Professional Documents
Culture Documents
Objectives
15 minutes for definition and clinical aspect of sepsis
Patophysiology of sepsis Intervention in septic patients SSC
Septic Shock
Hypotension (despite fluid resuscitation) plus hypoperfusion
SIRS / Sepsis
Bacteremia (septicemia)
Other
SIRS
Infection Fungal
Parasit. Vir. Other
Trauma
Sepsis
Burns Pancreatitis
Rapid activation of the innate immune response and release of a variety of humoral mediator
Human Immune Response to Sepsis caused by Injury/ Infection is orchestrated by complex interactions of soluble mediator and cellular elements
tissue injury
2. Release of Signaling Molecules
recognition
receptor
Phagocytosis
Signal transduction
Adherens
Uncontrolled activation of this protein cascades and release of inflammatory mediators result in systemic inflammation
COAGULATION CASCADE
Factor VIIIa PAI-1
Tissue Factor
Organisms
Monocyte
Factor Va
THROMBIN
TAFI
Suppressed fibrinolysis
Fibrin Fibrin clot
Neutrophil
IL-6
Tissue Factor
Inflammatory Response
Thrombotic Response
Fibrinolytic Response
cytokines
Formation of fibrin
procoagulant
Anti-coagulant tendency
Primary circulating cells that participate in septic response : mononuclear phagocyte & neutrophils
Support the role of T cell, B cell, and Natural Killer ( NK) cells Produced : Pro inflammatory mediators Anti inflammatory mediators Growth factors
Initial insult
Systemic reaction
SIRS CARS
Systemic spill over of anti inflammatory mediator Suppression of immune system CARS predominate Apoptosis death with minimal inflammation
Coagulation
Repair
Apoptosis of inflammatory cell Regeneration of parenchyma cell Angiogenesis Proliferation of epithelia and fibroblasts
Increased cortisol production Activation of sympathetic nervous system Reduction of active thyroid hormone
B. Transmitters
( Blood and lymphatics, peripheral nerves, CNS)
C. Effector site
Sympathetic nerv syst
Adrenal medula Epinephrn norepinephr
Hypothalamus
Kidney
Pancr islets
Renin, angiotens
Glukagon Aldostrn Insulin
ADH
Cortison, aldostr, G.H
Approach to Management
Sepsis
Severe Sepsis
Septic Shock
62%
28%
amputation
Severe Sepsis
Septic Shock
Chest 1992;101:1644.
Severe Sepsis
Septic Shock
Xigris (Drotrecogin)
Early Goal Directed Therapy
Severe Sepsis
Septic Shock
Steroids Drotrecogin
Early Goal Directed Therapy
Initial resuscitation and Infections Issues Indicates a strong recommendation we recommend Indicates a weak recommendation we suggest Initial resuscitation (first 6 hrs)
Initial Resuscitation
Begin resuscitation immediately in patients with hypotension or elevated serum lactate 4 mmol/L; do not delay pending ICU admission (1C) Resuscitation goals (1C)
CVP 812 mm Hg MAP 65 mm Hg Urine output 0.5 1 mL/kg/hr
Central venous (superior vena cava) oxygen saturation 70% or mixed venous 65% If venous oxygen saturation target is not achieved (2C)
Consider further fluid Transfuse packed red blood cells if required to hematocrit of 30% and/or Start dobutamine infusion, maximum 20g/kg/min
Diagnosis
Obtain appropriate cultures before starting antibiotics provided this does not significantly delay antimicrobial administration (1C)
Obtain two or more BCs One or more BCs should be percutaneous One BC from each vascular access device in place > 48 hrs Culture other sites as clinically indicated
Perform imaging studies promptly to confirm and sample any source of infection, if safe to do so (1C)
Antibiotic therapy
Begin intravenous antibiotics as early as possible and always within the first hour of recognizing severe sepsis (1D) and septic shock (1B) Broad-spectrum: one or more agents active against likely bacterial/fungal pathogens and with good penetration into presumed source (1B) Reassess antimicrobial regimen daily to optimize efficacy, prevent resistance, avoid toxicity, and minimize costs (1C) Consider combination therapy in Pseudomonas infections (2D)
Consider combination empiric therapy in neutropenic patients (2D) Combination therapy 35 days and de-escalation following susceptibilities (2D)
Duration of therapy typically limited to 710 days; longer if response is slow or there are undrainable foci of infection or immunologic deficiencies (1D) Stop antimicrobial therapy if cause is found to be noninfectious (1D)
Fluid Therapy
Fluid-resuscitation using crystalloids or colloids (1B) Target a CVP of 8 mm Hg (12 mm Hg if mechanically ventilated) (1C) Use a fluid challenge technique while associated with a hemodynamic improvement (1D) Give fluid challenges of 1000 mL of crystalloids or 300500 mL of colloids over 30 mins More rapid and larger volumes may be required in sepsisinduced tissue hypoperfusion (1D) Rate of fluid administration should be reduced if cardiac filling pressures increase without concurrent hemodynamic improvement (1D)
Vasopressor
Maintain MAP 65 mm Hg (1C) Norepinephrine and dopamine centrally administered are the initial vasopressors of choice (1C) Epinephrine, phenylephrine, or vasopressin should not be administered as the initial vasopressor in septic shock (2C) Vasopressin 0.03 units/min may be subsequently added to norepinephrine with anticipation of an effect equivalent to norepinephrine alone Use epinephrine as the first alternative agent in septic shock when blood pressure is poorly responsive to norepinephrine or dopamine (2B) Do not use low-dose dopamine for renal protection (1A) In patients requiring vasopressors, insert an arterial catheter as soon as practical (1D)
Inotropic
Use dobutamine in patients with myocardial dysfunction as supported by elevated cardiac filling pressures and low cardiac output (1C) Do not increase cardiac index to predetermined supranormal levels (1B)
Steroid
Consider intravenous hydrocortisone for adult septic shock when hypotension responds poorly to adequate fluid resuscitation and vasopressors (2C) ACTH stimulation test is not recommended to identify the subset of adults with septic shock who should receive hydrocortisone (2B) Hydrocortisone is preferred to dexamethasone (2B) Fludrocortisone (50 g orally once a day) may be included if an alternative to hydrocortisone is being used that lacks significant mineralocorticoid activity. Fludrocortisone if optional if hydrocortisone is used (2C) Steroid therapy may be weaned once vasopressors are no longer required (2D) Hydrocortisone dose should be 300 mg/day (1A) Do not use corticosteroids to treat sepsis in the absence of shock unless the patients endocrine or corticosteroid history warrants it (1D)
Consider rhAPC in adult patients with sepsisinduced organ dysfunction with clinical assessment of high risk of death (typically APACHE II 25 or multiple organ failure) if there are no contraindications (2B, 2C for postoperative patients). Adult patients with severe sepsis and low risk of death (typically, APACHE II 20 or one organ failure) should not receive rhAPC (1A)
OTHERS
Blood product administration Mechanical ventilation of sepsis-induced ALI/ARDS Sedation, analgesia, and neuromuscular blockade in sepsis Glucose control Renal replacement Bicarbonate therapy Deep vein thrombosis prophylaxis Stress ulcer prophylaxis Consideration for limitation of support
Source Control
Historical Perspective
Alfred Blalock (early 20th century) shock intravascular volume deficit Fleming (1920s) penicillin Surgical management of infection
Trephination 10,000yr old skull Egyptians, Babylonians, Greeks, Romans Ambroise Pare (15th century) drainage of abcess Appendiceal abcess incision & drainage (1530) First appendectomy by Groves 1883 Canada
unlikely randomized controlled trial intervention vs nonintervention is undertaken Source control should be individualized based on:
Diagnostic uncertainty Physiologic stability Premorbid health status Previous surgical interventions Surgeons experience & skill Available surgical facilities
Definitions of terms
Term Source control Definition All physical measures undertaken to eliminate a source of infection, control ongoing contamination, and restore premorbid anatomy and function
Sinus
Fistula Abcess
Drainage Debridement
Drainage
Converting a contained collection to a controlled fistula (to exterior) or sinus Drain must permit free flow of the abscess Minimum risk and physiologic derangement: percutaneous drainage Modern imaging: all collections can be visualized preoperatively In unstable and ill patient surgery for controlled sinus/fistula & removal of dead tissue only
Debridement
The process of removing nonviable tissue Directed against solid components that promote bacterial growth Demarcation between viable and nonviable tissue maybe not absolute at early stage Gentle debridement use wet to dry saline dressing
Debridement
Remove all necrotic tissue but minimize the resulting defects for easier reconstruction Bleeding from viable tissue is better than fail to debride necrotic material
Debridement
Necrotic bowel
Excision for necrotic bowel is more complex The benefits of resection must be weighed against the consequences of loss of bowel length The dilemma is usually best resolved by a planned second-look laparotomy
Debridement
Foreign body
Risks are minimal when urinary or vascular catheter is infected Risks are high when aortic graft or heart valve is infected
Definitive management
The ultimate aim of therapy:
to restore function with the least risk To correct the abnormality that created the infection
Biologic Rationale
Host defenses are occasionally incapable of combating the introduction of microbes and establishment of infection
When large number of microbes are present When host defenses are diminished Ongoing source of microbial contamination
Drainage
Percutaneous abscess drainage (PD) is preferred Indication of operative intervention
When PD has failed When absolute contraindications to PD
Device Removal
Make sure the diagnosis of infection is secure Determine whether device removal would pose a significant risk Assess complicating factors (virulence, immunosuppression) and the history (previous therapy failed) When in doubt, take it out
Definitive vs Temporizing
The judgement to select a temporizing vs definitive requires an integrated assessment of
The surgeons knowledge about the underlying disease Systemic host factors Severity of the local inflammatory response
Diffuse Peritonitis
Aggressive initial surgical source control : intraoperative lavage If source control not possible
Continuous lavage Laparostomy Planned reexploration Or combination of above
Timing of Intervention
As general principle: as soon as possible Rapid, minimally invasive, temporizing or palliative measures may be superior to definitive but lengthy, more traumatizing procedures
Conclusion
The key to success when treating surgical infections is timely intervention to stop the delivery of bacteria and adjuvants of inflamation/infection into the peritoneal cavity All others are useless if source control failed
Thank you