Acute (adult) respiratory distress syndrome

What is acute respiratory distress syndrome?

Acute respiratory distress syndrome (ARDS) is a common and devastating condition which can affect all adult patients - eg, medical, surgical and obstetric patients. It occurs when non-cardiogenic pulmonary oedema (secondary to acute damage to the alveoli) leads to acute respiratory failure.¹

The Berlin criteria are used for the diagnosis of ARDS in adults .²

How common is acute respiratory distress syndrome? (Epidemiology)³

Various population-based studies conducted before the COVID-19 pandemic, revealed a huge global variation in incidence - eg, South America (10.1 per 100,000 person-years), Europe, (17.9 per 100,000 person-years), Australia (34 per 100,000 person-years), USA (78.9 per 100,000 person-years). Even within Europe, considerable variation exists: 10.6 per 100,000 person-years in Finland, 17.9 per 100,000 person-years in Scandinavia, 25.5 per 100,000 person-years in Spain.

In the UK, in one prospective six-month study to determine the incidence and outcome of ARDS in a UK adult University Hospital ICU, 344 patients were admitted during the study period, of which 43 (12.5%) were determined to have acute respiratory distress syndrome.⁴

Causes of acute respiratory distress syndrome (aetiology)

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

Most common risk factors⁵

• Sepsis.

• Massive trauma with shock and multiple transfusions.

• Hypovolaemic shock.

• Pneumonia.

• Gastric aspiration.

Other risk factors

Pathophysiology²

Increased permeability of pulmonary microvasculature causes leakage of proteinaceous fluid across the alveolar-capillary membrane. This may be one manifestation of a more generalised disruption of endothelium, resulting in hypoxia and multiple organ failure. There is also a reduction in surfactant production.

Some patients progress to fibrosis, whilst others recover. The reason for this is not known. However, it is known that there is genetic variability between patients who respond to treatment (particularly corticosteroids) and those who do not. There is also evidence of inflammation in the lung tissue which can be seen on metabolic imaging methods.

Clinical features

• 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.

Investigations

• FBC, U&E, LFTs, amylase, clotting, CRP, blood cultures, ABG.

• CXR shows bilateral alveolar shadowing, often with air bronchograms.

• Other investigations as deemed by the clinical scenario - eg, echocardiography.

Diagnostic criteria²

According to the Berlin definition, ARDS is an acute form of diffuse lung injury occurring in patients with a predisposing risk factor, meeting the following criteria:

• Onset within one week of a known clinical insult or new/worsening respiratory symptoms.

• Presence of bilateral opacities on CXR, not fully explained by effusion, lobar/lung collapse, or nodules.

• Diagnosis of respiratory failure not fully explained by cardiac failure or fluid overload.

• Presence of hypoxaemia, as defined by a specific threshold of the PaO₂/FiO₂ ratio measured with a minimum requirement of positive end-expiratory pressure (PEEP) ≥5 cm H₂O.

Three categories of severity are identified:

• Mild (200 millimetres of mercury (mm Hg) < PaO₂/FiO₂ ≤ 300 mm Hg).

• Moderate (100 mm Hg < PaO₂/FiO₂ ≤ 200 mm Hg).

• Severe (PaO₂/FiO₂ ≤ 100 mm Hg).

Acute respiratory distress syndrome treatment and management⁶

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.

The large tidal volumes (10-15 mL/kg) produced by conventional ventilation plus reduced lung compliance in ARDS may lead to high peak airway pressures ± pneumothorax. PEEP increases oxygenation but at the expense of venous return, cardiac output, and perfusion of the kidneys and liver.

The Faculty of Intensive Care Medicine and Intensive Care Society Guideline Development Group developed guidelines for the management of patients with acute respiratory distress syndrome (ARDS) that are supported by the British Thoracic Society.⁸ They suggest that where mechanical ventilation is required, low tidal volumes (<6 ml/kg ideal body weight) and airway pressures (plateau pressure <30 cmH2O) are used. For patients with moderate/severe ARDS (PF ratio<20 kPa), prone positioning was recommended for at least 12 hours per day. Prone ventilation has been shown to improve alveolar gaseous exchange.⁹ However, a 2022 Cochrane review concluded that there was only low certainty evidence and could not make definitive recommendations. ¹⁰

By contrast, high frequency oscillation was not recommended and it was suggested that inhaled nitric oxide is also not used.

Permissive hypercapnia (allowing the patient's carbon dioxide level to rise) has had its advocates, but evidence suggests that the risks may well outweigh the benefits.¹¹

Circulatory support

Invasive haemodynamic monitoring with an arterial line and Swan-Ganz catheter may be helpful in monitoring pulmonary capillary wedge pressure and cardiac output.

Maintaining cardiac output and thus oxygen delivery usually needs inotropes (eg, dobutamine), vasodilators and blood transfusion. Fluid rehydration needs to be carefully balanced and in some cases negative fluid balance is the objective. This may require haemofiltration in extreme cases.

Extra-corporeal life support (ECLS) or extra-corporeal membrane oxygenation (ECMO) can both be used to support gas exchange in ARDS.¹²

Other therapies

There is a range of opinion on whether the benefits of corticosteroids in ARDS outweigh the risks and a 2019 Cochrane review found insufficient evidence to recommend their use. ¹³ .

Essentially, the treatment of ARDS has been supportive, and no emerging therapies have been identified which make any difference to the clinical outcome.¹⁴

Sepsis

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

Other supportive care

• Nutritional support - enteral feeding is better than parenteral feeding.

• Venous thromboembolism prevention with low molecular weight heparin.

• Gastric ulcer prevention with prophylactic medications.

Prognosis

• Mortality rate in acute respiratory distress syndrome can vary between 27-46 (and even 60%).¹

• A number of methods to determine prognosis have been developed including the use of:¹⁵

  • Clinical characteristics.

  • Physiological parameters and oxygenation.

  • Genetic polymorphisms and biomarkers.

  • Scoring systems.

• In most cases, survivors' lung function returns almost to normal. However, some may have reduced exercise capacity and neuropsychological disorders up to five years after their illness.¹⁶