SEVERE SEPSIS AND SEPTIC SHOCK Dr Mobaien A
SEVERE SEPSIS AND SEPTIC SHOCK Dr. Mobaien A. R. MD - MPH By : Dr. A. R. Mobaien
1992 ﺗﻮﺍﻓﻖ ﻧﺎﻣﻪ n n The Society of Critical Care Medicine The American College of Chest Physicians By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
Mechanisms that sense bacteria and initiate host responses By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
Normal Systemic Responses to. Infection and Injury: Presumed Contributions to Host Defense By : Dr. A. R. Mobaien
pathogenesis the pathogenesis of severe sepsis may differ according to the: u infecting microbe, u the site of the primary infection, u the presence or absence of immune defects, u the prior physiologic status of the host. n Genetic factors may also be important. n By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
Inflammation-activated coagulation By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
PIRO Staging of Sepsis From Levy MM, Fink MP, Marshall JC, et al: 2001 SCCM/ESICM/ACCP/ ATS/SIS International sepsis definitions conference. Crit Care Med 2003; 31: 1250– 1256. By : Dr. A. R. Mobaien
CLINICAL MANIFESTATIONS patient’s underlying illness and primary infection n signs and symptoms develop may differ from patient to patient u the absence of fever is most common in: t neonates, t in elderly patients, t in persons with uremia or alcoholism. n By : Dr. A. R. Mobaien
Hyperventilation is often an early sign. n Disorientation, confusion, and other manifestations of encephalopathy may also develop early in the septic response n By : Dr. A. R. Mobaien
Plasma Lipids n n n High-density lipoprotein (HDL) and low-density lipoprotein (LDL) levels decrease Triglyceride, free fatty acid, and very low- density lipoprotein (VLDL) levels increase The decrease in serum cholesterol is almost entirely accounted for by lower concentrations of cholesterol esters in circulating HDL and LDL By : Dr. A. R. Mobaien
skin lesions may suggest specific pathogens. n n n cutaneous petechiae or purpura (Neisseria meningitidis) cutaneous lesion seen almost exclusively in neutropenic patients is ecthyma gangrenosum, usually caused by P. aeruginosa. Hemorrhagic or bullous lesions in who has recently eaten raw oysters suggest Vibrio vulnificus bacteremia patient who has recently suffered a dog bite may indicate bloodstream infection due to Capnocytophaga canimorsus Generalized erythroderma in a septic patient suggests the toxic shock syndrome due to S. aureus or S. pyogenes. By : Dr. A. R. Mobaien
Neisseria meningitidis By : Dr. A. R. Mobaien
Neisseria meningitidis By : Dr. A. R. Mobaien
n. P. aeruginosa. By : Dr. A. R. Mobaien
Vibrio vulnificus By : Dr. A. R. Mobaien
MAJOR COMPLICATIONS n n ARDS develops in 50% of patients with severe sepsis or septic shock. fluid volume overload or cardiac failure Depression of myocardial function, manifested as increased end diastolic and systolic ventricular volumes with a decreased ejection fraction, develops within 24 h in most patients with severe sepsis. refractory hypotension is usually due to a low systemic vascular resistance By : Dr. A. R. Mobaien
Renal Complications n n n Oliguria, azotemia, proteinuria, and nonspecific urinary casts Most renal failure is due to acute tubular necrosis some patients also have: u glomerulonephritis, u renal cortical necrosis, u interstitial nephritis By : Dr. A. R. Mobaien
Coagulation Thrombocytopenia (10 to 30%) n DIC ( lower than 50, 000/L) n By : Dr. A. R. Mobaien
Noninfectious etiologies of SIRS n n n n n pancreatitis, burns, trauma, adrenal insufficiency, pulmonary embolism, dissecting or ruptured aortic aneurysm, myocardial infarction, occult hemorrhage, cardiac tamponade, post-cardiopulmonary bypass syndrome, anaphylaxis, drug overdose. By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
blood cultures negative antibiotic administration, n the presence of slow-growing or fastidious organisms, n the absence of microbial invasion of the bloodstream n By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
TREATMENT By : Dr. A. R. Mobaien
TREATMENT Ø Ø Ø Respiratory Therapy Circulatory Therapy Transfusion of Erythrocytes and Erythropoietin Drugs Ø Antibiotics Ø Corticosteroids Ø Recombinant Human Activated Protein C Controversial Therapies in Septic Shock Ø Vasopressin Deficiency and Use of Vasopressin Ø Hyperglycemia and Intensive Insulin Therapy Ø Renal Dysfunction and Dialysis Ø Other Therapies(Deep vein thrombosis prophylaxis using low-dose heparin, Stress ulcer prophylaxis using H 2 -receptor antagonists, Enteral nutrition is generally safer and more effective than total parenteral nutrition By : Dr. A. R. Mobaien
CURRENT THERAPY n n n Identify the Cause and Source of Infection Initiate Appropriate Antibiotic Therapy Restore and Maintain Hemodynamic Function Support Oxygenation and Ventilation Antithrombotic, Profibrinolytic, Anti-inflammatory Therapy Metabolic Support t n Maintain early nutritional support. Maintain intestinal mucosa barrier function by enteral route, the preferred method. Control hyperglycemia to decrease infectious complications, may need IV insulin therapy. Prevent Complications of Critical Illness By : Dr. A. R. Mobaien
TREATMENT n Anticoagulant Agents u a. PC for use in adults ( >18 years of age) who meet the APACHE II ≥ 25 during the 24 h before initiation of a. PC infusion u Contraindications t Intracranial hemorrhage t platelet counts of < 30, 000/ m. L t meningitis By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
Definition of Sequential Organ Failure Assessment (SOFA) scores By : Dr. A. R. Mobaien
Empirical Antibiotic Options for Patients with Severe By : Dr. A. R. Mobaien Sepsis or Septic Shock
By : Dr. A. R. Mobaien
PROGNOSIS(30 day) Approximately 20 to 35% of patients with severe sepsis n 40 to 60% of patients with septic shock n Die By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
By : Dr. A. R. Mobaien
Sepsis By: Dr. Ahmadreza Mobaien MD - MPH By : Dr. A. R. Mobaien
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