated with hypotension notreversed by fluid resuscitation• Severe sepsis accounts for 9.3% of all deaths inthe US (Angus et al Crit Care Med 2001: 29)• Septic shock, the most severe manifestation ofsepsis, occurs in 2 to 20% of inpatients (Matot et alInt Care Med 2001:27)• Overall mortality for severe sepsis is 30% and50% for septic shock (Annane et AJRCCM 2003:168)and kills approximately 1400 people worldwidedailyRD 5/12

Epidemiology ofSepsis in the USSepticshock(severe sepsisplus refractoryhypotension)200,000 casesCrudemortality45%Number ofdeaths annually90,000Severe sepsis(sepsis plus organ failure)300,000 cases20%60,000Sepsis(systemic inflammatory response syndromeplus evidence of infection)400,000 cases15%60,000NEJM 2002; 347:966-67Total: 210,000RD 5/12

Sepsis and Septic Shock DefinedSEPSIS• (+) infection (proven of suspected) plus thepresence of SIRS (on the basis of ≥ 2 of thefollowing):• Increased HR > 90/min• Increased RR > 20 or PaCO2 less than 32or use of MV• Increased temperature > 38C or decreasedtemperature < 36C• Increased WBC (>12,000) or decreasedWBC (90% immature forms• Hyperglycemia, elevated CRP and procalcitoninLevy et al Crit Care Med 2003;31:1250-56RD 5/12

Supplemental oxygen endotrachealintubation and mechanical ventilationCentral venous and arterial catherizationSedation, paralysis(if intubated), or bothInitial Fluid Resuscitation:The Rivers Protocol8-12 mmHgCVP< 8 mmHgCrystalloidColloid< 65 mmHgMAP> 90 mmHg> 65 and < 90 mmHg< 70%ScvO 2Vasoactive agentsTransfusion of red cellsuntil hematocrit > 30%Inotropic agents> 70%< 70%NoYesGoalsachievedScvO 2Hospital admissionRivers et al NEJM 2001;345:1368-77)RD 5/12

Kaplan- Meier Estimates of Mortality and Causesof In-Hospital Death: Early Goal - Directed TherapyTable 3. Kaplan-Meier Estimate's of Mortality and Causes of Hospital Death*VariableIn-hospital mortalityAll patientsPatients with severe sepsisPatients with septic shockPatients with sepsis syndromeStandardTherapy59 (46.5)19 (30.0)40 (56.8)44 (45.4)No. (%)EarlyGoal-DirectedTherapy(N = 130)38 (30.5)9 (14.9)29 (42.3)35 (35.1)Relative Risk(95% Cl)0.58 (0.38-0.87)0.46 (0.21-1.03)0.60 (0.36-0.98)0.66 (0.42-1.04)P Value0.0090.060.040.0728-day mortality 61 (49.2) 40 (33.3) 0.58 (0.39-0.87) 0.0160-day mortality 70 (56.9) 50 (44.3) 0.67 (0.46-0.96) 0.03Causes of in-hospital deathSudden cardiovascular collapseMulti-organ failure25/199 (21.0)26/119 (21.8)12/17 (10.3)19/117 (16.2)----0.020.27Rivers et al NEJM 2001;345:1368-77)RD 5/12

Inotropic Therapy/Bicarbonate• Use dobutamine in patients with myocardialdysfunction as supported by elevatedcardiac filling pressures and low cardiacoutputTherapy• Do NOT increased cardiac index to predeterminedSUPRANORMAL levels• Bicarbonate should NOT be used hypoperfusioninducedlactic acidosisDellinger et al Surviving Sepsis Campaign: Crit Care Med2008; 36: 296-327RD 5/12

Steroids for Septic Shock? : Rationalefor Physiologic Dose• Relative adrenal insufficiency may be present in up to50% of patients with septic shock( Annane et al 2000: 283)• Systemic inflammation may lead to glucocorticoidreceptor resistance (Molijn et al J Clin Endocrinol Metab 1995; 80)• Patients with septic shock who had a reducedresponse to corticotropin (increase in plasmacortisol < 9 µg per deciliter) were likely to die(Rothwell et al Lancet 1991: 337)RD 5/12

CORTICUS Study: Placebo vsSteroids in Septic ShockKaplan-Meier Curve for The Time to Reversal of ShockSprung et al NEJM 2008; 358: 111-124RD 5/12

Probability of Survival and being DischargedHome after Randomization: Low Tidal Volume vsTraditional Tidal VolumeThe ARDS Network NEJM 2000; 342: 1301-1308RD 5/12

Low Tidal Volume Ventilation Strategy inPatients with ARDSMortality Among Patients with Pulmonary versus Nonpulmonary RiskFactors for ALI/ARDS: Efficacy of the Low VT Ventilation StrategyClinical riskfactorLow V T Ventilation*6 ml/kg (n = 473)Traditional V TVentilation 12 ml/kg (n= 429)All Patients †(n = 902)Pulmonary 32%76 / 23440%89 / 22036%165 / 454Nonpulmonary29%70 / 23940%84 / 20934%154 / 448Eisner et al AJRCCM 2001RD 5/12

Management of Patients with ARDS• Ventilate with “ lung protective strategy” – VT of 6 ml/kg,Pplat target of ≤ 30 cm H20, non-toxic FiO2 with more modestPaO2 goal of pO2 of at least 55 mm Hg or SpO2 of at least88%• Use of PEEP to improvement recruitment, to preventalveolar trauma and to decrease FiO2 requirement• Use of CVC (instead of PAC)• “Conservative” fluid management strategy (keep patient onthe “dry” side!) in patients who have no evidence of tissuehypoperfusion after initial fluid resuscitationARDSnet Publications, 2000, 2005RD 5/12

Septic Shock: The Critical First 6 Hours• Appropriate and prompt diagnosis of severesepsis and septic shock• Early-Goal Directed Therapy (1C)• Blood Cultures before antibiotic therapy, othercultures as needed (1C)• Administration of antibiotics within 1 hour ofdiagnosis of septic shock (1B)• Vasopressor preference for norepinephrine anddopamine (1C)• Low tidal volume, limitation of plateau pressureand the use of PEEP in ALI/ARDS (1B)• Use of stress dose steroids with hydrocortisoneas choice should be considered (2C)RD 5/12

RD 5/12