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Acute
respiratory distress syndrome
Definition
Consensus conference definition:
- acute onset
- a condition known to be
associated with the development of ARDS
- bilateral infiltrates on frontal CXR
- PAWP <18 if measured or absence of evidence of LA hypertension if not
- PaO2/FiO2
<200 mmHg (26 kPa)
Definition of acute lung injury
is the same except the severity of gas exchange impairment is less (PaO2
<300 mmHg)
Epidemiology
- Not well studied. Best estimate is about 3/100000/year with a mortality of
about 60%
- <20% of deaths are due to refractory respiratory failure
- Commonest causes:
- septic shock
- gastric aspiration
- Other causes include:
Develops very soon after the precipitating event. Usually within 12-72 hours
and often within 6 hours
Pathogenesis
- probably part of a systemic problem that is manifested in lung
- all aetiologies eventually lead to clinically similar responses and injury of
both epithelium and endothelium of lung. However it is conceptually useful to
consider 2 separate main mechanisms of injury: a direct insult to the lung
(primary ARDS) and
the effects of systemic inflammatory response on the lung (secondary ARDS)
- result of a complex interaction between:
- pro- and anti-inflammatory mediators
- resolution of inflammation as a result of apoptosis
- activation of coagulation cascade
- genetic pre-disposition
- mechanical injury from mechanical ventilation
- poor function of mechanisms responsible for clearing exuded fluid from
lungs
Effects on cardiac function
- increased pulmonary vascular resistance results in increased right
ventricular load. Cardiac output is maintained by an increase in RV stroke work,
pressure and volume until RV failure develops (rare)
- RV failure results in decreased LV output because of decreased LV preload.
Also ̃ back pressure on systemic venous and portal
venous systems
- LV function is depressed in septic shock
Multi-organ failure
- common "complication" of ARDS
- incidence of organ failure in ARDS:
- renal 40-55%
- hepatic 12%
- CNS 7-30% (confusion, coma, agitation, fits)
- GI failure 7-30% (haemorrhage, ileus, malabsorption, acalculous
cholecystitis, pancreatitis)
- haematological 0-26% (WBC < 1, platelets < 50, fibrinogen < 0.1
g/dl)
- cardiovascular 10-23% (cardiac index < 2 l/min/m2 or MAP
< 60 mmHg or reversible VF or asystole)
- mortality closely related to number of organ systems involved. Varies from
15-30% for lung alone to > 80% for three or more organs.
- not clear whether multiple organ failure is a consequence of ARDS or whether
ARDS is simply one manifestation of a more widespread disease process that shows
itself in the lung first because of the immediate requirements for gas exchange.
Current evidence favours the latter hypothesis.
Extracorporeal membrane oxygenation (ECMO)
- very expensive
- not associated with improved survival
Drug treatment
No treatment has been shown conclusively to be of benefit in ARDS
Cyclo-oxygenase inhibitors
- NSAIDs, especially ibuprofen improve shock and acute lung injury in models
of sepsis
- trend towards increased thoracic compliance and decreased airway pressures
in patients with sepsis syndrome treated with ibuprofen but not statistically
significant
- Antagonism of thromboxane with ketoconazole not found to be useful in
multi-centered randomized controlled trial
Corticosteroids
- Not useful in the acute management of ARDS
- May be of value in ARDS variants such as fat embolism
- Have been suggested as potential treatment for later "fibroproliferative"
phase. Very limited clinical data suggests that there may be a benefit.
Nitric oxide
- inhaled nitric oxide (40 ppm in air) reduces pulmonary hypertension and in
concentrations of 15-20 ppm decreases shunting and improves gas exchange in ARDS
by preferentially increasing blood flow to ventilated areas of the lung
- no systemic effects because nitric oxide scavenged rapidly by Hb
– 3 clinical trials have failed to show evidence of improved outcome in
patients treated with NO
Prostacyclin
- inhaled prostacyclin vasodilates as effectively as NO but does not confer as
much oxygenation benefit
Surfactant
- controlled trial of artificial surfactant failed to show an improvement in
outcome. However this was probably due to the fact that the delivery system
resulted in the surfactant being denatured
Cardiovascular management
- treatment aimed at reducing pulmonary capillary hydrostatic pressure causes
a reduction of pulmonary oedema formation in animal models of ARDS. There is
also some evidence to suggest that protocols which lead to negative fluid
balance improve outcome.
- however patients with severe ARDS may have decreased ventricular compliance
and preload reduction in these patients puts them at particular risk of falls in
cardiac output and oxygen delivery
- in severe ARDS PEEP may decrease RV output by increasing RV afterload.
Maintenance of RV output is usually achieved through the use of inotropes and
increasing preload. An alternative is to decrease RV afterload with PGE1 or
prostacyclin but this approach is limited by systemic hypotension and increasing
shunt fraction. Inhaled nitric oxide promising.
Prognosis
- immediate prognosis related to number of organ systems involved:
- lung only 15-30% mortality
- 2 organs 45-55%
- 3 or more > 80%
This figure rises to 100% if the multiple organ failure persists beyond 4
days
-
outcome also varies with the cause of ARDS. 90% of patients with ARDS
secondary to fat embolus survive whereas nearly 100% of patients with ARDS
following bone marrow transplantation die.
-
death is not usually due to respiratory failure.
Further reading
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