Acute Respiratory Distress
Syndrome
Definition
Acute respiratory distress syndrome (ARDS) is a
clinical syndrome of severe dyspnea of rapid onset,
hypoxemia, and diffuse pulmonary infiltrates
leading to respiratory failure.
Acute lung injury (ALI) is a less severe disorder but
has the potential to evolve into ARDS.
Epidemiology
The annual incidences of ALI and ARDS are
estimated to be up to 80/100,000 and
60/100,000, respectively.
Approximately 10% of all ICU admissions suffer
from acute respiratory failure, with ~20% of these
patients meeting criteria for ALI or ARDS.
Etiology
Most frequently reported surgical condition in ARDS : Trauma, pulmonary
contusion, multiple bone fractures, and chest wall trauma/flail chest.
The time course of ARDS
Exudative phase
Alveolar capillary endothelial cells & type I pneumocytes
(alveolar epithelial cells) are injured
Lost of the normally tight alveolar barrier to fluid and
macromolecules
Edema fluid (rich in protein) accumulates in the interstitial
and alveolar spaces
Significant concentrations of cytokines (e.g., IL-1, IL-8, and
TNF-α) and lipid mediators (e.g., leukotriene B4)
Exudative phase
In response to pro-inflammatory mediators, leukocytes
(especially neutrophils) traffic into the pulmonary
interstitium and alveoli.
Condensed plasma proteins aggregate with cellular debris
and dysfunctional pulmonary surfactant hyaline
membrane whorls
Pulmonary vascular injury also occurs early in ARDS, with
vascular obliteration by microthrombi and fibrocellular
proliferation
Proliferative phase
The initiation of lung repair, organization of alveolar
exudates, and a shift from a neutrophil- to a lymphocyte-
predominant pulmonary infiltrate.
As part of the reparative process, there is a proliferation of
type II pneumocytes along alveolar basement membranes.
These specialized epithelial cells synthesize new pulmonary
surfactant and differentiate into type I pneumocytes.
The presence of alveolar type III procollagen peptide
(marker of pulmonary fibrosis) is associated with a
protracted clinical course and increased mortality from
ARDS.
Fibrotic phase
The alveolar edema and inflammatory exudates are
converted to extensive alveolar duct and interstitial
fibrosis.
Acinar architecture is markedly disrupted, leading to
emphysema-like changes with large bullae.
Intimal fibroproliferation in the pulmonary
microcirculation leads to progressive vascular occlusion
and pulmonary hypertension.
The physiologic consequences include an increased risk
of pneumothorax, reductions in lung compliance, and
increased pulmonary dead space.
Diagnostic Criteria for ARDS
History
History of presenting complaint
Rapid breathing or difficult to breath
Association symptoms
Confusion, extreme tiredness,restlessness, agitation
Cough and fever (if your ARDS is caused by
pneumonia)
Past medical history and Drug History
Has patient been previously admitted to hospital with
similar symptoms?
Does patient have DM or Hipertension previously and
was patient compliant to medications?
Patient has any heart problems such as heart failure
previously?
Does the patient have asthma and is compliant to the
medications
Surgical history
Did the patient had any surgery done before?
Allergic history
Ask about all allergies including, for example, food,
inhaled allergens and drugs
Occupational and social history
Does the patient smoke, if yes how many years?
Occupational exposure to pollutions
Family history
Physical Examination
Inspection
Tachycardia and tachypnea (RR more than 30 to 40
breaths per minute)
Cyanosis (blue skin, lips, and nails caused by lack of
oxygen to the tissues) is often seen.
nasal flaring
Blood pressure may be normal or elevated initially,
then decreased in the later stages
Palpation
peripheral pulses reveals rapid
Percussion
Dull percussion noted
Auscultation
In the early stage, the lungs have decreased breath
sounds.
In the middle stages of ARDS, the patient may have
basilar crackles or even coarse crackles.
In the late stage of ARDS, if the disease has been left
untreated, the patient may have bronchial breath
sounds or little gas exchange with no breath sounds
When the patient is intubated and mechanically
ventilated, the lungs may sound extremely congested,
with wheezes and coarse crackles throughout
Investigation
Arterial blood gases usually detect an acute
respiratory alkalosis, hypoxemia, and an elevated
alveolar-arterial oxygen gradient. The hypoxemia is
generally due to physiological shunting.
Blood tests, including complete blood count and other
blood tests to look for signs of infection
Chest x-ray typically has bilateral alveolar infiltrates.
(The absence of pulmonary venous congestion, Kerley B
lines, cardiomegaly, and pleural effusions helps
distinguish ALI/ARDS from pulmonary edema).
Computed tomography (CT) reveals patchy
abnormalities that are more dense in dependent lung
zones.(also look for fluid in the lungs, signs of
pneumonia, or other lung problems)
Sputum cultures & analysis to see if bacteria or fungi
are present.
Bronchoscopy to analyze airways. A laboratory
examination may indicate presence of certain viruses or
cancer cells
Occasionally, an echocardiogram (heart ultrasound),
to rule out congestive heart failure
Complication
Infections such as nosocomial pneumonia
Pneumotorax causing lung collapse
Barotrauma
Renal failure
O2 toxicity
Tracheal ulceration
Blood clots lead to DVT
Pulmonary embolism
Management
Oxygenation
Continuous mechanical ventilatory - CMV with
intermittent positive pressure ventilation(IPPV).
If oxygenation cannot be maintain at adequate level
with FiO260%, use positive end expiratory pressure
(PEEP) 5-15cm H2O (0.5-1.5 kPa)
Use low tidal volume ventilation of < 7ml/kg to
minimize barotrauma.
A pH of >7.2 should be aim.
Fluid management
Must be carefully controlled to allow improvement of
systemic and pulmonary perfusion without aggravating
pulmonary oedema.
Use Swan-Ganz catheter, measuring pulmonary
capillary wedge pressure (PCWP) at 8-12cm H20.
IV frusemide should be used in patient with fluid
overload.
Check BP, peripheral perfusion, urine output.
Cardiac support
Optimal preload is achieved with fluid administration
according to the PCWP.
Inotropic agents such as dobutamine or dopamine, if
cardiac output cannot be maintained and urine output
is poor despite adequate hydration.
Specific therapy
Early corticosteroid does not prevent ARDS.
Corticosteroid use in proliferative phase may hasten
recovery.
Treatment of underlying causes and other
supportive measures
Thank You
