|EVIDENCE BASED DATA
|Year : 2007 | Volume
| Issue : 6 | Page : 550-551
M.D, FICS, FAMS, Senior Prof. & Head, Department of Anaesthesiology, R.N.T.Medical College, Udaipur (Raj.), India
|Date of Web Publication||20-Mar-2010|
25, Polo Ground, Udaipur (Raj.)
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Bajaj P. ARDS. Indian J Anaesth 2007;51:550-1
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  .
Whatever the insult, the acute inflammatory response in the lungs proceeds through two sequential phases : the exudative and the proliferative phase  . 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  . 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  . 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  . 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  . 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  . 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  . 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.
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