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Special Feature
April 2002

Image of the Month

Arch Surg. 2002;137(4):492. doi:
Answer: Acute Respiratory Distress Syndrome

Figure 1A, Chest radiograph shows a nondisplaced left clavicular fracture and mild increase in vascular markings. B, Postintubation chest radiograph shows a displaced left clavicular fracture and early bilateral patchy infiltrates.

In 1967, Ashbaugh et al1 first described acute respiratory distress syndrome (ARDS) in 12 patients with acute respiratory distress, cyanosis refractory to O2 therapy, decreased lung compliance, and diffuse infiltrates that were evident on the chest radiograph. Initially termed adult respiratory distress syndrome, it was subsequently renamed because the condition affects patients of any age. In 1988, an expanded definition was proposed that included a 4-point lung injury score based on the extent of chest radiographic abnormalities, the severity of hypoxemia, the degree of lung compliance, and the amount of positive end-expiratory pressure (PEEP).2 In 1994, the American-European Consensus Conference Committee proposed the current definition of ARDS.3 These criteria included an acute onset, bilateral infiltrates evident on chest radiographs, and either a pulmonary capillary wedge pressure of ≤18 mm Hg or the absence of clinical evidence of elevated left atrial pressure.3 This committee also proposed the term acute lung injury to describe those patients who have a "lesser form" of ARDS. Acute lung injury is defined by a PaO2/FIO2 ratio of ≤300 mm Hg, whereas in ARDS, the PaO2/FIO2 ratio has been set as ≤200 mm Hg.

Numerous risk factors for the development of ARDS have been identified. These causes can be subdivided into those associated with direct lung injury and indirect lung injury. Direct causes include aspiration, pneumonia, pulmonary contusion, inhalation injury, fat emboli, and near-drowning. Indirect causes include sepsis, shock, severe extrathoracic trauma, cardiopulmonary bypass, and multiple blood transfusions.4

Often progressive ARDS is characterized by 2 distinct stages.4 The initial acute, or exudative, phase is manifested by a rapid onset of respiratory failure. Arterial hypoxemia that is refractory to O2 therapy is characteristic. Radiographic changes are sometimes delayed, and the patchy or asymmetric infiltrates can be indistinguishable from those of cardiogenic pulmonary edema. Often, these radiographic findings underrepresent the profound degree of arteriopulmonary shunt that may develop in these patients. During the acute phase, there is diffuse alveolar damage with hyaline membrane deposition and hemorrhage, as well as progressive neutrophil and macrophage infiltration.5 Protein-rich fluid leaks into the interstitial spaces and the alveoli. Resultant surfactant abnormalities lead to increased surface tension within the alveoli, causing alveolar disruption and atelectasis.

After the acute lung injury phase of ARDS, some will have an uncomplicated course and resolution.6 In others, the disease progresses to a fibroproliferative stage that can be observed histologically as early as 5 to 7 days after ARDS onset.7 The fibroproliferative stage is characterized by infiltration of the interstitium with fibroblasts and other mesenchymal cells.8 Collagen deposition with decreased lung compliance and increased dead space results.

Mechanical ventilation remains the central supportive intervention in managing ARDS. Historically, a volume of 12 to 15 mL/kg was recommended in patients with ARDS; however, this high tidal volume may cause further injury to alveoli and lead to hyaline membrane formation.9 A recent large ARDS Network trial10 compared traditional mechanical ventilation with ventilation at a lower tidal volume. The subsequent mortality was significantly lower in the group treated with lower tidal volumes (approximately 6 mL/kg) than in the group treated with traditional tidal volumes. Lung recruitment and alveolar stabilization through the use of PEEP are also mainstays of ARDS management.11 Other means of intervention, including surfactant replacement,12 inhalation of nitric oxide,13 glucocorticoid administration,14 and inverse ratio ventilation, have been investigated by various groups, but with conflicting results.

Corresponding author: Shariq Sayeed, MD, University of Rochester Medical Center, Box SURG, 601 Elmwood Ave, Rochester, NY 14642 (e-mail: shariq_sayeed@urmc.rochester.edu).

Ashbaugh  DGBigelow  DBPetty  TLLevine  BE Acute respiratory distress in adults. Lancet. 1967;2319- 323Article
Murray  JFMatthay  MALuce  JMFlick  MR An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis. 1988;138720- 723Article
Bernard  GRArtigas  ABrigham  KL  et al.  The American-European Consensus Conference of ARDS. Am J Respir Crit Care Med. 1994;149818- 824Article
Ware  LBMatthay  MA The acute respiratory distress syndrome. N Eng J Med. 2000;3421334- 1349Article
Anderson  WRThielen  K Correlative study of adult respiratory distress syndrome by light, scanning, and transmission electron microscopy. Ultrastruct Pathol. 1992;16615- 628Article
Matthay  MAWiener-Kronish  JP Intact epithelial barrier function is critical for the resolution of alveolar edema in humans. Am Rev Respir Dis. 1990;1421250- 1257Article
Pratt  PCVollmer  RTShelburne  JDCrapo  JD Pulmonary morphology in a multihospital collaborative extracorporeal membrane oxygenation project, I: light microscopy. Am J Pathol. 1979;95191- 214
Fukuda  YIshizaki  MMasuda  YKimura  GKawanami  OMasugi  Y The role of intraalveolar fibrosis in the process of pulmonary structural remodeling in patients with diffuse alveolar damage. Am J Pathol. 1987;126171- 182
Dreyfuss  DBasset  GSoler  PSaumaon  G Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats. Am Rev Respir Dis. 1985;132880- 884
The Acute Respiratory Distress Syndrome Network, Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;3421301- 1308Article
Amato  MBPBarbas  CSMedeiros  D  et al.  Beneficial effects of the "open lung approach" with low distending pressures in acute respiratory distress syndrome: a prospective randomized study on mechanical ventilation. Am J Respir Crit Care Med. 1995;1521835- 1846Article
Anzueto  ABaughman  RPGuntupalli  KK  et al. for the Exosurf Acute Respiratory Distress Syndrome Sepsis Study Group, Aerosolized surfactant in adults with sepsis-induced acute respiratory distress syndrome. N Engl J Med. 1996;3341417- 1421Article
Dellinger  RPZimmerman  JLTaylor  RW  et al. and the Inhaled Nitric Oxide in ARDS Study Group, Effects of inhaled nitric oxide in patients with acute respiratory distress syndrome. Crit Care Med. 1998;2615- 23Article
Meduri  GUHeadley  ASGolden  E  et al.  Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial. JAMA. 1998;280159- 165Article