Acute respiratory distress syndrome medical therapy: Difference between revisions
No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | |||
{{Acute respiratory distress syndrome}} | {{Acute respiratory distress syndrome}} | ||
{{CMG}} | {{CMG}} | ||
==Overview== | ==Overview== | ||
==Medical Therapy== | |||
The possibilities of non-invasive ventilation are limited to the very early period of the disease or, better, to prevention in individuals at risk for the development of the disease ([[atypical pneumonia]]s, pulmonary contusion, major surgery patients). | The possibilities of non-invasive ventilation are limited to the very early period of the disease or, better, to prevention in individuals at risk for the development of the disease ([[atypical pneumonia]]s, pulmonary contusion, major surgery patients). | ||
| Line 9: | Line 11: | ||
Appropriate [[antibiotic]] therapy must be administered as soon as [[microbiological culture]] results are available. Empirical therapy ''may'' be appropriate if local microbiological surveillance is efficient. More than 60% ARDS patients experience a (nosocomial) pulmonary infection either before or after the onset of lung injury. | Appropriate [[antibiotic]] therapy must be administered as soon as [[microbiological culture]] results are available. Empirical therapy ''may'' be appropriate if local microbiological surveillance is efficient. More than 60% ARDS patients experience a (nosocomial) pulmonary infection either before or after the onset of lung injury. | ||
==Fluid management== | ===Fluid management=== | ||
Several studies have shown that pulmonary function and outcome are better in patients that lost weight or wedge pressure was lowered by [[diuresis]] or fluid restriction. | Several studies have shown that pulmonary function and outcome are better in patients that lost weight or wedge pressure was lowered by [[diuresis]] or fluid restriction. | ||
==Corticosteroids== | ===Corticosteroids=== | ||
Patients with ARDS do not benefit from high-dose corticosteroids. Meduri et al however did find significant improvement using modest doses. This is probably because of a suppression of ongoing inflammation during the fibroproliferative phase of ARDS. The initial regimen consists of [[methylprednisolone]] 2 mg/kg daily. After 3-5 days a response must be apparent. In 1-2 weeks the dose can be tapered to methylprednisolone 0.5-1.0 mg daily. In the absence of results steroids can be discontinued.<ref name=Meduri-ARDS>{{cite journal | author = Meduri G, Tolley E, Chrousos G, Stentz F | title = Prolonged methylprednisolone treatment suppresses systemic inflammation in patients with unresolving acute respiratory distress syndrome: evidence for inadequate endogenous glucocorticoid secretion and inflammation-induced immune cell resistance to glucocorticoids. | journal = Am J Respir Crit Care Med | volume = 165 | issue = 7 | pages = 983-91 | year = 2002 | id = PMID 11934726}}</ref> | Patients with ARDS do not benefit from high-dose corticosteroids. Meduri et al however did find significant improvement using modest doses. This is probably because of a suppression of ongoing inflammation during the fibroproliferative phase of ARDS. The initial regimen consists of [[methylprednisolone]] 2 mg/kg daily. After 3-5 days a response must be apparent. In 1-2 weeks the dose can be tapered to methylprednisolone 0.5-1.0 mg daily. In the absence of results steroids can be discontinued.<ref name=Meduri-ARDS>{{cite journal | author = Meduri G, Tolley E, Chrousos G, Stentz F | title = Prolonged methylprednisolone treatment suppresses systemic inflammation in patients with unresolving acute respiratory distress syndrome: evidence for inadequate endogenous glucocorticoid secretion and inflammation-induced immune cell resistance to glucocorticoids. | journal = Am J Respir Crit Care Med | volume = 165 | issue = 7 | pages = 983-91 | year = 2002 | id = PMID 11934726}}</ref> | ||
The recent NIH-sponsored ARDSnet LAZARUS study of corticosteroids for ARDS demonstrated that they are not efficacious in ARDS. | The recent NIH-sponsored ARDSnet LAZARUS study of corticosteroids for ARDS demonstrated that they are not efficacious in ARDS. | ||
==Nitric oxide== | ===Nitric oxide=== | ||
Inhaled [[nitric oxide]] (NO) potentially acts as selective pulmonary vasodilator. Rapid binding to [[hemoglobin]] prevents systemic effects. It should increase perfusion of better ventilated areas. There are no large studies demonstrating positive results. Therefore its use must be considered individually. | Inhaled [[nitric oxide]] (NO) potentially acts as selective pulmonary vasodilator. Rapid binding to [[hemoglobin]] prevents systemic effects. It should increase perfusion of better ventilated areas. There are no large studies demonstrating positive results. Therefore its use must be considered individually. | ||
Almitrine bismesylate stimulates chemoreceptors in carotic and aortic bodies. It has been used to potentiate the effect of NO, presumably by potentiating hypoxia-induced pulmonary vasoconstriction. In case of ARDS it is not known whether this combination is useful. | Almitrine bismesylate stimulates chemoreceptors in carotic and aortic bodies. It has been used to potentiate the effect of NO, presumably by potentiating hypoxia-induced pulmonary vasoconstriction. In case of ARDS it is not known whether this combination is useful. | ||
==Surfactant therapy== | ===Surfactant therapy=== | ||
To date no prospective [[Randomized controlled trial|controlled clinical trial]] has shown a significant mortality benefit of exogenous surfactant in ARDS. | To date no prospective [[Randomized controlled trial|controlled clinical trial]] has shown a significant mortality benefit of exogenous surfactant in ARDS. | ||
| Line 29: | Line 31: | ||
[[ | [[Category:Disease]] | ||
[[ | [[Category:Intensive care medicine]] | ||
[[ | [[Category:Pulmonology]] | ||
[[ | [[Category:Syndromes]] | ||
[[ | [[Category:Overview complete]] | ||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
Revision as of 00:17, 25 September 2012
|
Acute respiratory distress syndrome Microchapters |
|
Differentiating Acute respiratory distress syndrome from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Acute respiratory distress syndrome medical therapy On the Web |
|
American Roentgen Ray Society Images of Acute respiratory distress syndrome medical therapy |
|
Acute respiratory distress syndrome medical therapy in the news |
|
Blogs on Acute respiratory distress syndrome medical therapy |
|
Directions to Hospitals Treating Acute respiratory distress syndrome |
|
Risk calculators and risk factors for Acute respiratory distress syndrome medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Medical Therapy
The possibilities of non-invasive ventilation are limited to the very early period of the disease or, better, to prevention in individuals at risk for the development of the disease (atypical pneumonias, pulmonary contusion, major surgery patients).
Treatment of the underlying cause is imperative, as it tends to maintain the ARDS picture.
Appropriate antibiotic therapy must be administered as soon as microbiological culture results are available. Empirical therapy may be appropriate if local microbiological surveillance is efficient. More than 60% ARDS patients experience a (nosocomial) pulmonary infection either before or after the onset of lung injury.
Fluid management
Several studies have shown that pulmonary function and outcome are better in patients that lost weight or wedge pressure was lowered by diuresis or fluid restriction.
Corticosteroids
Patients with ARDS do not benefit from high-dose corticosteroids. Meduri et al however did find significant improvement using modest doses. This is probably because of a suppression of ongoing inflammation during the fibroproliferative phase of ARDS. The initial regimen consists of methylprednisolone 2 mg/kg daily. After 3-5 days a response must be apparent. In 1-2 weeks the dose can be tapered to methylprednisolone 0.5-1.0 mg daily. In the absence of results steroids can be discontinued.[1]
The recent NIH-sponsored ARDSnet LAZARUS study of corticosteroids for ARDS demonstrated that they are not efficacious in ARDS.
Nitric oxide
Inhaled nitric oxide (NO) potentially acts as selective pulmonary vasodilator. Rapid binding to hemoglobin prevents systemic effects. It should increase perfusion of better ventilated areas. There are no large studies demonstrating positive results. Therefore its use must be considered individually.
Almitrine bismesylate stimulates chemoreceptors in carotic and aortic bodies. It has been used to potentiate the effect of NO, presumably by potentiating hypoxia-induced pulmonary vasoconstriction. In case of ARDS it is not known whether this combination is useful.
Surfactant therapy
To date no prospective controlled clinical trial has shown a significant mortality benefit of exogenous surfactant in ARDS.
References
- ↑ Meduri G, Tolley E, Chrousos G, Stentz F (2002). "Prolonged methylprednisolone treatment suppresses systemic inflammation in patients with unresolving acute respiratory distress syndrome: evidence for inadequate endogenous glucocorticoid secretion and inflammation-induced immune cell resistance to glucocorticoids". Am J Respir Crit Care Med. 165 (7): 983–91. PMID 11934726.