Acute (Adult) Respiratory Distress Syndrome

Synonyms: Adult respiratory distress syndrome (ARDS); Acute lung injury (ALI).

Acute respiratory distress syndrome (ARDS) is a common and devastating condition which affects both medical and surgical patients. It occurs when noncardiogenic pulmonary oedema (secondary to acute damage to the alveoli) leads to acute respiratory failure.

Incidence is uncertain, but was reported as 17.9 per 100,000 for acute lung injury and 13.5 per 100,000 for ARDS in a Scandinavian study in 1994.¹

• Pulmonary: pneumonia; gastric aspiration; inhalation injury; vasculitis; contusion
• Non-pulmonary: shock; septicaemia; haemorrhage; multiple transfusions; DIC; acute pancreatitis; acute liver failure; trauma; head injury; fat embolism; burns; obstetric complications (eclampsia; amniotic fluid embolus); drugs/toxins (aspirin, heroin, paraquat)

Risk Factors

The more risk factors apply, the greater the chance of ARDS.

Commonest Risk Factors

• Sepsis
• Massive trauma with shock and multiple transfusions
• Hypovolaemic shock
• Pneumonia
• Gastric aspiration

Increased permeability of pulmonary microvasculature causes leakage of proteinaceous fluid across the alveolar-capillary membrane.² This may be one manifestation of a more generalized disruption of endothelium, resulting in hypoxia and multiple organ failure.

• Symptoms: History of relevant injury and increasing dyspnoea which may occur some time after the precipitating event.
• Signs: Cyanosis (reflecting hypoxia refractory to oxygen therapy), tachypnoea, tachycardia, peripheral vasodilatation; bilateral fine inspiratory crackles.

• FBC, U and E, LFTs, amylase, clotting, CRP, blood cultures, ABG.
• CXR shows bilateral alveolar shadowing, often with air bronchograms.
• Pulmonary artery catheter to measure pulmonary capillary wedge pressure (PCWP).

One consensus requires these 4 to exist:³

1. Acute onset
2. CXR: bilateral infiltrates
3. Pulmonary-artery wedge pressure18mmHg or a lack of clinical evidence of left atrial hypertension (i.e. CCF)
4. Refractory hypoxaemia: acute lung injury is present when ratio PaO2:FiO2<300; ARDS is present when PaO2: FiO2<200.

20-50% of acute lung injury patients will develop ARDS within 7 days.⁴

Admit to ITU, give supportive therapy and treat the underlying cause.

Respiratory support

In early ARDS continuous positive airway pressure (CPAP) with 40-60% oxygen may be adequate to maintain oxygenation. But most patients need mechanical ventilation.

Circulatory support

Circulatory support Invasive haemodynamic monitoring with an arterial line and Swan-Ganz catheter aids the diagnosis and may be helpful in monitoring PCWP and cardiac output.

Maintain cardiac output and oxygen delivery with inotropes (eg dobutamine 2.5-10μg/kg/min), vasodilators and blood transfusion. Consider treating pulmonary hypertension with low-dose (20-120ppm) nitric oxide, a selective pulmonary vasodilator.⁸ However, a recent systematic review and meta-analysis found that nitric oxide only provides a short improvement and does not affect survival. Furthermore, nitric oxide was associated with renal dysfunction.⁹ Haemofiltration may be needed in renal failure and to achieve a negative fluid balance.

Experimental therapies

More novel therapies currently in the experimental stages include activated protein C, granulocyte-macrophage colony-stimulating factor and the use of beta agonists to enhance alveolar fluid clearance.⁸

Sepsis

Identify organism(s) and treat accordingly. If clinically septic, but no organisms cultured, use empirical broad spectrum antibiotics. Avoid nephrotoxic antibiotics.

Nutritional support

Enteral is better than parenteral feeding. Steroids do not improve mortality in the acute phase but may be of benefit later on (>7 days), particularly if eosinophilia in blood or bronchial-alveolar-lavage (BAL).

Overall mortality is 50-75%. Prognosis varies with age of patient, cause of ARDS (pneumonia 86%, trauma 38%), and number of organs involved (3 organs involved for >1 week is invariably fatal). In most cases, survivors' lung function returns almost to normal within 6-12 months. There may be reduced vital capacity and some obstructive lung disease but these are usually asymptomatic.⁴ Interestingly, patients with acute lung injury have reduced exercise capacity up to two years after the episode and there is evidence to suggest long-term neurocognitive impairment.⁴