• Clinical science

Acute respiratory distress syndrome

Abstract

Acute respiratory distress syndrome (ARDS) is a severe inflammatory reaction of the lungs to pulmonary damage. Sepsis is the most common cause, but various other systemic or pulmonary factors – such as pneumonia or aspiration – can lead to ARDS. Patients initially present with acute onset cyanosis, dyspnea, and tachypnea. Over the course of the next weeks, most patients will improve significantly, although some progress to pulmonary fibrosis, which prolongs their hospital stay and delays resolution of symptoms. The chief finding in ARDS is hypoxemic respiratory failure with decreased arterial oxygen pressure, which usually progresses to hypercapnic respiratory failure. Chest x-ray typically shows diffuse bilateral infiltrates (“butterfly pattern”). Management of ARDS focuses on maintaining adequate oxygenation, which often requires intubation and (lung protective) mechanical ventilation, as nasal prongs and/or mask ventilation are insufficient. Moreover, any treatable causes of ARDS should be addressed. However, even if adequate treatment is initiated, ARDS remains an acutely life-threatening disease with a high mortality rate.

Etiology

Systemic causes

Primary damage to the lungs

Sepsis is the most common cause of ARDS!

References:[1][2][3][4]

Pathophysiology

References:[5][3][6][7]

Clinical features

  • Acute onset
  • Disease course
    • Most patients begin to improve after the first 1–3 weeks and symptoms usually resolve fully.
    • Some develop pulmonary fibrosis with prolonged resolution of symptoms and extended ventilator dependence.

References:[8][9][10]

Diagnostics

ARDS is a likely diagnosis in the presence of both typical causes and therapy-resistant hypoxemia. The diagnosis is further supported by characteristic findings on chest x-ray that are not explained by underlying cardiac disease.

References:[1][11][9]

Differential diagnoses

References:[9][1][12]

The differential diagnoses listed here are not exhaustive.

Treatment

Approach

  • The primary objective is achieving sufficient oxygen saturation (while avoiding oxygen toxicity).
  • Treat the underlying cause (e.g., sepsis).
  • Sedation (benzodiazepines, opioids)
  • If oxygenation is insufficient:
    • Noninvasive oxygenation (e.g., via masks and nasal tubes) can usually deliver a FiO2 of ∼ 70%.
    • Endotracheal intubation and lung protective ventilation can usually provide a FiO2 of 100% and should be administered early on in most patients. The goal is to achieve assisted spontaneous breathing with bilevel positive airway pressure (BiPAP) as soon as possible.

Lung protective ventilation

  • Description: Pressure-controlled ventilation with a low tidal volume and low peak inspiratory pressure to avoid further pulmonary damage. However, increasing the positive end-expiratory pressure (PEEP) is often necessary during treatment. With this type of ventilation, higher levels of CO2 can be tolerated (permissive hypercapnia).
  • Settings
    • Standard tidal volume ≅ 6 mL/kg body weight
    • FiO2 < 0.5 (< 50% in the gas mixture) to avoid oxygen toxicity
    • PEEP and FiO2 can be adjusted to recruit collapsed alveoli and guarantee sufficient oxygen saturation.
  • Goal: SaO2 > 90% (or PaO2 > 55 mm Hg)
  • Patients must be slowly weaned from ventilation.
  • If initial treatment fails, a number of additional measures can be employed (rescue therapy).
    • Increasing the inspiration/expiration ratio
    • High-frequency ventilation, high PEEP
    • Extracorporeal life support (ECLS)
    • Negative fluid balance through diuresis or restriction of fluid intake
    • In some cases, administration of nitrates (improves oxygenation for a short period)
    • In some cases, administration of methylprednisolone ( ↑ ventilator-free days)

A high respiratory rate and a low tidal volume are the principles of lung protective ventilation!

Extracorporeal life support (ECLS)

References:[1][13][14][15][16][17][18][19]

Prognosis

References:[5][20]