mods presentation final

8/12/2019 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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Who is at risk ?Notlimited to patientswith sepsis


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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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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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Loss of homeostasisbetween systemicinflammation and acounter balancing anti-inflammatory response

Loss of immune

compartmentalization


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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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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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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

mods presentation final

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