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Mosul Anesthesia & ICU

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Mosul Anesthesia & ICU

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    ARDS – Definition and Pathophysiology

    yagocom
    yagocom
    المشرف العام


    عدد الرسائل : 193
    العمر : 54
    تاريخ التسجيل : 2008-07-26

    ARDS – Definition and Pathophysiology Empty ARDS – Definition and Pathophysiology

    Post by yagocom Tue Aug 12, 2008 10:46 pm

    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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