mods presentation final
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Multiple Organ DysfunctionSyndrome
(MODS)
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History & Epidemiology
Tilney et al. 1973: First description
Fry et al. 1980: role of infection and temporalsequence of organ failure
LungLiverGastric Mucosakidney
(Variations of this sequence can occur !)
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History & Epidemiology
Who is at risk ?Notlimited to patientswith sepsis
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History & Epidemiology
One of the most common causes of death in non-coronary intensive care units
Prognosis related to severity of MODS and number
of involved organs
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History & Epidemiology
Angus et al. 2001:
Number oforgans
involved inMODS
Incidence Mortality
1 73.6% 21.2%
2 20.7% 44.3%
3 4.7% 64.5%
4+ 1% 76.2%
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Scoring systems
Multiple Organ Dysfunction Score
Sequential Organ Failure Assessment Score
Logistic Organ Dysfunction System
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Scoring systems
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Mediators and methods of organ dysfunction
Key concepts:
1. Dysregulated immune response
2. The role of the gut
3. Nosocomial or iatrogenic insults4. Complete recovery is possible therefore etiology
more likely to be functional (vs. structural)
5. Non uniform mechanisms
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1. Dysregulated immune response
Loss of homeostasisbetween systemicinflammation and acounter balancing anti-inflammatory response
Loss of immune
compartmentalization
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1. Dysregulated immune response
Role of uncontrolled infection ?
Triggers MODS
POSSIBLY not as important in the evolution of the
syndromewhy?
Vascular endothelial injury
Mediated by leukocyte derived mediators, platelet-leukocyte-fibrin thrombi and TNF-alpha.
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2. The role of the gut
1) Intestinal epithelial hyper permeability:
Common in critical illness
Detectable before the onset of the syndrome
2) Gut associated lymphoid tissue (GALT)Inadequate function
reduced mucosal IgA levels
Pneumonia
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2. The role of the gut
3) Enteric commensal bacteria
Gut derived sepsis(Alverdy et al.):
Disruption in microenvironmentactivation ofvirulence genes
1+2+3=loss of immune
compartmentalization
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Nosocomial and iatrogenic promoters of MODS
two hithypothesis:
1. Severe trauma + associated tissue hypoperfusion primes
leukocytes
2.Ventilator-associated pneumoniablood transfusion
abdominal compartment syndrome
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A few more potential mechanisms
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Respiratory system
Typically the first organ to be involved
Failure of normal gas exchange1. atelactasis, intravascular thrombosis or altered regional flow
ventilation/perfusion mismatch.
2. Increased capillary permeabilityalveolar floodingARDS (typeI & III)
Type IV respiratory failure: hypoperfusion of respiratory muscles inpatients in shock
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Respiratory system
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Respiratory system
Complications ?
Ventilator induced lunginjury
Solution ?
Low tidal volume (6ml/Kg)ventilation
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Renal
Acute kidney injury (AKI)
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Renal
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Renal
USA: 700,000 cases of sepsis each year, AKIcomplicates more than 50% of these.
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Cardiovascular
Acute cardiovascular derangements of MODS:
1. Generalized reduction in peripheral vascular tone
2.Generalized increase in capillary permeability
3.Alterations in regional blood flow to specific organs4.Microvascular plugging and stasis
5. Myocardial depression septic cardiomyopathy
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Cardiovascular
Reduce afterload
Increase preload
Improve myocardial contractility
Control heart rate and rhythm
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Gastrointestinal & Hepatic
G.I. Signs: nausea, vomiting, nasogastric aspiratescan beearly signs of regional circulatory failure
Splanchnic vasoconstrictiongut mucosal ischaemia
MODS G.I. manifestations:
1. Loss of gastric acid production2. Stress ulceration
3. Bleeding
4. Ischaemia
5. Pancreatitis
Early enteral nutrition most effective strategy for gutmucosal protection
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Gastrointestinal & Hepatic
Hepatic circulation compromised by the same factorswhich lead to splanchnic vasoconstriction
Release of inflammatory mediators from activated
Kupffer cells Typically manifests as ICU jaundiceand
cholestasis.
Shock livercentrilobular hepatocellular necrosis
Treatment is non-specific: enteral feeding, improvesplanchnic blood flow
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Hemostatic abnormalities
Cytokine prothrombotic abnormalities withinmicrocirculation
Inappropriate intravascular coagulation could be the
final pathway to organ dysfunctuion Disseminated intravascular coagulation: Powerful
predictor of subsequent organ dysfunction(Longitudinal study of 136 patients with multiple
trauma, Gando et al.)
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Neurological
Continuum of states ofreduced alertness
Coma
StuporSomnolence (drowsiness)
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Neurological
A reduced Glasgow Coma Score isthe most readily recognizablemanifestation of the neurologicaldysfunction of MODS.
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Neurological
Delerium:
1. Acute onset of changes or fluctuations in the courseof mental status
2. Inattention3. Disorganized thinking
4. Altered level of consciousness
80% of mechanically ventilated ICU patients
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Neurological
Hypoxic ischemic encephalopathy
Metabolic encephalopathies
Septic encephalopathy
Acute alteration in the level of consciousnessaccompanying severe sepsis
Most common in ICU
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Management
Recognize patients at greatest risk ! Individualized therapy
Minimize risk of progression to MODS
1. Optimization of supportive management of circulatory
and respiratory dysfunction2. Reducing the rate of protein catabolism
3. Early nutrition support by the enteral route
4. Selective, targeted use of antibiotics
5. Minimizing blood transfusions
Read Surviving sepsis campaignguidelines (2008)
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Case studies
Frank Cerra: typical clinical course of MODS in thesurgical patients
Stage 1: Acute event associated with hypotension
Stage 2: Active resuscitation (24hrs)Stage 3: Stable hypermetabolism (7-10 days)
Clinical onset of MODS: low grade fever, tachycardiaand dyspnea. Mental confusion. Patchy infiltrates on
chest X-ray. DIC and thrombocytopenia.
What next?
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Case studies
Pulmonary status worsensintubation and mechanicalventilation
Hyperdynamic circulation Urine urea nitrogen output is substantial Glucose intolerance and hyperlactatemia
7-10 days later Hyperbilirubinemia and increased serum creatinine Bacteremia Requires more inotropic support
Deterioration of renal function, worsening encephalopathyand G.I. BleedingStage 4: (14-21 days later) Renal failure requiring dialysisDeath: 21-28 days after the initial event
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