Definition
- ARDS is an acute pulmonary disorder characterized by diffuse
capillary leak resulting in wet lung and a constellation of
features secondary to it.
- This syndrome is associated with a multitude of clinical
conditions which primarily damage the lung or secondarily as part
of a systemic disorder.
Pathogenesis
- ARDS is the end result of acute alveolar injury caused by a vareity
of insults and probably initiated by different mechanisms.
- The initial injury most frequently affects the endothelium,
less frequently the alveolar epithelium.
- There are many types of injuries which lead to the ultimate, common
pathway, i.e., damage to the alveolar capillary unit.
- Injury produces increased vascular permeability,
edema, fibrin-exudation (hyaline
membranes).
- Organization and scarring follows.
- Endotoxin, neutrophils, and macrophages may also play key roles in
the pathogenesis of ARDS
- Leukocytes (primarily neutrophils) plays a key role in endothelial
damage.
- The capillary defect is produced by an interaction of inflammatory
cells and mediators, including leukocytes, cytokines, oxygen radicals,
complement and arachidonate metabolites, that damages the endothelium and
allows fluid and proteins to leak.
Pathology
Pathophysiology
- There is diffuse loss of Surfactant resulting in alveolar
atelectasis.
- Lung becomes stiff and less compliant. Lung
volumes decrease and minute ventilation increases as a compensatory
phenomenon.
- Tremendous intrapulmonary shunt develops as a
consequence of alveolar atelectasis, where there is no ventilation with
respect to perfusion.
Clinical Features
- A major event always precedes. Common major events
are Sepsis, Shock, Trauma, Gastric aspiration, acute blood loss and acute
Pancreatitis.
- Following a brief lag period of the major event,
patient develops hypoxia, tachypnea and rapidly progresses to acute
hypoxemic respiratory failure.
- Hypoxemia is refractory to therapy.
- CXR shows diffuse white out of lungs.
- Wedge pressure is normal indicating that it is
non-cardiogenic pulmonary edema.
Therapy
- Correction of the primary event that induced ARDS,
if possible.
- Ventilator support to provide adequate
oxygenation.
- PEEP is necessary to prevent alveolar atelectasis,
decrease shunt and improve oxygenation.
- Supportive care for nutrition and infections.
Prognosis
- Even with optimal therapy mortality is 60%.
- Patients who recover have almost normal pulmonary function. Some
diffusion defect can be residual.
- Hypoxemia is refractory to therapy.
- CXR shows diffuse white out of lungs.
- Wedge pressure is normal indicating that it is non-cardiogenic
pulmonary edema.
Therapy
- Correction of the primary event that induced ARDS, if possible.
- Ventilator support to provide adequate oxygenation.
- PEEP is necessary to prevent alveolar atelectasis, decrease
shunt and improve oxygenation.
- Supportive care for nutrition and infections.
Prognosis
- Even with optimal therapy mortality is 60%.
- Patients who recover have almost normal pulmonary function. Some diffusion defect
can be residual.