Acute Respiratory Distress Syndrome
From Pharmpedia
Acute Respiratory Distress Syndrome (ARDS) as the name suggests, is not a specific disease but an acute syndrome that usually follows severe, acute lung injury.
It is characterized pulmonary edema (in the absence of volume overload or depressed left ventricular function), refractory hypoxia, and decreased lung compliance, due to sudden and life-threatening lung failure. The alveoli get inflamed, leading to accumulation of fluid (pulmonary edema) and collapse. The alveolar collapse leads to defective gas exchange with attendant lack of oxygen to the body.
Although termed "adult," this syndrome can also occur in children where it is called as Infant Respiratory Distress Syndrome . Though there are some similarities with ARDS, the causes and treatment are different.
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Definition
ARDS is defined as an acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for cardiogenic pulmonary edema.
Incidence
The exact figure is not known but is estimated to occur in 1.5 to 75 cases per 100,000 persons.
Mortality and morbidity
Death from ARDS ranges from 35–50%.
Deaths usually result from oxygen lack leading to multisystem organ failure (including lung failure).
It may take up to one year for the lung to resume its normal function, in those who survive.
Causes
ARDS is precipitated by the following acute conditions that directly or indirectly injure the lung.
Direct lung injuries
Pneumonia - bacterial or viral*
Aspiration of stomach contents
Near drowning (salt as opposed to fresh water)
Trauma - Chest injury
Inhalation of smoke/ toxic gas (e.g. carbon monoxide)
- Severe Acute Respiratory Syndrome (SARS) is a viral pneumonia due to the SARS coronavirus. About 20% of patients suffering from SARS develop ARDS. Of those who require mechanical ventilation, about 25% die. Thus the SARS coronavirus must be added to the list of infections that cause ARDS.
Indirect lung injuries
Sepsis (a toxic condition resulting from spread of bacteria) – is the highest risk factor
Trauma - head injury or other multiple injuries
Shock – profound/prolonged
Massive blood transfusion
Burns
O2 toxicity
Acute hemorrhagic pancreatitis
Ingestion of certain drugs (overdose with tricyclic antidepressants, narcotics [e.g. heroin], other sedatives and salicylates)
Who are at more risk for ARDS?
Patients with chronic lung disease, chronic alcoholics, and patients over 65 years of age are usually the higher risk category prone for ARDS.
Pathophysiology
The onset of ARDS is within one to three days of the original illness or injury. The initial lung injury is poorly understood. Any of the various causes mentioned earlier initiate pulmonary endothelial and epithelial damage and subsequent increased permeability. Thus the alveoli and the accompanying blood vessels get damaged in ARDS.
It is suggested that activated white blood cells and platelets accumulate in blood vessels, the interstitium, and airspaces; they release mediators like prostaglandins, toxic oxygen radicals, proteolytic enzymes,
(such as tumor necrosis factor and interleukins), which injure cells, promote inflammation and fibrosis, and alter tone of the
bronchial muscles and vasoreactivity. In short there is an increase in pulmonary or circulatory pro-inflammatory cytokines. This
leads to fluid leaks into the lungs because of the increased permeability by the damaged blood vessels.
The accumulation of fluid in the alveoli prevents the normal gas
exchange (severe ventilation-perfusion mismatch), leading to respiratory failure and oxygen deficiency (severe hypoxia) with a
decrease in the Pao2/Fio2 ratio.
Clinical features
Dyspnea (difficulty in breathing) occurs first, usually with tachypnea (rapid), shallow respiration leading to respiratory alkalosis and tachycardia. These are the early and typical manifestations leading to severe hypoxia, and decreased lung compliance ultimately resulting in respiratory failure within 48 hours.
The skin may appear cyanotic or mottled (due to hypoxia) and may not improve with O2.
Auscultation may be normal or there may be crackles, rhonchi, or wheezes.
Diagnosis
Early diagnosis requires a high index of suspicion aroused by the onset of dyspnea in settings that predispose to ARDS.
A presumptive diagnosis can be made with the presentation features and chest x-ray.
Initial arterial blood gas analysis shows acute respiratory alkalosis: a very low PaO2 , a normal or low PaCO2, and an elevated pH.
Patients with a ratio of partial pressure of arterial oxygen to a fraction of inspired oxygen of 300 or less are considered to
have acute lung injury (ALI), whereas those patients with severe hypoxemia and a ratio of 200 or less are considered to have
ARDS.
Chest x-rays may show diffuse bilateral alveolar infiltrates resembling acute pulmonary edema, but ARDS often lack cardiomegaly, pleural effusions, and vascular redistribution. The changes seen on x-ray often lag many hours behind functional changes. The extremely low PaO2 often persists despite high concentrations of inspired O2 (FiO2), indicating pulmonary right-to-left shunting through atelectatic and consolidated lung units that are not ventilated.
Computed tomographic (CT) scans of the chest- Bilateral alveolar opacities are seen during the acute phase and Bilateral reticular opacities, reduced lung volumes and, occasionally, large bullae are CT findings during the fibroproliferative stage (later stage).
Pulmonary arterial wedge pressure (PAWP) is low (< 18 mm Hg) in ARDS Lung biopsy or lavage by bronchoscopy may be needed.
The American-European Consensus Conference defines ARDS as PaO2/FiO2< 200 (regardless of positive end-expiratory pressure), bilateral infiltration on frontal chest x-rays, and PAWP <= 18 mm Hg when measured or no clinical evidence of left atrial hypertension.
FiO2 is the percentage of oxygen in the air inhaled, either on or off the ventilator. FiO2 ranges are from 21% (eg in room air) to 100% (eg pure oxygen).
Differential Diagnosis
Pulmonary edema of heart failure – PAWP is high (> 20 mm Hg) in heart failure.
Pulmonary embolism - pulmonary angiography should be performed to rule out this.
Pneumocystis carinii pneumonia and other primary lung infections - especially in immunocompromised patients – Lung biopsy or lavage to confirm.
Treatment
The goal is to support the patient’s breathing till the lungs heal. The main mode of treatment is supportive care, in an intensive care unit (ICU), with hemodynamic monitoring, mechanical ventilation (with appropriate level of sedation to facilitate patient-ventilator synchrony and limit patient discomfort) and supplemental oxygen.
The use of positive end-expiratory pressure (PEEP) to diminish alveolar collapse and the use of low tidal volumes and limited levels of inspiratory filling pressures appear to be beneficial in diminishing the ventilator-associated lung injury. Recently it has been suggested that small, rather than large, breaths of air from a mechanical ventilator reduces the number of deaths by 22 percent.
Early identification and treatment of the underlying disorder is equally essential.
Supportive care also includes attempts to minimize the development of complications such as nosocomial infection, gastrointestinal bleeding, and thromboembolism. Stress ulcer prophylaxis, careful hand washing and full-barrier precautions (to reduce nosocomial infection risk), deep venous thrombosis prophylaxis, nutritional support (in most cases, enteral administration preferred).
Currently no approved pharmacological therapy for ARDS is available. Inhaled nitric oxide, a pulmonary vasodilator, (to improve ventilation-perfusion match), corticosteroids and exogenous surfactant treatments (to reduce inflammation and improve surfactant function) have so far not been shown to reduce mortality but still more studies are on way.
Survival following ARDS depends upon the cause, age of the patient and severity of the condition.
Recovery rate is better in younger people and those with fewer chronic health problems.
Death rate may be more in cases of sepsis than that due to trauma or pulmonary infection.
Milder forms of ARDS tend to have a better recovery chance. Many patients who survive ARDS have permanent, mild to moderate impairment of lung function with poor quality of life because many may need tracheostomy.
Prevention
No successful preventative measure has been identified.
References
Author
This is original article by Dr.Gurusamy Sivagnanam
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