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Yusuph-SIRS AND SEPSIS NPMCN. pdf
- 1. SIRS AND SEPSIS H.YUSUPH
- 2. LEARNING OUTCOMES INTRODUCTION DEFINITIONS PATHOGENESIS CLINICAL FEATURES EVALUATIONS MANAGEMENT
- 3. INTRODUCTION Sepsis andsepticaemia are not the same Sepsis is a complication of septicaemia While septicaemia refers to organisms or their toxins in the blood stream, sepsis is the body’s inflammatory response to these.
- 4. Criteria/Definition Terms SIRS is thepresence of 2 or more of the following: (a) Temperature <36∘C (96.8∘F) (hypothermia) or>38∘C (100.4∘F) (fever). (b) Heart rate >90 beats/min (tachycardia). (c) Respiratory rate >20 breaths/min (tachypnea). (d) WBC count <4000/mm3 (leucopaenia) or >12,000/mm3 (leukocytosis), or > 10 band cells SIRS SIRS+ identified or presumed focus of infection. Sepsis Sepsis + organ dysfunction* Severe Sepsis Sepsis + unexplained arterial hypotension. Septic Shock CONSENSUS CONFERENCE DEFINITIONS
- 5. DEFINITIONS CONTD. Sepsissyndrome (Severe sepsis): Association of sepsis with altered organ perfusion and/or altered organ function. Organ dysfunction can be identified by an acute change in the Sequential Organ Failure Assessment score (SOFA) of >2 points following infection. The baseline SOFA score can be assumed to be zero in patients not known to have pre-existing organ dysfunction Sepsis-2 (2001): Proven suspected infection in combination with a rise in SOFA score of at least 2 points compared to baseline OR two or more SIRS criteria and infection on the same day Sepsis-3 (2015): Life-threatening organ dysfunction caused by a dysregulated host response to infection. If not recognized early and managed promptly, it can lead to septic shock, multiple organ failure and death OR an increase in SOFA score of two or more in conjunction with an infection
- 9. Causes of sepsiscont. Developed Vs Developing Staph aureus, Enterococcus spp., strep. Pneumoniae are the leading G+ organism in high income countries Leading G- organisms include E.coli, K. Pneumoniae, Pseudomonas spp., and Acinetobacter baumanni Most common species in Africa – staphylococcus spp., salmonella spp, (predominantly NTS) and E-coli The organisms isolated in Nigeria are similar to those found in other parts of Africa.
- 10. Risk Factors Severewounds or burns Extremes of age Compromised immune system, which can occur from conditions, such as HIV, DM, malignancy, malnutrition, alcohol abuse or leukaemia, or from medical treatments such as chemotherapy or steroid therapy Major organ failures – liver, kidney and heart Urinary or intravenous catheter Mechanical ventilation Dental procedures
- 11. PATHOGENESIS Initiation of theinflammatory response The process begins with infection in one part of the body that triggers a localised inflammatory response. Appropriate source control and a competent immune system will, in most cases, contain the infection at this stage. However, if certain factors are present, the infection may become systemic. The causative factors are not fully elucidated but probably include: Genetic predisposition to sepsis (DEFA1/DEFA3) Large microbiological load High virulence of the organism Delay in source control (either surgical or antimicrobial) Resistance of the organism to treatment Patient factors (immune status, nutrition, frailty).
- 12. PATHOGENESIS Mediators arereleased from damaged cells (called ‘alarmins’) and these, coupled with direct stimulation of immune cells by the molecular patterns of the microorganism, trigger the inflammatory response. Once the inflammatory response is activated, immune cells such as macrophages release the inflammatory cytokines interleukin-2 (IL-2), IL- 6 and TNF-α, which, in turn, activate neutrophils. Activated neutrophils express adhesion factors and release various other inflammatory and toxic substances; the net effects are vasodilatation (via activation of inducible nitric oxide synthase enzymes) and damage to the endothelium. Neutrophils migrate into the interstitial space; fluid and plasma proteins will also leak through the damaged endothelium, leading to oedema and intravascular fluid depletion.
- 13. PATHOGENESIS Activation of thecoagulation system Damaged endothelium triggers the coagulation cascade (via tissue factor, factor VII, and reduced activity of proteins C and S) and thrombus forms within the microvasculature. A vicious circle of endothelial injury, intravascular coagulation and microvascular occlusion develops, causing more tissue damage and further release of inflammatory mediators. In severe sepsis, intravascular coagulation can become widespread (DIC) and usually heralds the onset of multi-organ failure.
- 14. CLINICAL FEATURES Symptoms usuallystart abruptly. Even in the first stages, a person can look very sick. The most common symptoms are: Fever with Chills/hypothermia (worse prognosis) Tachypnoea Tachycardia Vasodilatation, warm peripheries Bounding pulse Rapid capillary refill Hypotension, low diastolic pressure, widened pulse pressure Hyperglycaemia/hypoglycaemia Confusion Nausea and vomiting Red dots on the skin Oliguria Inadequate circulation Shock
- 15. EVALUATION/DIAGNOSIS It can bedifficult to find the exact cause of the infection. A wide range of tests may be required: Medical history: symptoms and physical examination –hypotension and body temperature Look for signs of conditions that more commonly occur along with septicemia: Pneumonia Meningitis Cellulitis Investigations: Blood culture Urine MCS/urinalysis Wound secretions and skin sores/Biopsies Respiratory secretions Endotoxin test Procalcitonin test SeptiCyte test
- 16. EVALUATION/DIAGNOSIS CONTD. FBC Chemistry Clotting profile Serumlactate -serial Oxygen saturation/carbon dioxide levels X-ray MRI CT scan Ultrasound SIRS-based definition
- 17. EVALUATION/DIAGNOSIS CONTD. NEWS2 tool PliNOSatest Presepsin CRP
- 18. Management General considerations Medical emergency ICU Vitalsigns should be closely monitored Samples for tests should be taken qSOFA –for assessment
- 19. Management Contd. The ‘SepsisSix’ (The UK Sepsis Trust) 1. Deliver high-flow oxygen 2. Take blood cultures 3. Administer intravenous antibiotics 4. Measure serum lactate and send full blood count 5. Start intravenous fluid replacement 6. Commence accurate measurement of urine output Treatment will depend on: Age Overall health – treat source of infection Extent of the condition Tolerance for certain medications
- 21. Management CONTD. Thesurviving sepsis campaign (SSC) -2001 SSC Updated in 2008 Use limited in SSA –limited resources, lack of awareness SSC is divided into 3 Initial resuscitation and infection management Haemodynamic support Other supportive therapies
- 22. Management CONTD. Initial resuscitationand infection management Care in the first six hours and meeting the following goals: CVP 8-12mmHg MAP ≥ 65mmHg Urine output ≥ 0.5ml/kg/hr CVO2 ≥ 70% Infection management –diagnosis, antibiotics and source control Haemodynamic support Blood transfusion intravenous fluids Vasopressors Other supportive therapies mechanical ventilation heparin or LMWH stress ulcer prophylaxis HD
- 23. Management CONTD. Antibiotics Initial treatment will usually use “broad-spectrum” antibiotics designed to work against a wide range of bacteria at once A more focused antibiotic may be used if the specific bacteria is identified. Antibiotic susceptibility pattern should be determined Bacterial resistance more common in the HIV-infected Antibiotic treatment guidelines – non-existent in most centres Multi-drug resistance is high Treating the source of the infection Kidney dialysis may be needed
- 24. Specific drugs DrugsTargeting Inflammatory Imbalance Cytokine Antagonists Pattern Recognition Receptors (PRR) Antagonist Pathogen-Associated Molecular Antagonists Drugs for Coagulopathy Recombinant Human Activated Protein (rhAPC) Recombinant Human Soluble Thrombosis Regulators Pentoxifylline Drugs Against Immune Function Inhibition Cytokines Co-Inhibiting Molecular Inhibitors
- 25. Complications AKI Tissue death –fingersor toes Permanent lung damage Permanent brain damage Immune system failure Damage to heart valves Death
- 26. Biomarkers of Sepsis Infection-Related Biomarkers Procalcitonin (PCT) C-Reactive Protein (CRP) Cytokines (TNF-α/IL-6) Biomarkers Related to Inflammation Activation and Immune Imbalance Monocyte Chemoattractant Protein-1 (MCP-1) Programmed Death Receptor-1 and Programmed Death Ligand-1 (PD-1/PD-L1) Soluble Triggering Receptor Expressed on Myeloid Cells-1 (sTREM-1) Complement Pathway Neutrophil Surface Receptor (CD64) MicroRNA (miRNA) Plasma Cell-Free DNA Presepsin (sCD14-ST) Biomarkers Related to Organ Dysfunction Angiopoietin (Ang) Matrix Metalloproteinases (MMPs)
- 27. CONCLUSION Sepsis stillremains a global problem It’s a complication of septicaemia It’s a life-threatening condition caused by a myriad of organisms Pathogenesis is not completely understood. Therefore, risk should be minimized qSOFA score can be used as a first line bedside tool to assess patients Emperic antibiotic therapy is the mainstay initially and hence knowledge of antimicrobial resistance and sensitivity patterns in the environment are paramount Patients require holistic therapy Sepsis specific drugs/Biomarkers are yet to be readily available
- 28. FURTHER READING JacobST, Moore CC, Banura P, Pinkerton R, Meya D, Opendi P, et al. Severe sepsis in two Ugandan Hospitals: a prospective observational study of management and outcomes in a predominantly HIV-1 infected population. PLoS One. 2009;4:1-11. Alebachew G, Brhanu T, Mengistu E, Yitayal S and Belay T. Etiologic agents of bacteria sepsis and their antibiotic susceptibility patterns among patients living with the Human immunodeficiency virus at Gondar university teaching hospital, Northwest Ethiopia. Biomedical Research Journal.2016;1-8. Adesida SA, Abioye OA, Bamiro BS, Amisu KO, Badaru SO, Coker AO. Staphylococcal bacteremia among human immunodeficiency virus positive patients at a screening centre in Lagos, Nigeria. Beni-Suef University Journal of Basic and applied Sciences. 2017;6(2):112-117. Oluyege AO, Ojo-Bola O and Olugbemi AA. Prevalence and antibiotics resistance pattern of blood culture isolates from human immunodeficiency virus (HIV) patients on highly active antiretroviral therapy (HAART) in Nigeria. Afr J Microbiol. 2015;9(13):910-914. Ogunsola FT, Arewa DG, Akinsete IE, Oduyebo OO, Akanmu AS, Odugbemi TO. Aetiology of bacteraemia among adult AIDS patients attending Lagos University Teaching Hospital (LUTH), Lagos, Nigeria. NigerPostgrad Med J 2009;16:186-92. Adeyemi IA, Akanmu AS, Bamiro BS, Obosi AC, and Inem AV. Bacterial blood stream infection in HIV- infected adult attending Lagos Teaching Hospital.Health PopulNutr. 2010;28(4):318- 326. Non-salmonella bacteremia among seropositive HIV patients attending three tertiary hospital in Nasarawa State, Nigeria. Journal of Natural Science Research. 2013;3(5):61-66.