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       Acute  Respiratory Distress Syndrome

        Dr Sampurna Roy MD

 


Syn: Adult Respiratory Distress Syndrome

              

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The most important cause of diffuse alveolar damage is the acute respiratory distress syndrome (ARDS).

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In this syndrome, a patient with apparently normal lungs suffers an insult and then develops rapidly progressive respiratory failure, characterized  by hypoxia and extensive radiologic opacities in both lungs.

Acute Respiratory Distress Syndrome (ARDS) is characterized by diffuse alveolar capillary damage, leading to severe pulmonary edema, respiratory failure and arterial hypoxemia refractory to oxygen therapy.

Respiratory failure, unresponsive to oxygen therapy, develops with diffuse bilateral infiltration on x-ray and frequent superimposed infections, resulting in death (more than 50 %).

Over the years there has been much debate about the term ARDS.

Some feel that the definition of rapidly progressive respiratory failure in a patient with apparently normal lungs is too broad, since it obviously encompasses many conditions in which a more specific diagnosis can be made, such as pneumonia of any sort, fat embolism, pulmonary thromboembolism, aspiration, inhalation of toxic gases etc.

Others have doubted the existence of ARDS related to trauma and have held that the pulmonary lesions are due to known causes, such as oxygen toxicity or hemodynamic pulmonary edema .

However, there is now little doubt that ARDS is a useful term and that it is not simply due to oxygen or hemodynamic pulmonary edema.

 It should be recognized that the syndrome of ARDS exists and is multifactorial and that it is appropriate to qualify the term as ARDS due to specific conditions, such as nonthoracic trauma, inhalation of toxic gases, aspiration etc.  In addition, oxygen toxicity produces similar lesions, and an idiopathic category should also be recognized.

 The overall medical costs are enormous, since mangement requires high technology and intensive care.

The syndrome was first recognized as an entity during the Vietnam War as a result of effective resuscitation techniques for seriously injured combatants.

 Typically nonthoracic trauma or infection leads to hemodynamic shock, from which the patient is resuscitated.

However, recovery is inturrupted by respiratory symptoms (Eg. tachypnea, dyspnea, and hypoxemia) and a chest radiograph shows diffuse bilateral infiltrates, which progresses to virtually complete opacification.

The patient requires ventilatory assistance and increasing amounts of oxygen.

The lungs become stiff (decreased compliance), and increasing end-expiratory pressures are required, until the patient needs 100% oxygen to maintain tissue oxygenation.

 Half of all patients with Acute Respiratory Distress Syndrome (ARDS) die.

           

 ARDS has been studied in patients and in animal models.

The important early event is leakiness of endothelial capillaries, with morphologic loosening of the intercellular junctions. At this stage respiratory failure is not apparent.

Then, 24 to 48 hours after the initial insult, pulmonary edema and resultant hypoxemia ensue in the exudative phase.

The next stage is diffuse alveolar damage, in which necrosis of type I epithelial cells and hyaline membranes that line the air spaces are prominent.

In the proliferative phase, type II cells multiply to reconstitute the alveolar lining and an interstitial inflammatory infiltrate of mononuclear cells is accompanied by proliferation of fibroblasts.

All these conditions are present 4 to 7days after the insult, and the patient usually dies in severe respiratory failure.

 If the patient survives, the lesions may heal with resorption of the alveolar exudates and hyaline membranes and restitution of the normal alveolar epithelium.

Fibroblastic proliferation ceases and the extra collagen is metabolized.

It is well documented that patients with ARDS who recover have normal pulmonary function.

Alternatively, more fibrous tissue is laid down and the lung then becomes remodeled to produce the “honeycomb lung” - multiple cyst-like spaces throughout the lung, separated from each other by fibrous tissue and lined by type II cells, bronchiolar epithelium, or squamous cells . The resemblance of the honeycomb lung to the end stage of fibrosing alveolitis is rarely more than superficial.

Following ARDS there is more active fibroblastic proliferation and less dense scarring. Bronchiolar epithelium lining is less promonent and secretions are not present in the spaces.

Occasionally, an appearance similar to bronchopulmonary dysplasia develops.

In ARDS produced by the inhalation of toxic gases or near-drowning, the damage occurs primarily at the alveolar epithelial surface.As indicated, the alveolar epithelial junctions are usually very tight ; damage to the epithelium results in exudation of fluid and proteins from the interstitium into the alveolar spaces. Endothelial damage may or may not occur in ARDS that is due to inhalation of toxic substances, but the sequence of events is similar to that due to endothelial damage in ARDS that follows trauma or septicemia.

Mechanism of injury:  

1. Oxygen-derived free radicals, especially in the toxicity induced by prolonged exposure (e.g. in respirators) to high concentrations of oxygen or other toxins (e.g.- paraquat).

2. Aggregation of activated neutrophils in the pulmonary vasculature. Clinical studies have shown that a reduced number of neutrophils in the blood of patients with risk factors for ARDS is a good predictor for the development of the syndrome. This finding suggests that increased numbers of neutrophils are sequestered in the pulmonary capillary bed. These neutrophils damage epithelium by secreting several types of injurious factors, including oxygen-derived free radicals and lysosomal enzymes (proteases). It also secretes arachidonic acid metabolites that induce neutrophil aggregation.

3. Activation of lung macrophages, which release oxidants, proteases and proinflammatory cytokines (e.g. IL-8).

4. Loss or damage to surfactant, contributing to atelectasis, which (in combination with pulmonary edema) results in the stiff lungs characteristic of ARDS.

Diagnostic studies in patients with acute respiratory distress syndrome.Semin Thorac Cardiovasc Surg. 2006 Spring;18(1):2-7

Acute respiratory distress syndrome (ARDS) is a clinical-radiological diagnosis. Clinical diagnosis comprises severe hypoxemia assessed by arterial oxygen tension/fraction of inspired oxygen ratio of less than 200 and bilateral infiltrate on a chest radiograph in the absence of left atrial hypertension. The sensitivity and specificity of the clinical diagnosis vary based on the underlying etiology for ARDS. Except for presence of bilateral infiltrate on chest radiograph and severe hypoxemia on arterial blood gas, most diagnostic studies are used to exclude mimics of ARDS and potentially modify treatment. Computerized tomography of the chest is helpful in understanding the extent of the disease and is more sensitive in identifying pneumomediastinum and pneumothoraces seen frequently in patients with ARDS, which can be missed on a chest radiograph, especially if they are small in size. Measurements of alveolar dead space ventilation fraction can be helpful in determining the prognosis in individuals with ARDS. Bronchoalveolar lavage, transbronchial lung biopsy, and open lung biopsies can be safely performed in patients with ARDS. Bronchoalveolar lavage fluid in patients with ARDS shows neutrophil predominance with increased edema fluid to serum protein ratio. Diffuse alveolar damage, a pathognomic of ARDS, is seen on histopathology on transbronchial lung biopsy or open lung biopsy. Most common complications of these procedures include transient hypoxemia, respiratory acidosis, and pneumothorax with occasional persistent air leak. The potential risk of diagnostic studies should be balanced against the possible foreseeable benefits of the diagnostic studies.

          

 Summary of Pathogenesis and Pathological features:

Pathogenesis:

The basic lesion is diffuse damage to the alveolar wall, initially involving the capillary endothelium but eventually the epithelium as well. Damage leads to the acute stage of ARDS with increased capillary permeability and edema, fibrin exudation, formation of hyaline membrane (composed of necrotic epithelial cell debris and exuded proteins), and septal inflammation.

Pathological features:

In the acute stage:

Gross features:  lungs are diffusely firm, red, boggy, and heavy.

Microscopic features:  Shows diffuse alveolar damage with interstitial and intra-alveolar edema, hyaline membranes and acute inflammation.

In the proliferative/organizing stage:

There are patchy areas of intersititial fibrosis and type-II epithelial proliferation, frequently, in fatal cases with superimposed bacterial infection.

                        

 
 June 2010

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Before 1992, the acronym ARDS represented the adult respiratory distress syndrome. The American-European Consensus Committee on ARDS standardized the definition in 1994 and renamed it acute rather than adult respiratory distress syndrome because it occurs at all ages. The term acute lung injury (ALI) was also introduced at that time. The committee recommended that ALI be defined as "a syndrome of inflammation and increased permeability that is associated with a constellation of clinical, radiologic, and physiologic abnormalities that cannot be explained by, but may coexist with, left atrial or pulmonary capillary hypertension.

Ref:  Report of the American-European consensus conference on ARDS: definitions, mechanisms, relevant outcomes and clinical trial coordination. Intensive Care Med 1994;20:225-32.

Abstracts:

Lung biopsy in ARDS: is it worth the risk?
Crit Care. 2006;10(4):160.

Pathology of acute lung injury and acute respiratory distress syndrome: a clinical-pathological correlation.
Clin Chest Med. 2006 Dec;27(4) :571-8;
 

Validity of the diagnostic criteria of the acute respiratory distress syndrome.Med Intensiva. 2006 ;30(5):212-7

Comparison of clinical criteria for the acute respiratory distress syndrome with autopsy findings.Ann Intern Med. 2004 Sep 21;141(6):440-5

Sepsis syndrome, the adult respiratory distress syndrome, and nosocomial pneumonia. A common clinical sequence.Clin Chest Med. 1990 Dec;11(4):633-56

Host responses in mediating sepsis and adult respiratory distress syndrome.Semin Respir Infect. 1990 Sep;5(3):233-47

Why do patients who have acute lung injury/acute respiratory distress syndrome die from multiple organ dysfunction syndrome? Implications for management.
Clin Chest Med. 2006 Dec;27(4): 725-31;

Genetic epidemiology of acute respiratory distress syndrome: implications for future prevention and treatment.
Clin Chest Med. 2006 Dec;27(4): 705-24;

Clinical epidemiology of acute lung injury and acute respiratory distress syndrome: incidence, diagnosis, and outcomes.Clin Chest Med. 2006 Dec;27(4):549-57; abstract vii

Epidemiology of acute lung injury and acute respiratory distress syndrome.Semin Respir Crit Care Med. 2006 Aug;27(4):327-36

Epidemiology of ARDS.Minerva Anestesiol. 2006 Jun;72(6):473-7

Acute respiratory distress syndrome: frequency, clinical course, and costs of care.Crit Care Med. 1999 Nov;27(11):2367-74

Role of nonbronchoscopic lavage for investigating alveolar inflammation and permeability in acute respiratory distress syndrome.Crit Care Med. 2006 Jan;34(1):57-64

Open-lung biopsy in patients with acute respiratory distress syndrome.Anesthesiology. 1998 Apr;88(4):935-44

Open lung biopsy in early-stage acute respiratory distress syndrome.Crit Care. 2006;10(4):R106


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