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 ARDS – Definition and Pathophysiology

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عدد الرسائل : 199
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تاريخ التسجيل : 27/07/2008

مُساهمةموضوع: ARDS – Definition and Pathophysiology   الأربعاء أغسطس 13, 2008 3:46 am

Acute lung injury (ALI) and adult respiratory distress syndrome (ARDS) develop in response to lung injury. A wide variety of precipitating causes are recognised (Tables 1a and 1b). Severe sepsis is the leading cause, followed by pneumonia, aspiration of gastric contents, massive blood transfusion, multiple trauma and pregnancy-related ARDS. ALI and ARDS develop very soon after the precipitating event, usually within 12-72 hours and often within 6 hours. In 1994, The American-European Consensus Conference Committee proposed definitions for ALI and ARDS (Table 2). It can be seen that ALI is a continuum of injury. When the oxygenation abnormality is more severe, the condition is termed ARDS. There are estimated to be about 3/100,000 cases of ARDS each year. Recent improvements in critical care have seen a reduction in the mortality of ARDS but it still remains at about 50% for the general population and 25% if it is pregnancy related. Fewer than 20% of deaths are due to refractory respiratory failure. This emphasises the importance of identifying and treating the precipitating cause.

Table 1a. Causes of ARDS

Septic shock

Gastric aspiration

Pre-eclampsia

Amniotic fluid embolus

Shock of any aetiology

Major trauma

Massive blood transfusion

Severe acute pancreatitis

Drug overdose

Pneumonia

Raised ICP

High inspired oxygen concentration

Pulmonary contusion

Near drowning

Cardiopulmonary bypass

Inhalation toxic fumes

Massive burns




Typical radiological appearances of ARDS




Acute phase

Pulmonary oedema

Normal vascular pedicle

No cardiomegaly or upper lobe blood diversion

Septal lines usually absent




Subacute phase

Progressive lung destruction and transition from alveolar to interstitial opacities




Chronic phase

Fibrosis

Focal emphysema



Table 3. The clinical and pathological phases of ARDS






Initial phase

Lasts 3-5 days

Severe oxygenation defect

Reduced lung compliance

Bilateral pulmonary infiltrates

Endothelial and epithelial cell injury

Leak of protein-rich oedema fluid in interstitium and air spaces.

Abnormal surfactant/inactivation of surfactant

Neutrophil sequestration and migration in lung




Sub-acute

Starts 5-7 days after onset of ARDS

Persistent oxygenation defect

Persistently reduced lung compliance

Increased alveolar dead space

Interstitial fibrosis with proliferation of type II alveolar cells

Widespread disruption of the pulmonary micro-circulation.




Chronic

Starts about 14 days after initial insult

Persistent low lung compliance

Increase in dead space ventilation

Extensive pulmonary fibrosis

Obliteration of normal alveolar architecture

Widespread emphysema and discrete bullae.




Focus on clinical manifestations and outcome from ARDS
At the bedside, the patient is clearly in respiratory distress. Although orthopneoa may be present, the other features of congestive heart failure are seldom present. Chest X-ray reveals diffuse, bilateral infiltrates that are often patchy and asymmetric (Table 4). Arterial blood gases reveal hypoxaemia that is often refractory to oxygen therapy. An initial respiratory alkalosis invariably leads to hypercapnia as dead space ventilation increases and muscle fatigue sets in. As ARDS evolves, the cardiovascular system is commonly affected and multi-organ failure invariably ensues. Over half the patients will develop associated renal failure. Immediate prognosis is related to the number of organ systems involved. In the general population, patients with only lung involvement have 15-30% mortality. If three or more organs are involved, this becomes greater than 80%. If the multi-organ failure persists beyond 4 days, mortality is 100%.
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