Understanding Sepsis: Terminology, Etiology, Pathophysiology, Clinical Presentation, Complications, Diagnosis and Management
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Sepsis, Septic Shock, SIRS - Undergraduate level
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Understanding Sepsis: Terminology, Etiology, Pathophysiology, Clinical Presentation, Complications, Diagnosis and Management
- 2. OUTLINE • Terminology • Etiology • Pathology • Clinical presentation • Complications • Investigations • Management • Prevention
- 3. 3
- 4. Infection • Invasion of normally sterile host tissue by microorganisms 4
- 5. BacterAemia • Presence of bacteria in blood • Evidenced by positive blood culture 5
- 6. Septicemia • Presence of microbes or toxins in blood 6
- 7. SIRS • Two or more of the following conditions: – Fever or hypothermia – Tachypnea – Tachycardia – Leukocytosis or leukopenia or >10% bands • Infectious / Noninfectious 7
- 8. Sepsis • SIRS with proven or suspected microbial etiology 8
- 9. Severe sepsis • Sepsis with signs of one or more organ dysfunction – Cardiovascular: hypotension that responds to administration of IV fluids – Renal – Respiratory – Hematologic – Unexplained metabolic acidosis 9
- 10. Septic shock • Sepsis with –Hypotension, for at least 1 h, despite adequate fluid resuscitation –Need for vasopressors 10
- 11. MODS- Multiorgan dysfunction • Dysfunction of >1 organ • Requiring intervention to maintain homeostasis 11
- 12. • Septicemia can be a response to any class of microorganism ETIOLOGY Harrison’ s Internal Medicine 18th edition
- 13. ETIOLOGY • Blood cultures are positive: – 20–40% of Severe sepsis cases – 40–70% of septic shock cases • Of cases with positive blood cultures, – 40% -gram-positive bacteria, – 35% -gram-negative bacteria, – 11 % - Poly-microbial – 7% - fungi – < 5% - classic pathogens Harrison’ s Internal Medicine 18th edition
- 14. PATHOPHYSIOLOGY
- 15. 15
- 16. Bacteria LP S Phagocyte Toxin Recognition by the Host
- 17. LBPBacteria LP S Phagocyte MD- 2 TLR- 4 TLR4 – transmembrane protein, transmits the LPS recognition signal to the interior of the cell, where signal transduction and gene transcription pathways promote the production and/or secretion of numerous molecules that mediate the inflammatory response LP S MD-2 Extracellular protein which binds the lipid A moiety of LPS Toxin Recognition by the Host Signaling complex Mandell Principles of Infectious Disease
- 18. Inflammatory response to sepsis 19
- 20. • CLINICAL MANIFESTATIONCLINICAL MANIFESTATION
- 21. • Patients usually manifests symptoms and signs related to primary infection. • Manifestations of Systemic Inflammatory Response • Evidence of shock • (-) fever: most common in neonates, elderly patients and in persons with uremia or alcoholism Harrison’ s Internal Medicine 18th edition
- 22. • Hyperventilation • Encephalopathy • Hypotension • DIC, ischemic necrosis of peripheral tissues (e.g., digits) • Skin: hemorrhagic lesions, bullae, cellulitis • Gastrointestinal • Hypoxemia Harrison’ s Internal Medicine 18th edition
- 23. MAJOR COMPLICATIONS l. Cardiopulmonary Complications – Acute respiratory distress syndrome – Hypotension – Decrease Myocardial function II. Renal Complications o Oliguira o Azotemia o Proteinuria o Nonspecific casts
- 24. III. Coagulopathy • Thrombocytopenia • Platelet usually very low <50,000/uL in patient with DIC IV. Neurological Complications • DDX: Guillain-Barre syndrome, metabolic disturbance, toxin activity MAJOR COMPLICATIONS Harrison’ s Internal Medicine 18th edition
- 26. • CBC • Renal function • LFTs • Blood Glucose • Clotting screen, including D-dimer and fibrinogen • Blood cultures • Radiology - CXR, abdominal USG, CT • Serum lactate • Arterial blood gases • Lumbar puncture, bronchoscopy, laparoscopy, lymph node biopsy, etc.
- 28. Harrison’ s Internal Medicine 18th edition Treatment:
- 29. Supportivecare Resuscitation Intravenous rehydration Monitoring the patient Intravenous insulin if required Intravenous hydrocortisone
- 30. Specifictherapy Intravenous antimicrobials Vasopressin Inotropes (dobutamine if cardiac dysfunction) Surgery eg, wound debridement, abscess drainage Bed sores management and prevention
- 31. Other measures • Nutritional supplementation • Prophylactic heparinization (DVT prphylaxis) • Blood transfusion – When Hb < 7 g/dl – Target level 9 g/dl 32
- 32. Other measures: cont… • Bicarbonate(for acidosis) • Fresh frozen plasma and platelets • Ventilatory support • Hemodialysis or hemofiltration 33
- 33. Ongoing trials • IV Ig • Endotoxin antagonist (eritoran) • GM CSF 34
Editor's Notes
- These mediators include cytokines (in particular, tumor necrosis factor [TNF]; interleukin [IL]-1â, IL-12); chemokines (IL-8, macrophage inflammatory protein [MIP]-1á); lipid mediators (prostaglandins, leukotrienes); and others, and they result in the familiar elements of local inflammation: increased capil- lary permeability and blood flow, infiltration of neutrophils, and pain. In addition, local deposition of fibrin that is initiated by the expression of tissue factor on activated macrophages and endothelial cells helps wall off the infected tissue and provides an important impediment to bloodstream invasion. Although neutrophils circulate in the bloodstream, they carry out phagocytosis largely in tissue spaces, where they can attach to extracel- lular matrix, spread out, get traction, and ingest. Because phagocytes may regurgitate the contents of their lysosomes as they eat, limiting this activity to local tissues minimizes the release of digestive enzymes and oxidants into the circulating blood. The major inherited mecha- nisms for killing microbes in the blood are soluble molecules: the mannose-binding lectin and C-reactive protein (CRP) pathways for activating complement, the alternative complement pathway, antibac- terial proteins (such as bactericidal permeability-increasing protein [BPI]), and natural IgM antibodies. Increased capillary permeability allows these molecules to diffuse into tissues where there is local inflammation.
- These mediators include cytokines (in particular, tumor necrosis factor [TNF]; interleukin [IL]-1â, IL-12); chemokines (IL-8, macrophage inflammatory protein [MIP]-1á); lipid mediators (prostaglandins, leukotrienes); and others, and they result in the familiar elements of local inflammation: increased capil- lary permeability and blood flow, infiltration of neutrophils, and pain. In addition, local deposition of fibrin that is initiated by the expression of tissue factor on activated macrophages and endothelial cells helps wall off the infected tissue and provides an important impediment to bloodstream invasion. Although neutrophils circulate in the bloodstream, they carry out phagocytosis largely in tissue spaces, where they can attach to extracel- lular matrix, spread out, get traction, and ingest. Because phagocytes may regurgitate the contents of their lysosomes as they eat, limiting this activity to local tissues minimizes the release of digestive enzymes and oxidants into the circulating blood. The major inherited mecha- nisms for killing microbes in the blood are soluble molecules: the mannose-binding lectin and C-reactive protein (CRP) pathways for activating complement, the alternative complement pathway, antibac- terial proteins (such as bactericidal permeability-increasing protein [BPI]), and natural IgM antibodies. Increased capillary permeability allows these molecules to diffuse into tissues where there is local inflammation.
- Ex: Pneumonia ( cough, dypnea, productive sputum) Fever, chills, hypothermia, Hypotension, lactic acidemia, progressive organ system dysfunction. S/S rate differ from px to px • Different variations, too • Some sepsis are normo or hypothermic • Absence of fever MOST COMMON
- Hyperventilation – earliest sign Encephalopathy (disorientation, confusion) Hypotension DIC, acrocyanosis, ischemic necrosis of peripheral tissues (e.g., digits) • Skin: hemorrhagic lesions, bullae, cellulitis. Skin lesions may suggest specific pathogens—e.g., petechiae and purpura with Neisseria meningitidis, ecthyma gangrenosum with Pseudomonas aeruginosa. • Gastrointestinal: nausea, vomiting, diarrhea, ileus, cholestatic jaundice • Hypoxemia: ventilation-perfusion mismatchand increased alveolar capillary permeability with increased pulmonary water content
- Acute respiratory distress syndrome VQ mismatch → fall in arterial PO2 early in course Inc alveolar capillary permeability ↓ pulmonary water content ↓ decrease compliance and interferes with gas exchange (progressive diffuse pulmonary infiltrates and arterial hypoxemia (PaO2/FIO2 <200)) is ARD which develops in 50% of pts with severe sepsis or septic shock. Hypotension: Normal or increased cardiac output and decreased systemic vascular resistance distinguish septic shock from cardiogenic or hypovolemic shock. a. generalized maldistribution of blood flow and blood volume b. hypovolemia (dt diffuse capillary leakage of intravascular fluid) c. Dehydration from atecedent dse or insensible fluid losses, v/d, and polyuria Myocardial function is depressed manifested with Decreased Ejection fraction • Increased end-diastolic and systolic ventricular volumes *CO normal even if decrease Ejection Fraction because of ventricular dilatation which permits normal stroke volume Renal complications 2) Renal Complications • Oliguira • Azotemia • Proteinuria • Nonspecific casts • Polyuric (Hypergly can exacerbate) • Most renal failure dt ATN induced by hypotension or capillary injury • Some may have glomerulonephritis, renal cortical necrosis or interstitial nephritis • Drug induced renal damage can complicate therapy