Acute respiratory distress syndrome medical therapy: Difference between revisions
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==Overview== | ==Overview== | ||
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Latest revision as of 03:48, 20 July 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Brian Shaller, M.D. [2]
Overview
The majority of medical therapies for ARDS are aimed at treating its underlying cause (e.g., antimicrobials for infection).
Medical Therapy
Although patients with ARDS often require aggressive medical therapies aimed at treating their underlying illness, there are few medical therapies (beyond mechanical ventilation and other strategies to improve oxygenation) that address the physiologic derangements of ARDS itself.
Fluid management
Removal of excess fluids via diuresis or renal replacement therapy (typically continuous renal replacement therapy or hemodialysis) in patients with concomitant volume overload due to heart failure or renal dysfunction is recommended, however, these interventions are of little or no benefit in patients who are not volume-overloaded (i.e., euvolemic).
Corticosteroids
While patients with adrenal insufficiency and ARDS should receive stress-dosed glucocorticoid replacement therapy, glucocorticoids by themselves have not been demonstrated to improve survival and may increase mortality in ARDS. The lack of benefit of glucocorticoid therapy for ARDS was demonstrated in the LaSRS (pronounced Lazarus) Trial (conducted by the NIH-NHLBI ARDS Clinical Trials Network from 1997 to 2003) – a multicenter randomized, controlled trial comparing methylprednisolone versus placebo for 21 days in patients with moderate-to-severe ARDS. Patients in the methylprednisolone arm experienced more ventilator-free, shock-free, and ICU-free days by follow-up day 28; however, no survival benefit was observed and a significantly higher mortality rate was observed at 60 and 180 days in patients who received methylprednisolone more than 14 days after the onset of ARDS.[1]
Inhaled Pulmonary Vasodilators
Inhaled pulmonary vasodilators (medications that dilate the vessels of pulmonary arterial circulation) have been used to improve hypoxemia by reversing ventilation/perfusion (V/Q) mismatching, however, studies of inhaled nitric oxide (iNO) and inhaled prostacyclin have not demonstrated a survival benefit to these therapies.[2][3][4][5] It is important to monitor the platelet count when initiating treatment with inhaled prostacyclin due to the low risk of thrombocytopenia.
References
- ↑ Steinberg KP, Hudson LD, Goodman RB, Hough CL, Lanken PN, Hyzy R; et al. (2006). "Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome". N Engl J Med. 354 (16): 1671–84. doi:10.1056/NEJMoa051693. PMID 16625008.
- ↑ Taylor RW, Zimmerman JL, Dellinger RP, Straube RC, Criner GJ, Davis K; et al. (2004). "Low-dose inhaled nitric oxide in patients with acute lung injury: a randomized controlled trial". JAMA. 291 (13): 1603–9. doi:10.1001/jama.291.13.1603. PMID 15069048.
- ↑ Adhikari NK, Dellinger RP, Lundin S, Payen D, Vallet B, Gerlach H; et al. (2014). "Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: systematic review and meta-analysis". Crit Care Med. 42 (2): 404–12. doi:10.1097/CCM.0b013e3182a27909. PMID 24132038.
- ↑ Walmrath D, Schneider T, Schermuly R, Olschewski H, Grimminger F, Seeger W (1996). "Direct comparison of inhaled nitric oxide and aerosolized prostacyclin in acute respiratory distress syndrome". Am J Respir Crit Care Med. 153 (3): 991–6. doi:10.1164/ajrccm.153.3.8630585. PMID 8630585.
- ↑ Zwissler B, Kemming G, Habler O, Kleen M, Merkel M, Haller M; et al. (1996). "Inhaled prostacyclin (PGI2) versus inhaled nitric oxide in adult respiratory distress syndrome". Am J Respir Crit Care Med. 154 (6 Pt 1): 1671–7. doi:10.1164/ajrccm.154.6.8970353. PMID 8970353.