Download Free Medical What is new in management of Surgical Infection PowerPoint Presentation

What is new in management of Surgical Infection PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "What is new in management of Surgical Infection" by Prof. Ravi Kant.

This medical PowerPoint presentation talks about advancements in the management of surgical infections in recent years.

Tags : Surgical Infection, Antibiotic Stewardship, Enhanced Recovery After Surgery (ERAS), Wound Management, Minimally Invasive Surgery, critical care medicine, critical care medicine PowerPoint presentation

Published on : Mar 31, 2023 | Views : 1377 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

What is new in management of Surgical Infection Prof. Ravi Kant
Slide 2-

Contents: Introduction Types of surgical infections Definition of SSI Types SSI Recent management of SSI sepsis Peritonitis
Slide 3-

Soft tissue/wound Infictions. Third most reported nosocomial infections 16% of all reported nosocomial infections Most common surgical patient nosocomial infection (38%)
Slide 4-

2/3 involved surgical incision 1/3 deep structures accessed by incision Deaths in patients with nosocomial infections—77% related to infection. Soft tissue/wound Infictions. EWMA Journal 2005; 5(2): 11-15.
Slide 5-

Introduction < 1900= 70-80% mortality for wound infection >1900: Ignaz Semmelweis and Joseph Lister = antiseptic surgery
Slide 6-

Introduction Surgery, trauma, non-trauma local invasion can lead to bacterial insult. Once present, bacteria, initiate the host defense processes. Inflammatory mediators (kinins, histamine, etc.) PMN’s arrive, etc.
Slide 7-

Introduction Surgical infections surgical wound itself or in other systems in the patient. They can be initiated not only by “damage” to the host but also by changes in the host’s physiologic state.
Slide 8-

Infections Two main types Community-Acquired Hospital-Acquired
Slide 9-

Community-Acquired Skin/soft tissue Cellulitis: Group A strep Abcess/furuncle: Staph aureus Necrotizing: Mixed Hiradenitis suppurativa:Staph aureus Lymphangitis: Staph aureus
Slide 10-

Cellulitis
Slide 11-

Furuncle
Slide 12-

Necrotizing
Slide 13-

Hiradenitis
Slide 14-

Lymphangitis
Slide 15-

Breast Abscess
Slide 16-

Peri-rectal abscess
Slide 17-

Gas Gangrene
Slide 18-

Paronychia
Slide 19-

Diabetic foot infection
Slide 20-

Biliary Tract Usually result from obstruction Usual suspects: E. coli, Klebsiella, Enterococci Acute Cholecystitis GB empyema Ascending cholangitis
Slide 21-

Community-Acquired Viral Hepatitis HIV/AIDS Tetanus
Slide 22-

Hospital-Acquired Post-operative At the surgical site Systemic.
Slide 23-

Infected Vascular Graft Inguinal incision is independent risk factor Length of case and blood loss Prosthetic grafts 10%-20% S. Aureus
Slide 24-

Gas gangrene Beta hemolytic strept Clostridial perfringes (gram pos rods) rare 50% polymicrobial Rapid lysis of tissues with relatively little response from host Endotoxin
Slide 25-

Gas gangrene Aggressive debridement & antibiotics Repeat antibiotics
Slide 26-

Catheter Sepsis 80% of cases, colonized catheters had been inserted by inexperienced and experienced residents Key is to identify before sepsis develops Stapylococcus epidermis, S. Aureus, yeast
Slide 27-

Burn Infections Necrotic tissue readily colonized High bacteria counts are NOT a reliable indication of an infected burn Histological examination to determine invasiveness TX: debridement and antibiotics
Slide 28-

Hospital-Acquired Pulmonary Pneumonia Non-ventilator associated Ventilator associated Aspiration
Slide 29-

Hospital-Acquired Urinary Tract Diagnosis Usual suspects Pseudomonas, Serratia, other
Slide 30-

Hospital-Acquired Foreign-body associated Sites Catheters Lines Prosthetics/grafts
Slide 31-

Hospital-Acquired Wound infection & SSI.
Slide 32-

Surgical wounds are healing by 1) Primary intention 2) Secondary intention 3) Delayed primary intention
Slide 33-

Incidence of SSIs →closure/delayed closure of an infected wound [Gottrup, F. Wound healing and principles of wound closure. In: Holström H, Drzewieck KT (Eds). The Scandinavian Handbook of Plastic Surgery. Malmoe: Studenterliteraturen, 2005
Slide 34-

Definition of SSI The CDC : =< 30 days of surgery (or within a year in the case of implants) Mangram . Guideline for prevention of surgical site infection, 1999. Infect Control Hosp Epidemiol 1999;
Slide 35-

classificationincisionalsurgical site infections Superficial Deep Organ/space
Slide 36-

superficial incisional surgical site infections < 30 days of procedure involve only the skin or subcutaneous tissue around the incision. Mangram . Guideline for prevention of surgical site infection, 1999. Infect Control Hosp Epidemiol 1999
Slide 37-

Deep incisional surgical site infections < 30 days of procedure (or one year in the case of implants) are related to the procedure involve deep soft tissues, such as the fascia and muscles. Mangram . Guideline for prevention of surgical site infection, 1999. Infect Control Hosp Epidemiol 1999
Slide 38-

ASEPSIS WOUND SCORING SYSTEM [ Wilson AP, Lancet 1986
Slide 39-

ppt slide no 39 content not found
Slide 40-

ppt slide no 40 content not found
Slide 41-

Southampton wound scoring system [Bailey IS, BMJ 1992; 304: 469-71
Slide 42-

ppt slide no 42 content not found
Slide 43-

Risk Factors Surgical factors Patient-specific factors local systemic
Slide 44-

Factors influencing SSIsPatient Risk Factors Local: High bacterial load Wound hematoma Necrotic tissue Foreign body Obesity Systemic: Advanced age Shock Diabetes Malnutrition Alcoholism Steroids Chemotherapy Immuno-compromise
Slide 45-

Factors influencing SSIs Antibiotics Prophylactic Therapeutic
Slide 46-

Factors influencing SSIs Surgical Risk Factors Type of procedure Degree of contamination Duration of operation Urgency of operation skin preparation operating room environment Antibiotic prophylaxis EWMA Journal 2005; 5(2): 11-15.
Slide 47-

Berard F, Gandon J, Ann Surg 1964
Slide 48-

Reduce hemoglobin A1c levels to <7% before operation Evidence Class II data References Anderson DJ, Kaye KS, Classen D, et al. Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Epidemiol 2008;
Slide 49-

Smoking cessation 30 d before operation Evidence Class II data References Anderson DJ, Kaye KS, Classen D, et al. Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Epidemiol 2008
Slide 50-

Remove hair only if it will interfere with the operation; hair removal by clipping immediately before the operation or with depilatories; no pre- or perioperative shaving of surgical Evidence Class I data References Kjønniksen I. Preoperative hair removal– a systematic literature review. AORN J 2002
Slide 51-

Use an antiseptic surgical scrub or alcohol-based hand antiseptic for preoperative cleansing of the operative team members’ hands and forearms Evidence Class II data References Anderson DJ. Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Epidemiol 2008;
Slide 52-

Prepare the skin around the operative site with an appropriate antiseptic agent, including preparations based on alcohol, chlorhexidine, or iodine/iodophors Evidence Class II data References Anderson . Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Epidemiol 2008;
Slide 53-

Administer prophylactic antibiotics for most clean-contaminated and contaminated procedures, and selected clean procedures use antibiotics appropriate for the potential pathogens Evidence Strong Class I data References Springer R. The Surgical care improvement project-focusing on infection control.Plast Surg Nurs 2007;
Slide 54-

Administer prophylactic antibiotics within1 h before incision (2 h for vancomycin and fluoroquinolones) Evidence Strong Class II data References Springer R. The Surgical care improvement project-focusing on infection control.Plast Surg Nurs 2007
Slide 55-

Use higher dosages of prophylactic antibioticsfor morbidly obese patients Evidence Limited Class II data References Springer R. The Surgical care improvement project-focusing on infection control.Plast Surg Nurs 2007
Slide 56-

Carefully handle tissue, eradicate dead space, and adhere to standard principles of asepsis Evidence Class III References Anderson DJ. Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Epidemiol 2008;
Slide 57-

Redose prophylactic antibiotics with short half-lives intraoperatively if operation is prolonged (for cefazolin if operation is >3 h) or if there is extensive blood loss Evidence Limited Class I, Class II data References Scher K. Studies on the duration of antibiotic administration for surgical prophylaxis Am Surg 1997
Slide 58-

Maintain intraoperative normothermiac Evidence Class I; some contradictory Class II data References Sessler DI, Akca O. Nonpharmacological prevention of surgical wound infections. Clin Infect Dis 2002
Slide 59-

Discontinue prophylactic antibiotics within 24 h after the procedure (48 h for cardiac surgery &liver transplant procedures) discontinue prophylactic antibiotics after skin closure Evidence Class I; meta-analyses support single dose regimens for prophylaxis References ASHP Therapeutic guidelines on antimicrobial prophylaxis in surgery. Am J Health Syst Pharm 1999
Slide 60-

Maintain serum glucose levels <200 mg/dL on PO Evidence Class II data References Anderson DJ. Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Epidemiol 2008
Slide 61-

Monitor wound for the development of SSI postoperative days 1 and 2d Evidence Class III data References Anderson DJ. Strategies to prevent surgical site infections in acute care hospitals. Infect Control Hosp Epidemiol 2008
Slide 62-

opening the wound I&D . For most patients who have had their wounds opened and adequately drained, antibiotic therapy is unnecessary. Treatment of SSI Stevens DL. Prguidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis 2005actice
Slide 63-

o use antibiotics only when there are significant systemic signs of infection (temperature higher than 38.5Cor heart rate greater than 100 beats/min) erythema extends more than 5 cm from the incision. Stevens DL. Prguidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis 2005actice Treatment of SSI
Slide 64-

Sepsis Sepsis: Commonly called a "blood stream infection.“ The presence of bacteria (bacteremia) or other infectious organisms or their toxins in the blood (septicemia) or in other tissue of the body.
Slide 65-

Sepsis Sepsis may be associated with clinical symptoms of systemic (bodywide) illness, such as fever, chills, malaise , low blood pressure, and mental status changes. Sepsis can be a serious situation, a life threatening disease calling for urgent and comprehensive care.
Slide 66-

Sepsis, Septic shock Signs of: Increased C.O. Altered O2 SATURATION. Metabolic acidosis (usually) Can lead to ---Death.
Slide 67-

Sepsis Sepsis remains a major clinical problem for 21st century marginal improvement in the mortality antibiotics are cornerstone 10% improvement in mortality Mac Arthur RD et al.Adequacy of early empiric antibiotic treatment in severe sepsis experience from MONARCS trial . Clin Infect Dis 2004;38(2):284-88
Slide 68-

Cytokines Release TNF , IL1 IL6,10 Protease ,PG PAF Endothelial injury Coagulopathy Tissue factor Fibrin clot Inhibit activity Protein C Antithrombin III Suppress fibrinolysis
Slide 69-

The aim Sepsis is condition diagnosed on the bases of clinical & laboratory parameters increased level of inflammatory mediators reflects global dysregulation of immune response Examine the latest evidence for the use of immuno-modulating drugs obtained from human clinical trials
Slide 70-

immune response is multi-faceted Aim : Eliminate invading object Maintain homeostasis Limit tissue damage
Slide 71-

Sepsis And host response More than adequate or Inadequate.
Slide 72-

Inadequate Host response Stimulation by Levamisole Pro inflammatory Cytokine interferon y Anti- prostaglandins (immunosuppressive mediators
Slide 73-

IL-10 IL- 10 administration improves survival following endotoxin challenge Live candida - block IL-10- improves survival
Slide 74-

More than adequate host response Anti-inflammatory cyotkines like Interleukin 10 Agents to neutralise tumor necrsois factor or interlekin -1
Slide 75-

Severity assessment PAC- initially Ultra low frequency ossillations in CO/global end diastolic vol -severity high Lactate levels –good severity predictor Low exogenous clearance – very early predictor of mortality C reactive protein – high risk of organ failure/ too slow to monitor
Slide 76-

Management of Sepsis Hemodynamic, respiratory stability Source control in sepsis Early enteral feed/intensive insulin therapy stress ulcer prophylaxis, and deep vein thrombosis Daily hemodalysis – better survival
Slide 77-

Early goal-directed therapy (EGDT) Oximetric central venous catheters were placed to measure central venous pressure (CVP) & CvO2 500-mL aliquots of isotonic crystalloid were given by bolus infusion to achieve a central venous pressure greater than 8 mm Hg. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;
Slide 78-

Early goal-directed therapy (EGDT) Mean arterial pressure was maintained at 65 mm Hg or higher with vasopressors. If the CvO2 saturation was still less than 70%, blood was transfused to a hematocritof 30. If the CvO2 saturation was still less than 70%, dobutamine was started. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;
Slide 79-

Early goal-directed therapy (EGDT) Mortality was significantly lower among patients randomized to EGDT (48.2% versus 33.3%, P 5 .01). Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;
Slide 80-

Sepsis it is complex process and the goal of immune therapy is identifying critical point of response to modulate it
Slide 81-

ppt slide no 81 content not found
Slide 82-

TNF TNF is an important mediator of sepsis Serum level correlate with outcome Immunotherapy : - Antibodies - Blocking receptor Calandra T et al.Prognostic values of tumor necrosis factor/cachectin,interlukin-1,interferon-alpha and interferon gamma in the serum of patients with septic shock. J Infec Dis 1990;161:982-87
Slide 83-

Blockade of tumor necrosis factor Improves outcome in E. coli septicemia. But increased mortality with cecal ligation and puncture.
Slide 84-

TNF antibody NEROCEPT : reduction of mortality 1st 3 days - dose dependant INTERSEPT : -reduce progression of sepsis - rapid resolution of shock
Slide 85-

TNF antireciptor: Recombinant receptor : - dose dependant increase in mortality - deleterious effect in human clinical trial Fisher CJ et al.Treatment of septic shock with the tumot necrosis factor receptor.Fc fusion protein .N Engl J Med 1996;334:1697-702
Slide 86-

Most widely known and used immunotherapy Blunt & potent anti-inflammatory Action : Prevent complement activation inhibit nitrous oxide synthatase Decrease proinflammatory cytokines inhibit neutrophil aggregation stabilise lysosomal membrane Steroids
Slide 87-

1960-90S No advantage 1997 increase mortality with high dose Beneficial for patient with adrenal insufficiency Currently “ 2nd generation trials” : - low & physiological dose - long duration - vasopressor dependant pt - no difference among corticotrophic dependant or non dependant Minneci PC et al Meta analysis:the effect of steroids on survival & shock during sepsis depend on the dose. Ann Intern Med 2004;141:47-57
Slide 88-

ppt slide no 88 content not found
Slide 89-

Inhibit thrombin and factor Xa low during sepsis d/t - impaired synthesis - consumption by DIC - degradation by elastase Abraham E et al.Efficacy and safety of tifacogen in severe sepsis: randomised controlled trial .JAMA 2003;290:238-47
Slide 90-

ppt slide no 90 content not found
Slide 91-

APC action Anticoagulant Anti-inflammatory inhibit transcription NF-kB reducing pro-inflammatory cytokines APC inactivate Va,VIIa Low level in sepsis cytokine-induced down-regulation of thrombomodulin Esmon CT. Inflammation & thrombosis : mutual regulation by protein C. Immunologist 1998;6:84-89
Slide 92-

ppt slide no 92 content not found
Slide 93-

48hrs /reduces mortalityiv 24 ug/ kg/hr x 96hrs Recombinant APC “ Dotrecogin alfa” : - Significant reduction of mortality - faster resolution cardiovascular & respiratory dysfunction PROWESS ( protein c worldwide evaluation in severe sepsis) multicentre study,2001 APC
Slide 94-

Vasopressor/ Inotropics The Surviving Sepsis guidelines recommended dopamine or norepinephrine as first line agents. Vasopressin should be considered an important adjunct vasopressor. Epinephrine may be considered as a second line agent. Matthew C. Byrnes, MDa,b,*, GregJ. Beilman, MDa
Slide 95-

INTENSIVE GLUCOSEMANAGEMENT Current international recommendations have been made to maintain blood glucose levels lower than150 mg/dL. Maintenance of blood glucose between 80 and 110 mg/dL may carry a significant risk of hypoglycemia.
Slide 96-

ppt slide no 96 content not found
Slide 97-

All of the mentioned immunotherapeutic strategies worked in animal models of sepsis but not always converted into patient Comorbidity Extreme ages organ dysfunction genetic polymorphism site of infection
Slide 98-

cautious multi-centre studies ! - differences resources - availability of intensive care bed
Slide 99-

ppt slide no 99 content not found
Slide 100-

Only APC has been shown to improve outcome in septic patient low steroid dose also worthy , should not restricted to corticotrophin hypo-responsive patient Sprung CL et al.Influence of alterations in foregoing life sustaining treatment practices on a clinical sepsis trial.Critical Care Medicine 1997;25:383-7
Slide 101-

most effective management of septic patient remains recognition support of organ dysfunction antibiotics remain the cornerstone of management
Slide 102-

Administration of AT III is not recommended in sepsis : no significance difference in mortality increase risk of bleeding KyberSept trial “ randomised controlled clinical trial “
Slide 103-

Peritonitis
Slide 104-

Classification Primary peritonitis Secondary peritonitis Tertiary peritonitis
Slide 105-

Secondary peritonitis is the most common form for surgeons
Slide 106-

Intra-abdominal sepsis... Diversion Nutrition Fluid & Electrolytes ABG Antibiotics
Slide 107-

Diversion Small Bowel : ileostomy Large bowel : colostomy More important than antibiotics
Slide 108-

Nutrition Enteral or parenteral (TPN)
Slide 109-

Any Question?
Slide 110-

References Awad, S., Palacio, C., Subramanian, A., Byers, P., Abraham, P., Lewis, D., & Young, E. (2009). Implementation of a methicillin-resistant staphylococcus aureus (MRSA) prevention bundle results in decreased MRSA surgical site infections. The American Journal of Surgery, 198(5), 607-610. doi:10.1016/j.amjsurg.2009.07.010 Bratzler, D. (2006). The surgical infection prevention and surgical care improvement project: Promises and pitfalls. The American Surgeon. 72(11). 1010-1016. Retrieved from http://www.highbeam.com/The+American+Surgeon/publications.aspx Centers for Disease Control and Prevention. (2008). Surgical site infections, frequently asked questions. Retrieved from: http://www.cdc.gov/ncidod/dhqp/FAQ_SSI.html Centers for Medicare & Medicaid Services. (2008). Medicare and Medicaid move aggressively to encourage greater patient safety in hospitals and reduce never events. Retrieved from http://www.cms.hhs.gov/apps/media/press/release.asp?Counter=3219&intNumPerPage=10&checkDate=&checkKey=&srchType=1&numDays=3500&srchOpt=0&srchData=&keywordType=All&chkNewsType=1%2C+2%2C+3%2C+4%2C+5&intPage=&showAll=&pYear=&year=&desc=&cboOrder=date
Slide 111-

References Chundamala, J., & Wright, J. (2007). The efficacy and risks of using povidone-iodine irrigation to prevent surgical site infection: An evidence-based review. Canadian Journal of Surgery. 50, 473-481. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/journals/505 Institute for Healthcare Improvement. (IHI). Surgical Site Infections. Retrieved from http://www.ihi.org/ihi/Topics/PatientSafety/SurgicalSiteInfections/SurgicalSiteInfectionsCaseForImprovement Joint Commission on Accreditation of Healthcare Organizations (JCAHO). 2004. Hospital National Patient Safety Goals. Retrieved from http://www.jointcommission.org/PatientSafety/NationalPatientSafetyGoals/04_npsgs.htm Kable, A., Gibberd, R., & Spigelman, A. (2004). Complications after discharge for surgical patients. ANZ Journal of Surgery, 74, 92-97. doi:10.1046/j.1445-2197.2003.02922.x. Mangram, A. J., Horan, T. C., Pearson, M. L., Silver, L. C., Jarvis, W. R., & The Hospital Infection Control Practices Advisory Committee. (1999). Guideline for prevention of surgical site infection. Infection Control and Hospital Epidemiology, 20, 247-278. Retrieved from http://www.cdc.gov/ncidod/dhqp/pdf/guidelines/SSI.pdf
Slide 112-

References Peden, A. & Vaughan, J. (2006). American Journal of Infection Control. Hand Hygiene, 34(5), E60. Retrieved from http://www.ajicjournal.org/handhygiene Odom-Forren, J. (2006). Preventing surgical site infections. Nursing Management, 36, 58-64. Retrieved from http://journals.lww.com/nursingmanagement/Pages/issuelist.aspx Ramos, A., Asenslo, A., Munez, E., Torre-Cisneros, J., Montejo, M., Aguado, J.,… Cisneros, J. (2008). Incisional surgical site infection in kidney transplantation. Reconstructive Urology, 72, 119-123. doi:10.1016/j.urology.2007.11.030 Wynne, R., Botti, M., Stedman, H., Holsworth, L., Harinos, M., Flavell, O., & Manterfield, C. (2004, January). Effect of three wound dressings on infection, healing comfort, and cost in patients with sternotomy wounds. Chest Journal, 125, 43-49. Retrieved from http://intl.chestjournal.org