ARDS, SARS, and Sepsis

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Last modified 01/06/2015

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ARDS, SARS, and Sepsis

Definition of Acute Respiratory Distress Syndrome (ARDS)

ARDS: A diffuse, heterogenous inflammatory response of the lungs, resulting in hypoxemia, consolidation, and decreased compliance.

The American-European Consensus Conference has provided the most precise definition of this syndrome (Box 23-1):

Although the aforementioned definition has become the most accepted definition of ALI/ARDS, it has been shown that alterations in FIO2 and PEEP can markedly affect the Pao2:FIO2 ratio, moving patients into and out of the classification of ALI or ARDS.

Others have used varying assessment mechanisms to define ARDS. The most commonly reported is the Murray lung injury score.

1. This score is based on four areas:

a. Chest radiograph Score
  (1) No consolidation 0
  (2) Consolidation confined to one quadrant 1
  (3) Consolidation confined to two quadrants 2
  (4) Consolidation confined to three quadrants 3
  (5) Consolidation confined to four quadrants 4
b. Hypoxemia Score
  (1) Pao2:FIO2 ≥300 0
  (2) Pao2:FIO2 225 to 299 1
  (3) Pao2:FIO2 175 to 224 2
  (4) Pao2:FIO2 100 to 174 3
  (5) Pao2:FIO2 <100 4
c. PEEP (if mechanically ventilated) Score
  (1) ≤5 cm H2O 0
  (2) 6 to 8 cm H2O 1
  (3) 9 to 11 cm H2O 2
  (4) 12 to 14 cm H2O 3
  (5) ≥15 cm H2O 4

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d. Respiratory system compliance (when ventilated) Score
  (1) ≥80 ml/cm H2O 0
  (2) 60 to 79 ml/cm H2O 1
  (3) 40 to 59 ml/cm H2O 2
  (4) 20 to 39 ml/cm H2O 3
  (5) ≤19 ml/cm H2O 4

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2. A score of 0 to 4 is given for each of the above available, and then scores are averaged.

3. ARDS is defined as a score >2.5; a mild to moderate injury is scored 0.1 to 2.5; and 0.0 indicates no lung injury.

It is important to remember that there is no test or measurement that can precisely define or identify ARDS. Diagnosis is always based on the signs and symptoms described previously.

Until a test is identified that can definitively diagnose ARDS there will continue to be controversy whether a patient truly has ARDS.

Many believe there is a genetic predisposition of ARDS and that one day an “ARDS gene” will be identified.

II Incidence and Mortality of ARDS

III Long-Term Outcome of ARDS

IV Causes of ARDS

Pathophysiology of ARDS

ARDS is characterized by diffuse alveolar damage and microvascular injury.

Three distinct phases of ARDS/ALI from a pathophysiologic perspective have been defined: Exudative phase, fibroproliferative phase, and resolution phase.

ARDS does not necessarily progress to the fibroproliferative phase; many patients rapidly move from the exudative phase to the resolution phase.

Exudative (acute) phase (Figure 23-1)

1. On histologic examination of the lung the following are observed:

2. The adhesion and activation of neutrophils lead to the secretion of proinflammatory mediators, potentially leading to more injury (see Figure 23-1; Table 23-1).

TABLE 23-1

Proinflammatory Mediators Associated with the Development of ARDS/ALI

Mediator Category Mediators
Tumor necrosis factors TNF-α, TNF-β
Interleukins IL-1β, IL-2, IL-6, IL-10, IL-12
Chemokines IL-8, MIP-1, MCP-1, growth-regulated peptides
Colony-stimulating factors G-CSF, GM-CSF
Interferon IFN-β

ARDS, Acute respiratory distress syndrome; ALI, acute lung injury.

From Wiedemann H: Systemic Pharmacolic Therapy of ARDS Resp Care Clin North Am 3:732, 1998.

3. The composition of pulmonary surfactant and its quantity are altered, increasing surface tension.

4. As the disease progresses deadspace ventilation increases.

5. Early in this exudative phase the major gas exchange issue is oxygenation. As this phase transitions into the fibroproliferative phase, ventilation generally becomes more of a problem.

6. The exudative phase generally lasts for approximately 3 to 7 days.

Fibroproliferative phase

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