History
Acute respiratory distress syndrome (ARDS) is characterized by the development of acute dyspnea and hypoxemia within hours to days of an inciting event, such as trauma, sepsis, drug overdose, massive transfusion, acute pancreatitis, or aspiration. In many cases, the inciting event is obvious, but, in others (eg, drug overdose), it may be harder to identify.
Patients developing ARDS are critically ill, often with multisystem organ failure, and they may not be capable of providing historical information. Typically, the illness develops within 12-48 hours after the inciting event, although, in rare instances, it may take up to a few days.
With the onset of lung injury, patients initially note dyspnea with exertion. This rapidly progresses to severe dyspnea at rest, tachypnea, anxiety, agitation, and the need for increasingly high concentrations of inspired oxygen.
Physical Examination
Physical findings often are nonspecific and include tachypnea, tachycardia, and the need for a high fraction of inspired oxygen (FiO2) to maintain oxygen saturation. The patient may be febrile or hypothermic. Because ARDS often occurs in the context of sepsis, associated hypotension and peripheral vasoconstriction with cold extremities may be present. Cyanosis of the lips and nail beds may occur.
Examination of the lungs may reveal bilateral rales. Rales may not be present despite widespread involvement. Because the patient is often intubated and mechanically ventilated, decreased breath sounds over 1 lung may indicate a pneumothorax or endotracheal tube down the right main bronchus.
Manifestations of the underlying cause (eg, acute abdominal findings in the case of ARDS caused by pancreatitis) are present.
In a septic patient without an obvious source, pay careful attention during the physical examination to identify potential causes of sepsis, including signs of lung consolidation or findings consistent with an acute abdomen. Carefully examine sites of intravascular lines, surgical wounds, drain sites, and decubitus ulcers for evidence of infection. Check for subcutaneous air, a manifestation of infection or barotrauma.
Because cardiogenic pulmonary edema must be distinguished from ARDS, carefully look for signs of congestive heart failure or intravascular volume overload, including jugular venous distention, cardiac murmurs and gallops, hepatomegaly, and edema.
Complications
Patients with ARDS often require high-intensity mechanical ventilation, including high levels of positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) and, possibly, high mean airway pressures; thus, barotrauma may occur. Patients present with pneumomediastinum, pneumothorax, or both. Other potential complications that may occur in these mechanically ventilated patients include accidental extubation and right mainstem intubation.
If prolonged mechanical ventilation is needed, patients may eventually require tracheostomy. With prolonged intubation and tracheostomy, upper airway complications may occur, most notably postextubation laryngeal edema and subglottic stenosis.
Because patients with ARDS often require prolonged mechanical ventilation and invasive hemodynamic monitoring, they are at risk for serious nosocomial infections, including ventilator-associated pneumonia (VAP) and line sepsis. The incidence of VAP in ARDS patients may be as high as 55% and appears to be higher than that in other populations requiring mechanical ventilation. Preventive strategies include elevation of head of the bed, use of subglottic suction endotracheal tubes, and oral decontamination.
Other potential infections include urinary tract infection (UTI) related to the use of urinary catheters and sinusitis related to the use of nasal feeding and drainage tubes. Patients may also develop Clostridium difficile colitis as a complication of broad-spectrum antibiotic therapy. Patients with ARDS, because of the extended intensive care unit (ICU) stay and treatment with multiple antibiotics, may also develop infections with drug-resistant organisms such as methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Enterococcus (VRE), or gram-negative organisms with extended-spectrum beta-lactamases.
In a study of survivors of ARDS, significant functional impairment was noted at 1 year, primarily related to muscle wasting and weakness. [13] Corticosteroid treatment and use of neuromuscular blockade are risk factors for muscle weakness and poor functional recovery.
Patients may have difficulty weaning from mechanical ventilation. Strategies to facilitate weaning, such as daily interruption of sedation, [16] early institution of physical therapy, attention to maintaining nutrition, and use of weaning protocols, may decrease the duration of mechanical ventilation and facilitate recovery.
Renal failure is a frequent complication of ARDS, particularly in the context of sepsis. Renal failure may be related to hypotension, nephrotoxic drugs, or underlying illness. Fluid management is complicated in this context, especially if the patient is oliguric. Multisystem organ failure, rather than respiratory failure alone, is usually the cause of death in ARDS.
Other potential complications include ileus, stress gastritis, and anemia. Stress ulcer prophylaxis is indicated for these patients. Anemia may be prevented by the use of growth factors (erythropoietin).
Although not mentioned often, survivors of ARDS often suffer from posttraumatic stress disorder (PTSD), prolonged myopathy limiting activities of daily living, and increased long-term mortality after apparent recovery. [17] These major postillness complications usually linger a minimum of 3 months, but several patients have persistent neurocognitive dysfunction 1-2 years afterward, independent of physiologic status and cardiopulmonary reserve. The management of these complications is primarily supportive and aided by the clinician having a keen awareness that such PTSD symptoms persist.
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Anteroposterior portable chest radiograph in patient who had been in respiratory failure for 1 week with diagnosis of acute respiratory distress syndrome. Image shows endotracheal tube, left subclavian central venous catheter in superior vena cava, and bilateral patchy opacities in mostly middle and lower lung zones.
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Photomicrograph from patient with acute respiratory distress syndrome (ARDS). Image shows ARDS in exudative stage. Note hyaline membranes and loss of alveolar epithelium in this early stage of ARDS.
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Portable chest radiograph in a patient with acute respiratory distress syndrome. The condition evolved over approximately 1 week.
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Portable chest radiograph in a patient with acute respiratory distress syndrome. The condition evolved over approximately 1 week.
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Portable chest radiograph in a patient with acute respiratory distress syndrome. The condition evolved over approximately 1 week.
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Photomicrograph from a patient with acute respiratory distress syndrome (ARDS). This image shows ARDS in the early proliferative stage. Note the type 2 pneumocytic proliferation, with widening of the septa and interstitial fibroblast proliferation.
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Photomicrograph from a patient with acute respiratory distress syndrome (ARDS). This image shows ARDS in the late proliferative stage. Note the extensive fibroblast proliferation, with incorporation of the hyaline membranes.
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Chest radiograph in a patient with acute respiratory distress syndrome (ARDS). The patient was treated with perflubron, which is used for partial liquid ventilation.
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Portable chest radiograph. This image shows bilateral opacities that are suggestive of ARDS.
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Computed tomography scan in a patient with suspected acute respiratory distress syndrome (ARDS). This image was obtained at the cardiac level with mediastinal window settings and shows bilateral pleural effusions instead of diffuse bilateral lung consolidation. In addition, the presence of some compression atelectasis in the lower lobes is observed.
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High-resolution computed tomography scan in a patient with acute respiratory distress syndrome. This image demonstrates a small right pleural effusion, consolidation with air-bronchograms, and some ground-glass-appearing opacities. The findings indicate an alveolar process, in this case, alveolar damage.
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ARDS, subacute 4x: low power view of lung in the organizing phase of ARDS. There is compression of alveoli by proliferating interstitial fibrous tissue but occasional hyaline membranes are still visible. Photomicrograph courtesy of Rodolfo Laucirica, M.D
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ARDS, subacute 20x: higher power view of an alveolus (center) lined by hyaline membranes with proliferating interstitial fibroblasts to the left and right of center. Photomicrograph courtesy of Rodolfo Laucirica, M.D
