- Clinical science
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.
(most common cause)
- E.g., secondary to trauma, infection or peritonitis
- Massive TRALI” for details) (See “
- Hematopoietic stem cell transplantation
- Medication (e.g., salicylic acid, tricyclic antidepressants, bleomycin)
- Recreational drug overdose (e.g., cocaine)
Primary damage to the lungs
- Inhaled toxins
- Pulmonary contusion
- Inhalation injury (e.g., inhalation of hyperbaric oxygen)
- Near drowning
- Fat embolism (e.g., through blunt trauma)
- Amniotic fluid embolism (e.g., during labor)
- Lung transplantation
Sepsis is the most common cause of ARDS!
Tissue damage (pulmonary or extrapulmonary) → release of inflammatory mediators (e.g., interleukin-1) → inflammatory reaction → injury to alveolar capillaries and endothelial cells leading to:
- Excess fluid in interstitium and on alveolar surface → pulmonary edema
- Exudation of neutrophils and protein-rich fluid (hyaline membrane) into the alveolar space → diffuse alveolar damage (DAD) to type I and type II pneumocytes → decrease in surfactant → intrapulmonary shunting → late stage: proliferation of type II pneumocytes and infiltration of fibroblasts → progressive interstitial fibrosis
- Impaired gas exchange, reduced compliance, hypertension and a right-to-left pulmonary shunt (increased shunt fraction) → hypoxemia → compensation through hyperventilation → respiratory alkalosis
- 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.
- Arterial blood gas
- Additional findings depend on the underlying cause (e.g., abnormal white blood count in sepsis) or associated complications (e.g., increased creatinine levels in acute tubular necrosis).
- Imaging: chest x-ray
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.
- Cardiogenic pulmonary edema: presents with signs of cardiac dysfunction (e.g., murmurs, jugular venous congestion)
- Acute exacerbations of interstitial lung diseases: examine patient history and past chest x-rays
- Transfusion-related acute lung injury (TRALI)
- Transfusion-associated circulatory overload (TACO): a rapid, high-volume infusion, which causes symptoms similar to ARDS
The differential diagnoses listed here are not exhaustive.
- 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.
- 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).
- 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)
- Definition: ECLS is a method of artificially supporting the circulatory system. In patients with severely reduced or no pulmonary function, the O2/CO2 exchange is achieved through the use of artificial lung membranes. Depending on the exact technique/machinery used, several other terms are employed as well (e.g., extracorporeal membrane oxygenation).
- Anticoagulation (usually IV heparin)
- Circulation variants