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ALL / Respiratory Medicine
Acute respiratory distress syndrome
Acute respiratory distress syndrome
Acute respiratory distress syndrome (ARDS) is caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli, i.e. non-cardiogenic pulmonary oedema. It is a serious condition that has a mortality of around 40% and is associated with significant morbidity in those who survive.Causes
- infection: sepsis, pneumonia
- massive blood transfusion
- trauma
- smoke inhalation
- acute pancreatitis
- Covid-19
- cardio-pulmonary bypass
Pathophysiology
- diffuse inflammatory alveolar-capillary injury
- increased alveolar-capillary membrane permeability
- leakage of protein-rich fluid into the alveoli
- non-cardiogenic pulmonary oedema
- pneumocyte damage
- damage to type I pneumocytes impairs gas exchange
- damage to type II pneumocytes reduces surfactant production
- alveolar consequences
- alveolar collapse
- reduced lung compliance
- formation of hyaline membranes
- physiological consequences
- severe ventilation-perfusion mismatch
- refractory hypoxaemia
Clinical features are typically of an acute onset and severe:
- dyspnoea
- elevated respiratory rate
- bilateral lung crackles
- low oxygen saturations
A chest x-ray and arterial blood gases are the key investigations.
Criteria (American-European Consensus Conference)
- acute onset (within 1 week of a known risk factor)
- pulmonary oedema: bilateral infiltrates on chest x-ray ('not fully explained by effusions, lobar/lung collapse or nodules)
- non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
- pO2/FiO2 < 40kPa (300 mmHg)
Management
- due to the severity of the condition patients are generally managed in ITU
- oxygenation/ventilation to treat the hypoxaemia
- general organ support e.g. vasopressors as needed
- treatment of the underlying cause e.g. antibiotics for sepsis
- certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS
+PassMedicine Notes
Acute respiratory distress syndrome (ARDS) is caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli, i.e. non-cardiogenic pulmonary oedema. It is a serious condition that has a mortality of around 40% and is associated with significant morbidity in those who survive.
Causes- infection: sepsis, pneumonia
- massive blood transfusion
- trauma
- smoke inhalation
- acute pancreatitis
- Covid-19
- cardio-pulmonary bypass
- diffuse inflammatory alveolar-capillary injury
- increased alveolar-capillary membrane permeability
- leakage of protein-rich fluid into the alveoli
- non-cardiogenic pulmonary oedema
- pneumocyte damage
- damage to type I pneumocytes impairs gas exchange
- damage to type II pneumocytes reduces surfactant production
- alveolar consequences
- alveolar collapse
- reduced lung compliance
- formation of hyaline membranes
- physiological consequences
- severe ventilation-perfusion mismatch
- refractory hypoxaemia
- dyspnoea
- elevated respiratory rate
- bilateral lung crackles
- low oxygen saturations
A chest x-ray and arterial blood gases are the key investigations.
Criteria (American-European Consensus Conference)- acute onset (within 1 week of a known risk factor)
- pulmonary oedema: bilateral infiltrates on chest x-ray ('not fully explained by effusions, lobar/lung collapse or nodules)
- non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
- pO2/FiO2 < 40kPa (300 mmHg)
- due to the severity of the condition patients are generally managed in ITU
- oxygenation/ventilation to treat the hypoxaemia
- general organ support e.g. vasopressors as needed
- treatment of the underlying cause e.g. antibiotics for sepsis
- certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS
