 | Acute respiratory distress syndrome: Encyclopedia II - Acute respiratory distress syndrome - Treatment
Acute respiratory distress syndrome - Treatment
Acute respiratory distress syndrome - General
Acute respiratory distress syndrome is usually treated with mechanical ventilation in the Intensive Care Unit. Ventilation is usually delivered through oro-tracheal intubation, or tracheostomy whenever prolonged ventilation (≥2 weeks) is deemed inevitable.
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.
The origin of infection, when surgically treatable, must be operated on. When sepsis is diagnosed, appropriate local protocols should be enacted.
Commonly used supportive therapy includes particular techniques of mechanical ventilation and pharmacological agents whose effectiveness with respect to the outcome has not yet been proven. It is now debated whether mechanical ventilation is to be considered mere supportive therapy or actual treatment, since it may substantially affect survival.
Acute respiratory distress syndrome - Mechanical ventilation
The overall goal is to maintain acceptable gas exchange and to minimize adverse effects in its application. Three parameters are used: PEEP (positive end-expiratory pressure, to maintain maximal recruitment of alveolar units), mean airway pressure (to promote recruitment and predictor of hemodynamic effects) and plateau pressure (best predictor of alveolar overdistention).
Conventional therapy aimed at tidal volumes (Vt) of 12-15 ml/kg. Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma (secondary lung injury). The National Institutes of Health (NIH) showed improved mortality when ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg. Low tidal volumes (Vt) may cause hypercapnia and atelectasis.[7]
Ventilation with low Vt may improve survival in ARDS, although the real goal seems to be a plateau pressure = 32 mmHg (4.3 kPa). To date, further reductions in pressures have not yielded significant benefits, probably because of the associated, more severe respiratory acidosis, caused by permissive hypercapnia. Although 6 mL·kg-1 were used in published trials, lower plateau pressures may be obtained at higher volumes (usually ≤ 10 mL·kg-1). There is no evidence that this higher range of Vt adversely affects outcome.
Volume-controlled intermittent mandatory ventilation has been the traditional, default mode of ventilation in ARDS patients. Pressure-controlled ventilation, biphasic positive airway pressure ventilation and newer modes may allow for better control of plateau pressures. This might prove especially true in patients who are not undergoing neuromuscular paralysis or very deep sedation.
A particular ventilation mode has yet to be proven more effective than others in ARDS, certain parameters have passed the test of science.
Acute respiratory distress syndrome - Positive end-expiratory pressure
Positive end-expiratory pressure (PEEP) must be used in mechanically-ventilated patients in order to contrast the tendency to collapse of affected alveoli.
Ideally, a 'perfect' PEEP would match the increased alveolar surface tension, caused by surfactant deficiency and external pressure (edema), thus restoring a normal time constant in all affected units.
However, because of the cited inherent inhomogeneity, surface tension varies, and so do PEEP requirements for the diseased units. Furthermore, high levels of PEEP may impair venous blood return to the right heart, although the actual impact of PEEP on hemodynamics is still debated.
The 'best PEEP' used to be defined as 'some' cmH2O above the lower inflection point (LIP) in the sigmoidal pressure-volume relationship curve of the lung. Recent research has shown that the LIP-point pressure is no better than any pressure above it, as recruitment of collapsed alveoli, and more importantly the overdistention of aerated units, occur throughout the whole inflation. Despite the awkwardness of most procedures used to trace the pressure-volume curve, it is still used by some to define the minimum PEEP to be applied to their patients. Some of the newest ventilators have the ability to automatically plot a pressure-volume curve. The possibility of having an 'instantaneous' tracing trigger might produce renewed interest in this analysis.
PEEP may also be set empirically. Some authors suggest performing a 'recruiting maneuver' (i.e., a short time at a very high continuous positive airway pressure, such as 50 cmH2O (4.9 kPa), to recruit, or open, collapsed unit with a high distending pressure) and then to increase PEEP to a rather high level before restoring previous ventilation. The final PEEP level should be the one just before the drop in PaO2 (or peripheral blood oxygen saturation) during a step-down trial.
PEEP 'stacks up' to Pl during volume-controlled ventilation. At high levels, it may cause significant overdistension of (and injury to) compliant, aerated units, and higher plateau pressures at the same Vt.
Intrinsic PEEP (iPEEP), or auto-PEEP, is not detected during normal ventilation. However, when ventilating at high frequencies, its contribution may be substantial, both in its positive and negative effects. There are 'underground', unproven claims that the Amato and NIH/ARDS Network studies got a positive result because of the high iPEEP levels reached by spontaneously breathing patients in low-volume assist-control ventilation. Whether or not that is true, it is a fact that iPEEP has been measured in very few formal studies on ventilation in ARDS patients, and its entity is largely unknown. Its measurement is recommended in the treatment of ARDS patients, especially when using high-frequency (oscillatory/jet) ventilation.
A compromise between the beneficial and adverse effects of PEEP is, as usual, inevitable.
Acute respiratory distress syndrome - Prone position
Distribution of lung infiltrates in acute respiratory distress syndrome is non-uniform. Repositioning into the prone position (face down) might improve oxygenation by relieving atelectasis and improving perfusion. However, although the hypoxemia is overcome there seems to be no effect on overall survival.[8][9]
Acute respiratory distress syndrome - 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. [10]
Acute respiratory distress syndrome - 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. [11][12]
Abstract presented from the ARDS-NET trial indicates no improvemeny in survival when steroids were given for ARDS
Acute respiratory distress syndrome - 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.[13]
Acute respiratory distress syndrome - Surfactant therapy
To date no prospective controlled clinical trial has shown a significant mortality benefit of exogenous surfactant in ARDS.[14]
Other related archives1988, Empirical, IRDS, Intensive Care Unit, Mechanical ventilation, Mortality, NIH, National Institutes of Health, Neutrophils, Positive end-expiratory pressure, acute renal failure, airways, alveolar, alveoli, antibiotic, arterial blood gas, aspiration, atelectasis, atypical pneumonias, barotrauma, blood, bronchi, capillaries, cells, chest X-ray, cmH2O, compliance, cytokines, diuresis, endothelial, epithelial, fibrosis, function, gas exchange, gradient, heart, hemodynamics, hemoglobin, hyaline, hypercapnia, hypoxemia, incidence, infant respiratory distress syndrome, infection, inflammation, intensive care unit, intensivists, interface, intubation, kPa, lobes, lung, lung transplantation, lymphocytes, major surgery, mechanical ventilation, mechanically ventilated, methylprednisolone, microbiological culture, mmHg, mortality, multiple organ failure, nitric oxide, nosocomial, overdose, oxygen, parenchyma, peripheral blood oxygen saturation, permissive hypercapnia, pneumonia, positive end-expiratory pressure, pressure, protocols, pulmonary artery catheter, pulmonary artery catheterization, pulmonary edema, pulmonary embolism, randomized controlled trials, resistance, respiratory acidosis, respiratory burst, sedation, sepsis, shear stress, shock, shortness of breath, shunt, sigmoidal, signal transduction, surface tension, surfactant, systemic inflammatory response syndrome, tachypnea, tidal volumes, tracheostomy, transfusions, trauma, venous blood, ventilator, ventilator-associated pneumonia
 Adapted from the Wikipedia article "Treatment", under the G.N U Free Docmentation License. Please also see http://en.wikipedia.org/wiki |
