Acute Lung Injury and ARDS

Posted by e-Medical PPT Saturday, October 1, 2011
Clinical Disorders Associated with the Development of ALI/ARDS
Direct insult
 Aspiration pneumonia
Less common
 Inhalation injury
 Pulmonary contusions
 Fat emboli
 Near drowning
 Reperfusion injury

Indirect insult
 Severe trauma
Less common
 Acute pancreatitis
 Cardiopulmonary bypass
 Transfusion-related TRALI
 Disseminated intravascular coagulation
 Head injury
 Drug overdose

Mortality from ARDS
ARDS mortality rates - 31% to 74%
The variability in the rates quoted is related to differences in the populations studied and in the precise definitions used.
The main causes of death are nonrespiratory causes (i.e., die with, rather than of, ARDS).
Respiratory failure has been reported as the cause of death in 9% to 16% of patients with ARDS.
Early deaths (within 72 hours) are caused by the underlying illness or injury, whereas late deaths are caused by sepsis or multiorgan dysfunction.
There is a controversy about the role of hypoxemia as a prognostic factor in adults. Nevertheless, in some studies, both Pao2/Fio2 ratio and Fio2 were variables independently associated to mortality.

One-year Outcomes in Survivors of the Acute Respiratory Distress Syndrome
Persistent functional limitation
Extrapulmonary diseases (primarily): Muscle wasting and weakness (corticosteroid-induced and critical-illness-associated myopathy) Entrapment neuropathy                                                
    Heterotopic ossification
Intrinsic pulmonary morbidity (5%): Bronchiolitis obliterans organizing pneumonia                                        
    Bronchiolitis obliterans

Ventilator-induced Lung Injury
Three different pathologic entities:
High-permeability type pulmonary edema
Mechanical over-inflation/distortion of lung structures
Lung inflammation “Biotrauma”

High-permeability type pulmonary edema
Main causative factor:
    End-inspiratory lung volume >> peak inspiratory pressure “volutrauma more appropriate than barotrauma”
Mechanisms altering the alveolar-capillary barrier permeability during MV involve:
         -    Increased transmural vascular pressure
         -    Surfactant inactivation
         -    Mechanical distortion and disruption of endothelial cells
         -    Regional activation of inflammatory cells

Mechanical overinflation/distortion of lung structures
Emphysema-like lesions, lung cysts, and bronchiectasis
These lesions predominate in nondependent and caudal lung regions
The degree of overinflation is dependent on:
-    Tidal volume
-    Peak airway pressure
-    Duration of mechanical ventilation
-    Time exposed to an Fio2 > 0.6

Lung inflammation “biotrauma”
Lung overinflation or overstretching produces regional and systemic inflammatoryresponse that may generate or amplify multiple-system organ failure.
Factors converting the shear stress applied to an injured lung into regional and systemic inflammation are still incompletely elucidated but could include:
-    Repetitive opening and collapse of atelectatic lung units
-    Surfactant alterations
-    Loss of alveolo-capillary barrier function
-    Bacterial translocation
-    Overinflation of health lung regions

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