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Acute respiratory distress syndrome (ARDS) was first described in 1967 by Ashbaugh, who described a syndrome of severe respiratory failure associated with pulmonary infiltrates, similar to infant hyaline membrane disease.
The 1994 American-European Consensus Committee defines ARDS as the acute onset of bilateral infiltrates on chest radiography, a partial pressure of arterial oxygen (PaO2) to fraction of inspired oxygen (FIO2) ratio of less than 200 mm Hg and a pulmonary artery occlusion pressure of less than 18, or the absence of clinical evidence of left arterial hypertension.
Put simply, ARDS is the presence of pulmonary edema in the absence of volume overload or depressed left ventricular function. This is distinguished from acute lung injury, which is similar to ARDS with the exception of a PaO2/FIO2 ratio of less than 300 mm Hg.
ARDS occurs in children as well as adults. The condition originates from a number of insults involving damage to the alveolocapillary membrane with subsequent fluid accumulation within the airspaces of the lung. Histologically, these changes have been termed diffuse alveolar damage.
The development of ARDS starts with damage to the alveolar epithelium and vascular endothelium resulting in increased permeability to plasma and inflammatory cells into the interstitium and alveolar space. Damage to the surfactant- producing type II cells and the presence of protein-rich fluid in the alveolar space disrupts the production and function of pulmonary surfactant leading to microatelectasis and impaired gas exchange.
Ultimately, regional variations in pulmonary perfusion, ventilation/perfusion (V/Q) mismatch with shunting of blood through unventilated alveoli, and increased alveolar-arterial oxygen gradient occur. Eventually, resorption of alveolar edema, regeneration of epithelial cells, proliferation and differentiation of type II alveolar cells, and alveolar remodeling occur.
Some patients have an uncomplicated course and rapid resolution, whereas others may progress to fibrosing alveolitis, which involves the deposition of collagen in alveolar, vascular, and interstitial spaces leading to poor lung compliance. Fibrosing alveolitis has been reported histologically as early as 5-7 days.
The mortality rate is approximately 30-40% in spite of maximal medical management and support. Deaths usually result from multisystem organ failure rather than lung failure alone.
Patients may present early in the course of the disease without symptoms or signs. Mild tachypnea may be the only manifestation. Severe respiratory distress eventually ensues. It comes on quickly and unexpectedly. Rales are frequently heard on auscultation of the lungs. However, examination findings may be surprisingly minimal when contrasted with chest radiographic findings. Signs of volume overload, such as a third heart sound (S3) on auscultation of the heart or jugular venous distention, should be noticeably absent.
A number of clinical conditions are associated with development of ARDS. Sepsis and the systemic inflammatory response syndrome (SIRS) are the most common predisposing factors associated with development of ARDS. These conditions may result from the indirect toxic effects of neutrophil-derived inflammatory mediators in the lungs.
Severe traumatic injury (especially multiple fractures), severe head injury, and pulmonary contusion are strongly associated with development of ARDS. Long bone fractures may give rise to ARDS through fat embolism. After severe head injury, ARDS is thought to result from a sudden discharge of the sympathetic nervous system, leading to acute pulmonary hypertension and injury to the pulmonary capillary bed. Pulmonary contusions cause ARDS through direct trauma to the lung.
Multiple transfusions are another important risk factor for ARDS, independent of the reason for transfusion or the coexistence of trauma. The incidence of ARDS increases with the number of units transfused. Preexisting liver disease or coagulation abnormalities further contribute to this risk.
Patients who have nearly drowned can develop ARDS. Development of ARDS is slightly more common with salt- water aspiration than with fresh-water aspiration. Infiltrates and hypoxia develop within 12-24 hours of the initial accident. Patients who are symptomatic after 6 hours of observation generally do well. Aspiration is particularly damaging to lung tissue, leading to an osmotic gradient that favors movement of water into airspaces of the lung. Aspiration may be visible with chest radiography, although the chest radiograph may be normal early in the course of the disease.
Smoke inhalation causes lung tissue damage from direct heat, toxic chemicals, and particulate matter carried into the lower lung. Patients with smoke inhalation initially may be asymptomatic. Patients with airway burns and/or exposure to carbon monoxide or toxic fumes should be monitored closely for development of ARDS, even if symptoms initially are absent.
Overdoses of narcotics (e.g.: heroin), salicylates, tricyclic antidepressants, and other sedatives have been associated with development of ARDS. (Overdoses of tricyclic antidepressants are the most common.) This risk is independent of the risk from concurrent aspiration. Other implicated toxins and drugs include tocolytic agents, hydrochlorothiazide, protamine, and interleukin-2 (IL-2).
ABG (arterial blood gas) usually reveals hypoxia. Respiratory alkalosis may be present early in the course of the disease; hypercarbia and respiratory acidosis develop as the disease progresses. Complete blood count (CBC), serum electrolytes, blood urea nitrogen (BUN), and creatinine should be ordered. Appropriate cultures in cases of severe ARDS without discernible cause should be obtained, as sepsis is by far the most common etiology.
The chest radiograph most often depicts bilateral diffuse infiltrates, normal-sized cardiac silhouette, and absence of vascular redistribution (e.g.: cephalization). Chest radiographic findings may be normal early in the course of the disease but may rapidly progress to complete whiteout of both lung fields.
Treatment of the patient is largely supportive. Intensive ventilatory support and hemodynamic monitoring are essential. The correct approach to the patient requires that the physician apply a cardiac monitor, a pulse-oximeter, and a time-cycled noninvasive BP cuff. He should start an IV line and administer fluids to hypotensive patients. As volume overload in the presence of ARDS may significantly worsen pulmonary edema, volume status must be reassessed continually. Patients must be placed on sufficient supplemental oxygen to keep the oxygen saturation above 90%. Endotracheal intubation should be performed if the oxygen saturation drops or if the patient develops fatigue or hypercarbia.
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