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EVIDENCE BASED DATA
Year : 2007  |  Volume : 51  |  Issue : 6  |  Page : 550-551 Table of Contents     

ARDS


M.D, FICS, FAMS, Senior Prof. & Head, Department of Anaesthesiology, R.N.T.Medical College, Udaipur (Raj.), India

Date of Web Publication20-Mar-2010

Correspondence Address:
Pramila Bajaj
25, Polo Ground, Udaipur (Raj.)
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Bajaj P. ARDS. Indian J Anaesth 2007;51:550-1

How to cite this URL:
Bajaj P. ARDS. Indian J Anaesth [serial online] 2007 [cited 2020 Oct 28];51:550-1. Available from: https://www.ijaweb.org/text.asp?2007/51/6/550/61199

The acute respiratory distress syndrome (ARDS) is a devastating injury to the lungs, characterized by dif­fuse pulmonary inflammation, hypoxemia, and respira­tory distress. Its mortality remains between 30% and 50%, despite early, aggressive and sometimes heroic in­tervention. Although in many cases complete recovery without sequelae is possible, in other cases ARDS may go on to a debilitating course requiring protracted venti­latory support, with high co-morbidity and mortality.

ARDS is usually considered as a homogenous en­tity in standard definitions and in many large studies that evaluate therapeutic interventions. However, it should really be considered the final common pathway of a very heterogenous group of insults.Although the injury is dif­fuse, it does not uniformly affect lung tissue and this non uniform distribution has important therapeutic conse­quences. There are also two broad etiologies of ARDS. In pulmonaryARDS, there is a primary lung injury (e.g., pneumonia) that involves the alveolar epitheliumand may be confined to single organ failure. In extrapulmonary ARDS, there is an insult-usually sepsis-at a remote lo­cation that reaches the capillary endothelium via a sys­temic inflammatory response syndrome, and lung failure becomes one more component of multisystem organ fail­ure. Although there are important differences in patho­physiology, outcome between ARDS of pulmonary and extrapulmonary origin does not appear to differ greatly [1] .

Whatever the insult, the acute inflammatory re­sponse in the lungs proceeds through two sequential phases : the exudative and the proliferative phase [2] . Al­though these phases are pathophysiologically quite dis­tinct, they may overlap temporally and even coexist in the same lung.

In 1994, the American-European Consensus Con­ference onARDS condensed the clinical features of this syndrome into a definition that forms the basis for all the investigation since performed [3] . Its criteria are 1) acute respiratory distress; 2) bilateral radiographic pulmonary infiltrates; 3) hypoxemia, defined as acute lung injury if the Pao 2 to FIO 2 (P:F) ratio is <300, or ARDS if <200; and 4) the absence of heart failure, as defined by a pul­monary artery occlusion pressure (PAOP) <18 mm Hg.

This definition is far from perfect. Respiratory dis­tress, characterized by tachypnea, dyspnea, and acute respiratory alkalosis not relieved by correcting hypox­emia, is common to many pulmonary processes. Bilat­eral radiologic infiltrates may be caused by cardiogenic edema, pneumonitis, and several other entities. The P:F ratio may be influenced by therapy, especially PEEP and the FIO 2 itself. It seems specious to separate "acute lung injury" from ARDS, when the former is in fact respon­sible for the latter. Heart failure may be present at PAOP <18 mm Hg and may coexist with ARDS. Nonetheless­although presently undergoing revision-this definition has stood the test of time and on pulmonary vasoconstric­tion, the benefit to oxygenation is quite variable, and may differ markedly between patients and even at different times in the same patient.Also, unlike the effect on PVR, there appears to be a "plateau" oxygenation response that reaches a maximum at 5-10 ppm. This may repre­sent diffusion of NO to less well-ventilated lung units where it would tend to reverse hypoxic pulmonary vaso­constriction.

Although in individual cases of severe ARDS, in­haled nitric oxide(INO) may provide striking improve­ment in oxygenation, there is no evidence that it improves overall mortality. In a large multinational European trial, 268 adults with acute lung injury in 43 hospitals, who had a P:F ratio of <165, were treated with INO [4] . Of these, 180 exhibited a positive response (>20% improvement in Pao 2 ), and were then randomized to no INO or INO at 2, 10, and 40 ppm.Although patients treated with INO had a significantly decreased incidence of severeARDS (2.2% vs 10.3%), there was no difference in the pri­mary end point, reversal of acute lung injury, or 30-day mortality (44% vs 40%). Because of these and other data, INO therapy is not advocated for the treatment of ARDS in the U.S.

An important first step in the treatment of ARDS is that the care team agrees on treatment goals for hy­poxemia. A logical initial goal is to achieve a Pao 2 >60 mm Hg (equivalent to Spo 2 >90%), because this is the upper inflection point of the hemoglobin dissociation curve-below this level, the saturation falls rapidly. Air­way pressure therapy should then be directed to achieve the lowest FIo 2 -ideally, <0.4-that will sustain a Pao 2> 60mm Hg. If the Fio 2 cannot be decreased, a further increase in airway pressure therapy is warranted, within the constraints described below. Once the Fio 2 can be decreased to <0.4, and oxygenation is stable for at least 12 h, airway pressure may gradually be withdrawn. An important caveat is that too rapid withdrawal may result in alveolar derecruitment and collapse that may be very difficult to recoup. For example, PEEP should be with­drawn in decrements no greater than 2 cm H 2 O every 6 h.

From the discussion above, it may be concluded that no single intervention has been demonstrated to de­crease mortality in ARDS, except use of low tidal vol­umes (but that is only in the context of comparing 6 ml.kg­ 1 vs 12 ml.kg -1 ). Indeed, there are few comparisons of one intervention versus another. In one such study, Dupont et al demonstrated that the prone position increased oxy­genation (P:F ratio) more than INO therapy [5] . However, Germann et al took this one step further : they demon­strated that the combination of the prone position with INO therapy improved oxygenation more than either in­tervention used alone [6] . Moreover, INO therapy also de­creased PVR, whereas prone position had no effect.

A logical extension of these observations is that we should be examining combined therapeutic ap­proaches and creating algorithms of therapy for ARDS, much like the evidenced-based guidelines included in the "Surviving Sepsis campaign" now advocated by the So­ciety of Critical Care Medicine [7] . One example is the report from the ICU group at the University of Vienna, Austria, a national referral center forARDS, on a strictly protocol-based approach [8] . All 84 of their patients were managed with a regimen that included sedation, early percutaneous tracheostomy, diuresis, continuous hemofiltration, and a step-wise treatment algorithm of PC-IRV, PEEP, permissive hypercapnia, INO therapy, and prone positioning. Nonresponders, defined as pa­tients who did not exhibit a 20% increase in Pao 2 within 96 h, were triaged to VV-ECMO. Their results are im­pressive: only 15% of patients required ECMO, and their overall survival rate was 80%; the survival rate in pa­tients who went on to ECMO was 62%. There is a les­son to be learned here.

 
   References Top

1.Agarwal R, Aggarwal AN, Gupta D, et al. Etiology and out­comes of pulmonary and extrapulmonary acute lung injury/ ARDS in a respiratoryICU in North India. Chest 2006;130:724­9.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Ware LB, Matthay MA. The acute respiratory distress syn­drome. N Engl J Med 2000;342:1334-49.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Bernard GR,Artigas A, Brigham KL, et al. Definitions, mecha­nisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994;149:818-24.  Back to cited text no. 3  [PUBMED]    
4.Lundin S, Mang H, Smithies M, et al. Inhalation of nitric oxide in acute lung injury:results of a European multicentre study. The European Study Group of Inhaled Nitric Oxide. Intensive Care Med 1999;25:911-19.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]  
5.Dupont H, Mentec H, Cheval C, et al. Short-term effect of inhaled nitric oxide and prone positioning on gas exchange in patients with severe acute respiratory distress syndrome. Crit Care Med 2000;28:304-8.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]  
6.Germann P, Poschl G, Leitner C, et al. Additive effect of nitric oxide inhalation on the oxygenation benefit of the prone posi­tion in the adult respiratory distress syndrome. Anesthesiol­ogy 1998;89:1401-6.  Back to cited text no. 6      
7.Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis cam­paign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004; 32:858-73.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Ullrich R, Lorber C, Roder G, et al. Controlled airway pressure therapy, nitric oxide inhalation, prone position, and extracor­poreal membrane oxygenation (ECMO) as components of an integrated approach to ARDS. Anesthesiology 1999;91:1577-86.  Back to cited text no. 8      




 

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