Treatment of patients with ARDS is primarily aimed at maintaining adequate oxygen delivery to vital organs and peripheral tissues, by means of respiratory and cardiovascular intervention, until lung injury resolves. Correction of anemia and the optimization of hemodynamic indices, with inotropes if necessary, may improve oxygen flux to systemic microvascular beds. Early assessment with CT indicates the extent and location of recruitable lung, and may also reveal loculated pneumothoraces or sources of infection (Fig 3). The correction of exacerbating factors is a key aspect of therapeutic strategy. Eradication of sepsis with appropriate antibiotics and drainage, if indicated, is essential. Prudent attention to hydration, nutrition, electrolyte, and acid-base balance is important. Physiotherapy assists sputum clearance and lung re-expansion in established acute respiratory failure.
Fig. 3 (a) CT appearance of ARDS. The bilateral dependent consolidation and ground glass appearance are consistent with acute disease. These are accompanied bilaterally by small pneumothoraces. (b) CT demonstration of a large anterior pneumothorax not visible on a plain chest radiograph.
The application and integration of the above techniques into a therapeutic strategy is clearly a matter of individual experience as randomized prospective trials are lacking, and this has hampered the widespread acceptance of lung-protective approaches to ventilation. Therefore empirically based intervention algorithms are inevitably the product of anecdotal experience. Figure4 illustrates one such approach to the management of refractory hypoxemia as a consequence of ARDS. The algorithm presented emphasizes the value of initial CT assessment and the importance of patient response to interventions. The recognition that deterioration of lung injury is often iatrogenic in origin has led to the adoption of pressure-controlled inverse ratio ventilation as our initial mode of ventilation in this group of patients. CT appearance and the etiology of any underlying process dictate further strategies to improve oxygenation, but individual patients combine distinct personal circumstances with precipitating illness, so that some flexibility in interpretation and management is required. A negative fluid balance is desirable and may produce improvements in gas exchange where edema is a prominent feature. Dependent atelectasis may be responsive to postural manipulations, but frequent switching between supine and prone positions may itself be hazardous. The use of pulmonary-selective vasodilators is commonplace, but their effects can be erratic and their impact on mortality is questionable. Pulsed steroids are administered to non-responders where there is evidence of fibroproliferation on CT scanning and no clinical or bronchoalveolar lavage evidence of sepsis. Several interventions suggested for use in non-responder groups remain unproven and await further scientific scrutiny. Therefore it is not possible to be dogmatic about these therapies, but their use in individual cases may be appropriate.
Fig. 4 Algorithm presenting a therapeutic strategy for managing acute respiratory failure secondary to acute respiratory distress syndrome: PC-IRV, pressure-controlled inverse ratio ventilation; HFJV, high-frequency jet ventilation; PGI2, prostacyclin; BAL, bronchoalveolar lavage; IVOX, intravascular oxygenator. The importance of early CT scanning is emphasized. Lung-protective modes of ventilation may reduce associated iatrogenic volutrauma. Patients with pneumonia or more than 72 h after the initiating insult do not usually respond to high-frequency ventilation.
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