Transcript Sepsis

System inflammatory
response syndrome and
sepsis for surgery patients
Surgery department №2
DSMA
System inflammatory response syndrome (SIRS) Sepsis — SIRS + septic site
SIRS
• Continuum of clinical pathophysiology
and severity
• Process rather than an event
• Mild dysfunction to frank organ failure
• Changes in the function of every organ
system mediated by the host immune
system.
SIRS
• Systemic Inflammatory Response Syndrome
Criteria (ACCP/SCCM Consensus)
– Temperature >38°C or <36°
– Heart rate >90 bpm
– Respiratory Rate>20 or PaCO2<32mmHg
– WBC>12,000/μl or <4,000/μl
Sepsis
• Sepsis: 2 or more– Tachycardia >90bpm
– Rectal temp>38°C or <36°C
– Tachypnea(>20bpm)
• With 1 or more
– Alteration in mental status
– Hypoxemia (PaO2<72mmHG at FiO20.21)
– Elevated plasma lactate
– Oligouria
Sepsis
classification by ethiology
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Gram (+)
Gram (-)
Aerobic
Anaerobic
Mycobacterial
Staphylococcus
Streptococcus
Mixt-sepsis
Sepsis
classification by primary focus
• Post-traumatic:
– burn
– wound
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Lung
Angiogenic
Cardiogenic
Abdominal:
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Biliary
Pancreatic
Intestinal
Peritoneal
Appendicular
• Soft-tissue inglammation
• Urological etc
Sepsis
classification by development with a time (stages)
• Toxemia
• Septicemia
• Septicopyemia
Sepsis
classification by clinical course
• Fulminant or the acutest
• Acute
• Chronic
Sepsis
classification by clinical severity
Sepsis
Severe sepsis – sepsis + organ dysfunction
Septic shock – sepsis + hypotension
(Multiple organ dysfunction)
Sepsis
• Severe Sepsis
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Tachycardia >90bpm
Rectal temp>38°C or <36°C
Tachypnea(>20bpm) or PaCO2<32mmHg
Hypotension despite fluid resuscitation
Presence of perfusion abnormalities: lactic
acidosis, oligouria, alteration in mental status
Sepsis
• Mediators of Sepsis
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Lipospolysaccharide (gram-negative bacteria)
Lipoteichoic acid (gram-positive bacteria
Peptidoglycan
Cytokines
• IL-1 – mediates systemic effects of infection
• IL-6 – effects liver function
• TNF-α- potentiates the activation of neutrophils and
macrophages
• IL-8 – regulates neutrophil function, mediates lung injury in
sepsis
Sepsis
• Mediators of Sepsis
– Complement
– Nitric Oxide
– Lipid Mediators: Chemotaxis, Cell activation,
Vascular Permeability
Phospholipase A2
PAF
Eicosanoids
Sepsis
• Mediators of Sepsis
– Adhesion Molecules
• Selectins
• Leukocyte Antigens
Sepsis
• Circulatory Manifestations
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Vasodilation
Tachycardia
Increased Cardiac Output
Depressed Myocardial Function
Increased Delivery
Decreased Extraction
Sepsis
• Circulatory Manifestations
– Downregulation of catecholamine receptors
– Increased local vasodilating substances
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Nitric oxide
Prostacyclin
Decreased Oxygen
Low pH
Increased anaerobic metabolism
Shunting
Sepsis
• Pulmonary Dysfunction
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Endothelial Injury
Interstitial Edema
Alveolar Edema
Neutrophil entrapment
Injury Type I pneumocyte
Hyperplasia Type II pneumocyte
Continued Neutrophil, monocyte, leukocyte and
platelet aggregation
Sepsis
• Other Organ Dysfunction
– GI
• Ileus
• Malabsorption
• Overgrowth of bacteria, Translocation
– Liver
– Renal
– CNS
Sepsis
• Organisms
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Lower Respiratory Tract Infections (25%)
Urinary Tract Infections (25%)
Gastrointestinal Infections (25%)
Soft Tissue Infections (15%)
Reproductive Organs (5%)
Sepsis
• Risk Factors
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Extremes of Age (<10 and >70 years)
Pre-existing Organ Dysfunction
Immunosuppression
Major Surgery, Trauma, Burns
Indwelling Devices
Prolonged Hospitalization
Malnutrition
Prior Antibiotic Treatment
Sepsis
• Principles for Management of Sepsis
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Early Recognition
Early and Adequate Antibiotic Therapy
Source Control
Early Hemodynamic Resuscitation and continued
support
– Drotrecogin Alpha (Apache II>25)
– Tight Glycemic Control
– Ventilatory Support
Sepsis
• Drotrecogin-alpha/Recombinant Human
Activated Protein C
– Reduced levels of anti-inflammatory mediators
– Activated Protein C
• Inhibits thrombosis
• Decreases inflammation
• Promotes fibrinolysis
– Side Effect: Bleeding
– PROWESS study group
• Lower mortality rate (24.7 vs. 30.8%)
Sepsis
• Steroids???
– Older trials used high doses
– Recent trials suggest low dose, with taper and tight
glycemic control may improve outcome
– Vasopressor-dependent shock
– Cosyntropin Stim Test-Relative Adrenal
Insufficiency (<9mcg/dL)
Sepsis
• Experimental Therapies
– Dopexamine- beta 2 adrenergic and dopaminergic
effects, NO alpha adrenergic activity
– Vasopressin- reduces inducible NO synthase,
upregulates endogenous catecholamine receptors
– Phosphodiesterase Inhibitors-ionotropic agents
with vasodilating actions
– Nitric Oxide Inhibitors- N-monomethyl-l-arginine
ARDS
• Frequent Complication in Sepsis(40%)
• Adult Respiratory Distress Syndrome
– Oxygenation abnormality: PaO2/FiO2 ratio less
than 200
– Bilateral opacities on CXR
– PAOP <18mm Hg or no evidence of L atrial
hypertension
ARDS
• Frequent Complication in Sepsis(40%)
• Adult Respiratory Distress Syndrome
– Oxygenation abnormality: PaO2/FiO2 ratio less
than 200
– Bilateral opacities on CXR
– PAOP <18mm Hg or no evidence of L atrial
hypertension
– Frequency of ARDS in sepsis 18-38%
– 16% patients die w/irreversible respiratory failure
ARDS
• Pathophysiology
– Injury to Alveolocapillary unit
– Exudative Phase
• Endothelial injury, immune cell infiltration, pneumocyte and
endothelial injury and necrosis
– Proliferative Phase
• Organization of exudate, myofibroblast proliferation
• Conversion of exudate to fibrous tissue
– Fibrotic Phase
• Remodeling of fibrosis, microcystic honeycomb formation and
traction bronchiectasis
ARDS
• Management
– Lung-Protective Strategy-Reduction of
Barotrauma
– TV 5ml/kg
– Longer inspiratory time
– Peak Inspiratory Pressure<35-40cmH2O
– Permissive Hypercapnea
– PEEP
Acute Renal Failure
• Increases Mortality in ICU 30%
• Physiology
– Glomerular Filtration dependent on perfusion
pressure (MAP 60-80mmHg)
– Less than 60mmHG
• Decreased flow
• Arterial dilation in pre-glomerular arterioles
(prostaglandins)
• Constriction of post-glomerular arterioles (angiotensin
II)
Acute Renal Failure
• As Renal Perfusion Falls
– Increased reabsorption in proximal tubules
• 90% water is reabsorbed (normal is 60%)
– Decreased fluid to the distal tubules
• Loss of potassium elimination
– Tubular cells dependent on aerobic respiration
• Ascending loop is most sensitive to ischemia
Acute Renal Failure
• Dose all drugs appropriately
• Correction of Metabolic Acidosis
– Isotonic Bicarbonate
– Cannot Correct Ongoing Hypoperfusion
• Renal Replacement Therapy
– Absolute indication
• Acidosis
• Hyperkalemia
• Uremia (relative)
Sepsis
• Principles for Management of Sepsis
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Early Recognition
Early and Adequate Antibiotic Therapy
Source Control
Early Hemodynamic Resuscitation and continued
support
– Drotrecogin Alpha (Apache II>25)
– Tight Glycemic Control
– Ventilatory Support