Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) is most simply define as 'leaky lung syndrome' or 'low-pressure (i.e. non-cardiogenic) pulmonary oedema'. It describes an acute, diffuse inflammator lung injury, often in previously healthy lungs (Fig. 41a) in response to a variety of direct (i.e. inhaled) or indirect (i.e. bloodborne) insults.
The internationally agreed criteria for diagnosis of ARDS are:
1. Severe hypoxaemia, Pao2/Fio2 <200, (±positive end-expiratory pressure (PEEP)), e.g. Pao2 (55 mmHg)/Fio2 (80% inspired O2) = 55/0.8 = 75
2. Bilateral diffuse pulmonary inﬁltrates on chest X-ray
3. Normal or only slightly elevated left atrial pressure (pulmonary artery occlusion pressure <18 mmHg).
Acute lung injury (ALI) is the precursor to ARDS. Apart from a lesser degree of hypoxaemia (Pao2/Fio2 <300), the criteria for diag- nosis are the same.
Epidemiology and prognosis
The incidence of ARDS is approximately 2-8 cases per 100 000 population per year, but its precursor ALI is much more common. ARDS mortality is generally high (>40%) but is determined by the precipitating condition ( 35% for trauma, 50% for sepsis and 80% for aspiration pneumonia). Age (>60 years) and sepsis are also associated with increased mortality. Early diagnosis and treatment may improve outcome. The cause of death is multiorgan failure (MOF), usually due to a combination of tissue hypoxia and overwhelming secondary infection. Less than 20% of patients die from hypoxaemia alone.
Pathogenesis (Fig. 41a and b) and causes (Fig. 41c)
During the acute inﬂammatory phase of ARDS, cytokine-activated neutrophils and monocytes adhere to pulmonary endothelium or alveolar epithelium, releasing inflammator mediators and proteolytic enzymes (Chapter 18). These damage the integrity of the alveolar-capillary membrane, increase permeability and cause alveolar oedema. Reduced surfactant production causes alveolar collapse and hyaline membrane formation. The loss of functioning alveoli and ventilation/perfusion mismatch leads to progressive hypoxaemia and respiratory failure. The subsequent late healing ﬁbroproliferative phase results in progressive pulmonary fibrosi and reduced compliance (stiff lungs). Associated pulmonary hypertension is partially due to activation of the coagulation cascade, with pulmonary capillary microthrombosis and regional hypoxic vasoconstriction.
The acute inﬂammatory phase lasts 3-10 days and results in hypoxaemia and MOF. It presents with progressive breathlessness, tachypnoea, central cyanosis, hypoxic confusion and lung crepitations. These symptoms and signs are in no way diagnostic and are shared with many other pulmonary conditions. During the later healing, ﬁbroproliferative phase, pulmonary fibrosi (lung scarring) and pneumothoraxes (Chapter 35) are common. Secondary chest and systemic infections complicate both phases.
Monitoring: Routine measurements include temperature, respiratory rate, O2 saturation and urine output. In addition, the arterial and central venous pressures, the cardiac output and occasionally the left atrial pressure (using a pulmonary artery catheter) are measured to assess ﬂuid balance and ensure adequate tissue oxygen delivery. Serial blood gas measurements are used to monitor gas exchange. Early detection of secondary pulmonary infection requires microbiological examination of sputum or bronchoalveolar lavage.
Radiological: Serial chest X-rays (CXRs) identify progression of diffuse bilateral pulmonary inﬁltrates. Similarly, early computed tomography (CT) scanning can identify diffuse patchy inﬁltrates with dependent consolidation; later scans reveal pneumothoraxes, pneumatoceles and ﬁbrosis.
The key to successful management of ARDS is to establish and treat the underlying cause. In the early stages, oxygen therapy and physiotherapy may suff ce. With progressive respiratory failure, non-invasive ventilation with continuous positive airway pressure (CPAP) or non-invasive positive pressure ventilation (NIPPY) or full mechanical ventilation and high-inspired oxygen concentrations may be required to maintain adequate ventilation and oxygenation. The high airways pressures needed to achieve normal tidal volumes during mechani- cal ventilation often result in lung damage (barotrauma), including pneumothorax and lung cysts. This ventilator-induced lung injury and oxygen toxicity (Fio2 >0.8) must be prevented, as these contribute to mortality and multiorgan failure (Fig. 41b).
The basic principles of mechanical ventilation are to limit pressureinduced damage, optimize oxygenation and avoid circulatory compromise (reduced cardiac output and blood pressure due to high intrathoracic pressures; see also Chapter 42). A 'protective lung ventilation strategy' of low tidal volumes (6 mL/kg) and low peak inspiratory pressures (<30 cmH2O) reduces lung damage, complications and mortality. Alveolar recruitment (of collapsed alveoli) is achieved with high positive end-expiratory pressures (PEEP >10 cmH2O) or long inspiratory-expiratory times. The CO2 retention ('permissive hypercapnia') resulting from this strategy of low tidal volume ventilation can be tolerated for long periods.
Excessive ﬂuid loading must be avoided, as this increases the alveolar floodin characteristic of ARDS. The aim must be to maintain adequate perfusion of other organs while using the lowest possible left atrial pressures. In the acute situation, diuretics may be essential to correct hypoxaemia by reducing extravascular lung water. Thereafter, combinations of systemic vasodilators (after load reduction of the left heart), inotropes and vasoconstrictor agents may be used to achieve adequate cardiac output and perfusion pressures at low left atrial fillin pressures.
Essential general measures include good nursing care, physiotherapy, nutrition and infection control. Reducing fever (shivering) and controlling anxiety with sedation decrease metabolic demand. No drug therapy has been consistently beneﬁcial in early ARDS, including steroids, anti-inflammator agents, anticytokines or surfactant therapy. However, 7-10 days after onset, steroid therapy may prevent the development of subsequent pulmonary fibrosis Inhaled nitric oxide and nursing the patient in the prone position improve gas exchange by increasing perfusion to ventilated areas of lung, but no survival benefi has been demonstrated (Fig. 41d). Extracorporeal membrane oxygenation (ECMO) techniques to oxygenate blood or remove CO are effective in children, but the benefi in adults has not been blished.