By : Dr.A.R.Mobaien Dr. Mobaien A.R. Dr. Mobaien A.R. MD - MPH SEVERE SEPSIS AND SEPTIC SHOCK

By : Dr.A.R.Mobaien تعاريف باكتريمي = به حضور باكتري زنده در خون كه با كشت خون مثبت ثابت شود سپتي سمي = به بيماري سيستميكي كه ناشي از گسترش ميكروب يا سموم انها از طريق جريان خون ايجاد شده

By : Dr.A.R.Mobaien نكته : براي بروز سپسيس ورود ميكروب به جريان خون ضروري نيست و گسترش موضعي يا عمومي عوامل ميكروبي و توكسين ها كافي هستند.

By : Dr.A.R.Mobaien توافق نامه 1992 The Society of Critical Care Medicine The American College of Chest Physicians

By : Dr.A.R.Mobaien SIRS = وجود دو مورد يا بيشتر از موارد زير : دماي بدن بيش از 38.3 يا كمتر از 36 درجه سانتي گراد ضربان قلب بيش از 90 ضربه در دقيقه تعداد تنفس بيش از 20 بار در دقيقه يا PaCO2 < 32 mmHg تعداد سلولهاي سفيد خون بيش از يا كمتر از 4000 در هر ميكروليتر يا سلول بلاست (Band Cell) خون بيش از 10%

By : Dr.A.R.Mobaien SEPSIS = پاسخ سيستميك به عفونت كه با دو يا بيشتر از وضعيتهاي فوق تظاهر مييابد بعبارتي SIRS + evidence of infection SEVERE SEPSIS = سپسيس همراه با ديسفونكسيون ارگان ها ، هيپوپرفيوژن كه شامل : اسيدوز لاكتيك ،اوليگوري ويا تغييرات حاد در وضعيت منتال SEPTIC SHOCK = سپسيس همراه با كاهش فشار خون ( فشار خون سيستوليك كمتر از 90 ميليمتر جيوه يا كاهش بيش از 40 ميليمتر جيوه از مقدار نسبت پايه در قبل ) عليرغم دادن مايع به اندازه كافي همراه با غير طبيعي بودن پرفيوژن بافتي كه ممكن است شامل اسيدوز لاكتيك ، اوليگوري ويا تغييرات حاد در وضعيت منتال باشد كه به درمان سريع با 500 سي سي مايع پاسخ نمي دهند If septic shock lasts for >1 hr and does not respond to pressor administration, the term refractory septic shock is often used.

By : Dr.A.R.Mobaien

Mechanisms that sense bacteria and initiate host responses

By : Dr.A.R.Mobaien

Normal Systemic Responses toInfection and Injury: Presumed Contributions to Host Defense

By : Dr.A.R.Mobaien pathogenesis the pathogenesis of severe sepsis may differ according to the: the pathogenesis of severe sepsis may differ according to the:  infecting microbe,  the site of the primary infection,  the presence or absence of immune defects,  the prior physiologic status of the host. Genetic factors may also be important.

By : Dr.A.R.Mobaien

Inflammation-activated coagulation

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 signs and symptoms develop may differ from patient to patient   the absence of fever is most common in:   neonates,   in elderly patients,   in persons with uremia or alcoholism.

By : Dr.A.R.Mobaien Hyperventilation is often an early sign. Hyperventilation is often an early sign. Disorientation, confusion, and other manifestations of may also develop early in the septic response Disorientation, confusion, and other manifestations of encephalopathy may also develop early in the septic response

Plasma Lipids High-density lipoprotein (HDL) and low-density lipoprotein (LDL) levels decrease High-density lipoprotein (HDL) and low-density lipoprotein (LDL) levels decrease Triglyceride, free fatty acid, and very low- density lipoprotein (VLDL) levels increase 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 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. 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 P. aeruginosa.

By : Dr.A.R.Mobaien Vibrio vulnificus

By : Dr.A.R.Mobaien MAJOR COMPLICATIONS 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 Oliguria, azotemia, proteinuria, and nonspecific urinary casts Oliguria, azotemia, proteinuria, and nonspecific urinary casts Most renal failure is due to Most renal failure is due to acute tubular necrosis some patients also have: some patients also have:  glomerulonephritis,  renal cortical necrosis,  interstitial nephritis

By : Dr.A.R.Mobaien Coagulation Thrombocytopenia (10 to 30%) DIC ( lower than 50,000/L)

By : Dr.A.R.Mobaien Noninfectious etiologies of SIRS 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

blood cultures negative antibiotic administration, the presence of slow-growing or fastidious organisms, the absence of microbial invasion of the bloodstream

By : Dr.A.R.Mobaien

TREATMENT

By : Dr.A.R.Mobaien TREATMENT   Respiratory Therapy   Circulatory Therapy   Transfusion of Erythrocytes and Erythropoietin   Drugs   Antibiotics   Corticosteroids   Recombinant Human Activated Protein C  Controversial Therapies in Septic Shock   Vasopressin Deficiency and Use of Vasopressin   Hyperglycemia and Intensive Insulin Therapy   Renal Dysfunction and Dialysis   Other Therapies(Deep vein thrombosis prophylaxis using low-dose heparin, Stress ulcer prophylaxis using H2-receptor antagonists, Enteral nutrition is generally safer and more effective than total parenteral nutrition

By : Dr.A.R.Mobaien Identify the Cause and Source of Infection Identify the Cause and Source of Infection Initiate Appropriate Antibiotic Therapy Initiate Appropriate Antibiotic Therapy Restore and Maintain Hemodynamic Function Restore and Maintain Hemodynamic Function Support Oxygenation and Ventilation Support Oxygenation and Ventilation Antithrombotic, Profibrinolytic, Anti-inflammatory Therapy Antithrombotic, Profibrinolytic, Anti-inflammatory Therapy Metabolic Support Metabolic Support   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 Prevent Complications of Critical Illness CURRENT THERAPY

By : Dr.A.R.Mobaien TREATMENT Anticoagulant Agents   aPC for use in adults ( >18 years of age) who meet the APACHE II ≥ 25 during the 24h before initiation of aPC infusion  Contraindications   Intracranial hemorrhage   platelet counts of < 30,000/  L   meningitis

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 Sepsis or Septic Shock

By : Dr.A.R.Mobaien

PROGNOSIS(30 day) Approximately 20 to 35% of patients with severe sepsis 40 to 60% of patients with septic shock Die

By : Dr.A.R.Mobaien

Sepsis By: Dr. Ahmadreza Mobaien MD - MPH