Shock is defined as a life-threatening, generalized maldistribution of blood flow resulting in failure to deliver and/or utilize adequate amounts of oxygen, leading to tissue dysoxia.
Hypotension [SBP < 90 mmHg, SBP decrease of 40 mmHg from baseline, or mean arterial pressure (MAP) < 65 mmHg], while commonly present, should not be required to define shock . Shock requires evidence of inadequate tissue perfusion on physical examination .
A clinical response arising from a nonspecific insult, including 2 of the following:
Temperature 38 o C or 36 o C
HR 90 beats/min
WBC count 12,000/mm 3 or 4,000/mm 3 or >10% immature neutrophils
SIRS Systemic Inflammatory Response Syndrome SIRS with a presumed or confirmed infectious process Sepsis SIRS Infection Severe Sepsis SEPTIC SHOCK Inflammatory response to microorganisms or invasion of normally sterile tissues
Crit Care Med 2000, 28(4):N105-N113 with modification Infection Immune Response Sepsis Uncontrolled Pro-inflammatory Mechanisms Dysregulated anti-inflammatory Mechanisms SIRS MODS/MOF
Why some patients do well others die ? Death Infection Toxins Host defenses Overwhelming infection Death Sepsis Excessive Survival MODS Adequate Coordinated Infection control Survival Why? Why? Unregulated Host factors Delayed therapy Genetic predisposition HLA class III genes TNF a gene promoter Inadequate
Final pathway in sepsis Sepsis is a disease of the microcirculation Vasoplegia , Cardiac dysfunction, Capillary leak Hypovolemia,Maldistribution Microemboli Microcirculatory Mitochondrial Dysfunction syndrome (MMDS) Cell death-Organ injury –MODS- Death
Why the microcirculation is important in shock .
It is where oxygen exchange takes place.
It plays a central role in the
During sepsis and shock it the first to go and last to recover.
Rescue of the microcirculation = resuscitation end-point
Oxygen Don’t Go Where the Blood Won’t Flow! From these two statements three things are obvious Early therapy before mitochondria gets damaged. Macro circulation should be optimised first. Micro circulation optimisation to prevent Mitochondrial injury is the target
War on Sepsis Society of Critical Care Medicine, European Society of Intensive Care Medicine, International Sepsis Forum + Institute of Healthcare Improvement
Even with the ‘best’ parameters it is not always easy to make the right decision.………
EGDT Suspected infection Blood cultures Obtain two or more BCs One or more BCs should be percutaneous One BC from each vascular access device in place more than equal to 48 hrs Culture other sites as clinically indicated. Other diagnostic/imaging as indicated Appropriate Empirical Antibiotics with in 1 hr/ source control Host factors/ local antibiogram/ suspected site Combination antibiotics/ right dose SBP< 90 even after 20-30ml/kg fluid or Lactate > 4mmol/l
Antibiotics Always look at you local organisms and resistance patterns Early antibiotic therapy Right dose
35 year old male patient brought to ICU with 3 day old perforation, Posted for emergency Lapratomy
Has chills with fever
Tachypneic- RR 40/mt, has respiratory distress,
Tense abdomen, bilateral crepts,
Spo2 on 89% on room air.
Pulse 130/mt well felt, BP 80/60 mm Hg, Restless,
WBC – 19,000 T.B 3.5, Enzymes Normal
SC-2.0 INR 2.0, Platelets 1.2 lac
Lactate 5.0 SCVO2 60%, K+4.5
1-2 litrs NS/ RL still hypotensive Add noradrenaline and adrenaline BP 130/70 mmHg, lactate 3 mmol/l, SCVO2 68% CVP 8 cms H20/ UO 1ml/kg/mt If he continues to improve for first 6 hrs I may plan to administer anesthesia for his surgery.