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SIRS and the Septic Response. Manoj Sayal, MD FRCSC March 5, 2008. Agenda. A brief review of SIRS (systemic inflammatory response syndrome) SIRS and it’s role in sepsis Definitions of the sepsis syndrome Current sepsis guidelines. Case 1.

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SIRS and the Septic Response

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SIRS and the Septic Response

Manoj Sayal, MD FRCSC

March 5, 2008

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  • A brief review of SIRS (systemic inflammatory response syndrome)

  • SIRS and it’s role in sepsis

  • Definitions of the sepsis syndrome

  • Current sepsis guidelines

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Case 1

  • 67yo male, presents to ER with 2 day history of N+V, abdo pain

  • In ER, looks unwell: HR 130, BP 80/60 RR 36 SPO2 84% on room air; supplemental O2 applied, sats increase to 92%

  • Diffusely tender abdomen, coarse air entry bilaterally

  • What now?

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Case 1

  • 2 large bore IV’s—normal saline 1 litre

  • Labs drawn

  • CXR (portable), EKG, ABGs

  • Diagnosis?

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Case 1

  • CXR: RLL infiltrate

  • WBC 22.4 Hb 108 Pl 98

  • Lytes normal; transaminases normal

  • Amylase 700

  • What now?

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Case 2

  • Same patient, but normal amylase

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Case 3

  • Same patient but involved in a major house fire, normal amylase

  • What’s wrong with each of these patients?

  • Does their management differ significantly (initially)?

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  • They are all manifesting evidence of the SIRS response

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SIRS for Dummies (or Surgeons)

  • Dysregulation of the normal response with massive and uncontrolled release of proinflammatory mediators creating a chain of events that leads to widespread tissue injury

  • Results in MODS (Multiple Organ Dysfunction Syndrome) that causes the extremely high morbidity and mortality in this situation

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  • SIRS is a clinical diagnosis, recognized by 2 or more of the following (in the appropriate setting):

    • Temp >38ºC or <35ºC

    • HR>90bpm

    • RR>20bpm or PaCO2<32mmHg

    • WBC>12, <4 or >10% immature (band) forms

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  • Causes

    • Acute pancreatitis, autoimmune disorders, vasculitis, thromboembolism, burns, surgery, pulmonary contusion, SEPSIS)

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  • How does this relate to infection or the response to infection?

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  • an inflammatory response to microorganisms or the invasion of normally sterile host tissue by these organisms


  • viable bacteria in the blood

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  • In sepsis, clinical signs of SIRS are present and are due to either a culture proven infection or a suspected infection

  • Clinical syndrome that complicates severe infection and represents the systemic response to the infection

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Severe Sepsis

  • Sepsis plus at least one of the following:

    • Areas of mottled skin

    • Capillary refill > 3 seconds

    • Urine output < 0.5cc/kg/hr for at least one hour or renal replacement therapy

    • Elevated lactate (>2 to 3)

    • Abrupt change in mental status

    • Abnormal EEG findings

    • Platelet count <100, 000

    • DIC

    • ARDS

    • Cardiac dysfunction

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Septic Shock

  • Severe sepsis plus at least one of the following:

    • MAP<65mmHg despite adequate fluid resuscitation

    • Maintaining MAP>60-65mmHg requires vasopressors:

      • Dopamine > 5μg/kg/min

      • Norepinephrine < 0.25μg/kg/min

      • Epinephrine < 0.25mg/min

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Refractory Septic Shock

  • Septic shock that requires higher doses of the ionotropes to keep the MAP>65mmHg:

    • Dopamine > 15μg/kg/min

    • Norepinephrine > 0.25μg/kg/min

    • Epinephrine >0.25mg/min

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Multiple Organ Failure/MODS

  • Presence of altered organ functions in an acutely ill patient such that homeostasis cannot be maintained without intervention

    • Primary: secondary to a well defined insult in which organ dysfunction occurs early and can be directly attributable to the insult itself (eg ARF from rhabdomyolysis)

    • Secondary: organ failure not in direct response to the insult itself but as a consequence of a host response to the insult (eg ARDS in pancreatitis)

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  • Note that NO positive blood cultures are needed in the definition

    • You only get positive cultures in 17-69% of all septic/septic shock patients

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  • Getting more frequent (increasing by 8% per year since the 1970’s) with increasing severity

  • 2% of all hospitalized patients

  • Up to 75% of all ICU patients

  • 20-50% mortality, depending on the degree:

    • SIRS alone 7%

    • Sepsis 16%

    • Severe sepsis 20%

    • Septic shock 46%

      Rangud-Feausto, MS et al,

      JAMA 1995; 273:117

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  • Characteristics that influence outcome in the septic patient include:

    • Host response: is the host able to mount a fever or WBC response?

    • Underlying disease: comorbidities (NIDDM, kidney failure, hepatic failure, cancer, EtOH abuse, immune suppression)

    • APACHE II score

    • Advanced age

    • Site of infection: Lung/gut 50% Urine 30%

    • Community acquired vs healthcare acquired

    • Organism involved

    • Antibiotics—timing and type

    • Rapidity and adequacy of response

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  • Process of malignant intravascular inflammation

  • Uncontrolled, unregulated, self-sustaining

  • Exaggerated response of the normal inflammatory response

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  • When tissue is injured, or infected, there is the simultaneous release of proinflammatory and antiinflammatory elements—the balance of these helps facilitate tissue repair and healing

  • Remote tissue injury may ensue when this equilibrium in the inflammatory process is lost and these mediators exert systemic effects

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  • The significant consequences of a systemic proinflammatory reaction include endothelial damage, microvascular dysfuntion, impaired tissue oxygenation and subsequent organ damage or injury

  • The consequences of an excessive antiinflammatory response include anergy and immunosuppression

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  • Normal inflammation involves the regulation of PMN rolling, adhesion, diapedesis, chemotaxis, phagocytosis and killing of invading bacteria

  • These processes are highly controlled through proinflammatory and antiinflammatory cytokines released by activated macrophages

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  • As a result of dysregulation of this process, an autodestructive process ensues to involve otherwise remote normal tissue and results in the sepsis syndrome

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  • This involves many factors:

    • Proinflammatory cytokines (TNFα, IL-6 etc)

    • Bacterial factors—direct effect of invading microorganisms or their toxic products:

      • Endotoxin (gm neg bacteria)

      • Cell wall components (peptoglycans, muramyl dipeptide, lipoteichoic acid)

      • Enterotoxins (staph), exotoxin (pseudomonas), M protein (GAS), toxic shock toxin etc

    • Complement activation (C5a)

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  • This results in cellular injury and subsequent organ dysfunction

  • The precise mechanism is not known, but proposed mechanisms include:

    • Cellular ischemia (O2 lack relative to need)

    • Direct cell injury by inflammatory mediators and other products of inflammation

    • Increased rate of apoptosis (programmed cell death)

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  • If the mediators balance each other out and the initial infectious insult is overcome, homeostasis will be restored

  • The initial insult may be so severe that it directly induces SIRS and MODS

  • In most patients, a balance is not established and one of the 2 predominates

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Specific Organ Involvement


  • Derangement in metabolic autoregulation occurs (process that matches O2 availability to need)

  • Vasoactive mediators are released that cause microvascular permeability and vasodilation (prostacyclin and NO)

  • Impaired compensatory secretion of ADH (vasopressin) may also contribute

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  • In central circulation, early manifestations include changes in systolic and diastolic ventricular function

  • Initially, CO increases to compensate for the vasodilation until the patient is no longer able to do so

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  • In the regional circulation, there is heterogeneity in normal distribution of blood flow and loss of regulation

  • The microcirculation is a key (if not the most important) target organ for injury in the sepsis syndrome

  • There is a decrease in the number of functional capillaries which causes an inability to extract O2 maximally

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  • Panendothelial activation leads to widespread tissue edema, which is rich in protein

  • Hypotension is the most serious expression of the circulatory dysfunction that results (reduced arterial tone, increased permeability)

  • Other changes include venous dilatation (decreasing venous return to the heart) and the release of myocardial depressant factors

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  • Endothelial injury leads to disturbed capillary blood flow and enhanced microvascular permeability and subsequent interstitial and alveolar edema

  • PMN entrapment amplifies this damage


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GI Tract

  • May provided positive feedback loop in injury from sepsis from various sources:

    • Bacterial overgrowth in UGI tract leading to VAP if patients not fed or prophylaxed

    • Translocation through gut wall of bacteria from circulatory abnormalities depressing the gut’s barrier funtion

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  • Liver dysfunction can worsen sepsis by preventing bacterial clearance

  • Can get reticuloendothelial system dysfunction from the sepsis syndrome

  • Increased LFT’s/transaminases

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  • ATN (systemic hypotension, direct renal vasoconstriction, cytokine release etc may all cause)

  • Likelihood of death increases dramatically if renal failure accompanies sepsis

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Nervous System

  • CNS: altered sensorium

  • PNS: peripheral neuropathy

    • Limb muscle weakness and atrophy

    • Reduced DTR’s

    • Loss of peripheral sensation to light touch and pin prick

    • Preservation of cranial nerve function

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  • Thrombocytopenia

  • DIC

  • Hyponatremia

  • Anemia

  • Elevated or decreased WBC

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  • Try to get the patient back to homeostasis as quickly and safely as possible

  • Fluid is your best ionotrope…do not be afraid of it

  • “Hit them early, hit them hard”

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  • Early Goal Directed Therapy in the Treatment of Severe Sepsis and Septic Shock

    Emmanuel Rivers, NEJM 2001

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  • Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008

    Crit Care Med 2008 Vol 36 No 1

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Initial resuscitation (within first 6h)

  • Begin resuscitation immediately in patients with hypotension or elevated lactate (>4)—do not delay until pending ICU admission

  • Resuscitation goals

    • CVP 8-12 mmHg

    • MAP >65 mmHg

    • U/O > 0.5ml/kg/hr

    • SVC O2 sat >70%

  • If venous O2 sat not achieved, consider futher fluid, PRBC (to keep Hct >30%) or dobutamine

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  • Obtain appropriate cultures providing it does not delay antibiotic administration

  • 2 or more BCs

  • One BC from each access device >48hr old

  • Other sites as indicated

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  • As early as possible and always within 1hr

  • Broad spectrum, covering all likely pathogens then narrow as clinically indicated

  • Stop if not infectious cause, otherwise 7-10 days

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Source Control

  • Identify anatomic site of infection as soon as possible (within 6hr of presentation)

  • Choose source control with max efficacy and min physiologic upset

  • Remove all intravascular devices if potentially infected

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Fluid Therapy

  • Crystalloid or colloid

  • Use fluid challenge technique while associated with hemodynamic improvement

  • 1000cc crystalloid or 300-500cc colloid over 30 mins

  • Rate of fluid administration should be reduced if cardiac filling pressures increase without concurrent hemodynamic improvement

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  • Maintain MAP > 65mmHg

  • Norepinephrine or dopamine initially

  • Then can add epinephrine or vasopressin

  • Art line when practical

  • No low-dose dopamine for renal protection


  • Dobutamine in patients with depressed myocardial function

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  • Low dose in patients who respond poorly to fluids and vasopressors

  • No ACTH stim test needed

  • Use HC with or without FC

  • Stop once patient is off vasopressors

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Activated Protein C

  • Consider in patients with sepsis induced organ dysfunction and high risk of death (APACHE II >24 or MODS) if there are no contraindications

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Blood Product Administration

  • Give RBC if Hb < 70 to target 70-90

  • Do not use FFP unless there is bleeding or planned invasive procedures

  • Give platelets when counts are <5000, or between 5000 and 30000 and there is significant bleeding risk

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Mechanical Ventilation

  • Lung protective strategies, using ARDSnet guidelines

  • SBT’s once patient ready for them

  • HOB at 30-45 degrees

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  • Sedation as necessary

  • DVT/Stress ulcer prophylaxis

  • Glucose control (keep 5-8.3)

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  • A large and diverse topic

  • Will be a common occurrence in any surgical practice

  • Needs to be recognized and dealt with quickly to minimize morbidity and mortality

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