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.
Clinical features
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.
Investigations
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.
Management
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.
