Showing posts with label ARDS. Show all posts
Showing posts with label ARDS. Show all posts

ARDS

ARDS
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
  • 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 toacute 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.

Therapy

  • Whole lung lavage under general anesthesia is the only option for therapy.Dramatic improvement in symptoms follows whole lung lavage.
  • Relapses occur and repeated lavage may be necessary.
  • Some develop interstitial fibrosis and cor-pulmonaleLung transplant is a last resort option to patients with fibrosis.

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