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INFECTION AND SEPSIS Surrounded by pathogens Infection is the exception Protective from infection Physical barriers Chemical barriers Immunological function Physical and Chemical Barriers to Infection Skin stronger in hands and feet sebaceous secretions lower pH Mucous membranes ciliary function mucous barrier acid mileu in stomach Barriers breached in Surgery Barriers Breached in Trauma Immune Defense Humoral defense antibodies complement Cellular defense Cytokines potential for deleterious effects Interaction of mechanisms Breakdown of Host Defense Physical, chemical and immunological breakdown -act synergistically e.g. patient with diabetes immunosuppresion surgery Potential for deleterious effects Fourniers Gangrene Commensal Microbial Flora Important for immune development Occupy binding sites for pathogens Provide mucobacterial barrier Anerobic bacteria present in greatest quantity in GIT Greatest diversity Prevent invasion by gram neg. aerobes Breakdown of Host Defense - GIT Flora Transmigration of bacteria Lack of feeding Overuse of antibiotics Absence of bile Protein malnutrition Immune deficiency ICU patient fed enteraly To preserve GIT integrity Infection Manifestation Local signs Systemic signs Fever, somnolence, confusion, ileus, hypotension Lab tests pain,redness,swelling, warmth loss of function TW,polymorphs, Cultures Non infective- causes may manifest as infection Common Infections Wound infection Initial inoculum overwhelms host defense Occurs at 5 - 7 days post op Factors host - immune suppression, DM, renal failure surgeon - technique environment - contamination Common Infections Types of Wounds 1. Clean - no viscus, no sterile breach 2. Clean contaminated - controlled entry into viscus 3. Contaminated - emergency bowel resection, perforated appendix 4. Dirty - heavy contamination / long duration Antibiotics used type 2 as prophylaxis type 3,4 as treatment Wound Closure Wounds Closure by primary intention secondary intention Timing of closure delayed primary closure secondary closure Closure by Secondary Intention Intraabdominal Infection Defense Bacterial clearance - stomata between mesothelial cells under diaphragm lead to lymph vessels Phagocytosis - both resident and recruited phagocytes Sequestration - by fibrin rich inflammatory exudate, with omentum/viscera Intraabdomianal Infection Signs of peritonitis Pain Posture sharp in character, well localised at first spreads to surrounding areas involuntary guarding, rigidity absent bowel sounds lying still, rapid breathing ,no movement General condition ill, septic, dehydrated, hypotension Intraabdominal Infection Usually viscus perforation Isolates colon worse than upper GIT aerobic - E. Coli, klebsiella other enterobacter, strep, enterococci, proteus, pseudomonas anaerobic - bacteroides, Clostridium Treatment is surgical and aggressive antibiotic treatment Enterocutaneous Fistula Common Post Surgical Infections Pneumonia Protein malnourished upper abdominal wounds ® poor cough bed bound - atelectasis elderly ventilator Occurs from 3 days post op careful clinical exam,CXR Routine chest physiotherapy Common Post Surgical Infections Urinary Tract Infection catheters dehydration Remove catheters early Ensure hydration Antimicrobial therapy Common Post Surgical Infections Catheter and prosthetic devices I/v canulas central lines mesh Skin organisms- S aureus, S epidermidis Aseptic technique Remove if infected Less Common Post Surgical Infections Necrotising soft tissue infection Parotitis Sinusitis Tonsillitis Treatment of Infection General principles incise and drain pus antibiotics as needed debride dead tissue remove foreign bodies Antibiotic Therapy Prophylaxis Short course to prevent infection Must be on board before contamination Antibiotics with activity against expected inoculation organisms Avoid extended spectrum agents Post op benefit not proven Topical antibiotics - not proven Antibiotic Therapy Empirical therapy based on clinical information search for source must continue limit duration of empirical therapy use known institution pattern of infection multi agent vs broad agent Antibiotic Therapy Directed therapy target identified pathogens choose suitable efficacy /minimal toxicity agent cover aerobic and anaerobic if likelihood exist for both extended spectrum as last resort Multiple System Organ Failure AKA - Gram neg. bacterial sepsis 30% mortality Healthy and compromised host 3-13 cases per 1000 admissions Nosocomial Multiple System Organ Failure Factors Host compromise Elderly, disability Malnutrition Antimicrobial therapy Major surgery Cavity manipulation Immunosuppression e.g. steroids MSOF Fever Acidosis, hypoxemia Disordered oxygen and substrate use Hyperglycaemia Decreased systemic vascular resistance Elevated cardiac output Hypotension MSOF Evidence for LPS - endotoxin LPS O antigen - specific for each organism core LPS membrane lipid A LPS - EFFECTS non specific polyclonal b cell proliferation macrophage activation, cytokine release hypotension, hypoxemia bacterial translocation complement and coagulation activation platelet and white cell margination LPS - Mechanism Direct effect of bacteria Indirect (mediated) effect trigger macrophages to release TNFa, IL-1, IL-6, aIFN TNFa, IL-1, - primary mediators but may be deleterious in large amounts aIFN- causes continued activation of macrophages Permeability defects in microcirculation ARDS, GUT, Hepatic, renal failure Problem A 23 year old man had a perforated appendix. Three days post op this was his temperature chart. What is your interpretation. Problem What is your choice for antibiotic prophylaxis for colorectal surgery biliary surgery upper GI surgery Problem A 75 year old diabetic had an operation for perforated diverticular disease. His wound was found to be infected on the 5th POD. What factors may have contributed to this?