eMedicine Specialties > Critical Care > Medical Topics

Acute Respiratory Distress Syndrome: Treatment & Medication

Author: Eloise M Harman, MD, Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, University of Florida College of Medicine
Contributor Information and Disclosures

Updated: Nov 4, 2009

Treatment

Medical Care

No specific therapy for acute respiratory distress syndrome (ARDS) exists. Treatment of the underlying condition is essential, along with supportive care and appropriate ventilator and fluid management. Because infection is often the underlying cause of ARDS, careful assessment of the patient for infected sites and institution of appropriate antibiotic therapy are essential. In some instances, removal of intravascular lines, drainage of infected fluid collections, or surgical debridement or resection of an infected site, such as the ischemic bowel, may be necessary because sepsis-associated ARDS does not resolve without such management. However, large tidal volume (>6 mL/kg ideal body weight) worsens outcome. Other important interventions in sepsis might include early goal-directed therapy, tight glucose control, use of drotrecogin alpha in appropriate patients with severe sepsis, and avoidance of complications by means of prophylaxis for deep venous thrombosis and stress ulcer. The use of stress dose steroids in patients with septic shock did not change survival in a recently reported controlled trial.10  With the development of the NIH-sponsored ARDS Clinical Trials Network, large well-controlled trials of ARDS therapies have been completed. Thus far, the only treatment found to improve survival rates in such a study is a mechanical ventilation strategy using low tidal volumes.

Fluid management

Separating out initial resuscitation, as used for early goal directed therapy, and maintenance fluid therapy is important. Several small trials have demonstrated improved outcome for ARDS in patients treated with diuretics or dialysis to promote a negative fluid balance in the first few days.

An ARDS Clinical Trials Network study of fluid conservative versus fluid liberal strategies in the management of patients with ARDS/ALI did not demonstrate a statistically significant difference in 60 day mortality when patients were stratified into either group 72 hours after presenting in ARDS.11 However, patients treated with the fluid conservative strategy had an improved oxygenation index and lung injury score and an increase in ventilator-free days, without an increase in nonpulmonary organ failures.

Note that the fluid conservative group actually had an even rather than negative fluid balance over the first seven days, leading to the thought that the benefit may have been underestimated. Maintaining a low-normal intravascular volume may be facilitated by hemodynamic monitoring with a central venous or Swan-Ganz catheter, aiming for a CVP or pulmonary capillary wedge pressure at the lower end of normal. Maintaining mean arterial pressure of 65-70 or more may then require pressor administration. Closely monitor urine output and administer diuretics to facilitate a negative fluid balance. In oliguric patients, hemodialysis with ultrafiltration or continuous veno-venous hemofiltration/dialysis (CVVHD) may be required.

Noninvasive ventilation

Because intubation and mechanical ventilation may be associated with an increased incidence of complications, such as barotrauma and nosocomial pneumonia, noninvasive ventilation by means of a full face mask attached to a ventilator delivering continuous positive airway pressure (CPAP) with or without ventilator breaths or inspiratory pressure support (ie, noninvasive positive pressure ventilation [NIPPV]) in patients with milder ARDS may be advantageous. Noninvasive ventilation has been studied best in patients with hypercapnic respiratory failure caused by chronic obstructive pulmonary disease (COPD) or neuromuscular weakness; however, in a small series of patients with ARDS, some patients may have avoided intubation using this technique. This may be especially useful in immunocompromised patients.

Contraindications to NIPPV include a diminished level of consciousness or other causes of decreased airway protection reflexes, inadequate cough, vomiting or upper gastrointestinal bleeding, inability to properly fit the mask, poor patient cooperation, and hemodynamic instability.

Mechanical ventilation

The goals of mechanical ventilation in ARDS are to maintain oxygenation while avoiding oxygen toxicity and complications of mechanical ventilation. Generally, maintain oxygen saturations in the range of 85-90%, with a goal of diminishing inspired oxygen concentrations to less than 65% within the first 24-48 hours. This almost always necessitates the use of moderate-to-high levels of PEEP.

Mechanical ventilation may promote the development of acute lung injury. Evidence now indicates that a protective ventilation strategy using low tidal volumes improves survival rates compared with conventional tidal volumes. In a study conducted by the ARDS Network, patients with ALI and ARDS were randomized to mechanical ventilation at a tidal volume of 12 mL/kg of predicted body weight and an inspiratory pressure of 50 cm H2 O or less versus a tidal volume of 6 mL/kg and an inspiratory pressure of 30 cm H2 O or less. The study was stopped early after interim analysis of 861 patients demonstrated that subjects in the low tidal volume group had a significantly lower mortality rate, 31% versus 39.8%.12

While previous studies employing low tidal volumes allowed patients to be hypercapnic (permissive hypercapnia) and acidotic to achieve the protective ventilation goals of low tidal volume and low inspiratory airway pressure, the ARDS Network Study allowed increases in respiratory rate and administration of bicarbonate to correct acidosis. This may account for the positive outcome in this study compared to earlier studies that had failed to demonstrate a benefit. Thus, mechanical ventilation with a tidal volume of 6 mL/kg predicted body weight is recommended, with adjustment of the tidal volume to as low as 4 mL/kg if needed to limit the inspiratory plateau pressure to 30 cm H2 O or less. Increase the ventilator rate and administer bicarbonate as needed to maintain the pH at a near normal level (7.3).

In the ARDS Network Study, patients ventilated with lower tidal volumes required higher levels of PEEP (9.4 vs 8.6 cm H2 O) to maintain oxygen saturation at 85% or more. Some authors have speculated that the higher levels of PEEP may also have contributed to the improved survival rates. However, a subsequent ARDS study network trial of higher versus lower PEEP levels in patients with ARDS showed no benefit from higher PEEP levels, either in terms of survival or duration of mechanical ventilation.

  • Positive end-expiratory pressure or continuous positive airway pressure
    • ARDS is characterized by severe hypoxemia. When oxygenation cannot be maintained despite high inspired oxygen concentrations, the use of CPAP or PEEP usually promotes improved oxygenation, allowing for tapering of the FIO2. With PEEP, positive pressure is maintained throughout expiration, but when the patient inhales spontaneously, airway pressure decreases to below zero to trigger airflow. With CPAP, a low-resistance demand valve is used to allow positive pressure to be maintained continuously. Positive pressure ventilation increases intrathoracic pressure and, thus, may decrease cardiac output and blood pressure. Because mean airway pressure is greater with CPAP than PEEP, CPAP may have a more profound effect on blood pressure.
    • In general, patients tolerate CPAP well, and CPAP is usually used rather than PEEP. The use of appropriate levels of CPAP is thought to improve the outcome in ARDS. By maintaining the alveoli in an expanded state throughout the respiratory cycle, CPAP may decrease shear forces that promote ventilator-associated lung injury.
    • The best method for finding the optimal level of CPAP in patients with ARDS is controversial. Some favor the use of just enough CPAP to allow reduction of the FIO2 below 65%.
      • Another approach, favored by Amato and associates is the so-called open lung approach, in which the appropriate level is determined by the construction of a static pressure volume curve.13 This is an S-shaped curve, and the optimal level of PEEP is just above the lower inflection point. Using this approach, the average PEEP level required is 15.
      • However, as noted above, an ARDS Network study of higher versus lower PEEP levels in ARDS demonstrated no advantage to use of higher PEEP levels. In this study, PEEP level was determined by how much inspired oxygen was required to achieve a goal oxygen saturation of 88-95% or goal PO2 of 55-80 mm Hg. The PEEP level averaged 8 in the lower PEEP group and 13 in the higher PEEP group. No difference was shown in duration of mechanical ventilation or survival to hospital discharge.14
  • Pressure-controlled ventilation and high frequency ventilation
    • If high inspiratory airway pressures are required to deliver even low tidal volumes, pressure-controlled ventilation (PCV) may be initiated. In this mode of mechanical ventilation, the physician sets the level of pressure above CPAP (delta P) and the inspiratory time (I-time) or inspiratory/expiratory (I:E) ratio. The resultant tidal volume depends on lung compliance and increases as ARDS improves. PCV may also result in improved oxygenation in some patients not doing well on volume-controlled ventilation (VCV). If oxygenation is a problem, longer I-times, such that inspiration is longer than expiration (inverse I:E ratio ventilation) may be beneficial. Ratios as high as 4:1 have been used. PCV, using lower peak pressures, may also be beneficial in patients with bronchopleural fistulae, facilitating closure of the fistula.
    • Evidence indicates that PCV may be beneficial in ARDS, even without the special circumstances noted. In a multicenter controlled trial comparing VCV to PCV in patients with ARDS, Esteban found that PCV resulted in fewer organ system failures and lower mortality rates than VCV, despite use of the same tidal volumes and peak inspiratory pressures.15 A larger trial is needed before a definite recommendation is made.
    • High frequency ventilation (jet or oscillatory) is a ventilator mode that uses low tidal volumes and high respiratory rates. With the knowledge that distension of alveoli is one of the mechanisms promoting ventilator-associated lung injury, high frequency ventilation would be expected to be beneficial in ARDS. Results of clinical trials in adults have generally demonstrated early improvement in oxygenation when compared with conventional ventilation but no improvement in survival. In the largest randomized controlled trial, 148 adults with ARDS were randomized to conventional ventilation or high frequency oscillatory ventilation (HFOV). The HFOV group had early improvement in oxygenation that did not persist beyond 24 hours. The 30-day mortality in the HFOV group was 37% compared with 52% in the conventional ventilation group, but this difference was not statistically significant.16 This mode of ventilation may be the most useful for patients with bronchopleural fistulae.
    • Partial liquid ventilation has also been tried in ARDS and in a randomized controlled trial in which it was compared with conventional mechanical ventilation, resulted in increased morbidity (pneumothoraces, hypotensions, and hypoxemic episodes), and a trend toward higher mortality.17
  • Prone position
    • Although, 60-75% of patients with ARDS have significantly improved oxygenation when turned from the supine to the prone position, no survival benefit exists for patients treated in the prone position. When the prone position is used, the improvement in oxygenation is rapid and often significant enough to allow reductions in FIO2 or level of CPAP. The prone position is safe, with appropriate precautions to secure all tubes and lines, and does not require special equipment. The improvement in oxygenation may persist after the patient is returned to the supine position and may occur on repeat trials in patients who did not respond initially.
    • Possible mechanisms for the improvement noted are recruitment of dependent lung zones, increased functional residual capacity (FRC), improved diaphragmatic excursion, increased cardiac output, and improved ventilation-perfusion matching.
      • Despite improved oxygenation with the prone position, randomized controlled trial of the prone position in ARDS have not demonstrated improved survival. In an Italian study, the survival rate to discharge from the ICU and the survival rate at 6 months were unchanged compared with patients who underwent care in the supine position, despite a significant improvement in oxygenation.18 This study was criticized because patients were kept in the prone position for an average of only 7 hours per day.
      • However, in a subsequent French study in which patients were in the prone position for at least 8 hours per day, no benefit was shown to the prone position in terms of 28 day or 90 day mortality, duration of mechanical ventilation, or development of ventilator-associated pneumonia.19

Surgical Care

The treatment of acute respiratory distress syndrome (ARDS) is medical. Surgical intervention may be required for some of the underlying causes of ARDS, as previously noted. In patients requiring prolonged mechanical ventilation, tracheostomy is eventually required.

Extracorporeal membrane oxygenation (ECMO) was demonstrated in a large multicenter trial in the 1970s not to improve the mortality rate in ARDS. Still, it remains a potential heroic measure in select cases.

Consultations

Treatment of patients with acute respiratory distress syndrome (ARDS) requires special expertise with mechanical ventilation and management of critical illness. Thus, consult a physician specializing in pulmonary medicine or critical care.

Diet

Institution of nutritional support after 48-72 hours of mechanical ventilation usually is recommended. Unless contraindicated because of an acute abdomen, ileus, gastrointestinal bleeding, or other conditions, enteral nutrition via a feeding tube is preferable to intravenous hyperalimentation. A low-carbohydrate high-fat enteral formula containing components that are anti-inflammatory and vasodilating (eicosapentaenoic acid and linoleic acid) with antioxidants has been demonstrated in some studies to improve outcome in ARDS.20,21 In a prospective, randomized study of ARDS patients fed with an enteral nutrition formula containing antioxidants, eicosapentaenoic acid, and gamma-linoleic acid compared with a standard isocaloric formula, Pontes-Arruda demonstrated improved survival and oxygenation in patients receiving the specialized diet.

Activity

Patients with acute respiratory distress syndrome (ARDS) are at bedrest. Frequent position change and passive and, if possible, active range of motion activities of all muscle groups should be started immediately. Elevation of the head of the bed to a 45° angle is recommended to diminish the development of ventilator-associated pneumonia.

Medication

No drug has proved beneficial in the prevention or management of ARDS. The early administration of corticosteroids in septic patients does not prevent the development of ARDS. Numerous pharmacologic therapies, including the use of inhaled synthetic surfactant, intravenous antibody to endotoxin, ketoconazole, and ibuprofen, have been tried and are not effective.22 Small sepsis trials suggest a potential role for antibody to TNF and recombinant IL-1 receptor antagonist. Inhaled nitric oxide (NO), a potent pulmonary vasodilator seemed promising in early trials, but in larger controlled trials, did not change mortality rates in adults with ARDS.23,24

It was thought that there might be a role for high-dose corticosteroid therapy in patients with late (fibroproliferative phase) ARDS, because of apparent benefit in small trials.25 However, an ARDS Study Network trial of methylprednisolone for patients with ARDS persistent for at least 7 days demonstrated no benefit in terms of 60-day mortality.26 Patients treated late, 14 days after onset, had worsened mortality with corticosteroid therapy. Although no survival advantage was shown in patients treated with methylprednisolone, short-term clinical benefits included improved oxygenation and increased ventilator-free and shock-free days. Patients treated with corticosteroids were more likely to experience neuromuscular weakness, but the rate of infectious complications was not increased.

Corticosteroids

Development of the late phase of ARDS may represent continued uncontrolled inflammation and corticosteroids may be considered a form of rescue therapy that may improve oxygenation and hemodynamics but does not change mortality, except that corticosteroids increase mortality in patients with ARDS for more than 14 days.


Methylprednisolone (Solu-Medrol)

High-dose methylprednisolone has been used in trials of patients with ARDS who have persistent pulmonary infiltrates, fever, and high oxygen requirement despite resolution of pulmonary or extrapulmonary infection. Pulmonary infection is assessed with bronchoscopy and bilateral BAL and quantitative culture.

Adult

2 mg/kg of predicted body weight IV loading dose followed by 0.5 mg/kg of predicted body weight q6h

Pediatric

Not established

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Documented hypersensitivity; documented ARDS for >14 d; active tuberculosis; uncontrolled bacterial, viral, fungal infection

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Depo-Medrol contains benzyl alcohol which is potentially toxic when administered locally to neural tissue; administration of Depo-Medrol by other than indicated routes, including the epidural route, has been associated with reports of serious medical events including arachnoiditis, meningitis, paraparesis/paraplegia, sensory disturbances, bowel/bladder dysfunction, seizures, visual impairment including blindness, ocular and periocular inflammation, and residue or slough at injection site

More on Acute Respiratory Distress Syndrome

Overview: Acute Respiratory Distress Syndrome
Differential Diagnoses & Workup: Acute Respiratory Distress Syndrome
Treatment & Medication: Acute Respiratory Distress Syndrome
Follow-up: Acute Respiratory Distress Syndrome
Multimedia: Acute Respiratory Distress Syndrome
References
[ CLOSE WINDOW ]

References

  1. Ashbaugh DG, Bigelow DB, Petty TL. Acute respiratory distress in adults. Lancet. Aug 12 1967;2(7511):319-23. [Medline].

  2. Luhr OR, Antonsen K, Karlsson M. Incidence and mortality after acute respiratory failure and acute respiratory distress syndrome in Sweden, Denmark, and Iceland. The ARF Study Group. Am J Respir Crit Care Med. Jun 1999;159(6):1849-61. [Medline].

  3. Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, Neff M. Incidence and outcomes of acute lung injury. N Engl J Med. Oct 20 2005;353(16):1685-93. [Medline].

  4. Davidson TA, Caldwell ES, Curtis JR. Reduced quality of life in survivors of acute respiratory distress syndrome compared with critically ill control patients. JAMA. Jan 27 1999;281(4):354-60. [Medline].

  5. Davey-Quinn A, Gedney JA, Whiteley SM. Extravascular lung water and acute respiratory distress syndrome--oxygenation and outcome. Anaesth Intensive Care. Aug 1999;27(4):357-62. [Medline].

  6. Herridge MS, Cheung AM, Tansey CM. One-year outcomes in survivors of the acute respiratory distress syndrome. N Engl J Med. Feb 20 2003;348(8):683-93. [Medline].

  7. [Best Evidence] The NHLBI ARDS Clinical Trials Network. Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. N Engl J Med. May 25 2006;354(21):2213-24. [Medline].

  8. Connors AF Jr, Speroff T, Dawson NV. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA. Sep 18 1996;276(11):889-97. [Medline].

  9. Murray JF, Matthay MA, Luce JM. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis. Sep 1988;138(3):720-3. [Medline].

  10. [Best Evidence] Sprung CL, Annane D, Keh D, Moreno R, Singer M, Freivogel K. Hydrocortisone therapy for patients with septic shock. N Engl J Med. Jan 10 2008;358(2):111-24. [Medline].

  11. [Best Evidence] The NHLBI ARDS Clinical Trials Network. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. Jun 15 2006;354(24):2564-75. [Medline].

  12. 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. May 4 2000;342(18):1301-8. [Medline].

  13. Amato MB, Barbas CS, Medeiros DM. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med. Feb 5 1998;338(6):347-54. [Medline].

  14. Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, Ancukiewicz M. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. Jul 22 2004;351(4):327-36. [Medline].

  15. Esteban A, Alia I, Gordo F. Prospective randomized trial comparing pressure-controlled ventilation and volume-controlled ventilation in ARDS. For the Spanish Lung Failure Collaborative Group. Chest. Jun 2000;117(6):1690-6. [Medline].

  16. Derdak S, Mehta S, Stewart TE. High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial. Am J Respir Crit Care Med. Sep 15 2002;166(6):801-8. [Medline].

  17. Kacmarek RM, Wiedemann HP, Lavin PT. Partial liquid ventilation in adult patients with acute respiratory distress syndrome. Am J Respir Crit Care Med. Apr 15 2006;173(8):882-9.

  18. Gattinoni L, Tognoni G, Pesenti A. Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J Med. Aug 23 2001;345(8):568-73. [Medline].

  19. Guerin C, Gaillard S, Lemasson S. Effects of systematic prone positioning in hypoxemic acute respiratory failure: a randomized controlled trial. JAMA. Nov 17 2004;292(19):2379-87.

  20. Gadek JE, DeMichele SJ, Karlstad MD. Effect of enteral feeding with eicosapentaenoic acid, gamma-linolenic acid, and antioxidants in patients with acute respiratory distress syndrome. Enteral Nutrition in ARDS Study Group. Crit Care Med. Aug 1999;27(8):1409-20. [Medline].

  21. Pontes-Arruda A, Aragão AM, Albuquerque JD. Effects of enteral feeding with eicosapentaenoic acid, gamma-linolenic acid, and antioxidants in mechanically ventilated patients with severe sepsis and septic shock. Crit Care Med. Sep 2006;34(9):2325-33. [Medline].

  22. Cepkova M, Matthay MA. Pharmacotherapy of acute lung injury and the acute respiratory distress syndrome. J Intensive Care Med. May-Jun 2006;21(3):119-43. [Medline].

  23. Dellinger RP, Zimmerman JL, Taylor RW. Effects of inhaled nitric oxide in patients with acute respiratory distress syndrome: results of a randomized phase II trial. Inhaled Nitric Oxide in ARDS Study Group. Crit Care Med. Jan 1998;26(1):15-23. [Medline].

  24. Griffiths MJ, Evans TW. Inhaled nitric oxide therapy in adults. N Engl J Med. Dec 22 2005;353(25):2683-95.

  25. Meduri GU, Chinn AJ, Leeper KV. Corticosteroid rescue treatment of progressive fibroproliferation in late ARDS. Patterns of response and predictors of outcome. Chest. May 1994;105(5):1516-27. [Medline].

  26. [Best Evidence] Steinberg KP, Hudson LD, Goodman RB, Hough CL, Lanken PN, Hyzy R. Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome. N Engl J Med. Apr 20 2006;354(16):1671-84. [Medline].

  27. Abraham E, Matthay MA, Dinarello CA. Consensus conference definitions for sepsis, septic shock, acute lung injury, and acute respiratory distress syndrome: time for a reevaluation. Crit Care Med. Jan 2000;28(1):232-5. [Medline].

  28. Albert RK. The prone position in acute respiratory distress syndrome: where we are, and where do we go from here. Crit Care Med. Sep 1997;25(9):1453-4. [Medline].

  29. Anzueto A, Baughman RP, Guntupalli KK. Aerosolized surfactant in adults with sepsis-induced acute respiratory distress syndrome. Exosurf Acute Respiratory Distress Syndrome Sepsis Study Group. N Engl J Med. May 30 1996;334(22):1417-21. [Medline].

  30. Artigas A, Bernard GR, Carlet J. The American-European Consensus Conference on ARDS, part 2. Ventilatory, pharmacologic, supportive therapy, study design strategies and issues related to recovery and remodeling. Intensive Care Med. Apr 1998;24(4):378-98. [Medline].

  31. Bachofen M, Weibel ER. Alterations of the gas exchange apparatus in adult respiratory insufficiency associated with septicemia. Am Rev Respir Dis. Oct 1977;116(4):589-615. [Medline].

  32. Bachofen M, Weibel ER. Structural alterations of lung parenchyma in the adult respiratory distress syndrome. Clin Chest Med. Jan 1982;3(1):35-56. [Medline].

  33. Bernard GR, Artigas A, Brigham KL. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. Mar 1994;149(3 Pt 1):818-24. [Medline].

  34. Brochard L, Roudot-Thoraval F, Roupie E. Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. The Multicenter Trail Group on Tidal Volume reduction in ARDS. Am J Respir Crit Care Med. Dec 1998;158(6):1831-8. [Medline].

  35. Chesnutt AN, Matthay MA, Tibayan FA. Early detection of type III procollagen peptide in acute lung injury. Pathogenetic and prognostic significance. Am J Respir Crit Care Med. Sep 1997;156(3 Pt 1):840-5. [Medline].

  36. Doyle RL, Szaflarski N, Modin GW. Identification of patients with acute lung injury. Predictors of mortality. Am J Respir Crit Care Med. Dec 1995;152(6 Pt 1):1818-24. [Medline].

  37. Folkesson HG, Matthay MA, Westrom BR. Alveolar epithelial clearance of protein. J Appl Physiol. May 1996;80(5):1431-45. [Medline].

  38. Greene KE, Wright JR, Steinberg KP. Serial changes in surfactant-associated proteins in lung and serum before and after onset of ARDS. Am J Respir Crit Care Med. Dec 1999;160(6):1843-50. [Medline].

  39. Hickling KG, Walsh J, Henderson S. Low mortality rate in adult respiratory distress syndrome using low- volume, pressure-limited ventilation with permissive hypercapnia: a prospective study. Crit Care Med. Oct 1994;22(10):1568-78. [Medline].

  40. Hudson LD. Protective ventilation for patients with acute respiratory distress syndrome. N Engl J Med. Feb 5 1998;338(6):385-7. [Medline].

  41. Hudson LD, Milberg JA, Anardi D. Clinical risks for development of the acute respiratory distress syndrome. Am J Respir Crit Care Med. Feb 1995;151(2 Pt 1):293-301. [Medline].

  42. Hudson LD, Steinberg KP. Epidemiology of acute lung injury and ARDS. Chest. Jul 1999;116(1 Suppl):74S-82S. [Medline].

  43. Humphrey H, Hall J, Sznajder I. Improved survival in ARDS patients associated with a reduction in pulmonary capillary wedge pressure. Chest. May 1990;97(5):1176-80. [Medline].

  44. Kress JP, Pohlman AS, O''Connor MF. Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation. N Engl J Med. May 18 2000;342(20):1471-7. [Medline].

  45. Laufe MD, Simon RH, Flint A. Adult respiratory distress syndrome in neutropenic patients. Am J Med. Jun 1986;80(6):1022-6. [Medline].

  46. Marik PE, Krikorian J. Pressure-controlled ventilation in ARDS: a practical approach. Chest. Oct 1997;112(4):1102-6. [Medline].

  47. Martin C, Papazian L, Payan MJ. Pulmonary fibrosis correlates with outcome in adult respiratory distress syndrome. A study in mechanically ventilated patients. Chest. Jan 1995;107(1):196-200. [Medline].

  48. Martinet Y, Menard O, Vaillant P. Cytokines in human lung fibrosis. Arch Toxicol Suppl. 1996;18:127-39. [Medline].

  49. Matthay MA. Conference summary: acute lung injury. Chest. Jul 1999;116(1 Suppl):119S-126S. [Medline].

  50. Matthay MA, Folkesson HG, Verkman AS. Salt and water transport across alveolar and distal airway epithelia in the adult lung. Am J Physiol. Apr 1996;270(4 Pt 1):L487-503. [Medline].

  51. Matthay MA, Wiener-Kronish JP. Intact epithelial barrier function is critical for the resolution of alveolar edema in humans. Am Rev Respir Dis. Dec 1990;142(6 Pt 1):1250-7. [Medline].

  52. Matthay MA, Zimmerman GA. Acute lung injury and the acute respiratory distress syndrome: four decades of inquiry into pathogenesis and rational management. Am J Respir Cell Mol Biol. Oct 2005;33(4):319-27. [Medline].

  53. McHugh LG, Milberg JA, Whitcomb ME. Recovery of function in survivors of the acute respiratory distress syndrome. Am J Respir Crit Care Med. Jul 1994;150(1):90-4. [Medline].

  54. McIntyre RC Jr, Pulido EJ, Bensard DD. Thirty years of clinical trials in acute respiratory distress syndrome. Crit Care Med. Sep 2000;28(9):3314-31. [Medline].

  55. Milberg JA, Davis DR, Steinberg KP. Improved survival of patients with acute respiratory distress syndrome (ARDS): 1983-1993. JAMA. Jan 25 1995;273(4):306-9. [Medline].

  56. National Heart Lung and Blood Institue. Task force on Problems, Research, Approaches, Needs: The Lung Program Washington, DC, Department of Health, Education, and Welfare. Publication No. (N111) 73-432. 1972;165-180.

  57. Petty TL, Ashbaugh DG. The adult respiratory distress syndrome. Clinical features, factors influencing prognosis and principles of management. Chest. Sep 1971;60(3):233-9. [Medline].

  58. Pittet JF, Mackersie RC, Martin TR. Biological markers of acute lung injury: prognostic and pathogenetic significance. Am J Respir Crit Care Med. Apr 1997;155(4):1187-205. [Medline].

  59. Slutsky AS, Tremblay LN. Multiple system organ failure. Is mechanical ventilation a contributing factor?. Am J Respir Crit Care Med. Jun 1998;157(6 Pt 1):1721-5. [Medline].

  60. Spragg RG. Surfactant replacement therapy. Clin Chest Med. Sep 2000;21(3):531-41, ix. [Medline].

  61. Spragg RG, Lewis JF, Walmrath HD. Effect of recombinant surfactant protein C-based surfactant on the acute respiratory distress syndrome. N Engl J Med. Aug 26 2004;351(9):884-92.

  62. Steinberg KP, Hudson LD. Acute lung injury and acute respiratory distress syndrome. The clinical syndrome. Clin Chest Med. Sep 2000;21(3):401-17, vii. [Medline].

  63. Tobin MJ. Culmination of an era in research on the acute respiratory distress syndrome. N Engl J Med. May 4 2000;342(18):1360-1. [Medline].

  64. Tomashefski JF Jr. Pulmonary pathology of the adult respiratory distress syndrome. Clin Chest Med. Dec 1990;11(4):593-619. [Medline].

  65. Troncy E, Collet JP, Shapiro S. Inhaled nitric oxide in acute respiratory distress syndrome: a pilot randomized controlled study. Am J Respir Crit Care Med. May 1998;157(5 Pt 1):1483-8. [Medline].

  66. Ware LB. Prognostic determinants of acute respiratory distress syndrome in adults: impact on clinical trial design. Crit Care Med. Mar 2005;33(3 Suppl):S217-22.

  67. Ware LB, Matthay MA. Maximal alveolar epithelial fluid clearance in clinical acute lung injury: an excellent predictor of survival and the duration of mechanical ventilation. Am J Respir Crit Care Med. 1999;159:Supplement: A694. Abstract.

  68. Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med. May 4 2000;342(18):1334-49. [Medline].

  69. Weis CM, Wolfson MR, Shaffer TH. Liquid-assisted ventilation: physiology and clinical application. Ann Med. Dec 1997;29(6):509-17. [Medline].

  70. Wiener-Kronish JP, Albertine KH, Matthay MA. Differential responses of the endothelial and epithelial barriers of the lung in sheep to Escherichia coli endotoxin. J Clin Invest. Sep 1991;88(3):864-75. [Medline].

  71. Zilberberg MD, Epstein SK. Acute lung injury in the medical ICU: comorbid conditions, age, etiology, and hospital outcome. Am J Respir Crit Care Med. Apr 1998;157(4 Pt 1):1159-64. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

acute respiratory distress syndrome, ARDS, adult respiratory distress syndrome, acute lung injury, ALI, diffuse alveolar damage, noncardiogenic pulmonary edema, diffuse alveolar injury, bilateral pulmonary infiltrates

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Eloise M Harman, MD, Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, University of Florida College of Medicine
Eloise M Harman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American Medical Women's Association, American Thoracic Society, Phi Beta Kappa, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Cory Franklin, MD, Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science; Director, Division of Critical Care Medicine, Cook County Hospital
Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, FCCP, FCCM, Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair, Academic Affairs, University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center
Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Association of University Anesthetists, Shock Society, and Society of Critical Care Medicine
Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting; Applied Physiology, Ltd Honoraria Consulting; Cheetah Medical Consulting fee Consulting

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.