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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

SIRS and the Septic Response

Manoj Sayal, MD FRCSC

March 5, 2008

agenda
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
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?
case 14
Case 1
  • 2 large bore IV’s—normal saline 1 litre
  • Labs drawn
  • CXR (portable), EKG, ABGs
  • Diagnosis?
case 15
Case 1
  • CXR: RLL infiltrate
  • WBC 22.4 Hb 108 Pl 98
  • Lytes normal; transaminases normal
  • Amylase 700
  • What now?
case 2
Case 2
  • Same patient, but normal amylase
case 3
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)?
sirs for dummies or surgeons
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
slide10
SIRS
  • 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
slide11
SIRS
  • Causes
    • Acute pancreatitis, autoimmune disorders, vasculitis, thromboembolism, burns, surgery, pulmonary contusion, SEPSIS)
slide12
SIRS
  • How does this relate to infection or the response to infection?
definitions
Definitions

Infection

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

Bacteremia

  • viable bacteria in the blood
definitions14
Definitions

Sepsis

  • 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
definitions15
Definitions

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
definitions16
Definitions

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
definitions17
Definitions

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
definitions18
Definitions

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)
definitions19
Definitions
  • 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
sepsis
Sepsis
  • 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

sepsis21
Sepsis
  • 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
sepsis pathogenesis
Sepsis--Pathogenesis

Pathogenesis

  • Process of malignant intravascular inflammation
  • Uncontrolled, unregulated, self-sustaining
  • Exaggerated response of the normal inflammatory response
sepsis pathogenesis23
Sepsis--Pathogenesis
  • 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
sepsis pathogenesis24
Sepsis--Pathogenesis
  • 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
sepsis pathogenesis25
Sepsis--Pathogenesis
  • 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
sepsis pathogenesis26
Sepsis--Pathogenesis
  • As a result of dysregulation of this process, an autodestructive process ensues to involve otherwise remote normal tissue and results in the sepsis syndrome
sepsis pathogenesis27
Sepsis--Pathogenesis
  • 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)
sepsis pathogenesis28
Sepsis--Pathogenesis
  • 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)
sepsis pathogenesis29
Sepsis--Pathogenesis
  • 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
specific organ involvement
Specific Organ Involvement

Circulation

  • 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
slide31
Circulation
  • 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
slide32
Circulation
  • 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
slide33
Circulation
  • 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
slide34
Lung
  • Endothelial injury leads to disturbed capillary blood flow and enhanced microvascular permeability and subsequent interstitial and alveolar edema
  • PMN entrapment amplifies this damage
  • ALI/ARDS
slide35
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
slide36
Liver
  • Liver dysfunction can worsen sepsis by preventing bacterial clearance
  • Can get reticuloendothelial system dysfunction from the sepsis syndrome
  • Increased LFT’s/transaminases
slide37
Kidney
  • ATN (systemic hypotension, direct renal vasoconstriction, cytokine release etc may all cause)
  • Likelihood of death increases dramatically if renal failure accompanies sepsis
slide38
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
slide39
Blood
  • Thrombocytopenia
  • DIC
  • Hyponatremia
  • Anemia
  • Elevated or decreased WBC
treatment
Treatment
  • 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”
treatment41
Treatment
  • Early Goal Directed Therapy in the Treatment of Severe Sepsis and Septic Shock

Emmanuel Rivers, NEJM 2001

treatment42
Treatment
  • Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008

Crit Care Med 2008 Vol 36 No 1

treatment43
Treatment

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
treatment44
Treatment

Diagnosis

  • 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
treatment45
Treatment

Antibiotics

  • 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
treatment46
Treatment

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
treatment47
Treatment

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
treatment48
Treatment

Vasopressors

  • Maintain MAP > 65mmHg
  • Norepinephrine or dopamine initially
  • Then can add epinephrine or vasopressin
  • Art line when practical
  • No low-dose dopamine for renal protection

Ionotropes

  • Dobutamine in patients with depressed myocardial function
treatment49
Treatment

Steroids

  • 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
treament
Treament

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
treatment51
Treatment

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
treatment52
Treatment

Mechanical Ventilation

  • Lung protective strategies, using ARDSnet guidelines
  • SBT’s once patient ready for them
  • HOB at 30-45 degrees
treatment53
Treatment

Others

  • Sedation as necessary
  • DVT/Stress ulcer prophylaxis
  • Glucose control (keep 5-8.3)
summary
Summary
  • 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
ad