Acute Respiratory Distress Syndrome (ARDS)

OVERVIEW

Acute Respiratory Distress Syndrome (ARDS) is an acute diffuse, inflammatory lung injury, leading to
increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue with
hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased
physiological dead space and decreased lung compliance.
The term acute lung injury (ALI) has been discarded
See ARDS Definitions

DEFINITION

The Berlin Definition (2013)

acute, with onset over 1 week or less

bilateral opacities consistent with pulmonary edema must be present; they may be detected on CT or
chest radiograph
PF ratio <300mmHg with a minimum of 5 cmH20 PEEP
must not be fully explained by cardiac failure or fluid overload, in the physicians best estimation using
available information an objective assessment (e.g. echocardiogram) should be performed in most
cases if there is no clear cause such as trauma or sepsis.

SEVERITY

ARDS is categorized as being mild, moderate, or severe:

ARDS Severity PaO2/FiO2* Mortality**

Mild 200 300 27%

Moderate 100 200 32%

Severe < 100 45%

*on PEEP 5+; **observed in cohort

RISK FACTORS

Direct Indirect

pneumonia (46%) non-pulmonary sepsis (25%)

aspiration of gastric contents (29%) multiple trauma (41%)
lung contusion (34%) massive transfusion (34%)
fat embolism pancreatitits (25%)
near drowning cardiopulmonary bypass
inhalational injury
reperfusion injury
PATHOPHYSIOLOGY

Classical phases

Injury
Exudative alveolar capillary membrane disruption with inflammatory cell infiltrate and high protein
exudate to form hyaline membranes
Proliferative proliferation of abnormal Type II alveoli cells and inflammatory cells
Fibrotic infiltration with fibroblasts which replace alveoli and alveolar ducts with fibrosis
Resolution slow and incomplete repair and restoration of architecture

Complex interplay:

(1) pulmonary oedema from damage to the alveolocapillary barrier

(2) inflammatory infiltrates
(3) surfactant dysfunction

The alveolocapillary barrier

damage with bidirectional flow (proteins and fluid in to alveoli, surfactant and alveolar cytokines into
plasma)
surfactant dysfunction
proliferation of type II cells
-> the balance between repair and fibrosing alveolitis

Inflammatory infiltrates

migration of neutrophils into alveoli with activation -> release of oxygen species, cytokines, eicasanoids,
proteases -> tissue damage
pulmonary endothelial cells, platelets, interstitial and alveolar macrophages also play important roles in
alveolar inflammation.

Surfactant dysfunction

decreased activity -> decrease in pulmonary compliance

caused by increased binding by plasma proteins and decreased production

Effects

hypoxaemia (V/Q mismatch, impaired hypoxic pulmonary vasoconstriction)

increase in dependent densities (surfactant dysfunction, alveolar instabilities)
decreased compliance (surfactant dysfunction, decreased lung volume, fibrosis)
collapse/consolidation (increased compression of dependent lung)
increased minute ventilation (increased in alveolar dead space)
increased work of breathing (increased elastance, increased minute volume requirement)
pulmonary hypertension (vasoconstriction, microvascular thrombi, fibrosis, PEEP)

MANAGEMENT

General
 diagnosis and appropriate treatment to minimise physiological impact of cause (drain collection,
antibiotics, resuscitate, splint fractures)
feed
standard ICU prophylaxis

Mechanical ventilation

ARDS Network protective lung ventilation strategy (from the ARMA study)
controlled ventilation
TV 6mL/kg
avoid overstretch (volutrauma) and inadequate recruitment (atelectrauma)
PEEP
Plateau pressure <30 cmH20 (higher than this contributes to VILI from overstretching and
hyperinflation of the functional baby lung)
mode of ventilation: generally no difference
PCV tends to be used c/o plateau pressure approximates peak pressure, with VC plateau pressure
needs to be measured
no role for inverse ratio ventilation (I:E ratio > 1) -> increased mean airway pressure +
haemodynamic instability + regional hyperinflation
oxygenation target: SpO2 > 90%, PaO2 >60mmHg
carbon dioxide target: ARDSnet aimed for a normal CO2 -> but lung is exposed to repeated tidal stretch,
ideally hypercapnia should be minimised but there isnt compelling data to suggest it is harmful unless
there is an obvious reason (raised ICP, pregnancy).

Other techniques to improve oxygenation

prone posture: improves oxygenation and mortality in severe ARDS

recruitment manoeuvres (e.g. PEEP 30-40cmH2O held for 30 seconds or staircase recruitment
manouvre) -> can improve oxygenation but controversial, not everyone responds
inhaled iNO: optimisation of V/Q mis-match, 1-60ppm, on 40-70% will respond, monitor for metHb
inhaled prostacycline (PGI2): optimisation of V/Q mis-match, 1-50ng/kg/min, as effective as iNO

Pharmacological therapy

surfactant replacement therapy: theoretically good, improves oxygenation but no improvement in

mortality, problems with distribution to alveoli
glucocorticoids: improvement in ventilator free days and shock, no improvement in mortality and
increase in weakness
ketoconazole: antifungal that inhibits thromboxane synthase and 5-lipooxygenase -> early data but not
confirmed.
others: cytokine antagonism, NSAIDS, scavengers of O2 radicals, lisofylline -> no success, APC in
sepsis

Seek and treat underlying causes and complications

PROGNOSIS

pulmonary function returns to normal at 6-12 months in survivors

occasionally patient have severe restrictive lung disease
although this is the case, many patient have a severe reduction and pulmonary QOL -> depression,
anxiety and PTSD are common
patient often have cognitive impairment -> these correlate with the period and severity of hypoxia