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Respiratory Alterations and Management 363

AETIOLOGY
ARDS is a characteristic inflammatory response of the TABLE 14.8 Direct and indirect causes of acute
lung to a wide variety of insults. Approximately 200,000 lung injury 9
patients are diagnosed annually in the USA with ARDS,
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accounting for 10–15% of ICU admissions. Commonly Direct lung injury Indirect lung injury
associated clinical disorders can be separated into ● Pneumonia ● Sepsis
9
those that directly or indirectly injure the lung (see ● Aspiration of gastric contents ● Multiple trauma
Table 14.8). ● Pulmonary contusion ● Cardiopulmonary
● Fat, amniotic fluid, or air embolus bypass
The most common cause of indirect injury resulting in ● Near drowning ● Drug overdose
ALI/ARDS is sepsis, followed by severe trauma and hae- ● Inhalational injury (chemical or ● Acute pancreatitis
smoke)
modynamic shock states. Transfusion-related ALI (TRALI) ● Reperfusion pulmonary oedema ● Transfusion of blood
products
is not common but is observed in ICU. ARDS arising
from direct injury to the lung is most commonly seen in
patients with pneumonia. An individual’s risk of develop-
ing ARDS increases significantly when more than one
predisposing factor is present. 6 chest X-ray. The Murray Lung Injury Score was developed
as a method for clarifying and quantifying the existence
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PATHOPHYSIOLOGY and severity of the disease. The American-European
Inflammatory damage to alveoli from inflammatory Consensus Conference on ARDS provided the following
mediators (released locally or systemically) causes a definition:
change in pulmonary capillary permeability, with result- ● acute onset of arterial hypoxaemia (PaO 2 :FiO 2 ratio
ing fluid and protein leakage into the alveolar space and < 200)
pulmonary infiltrates. Dilution and loss of surfactant ● bilateral infiltrates on radiography without evidence
causes diffuse alveolar collapse and a reduction in pul- of left atrial hypertension or congestive cardiac failure.
monary compliance and may also impair the defence
mechanisms of the lungs. Intrapulmonary shunt is con- The spectrum of disease was also acknowledged and the
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firmed when hypoxaemia does not improve despite sup- term ALI was introduced to describe patients with a less
plemental oxygen administration. The characteristic severe but clinically similar form of respiratory failure
6
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course of ARDS is described as having three phases: 6,45 (PaO 2 :FiO 2 ratio <300). It has been suggested that these
definitions require review as they include such a broad,
1. Oedematous phase: involves an early period of heterogenous group of patients that has limited investiga-
alveolar damage and pulmonary infiltrates result- tion of appropriate management strategies. This may also
ing in hypoxaemia. This phase is characterised by be because the interventions studied were ineffective, but
migration of neutrophils into the alveolar com- it is just as likely that the broadly inclusive definition of
partment, releasing a variety of substances includ- ARDS captures a heterogeneous group of patients that
ing proteases, gelatinases A and B, and reactive respond differently to current therapies. 48
nitrogen and oxygen species that damage the
alveoli. Further damage is caused by resident alveo- CLINICAL MANIFESTATIONS
lar macrophages and release of proinflammatory While no specific test exists to determine whether a
cytokines that amplify the inflammatory response patient has ARDS, it should be considered in any patient
in the lung. Significant ventilation–perfusion with a predisposing risk factor who develops severe
(intrapulmonary shunt) mismatch evolves causing hypoxaemia, reduced compliance and diffuse pulmonary
hypoxaemia. infiltrates on a chest X-ray. ARDS usually occurs 1–2
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2. Proliferative phase: begins after 1–2 weeks as pul- days following onset of a presenting condition and is
monary infiltrates resolve and fibrosis and remod- characterised by rapid clinical deterioration. Common
elling occurs. This phase is characterised by reduced symptoms include severe dyspnoea, dry cough, cyano-
alveolar ventilation and pulmonary compliance sis, hypoxaemia requiring rapidly-escalating amounts of
and ventilation–perfusion mismatch. Reduced supplemental oxygen and persistent coarse crackles on
compliance (stiff lungs) causes further atelectasis auscultation. 6
in the mechanically ventilated patient as alveoli are
damaged by increased volume and/or pressure on Assessment
inspiration.
3. Fibrotic phase: the final phase where alveoli A patient with ARDS requires ongoing monitoring of
become fibrotic and the lung is left with oxygenation and ventilation through ABG analysis and
emphysema-like alterations. pulse oximetry and monitoring of PaCO 2 to assess per-
missive hypercapnia. Monitoring of ventilatory pressures
and volumes ensures that additional lung injury is pre-
DIAGNOSIS vented. As many patients with ARDS require cardiovascu-
A standardised definition of ARDS was first described in lar support, assessment of haemodynamics and peripheral
1988, with three clinical findings; hypoxia, decreased pul- perfusion is important to ensure oxygen delivery to cells
monary compliance and diffuse infiltrates observed on a is achieved. 6