Acute respiratory distress syndrome (ARDS)
Acute respiratory distress syndrome (ARDS)
D E FI N I T ION
Syndrome of acute and persistent lung inflammation with increased vascular
permeability. Characterized by:
. acute onset;
. bilateral infiltrates consistent with pulmonary oedema;
. hypoxaemia: PaO2/FiO2200mmHg regardless of the level of positive end-expiratory
pressure (PEEP);
. no clinical evidence for " left atrial pressure (pulmonary capillary wedge pressure
(PCWP)18 mmHg).
. ARDS is the severe end of the spectrum of ‘acute lung injury’ (ALI).
AETIOLOGY
Severe insult to the lungs or other organs induces the release of inflammatory
mediators, increased capillary permeability, pulmonary oedema, impaired gas exchange
and # lung compliance. Common causes include: sepsis, aspiration, pneumonia, pancreatitis,
trauma/burns, transfusion (massive, transfusion-related lung injury), transplantation
(bone marrow, lung) and drug overdose/reaction.
Patients progress through three pathologic stages: exudative, proliferative and fibrotic stage.
EPIDEMIOLOGY
Annual UK incidence1 in 6000.
HISTORY
Rapid deterioration of respiratory function, dyspnoea, respiratory distress,
cough, symptoms of aetiology.
EXAMINATION
Cyanosis, tachypnoea, tachycardia, widespread inspiratory crepitations.
Hypoxia refractory to oxygen treatment.
Signs are usually bilateral but may be asymmetrical in early stages.
INVESTIGATIONS
CXR:
Bilateral alveolar and interstitial shadowing.
Blood:
FBC, U&E, LFT, ESR/CRP, amylase, clotting, ABG, blood culture, sputum culture.
Plasma BNP < 100 pg/mL may distinguish ARDS/ALI from heart failure, but higher levels can
neither confirm heart failure nor exclude ARDS/ALI in critically ill patients.
Echocardiography:
Severe aortic or mitral valve dysfunction or # LVEF favours haemodynamic
oedema over ARDS.
Pulmonary artery catheterization:
PCWP18mmHg(however " PCWP does not exclude
ARDS as patients with ARDS may have concomitant left ventricular dysfunction).
Bronchoscopy:
If the cause cannot be determined from the history, and to exclude
differentials, e.g. diffuse alveolar haemorrhage (frothy blood in all airways, haemosiderin-
laden macrophage from lavage fluid), lavage fluid for microbiology (mycobacteria,
Legionella pneumophila, Pneumocystis, respiratory viruses) and cytology (eosinophils,
viral inclusion bodies and cancer cells).
MANAGEMENT
Respiratory support:
Supplemental oxygen (FiO2: 50–60%). Almost all patients require
intubation and mechanical ventilation.
Fully supported volume limited and pressure limited modes are both acceptable. The tidal
volume, respiratory rate, PEEP and FiO2 are managed according to the strategy of low tidal
volume ventilation (LTVV). The rationale for LTVV is that smaller tidal volumes are less
likely to generate alveolar overdistension and ventilator-associated lung injury. LTVV
frequently requires ‘permissive hypercapnic ventilation’, a ventilatory strategy that
accepts alveolar hypoventilation in order to maintain a low alveolar pressure and minimize
the complications of alveolar overdistension. The lowest plateau airway pressure possible
should be targeted.
Sedation and analgesia:
To improve tolerance of mechanical ventilation and to # oxygen
consumption. Neuromuscular blockade should be used only when sedation alone is
inadequate.
***********************
***********************
ليست هناك تعليقات:
إرسال تعليق