Respiratory Distress is defined as the presence of bilateral pulmonary infiltrates on chest radiograph, impaired oxygenation resulting in a PaO₂ to fraction of inspired oxygen (FIO₂) ratio of less than 200, and absence of elevated pulmonary arterial occlusion pressure (PAOP) or left atrial pressure. Stated another way, ARDS is the presence of pulmonary edema in the absence of volume overload or depressed left ventricular function.

                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.

• Mild tachypnea may be the only manifestation.

• Severe respiratory distress eventually ensues.

Physical:

• Rales most often are heard with auscultation of the lungs, although, surprisingly, findings usually are minimal compared to 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.

Causes:

• 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. In association with head injury, ARDS is thought to ensue from a sudden discharge of the sympathetic nervous system, resulting in 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 (eg, 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).