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Objectives

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Objectives

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    1. Objectives Understand the current nomenclature Know the local organisms Understand the spectrum of presenting illness Get a handle on the basic treatment Introduce novel treatments

    2. The Increasing Importance of the Intensive Care Unit

    3. Distribution of major sites of infection in medical ICU’s

    4. Nosocomial troika …….. S.aureus E.coli Pseudomonas aeruginosa

    5. Eight most common pathogens associated with nosocomial infection in an ICU, NNIS January 1989 - July 1998

    6. High Risk Patients For Sepsis Post op / post procedure / post trauma Post splenectomy (encapsulated organisms) Cancer Transplant / immune supressed Alcoholic / Malnourished For Dying Genetic predisposition (e.g. meningococcus) Delayed appropriate antibiotics Yeasts and Enterococcus Site For Both Cultural or religious impediment to treatment

    9. Definitions Sepsis = SIRS + Infection SIRS = 2/4 of Temp >38 or <36 HR >90 Respiratory Rate >20 or PaCO2 <32 (4.3kPa) WCC >12 or <4 or >10% bands Infection = either Bacteraemia (or viraemia/fungaemia/protozoan) Septic focus (abscess / cavity / tissue mass)

    10. Definitions Cont. Severe sepsis = Sepsis + Organ Dysfunction Organ Dysfunction = Any of SBP <90 or 40 <usual or inotrope to get MAP 90 BE <-5mmol/L Lactate >2mmol/L Oliguria <30ml/hr for 1 hour Creatinine >0.16mmol/L Toxic confusional state FIO2 >0.4 and PEEP >5 for oxygenation

    11. Definitions Cont. Septic Shock = Severe sepsis + Hypotension Hypotension = either SBP <90 or 40<usual Inotrope to get MAP >90

    13. Mortality Increases in Septic Shock Patients

    14. Dear SIRS I don’t like you...

    15. Definitions Cont.

    16. Differential Diagnosis Pancreatitis Ischeamic Gut Hypovolaemic shock GI bleed / AAA rupture / ectopic / dehydration Cardiogenic shock AMI / Myocarditis / Tamponade PE Toxic Shock Syndromes Staph Aureus Group A Strep Addisonian crisis (note relative adrenocorticoid insufficiency in many septic patients) Thyroid Storm Toxidromes Anticholinergic / serotoninergic

    17. Investigations Basic WBC Platelets Coags Renal function Glucose Albumin LFT ABG Specific ?Source Urine CxR Blood Cultures x 2 LP Aspirate Biopsy

    18. Clinical progression and laboratory results Patient’s fever persists to hospital Day 7 and he develops new pulmonary infiltrates Blood pressure remains stable Peripheral WBC count increases to 18.2 x 109/L (18 200/ľL) with 50% mature polymorphonuclear leukocytes and 30% bands

    20. Key learning points It is important to select appropriate antibiotics Administer antibiotics at the right dose for the appropriate duration Cultures should be obtained to confirm the microbiological diagnosis — nosocomial pathogens not previously encountered may cause infections

    21. THE EARLIEST , THE BETTER

    25. MOST COMMON SIGNS OF SEPSIS Fever (sometimes hypothermia), chills Increased serum concentration of C reactive protein (CRP) and procalcitonin (PCT), altered white blood cell count, increased interleukin 6 (IL-6), IL-8…… Increased heart rate, increased cardiac output, low systemic vascular resistance, increased oxygen consumption, low oxygen extraction ratio (OER) Tachypnea, low PaO2/FiO2 Altered skin perfusion, reduced urine output alterations in coagulation parameters, increases D-dimers, low protein C , low antithrombin, increased prothrombin time/activated partial thromboplastin time Increased insulin requirements unexplained alterations in mental status Increased urea and creatinine, low platelet count or other coagulation abnormalities, hyperbilirubinemia Vincent JL: “Sepsis definitions” Lancet Infect Dis 2002, 2:135

    26. Cytokines Kinetics

    28. Treatment Specific Antibiotics Empiric based on source Know local pathogens Use the RMO guidelines / pharmacy handbook for best guess treatment Ideal to get cultures 1st but do not delay antibiotics Surgery Get the pus out! All of it! Early definitive care will improve survival

    29. Treatment Supportive Oxygenate / Ventilate (6ml/kg) Volume Will need more than ‘maintenance’ + replace losses with like fluid Colloid v Chrystalloid (SAFE trial awaited – know the results!) Inotropes Noradrenalin is inotrope of choice, dopamine next Early ICU referral

    30. Treatment Supportive Electrolyte homeostasis THAM for pH <7.2 1-2mL / kg over 20min Address co-morbidities ß-Blocker & reduced inotropy DM / COAD Alcoholism / malnutrition / steroids Stop nephrotoxins (NSAIDs) Early ICU referral

    31. ANTIBIOTICS IN SEPSIS 1

    33. TREATMENT OPTIONS FOR INFECTIONS DUE TO EXTENDED –SPECTRUM ß-LACTAMASE (ESBL) PRODUCING ORGANISMS

    34. Possible empiric antibiotic choice in severe sepsis

    35. CONCENTRATION DEPENDENT vs INDEPENDENT BEHAVIOR OF ANTIBIOTICS CONCENTRATION DEPENDENT (TIME INDEPENDENT) The rate and extent of bacterial kill and the PAE all increase as the antibiotic concentration increase A) aminoglycosides B) fluoroquinolones C) metronidazole CONCENTRATION INDEPENDENT (TIME DEPENDENT) Once a threshold concentration of these antibiotics is achieved , further increases in antibiotic concentration do not result in an appreciably increased rate or extent of bacterial kill or an extension of the PAE A) ß-lactam antibiotics B) vancomycin C) Monobactam (aztreonam) ? D) Carbapenem (imipenem) ?

    37. Biofilm , Antimicrobial Resistance and Infections Stimulation of Staphylococcus epidermidis growth and biofilm formation by catecholamine inotropes The ability of catecholamine inotropic drugs to stimulate bacterial proliferation and biofilm formation may be an aetiological factor in the development of intravascular catheter colonisation and catheter related infection. The removal of iron from trasferrin for subsequent use by S. epidermidis is a possible mechanism by which catecholamine inotropes stimulate bacterial growth as biofilms Lancet 2003; 361:130-135 Singh PK, Parsek MR, Greenberg EP, Welsh MJ A component of innate immunity prevents bacterial biofilm development . Nature 2002; 417:552-5 Drenkard E, Ausubel FM Psedomonas biofilm formation and antibiotic resistance are linked to phenotypic variation. Nature 2002; 416:740-3

    38. La terapia antibiotica empirica deve essere appropriata, altrimenti la mortalitŕ aumenta. L’esame dei fattori di rischio, l’epidemiologia, il controllo delle coltivazioni di sorveglianza e delle colonizzazioni č importantissimo, assieme alla diagnosi clinica dell’infezione probabile. E’ necessario sottolineare che l’appropriatezza non č solo determinata dall’aver “indovinato” gli antibiotici, ma anche dalla precocitŕ della somministrazione, dal dosaggio adeguato e battericidaLa terapia antibiotica empirica deve essere appropriata, altrimenti la mortalitŕ aumenta. L’esame dei fattori di rischio, l’epidemiologia, il controllo delle coltivazioni di sorveglianza e delle colonizzazioni č importantissimo, assieme alla diagnosi clinica dell’infezione probabile. E’ necessario sottolineare che l’appropriatezza non č solo determinata dall’aver “indovinato” gli antibiotici, ma anche dalla precocitŕ della somministrazione, dal dosaggio adeguato e battericida

    43. TO PRESERVE VITAL ORGAN PERFUSION AND TO MAINTAIN TISSUE OXYGENATION SUPPORTIVE THERAPY - Haemodynamic support Early goal directed therapy - Respiratory support Protective ventilation strategy MANAGEMENT OF COAGULOPATHY

    46. THE KIDNEY IN SEPSIS Renal failure developing in the ICU carries a poor prognosis while combined renal and respiratory failure carries a considerably worse prognosis than respiratory failure alone In the absence of disease modifying therapies, it is impossible to measure the impact on mortality for preventing acute renal failure Renal salvage with furosemide, while having some theoretical benefits on reducing tubular cell energy consumption and flushing of debris out of tubules and ducts, has never been shown convincingly to improve either renal function or survival Similarly , the use of dopamine to increase renal flow is probably not advantageous and may be detrimental De Mendoca A,Vincent JL,Suter PM et al (2000) Acute renal failure in the ICU:risk factors and outcome evaluated by the SOFA score. Intensive Care Med 26:915-921 Sweet SJ, Glenney CU, Fitzgibbons JP, Friedman P, Teres D (1981) Synergistic effect of acute renal failure and respiratory failure in the surgical intensive care unit. Am J Surg 141:492-496 Brezis M, Agmon Y, Epstein FH (1994) Determinants of intrarenal oxygenation. I. Effects of diuretics. Am J Physiol 267: F1059-F1062 Bellomo R, Chapman M, Finfer S, Hicking K, Myburgh J (2000) Low dose dopamine in pazienta with early renal dysfunction: a placebo controlled randomized trial. Australian and New Zealand Intensive Care Society (ANZIC) Clinical Trial Group. Lancet 356:2139-2143 Galley HF (2000) Renal dose dopamine: will the message now get through? Lancet 356:2112-2113

    49. Questi possono essere i potenziali effetti dei corticosteroidi durante lo shock settico. E’ perň importante dire che il corticosteriode deve essere usato a dosi ridotte, cosidette stress doses , ovvero dosi che non superino i 300 mg al giorno in perfusione continua. Ancora piů serio sarebbe misurare la cortisolemia di base, senza effettuare un ritmo circadiano, e poi somministrare ACTH e poi ripetere la cortisolemia per vewdere se esiste una insufficienza relativa della surrenale. Il cortisone dovrebbe essere somministrato in caso di insufficienza relativa surrenalica, e dovrebbe essere valutato anche l’outcome surrogato della progressiva diminuzione del supporto con vasopressore.Questi possono essere i potenziali effetti dei corticosteroidi durante lo shock settico. E’ perň importante dire che il corticosteriode deve essere usato a dosi ridotte, cosidette stress doses , ovvero dosi che non superino i 300 mg al giorno in perfusione continua. Ancora piů serio sarebbe misurare la cortisolemia di base, senza effettuare un ritmo circadiano, e poi somministrare ACTH e poi ripetere la cortisolemia per vewdere se esiste una insufficienza relativa della surrenale. Il cortisone dovrebbe essere somministrato in caso di insufficienza relativa surrenalica, e dovrebbe essere valutato anche l’outcome surrogato della progressiva diminuzione del supporto con vasopressore.

    52. OTHER SUPPORTIVE THERAPY IN SEPSIS 1 Deep Vein Thrombosis (DVT) in septic patients and the high percentage of sepsis /infected patients included in studies that have demonstrated efficacy of DVT prophylaxis in general, septic patients should be treated with DVT prophylaxis. Even though there is not a randomized study that establishes the impact of DVT prophylaxis on morbidity and mortality specifically in septic patients, the significant number of septic patients included in the populations of patients enrolled in other prospective randomized trials supports that the use of DVT prophylaxis reduces morbidity and mortality in septic patients.

    55. Conceptual models of multiple organ dysfunction syndrome

    56. Novel Therapies Summary Reducing mortality in sepsis: new directions This is highly recommended reading, concise reviews of Low tidal volume ventilation Early goal directed therapy Drotrecogin alfa (activated) Moderate dose corticosteroids Tight control of blood sugar

    57. Novel Therapies NAC Crit. Care. Med. 2003 31 (11) 2574-78 Nuclear factor-?B controls expression inflammatory mediators NAC inhibits NFKB in vitro Pilot trial 20 patients, randomised 72 hrs NAC or placebo IL-8 suppressed (may be implicated in lung injury) Recommend larger human trials

    58. Summary Sepsis may be obvious or subtle early There is a high mortality and morbidity Have a high index of suspicion Know local organisms / susceptibilities Take appropriate cultures Treat early and aggressively Investigate early and aggressively Refer early and aggressively Be aware of new developments

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