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Acute Lung Injury

Introduction 2. What is Acute Lung Injury/ARDS? 3. What is the pathological basis of Acute Lung Injury? 4. How do I treat a patient with Acute Lung Injury? What do I do if the patient remains severely hypoxic in spite of maximal ventilatory support? 6. What is the "Open Lung" approach to ARDS? 7. What is the advantage of using pressure controlled ventilation in ARDS? 8. What is Ventilator Induced Lung Injury? 9. What is the role of steroids in ARDS? 10. Key Points
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1. Acute Lung Injury Introduction

Acute Lung Injury (ALI) is a distinct form of acute respiratory failure characterized by diffuse pulmonary infiltrates, progressive hypoxemia, reduced lung compliance and normal hydrostatic pressures

In 1967 Ashbaugh and colleagues (1) (2)published a case series in the Lancet which described a clinical syndrome, which they (later) termed Adult Respiratory Distress Syndrome (ARDS) (3). The 12 patients involved complained of acute respiratory distress, cyanosis refractory to oxygen therapy, decreased lung compliance and diffuse pulmonary infiltrates on chest x-ray. Trauma doctors involved in treating victims of war had long been familiar with this syndrome, which came to be known as wet lung, shock lung or Danang lung. This problem had been identified during World War II but with the advent of advanced trauma (M.A.S.H. units during the Vietnam war) the prevalence of this form of respiratory failure was truly recognized. Over the past 30 or so years, this syndrome has come to be one of the central problems of intensive care: lung injury arising from a variety of different etiologies, each characterized by bilateral diffuse infiltrates on x-ray, hypoxemia, and non-cardiogenic pulmonary edema. Learning Objectives

To understand the pathology and pathophysiology of ALI/ARDS To devise a ventilation strategy for these patients. To introduce the concept of ventilator induced lung injury To address adjunct and rescue therapy for patients with resistant hypoxemia

2. Acute Lung Injury What is it?


The definition of the syndrome was clarified by a 1992 American-European Consensus Conference (4). The term Acute Lung Injury has been used as an umbrella term for hypoxemic respiratory failure, a severe version of which is Acute Respiratory Distress Syndrome (ARDS). The characteristics follow: Bilateral pulmonary infiltrates on chest x-ray Pulmonary Capillary Wedge Pressure <18mmHg PaO2/FiO2* <300 = ALI PaO2/FiO2 <200 = ARDS Although not strictly part of the definition, there is widespread airway collapse (low lung volumes), surfactant deficiency and reduced lung compliance.

Classic Chest X Ray of a patient with ARDS, although the lung injury appears diffuse, when you look at the CT scan of the same patient on the right you can see that the lower lobes are densely consolidated and the upper lobes relatively spared. Nevertheless, this patient was severely hypoxic, and responded well to prone positioning.

What causes it?

ALI is caused by any stimulus of local or systemic inflammation, principally sepsis

ALI is most often seen as part of a systemic inflammatory process, particularly systemic sepsis, where the lung manifestations parallel those of other tissues widespread destruction of the capillary endothelium, extravascation of protein rich fluid and interstitial edema. In addition, the alveolar basement membrane is damaged, and fluid seeps into the airspaces, stiffening the lungs and causing ventilation-perfusion mismatch (5). Other causes of ARDS are listed below, as you can see, this is a mixture of virtually every disorder seen in ICU.

References
(1) Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet 1967; 2(7511):319-323. (2) Petty TL. In the Cards was ARDS. (How we discovered the acute respiratory distress syndrome). Am J Respir Crit Care Med 2001; 163(3):602-603. (3) Bigelow DB, Petty TL, Ashbaugh DG, Levine BE, Nett LM, Tyler SW. Acute respiratory failure. Experiences of a respiratory care unit. Med Clin North Am 1967; 51(2):323-340. (4) Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L et al. The AmericanEuropean Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994; 149(3 Pt 1):818-824. (5) Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med 2000; 342(18):1334-1349.

Acute Lung Injury Pathology

There are two major stages the acute phase characterized by disruption of the alveolar-capillary interface, leakage of protein rich fluid into the interstitium and alveolar space and extensive release of cytokines and migration of neutrophils. A later reparative phase is characterized by fibroproliferation, and organization of lung tissue If resolution does not occur, disordered collagen deposition occurs leading to extensive lung scarring.

CLICK HERE OR ON THE THUMBNAIL TO VIEW THE PICTURE GALLERY

The core pathology is disruption of the capillary-endothelial interface: this actually refers to two separate barriers the endothelium and the basement membrane of the alveolus. In the acute phase of ALI, there is increased permeability of this barrier, and protein rich fluid leaks out of the capillaries. There are two types of alveolar epithelial cells Type 1 pneumocytes represent 90% of the cell volume, and are easily damaged. Type 2 pneumocytes are more resistant to damage, which is important as these cells produce surfactant, transport ions and proliferate and differentiate into Type 1 cells.

The damage to the endothelium and the alveolar epithelium results in the creation of an open interface between the lung and the blood, facilitating the spread of micro-organisms from the lung systemically, stoking up a systemic inflammatory response. Moreover, the injury to epithelial cells handicaps the lungs ability to pump fluid out of airspaces. Fluid filled airspaces, loss of surfactant, microvascular thrombosis and disorganized repair (which leads to fibrosis) reduces resting lung volumes (decreased compliance), increasing ventilation-perfusion mismatch, right to left shunt and the work of breathing. In addition, lymphatic drainage of lung units appears to be curtailed stunned by the acute injury: this contributes to the build up of extravascular fluid. Some patients rapidly recover from acute lung injury, and have no permanent sequelae. Prolonged inflammation and destruction of pneumocytes leads to fibroblastic proliferation, hyaline membrane formation and lung fibrosis. This fibrosing alveolitis may become apparent as early as five days after the initial injury. Subsequent recovery may be characterized by reduced physiologic reserve, and increased susceptibility to further lung injuries. Extensive microvascular thrombosis may lead to pulmonary hypertension, myocardial dysfunction and systemic hypotension. Finally, it is essential to understand that although ALI is a diffuse process, it is also a heterogeneous process, and not all lung units are affected equally: normal and diseased tissue may exist side-by-side.

Acute Lung Injury Treatment

The cornerstone of treatment is to keep the PaO2 >60mmHg, without causing injury to the lungs with excessive O2 or volutrauma. Pressure control ventilation is more versatile than volume control, although breaths should be volume limited, to prevent stretch injury to the alveoli. In general tidal volumes should not exceed 6ml/kg and plateau pressure should not exceed 30cmH2O. However tidal volumes of 4ml/kg should be delivered irrespective of airway pressure. The management of patients with respiratory failure goes beyond ventilation strategies, we must have a holistic multisystem approach: I like to remind residents of the ABCDEFG mnemonic. A= Airway, establish an patient airway, intubate as necessary.

B = Breathing, commence mechanical ventilation and obtain an adequate minute volume to maintain oxygen delivery. C = D= E= Circulation: blood pressure, pulse, intravascular volume fluid resuscitation and vasopressors as necessary Diagnosis, find the underlying problem and control the source. Empiric therapy, for example antimicrobials for sepsis

FG = Feed the Gut, to prevent villus atrophy and bacterial translocation The principles of mechanical ventilation are simple: 1. Give enough oxygen to keep the PaO2 over 60mmHg preferably, and over 50mmHg at the very least. 2. Avoid volutrauma and barotrauma, by keeping the tidal volumes in the 4-6ml/kg range and the airway plateau pressure below 30 - 35cmH2O (the tidal volume should not be less than 4ml/kg, irrespective of airway pressure). The PaO2 is a function of the FiO2, the PEEP level, the mean airway pressure and the minute ventilation. The tidal volume, depending on what mode of ventilation is used, is determined by the pressure control level (in pressure controlled modes) or the tidal volume dialed up on the ventilator (in volume controlled modes). There is no clear evidence that any particular mode or strategy improves outcome in ALI, except for controlling tidal volumes and airway pressures. What follows is a suggested starting strategy:

1. Start with a high FiO2 (use the same FiO2 on the patient following intubation as before). 2. Set the CPAP/PEEP level if the patient has a P/F ratio of 200-300 start with CPAP/PEEP of 5cmH2O, if the P/F ratio is <200, use a CPAP/PEEP of 10cmH2O. 3. For inspiratory support, use a decelerating flow pattern, with a tidal volume of 5-6ml/kg, of if pressure control is being used, a pressure limit which gives a tidal volume of 5-6ml/kg (1). Please see tutorials on ventilator strategy.
It is important to note that ARDS is a disease of altered lung compliance. This is reduced due to the presence of large quantities of extravascular lung water. However, chest wall compliance may also be low - in patients who are edematous, have had massive fluid resuscitation or have abdominal hypertension. In this situation, the chamber in which the lungs are inflating (the chest), bears more resemblance to a brick wall than a rib cage with muscles. Higher inflation pressures are required to inflate the lungs in these circumstances and higher PEEP is required to maintain FRC.

The choice of mode of ventilation is institution specific. The majority of intensive care units in the United States continue to use volume controlled modes of ventilation to treat ARDS. Severe hypoxemia is managed by increasing mean airway pressure by escalating levels of PEEP and rapid respiratory rates. The logic behind increasing mean airway pressure is that much of the ventilation perfusion mismatch contributing to hypoxia occurs at end expiration (click here for more information). Although the majority cases can be managed in this way, more versatile modes are available, under the pressure control umbrella. Pressure control modes have the advantage of allowing us manipulate the mean airway pressure by prolonging inspiration, and this may improve oxygenation without increasing peak or plateau pressures . In addition, pressure control may improve gas distribution at the end of inspiration, particularly where different lung units have different resistance patterns (ALI is, after all, a heterogeneous process). The drawback of prolonging inspiration, and, in effect, inverting the I:E ratio (2;3), is that the patient may experience a lot of discomfort, and requires deep sedation. Further, incomplete expiration tends to reduce CO2 elimination, and

the patient will develop permissive hypercapnia and respiratory acidosis. As we now know that ventilator induced lung injury causes much more trouble than respiratory acidosis, we do not consider the latter to be a major problem (4). Newer pressure control modes such as BiLevel / Airway Pressure Release ventilation have been developed to address the problem of patient discomfort in inverse ratio ventilation; with some success. References
(1) Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000; 342(18):1301-1308. (2) Armstrong BW, Jr., MacIntyre NR. Pressure-controlled, inverse ratio ventilation that avoids air trapping in the adult respiratory distress syndrome. Crit Care Med 1995; 23(2):279-285. (3) Tharratt RS, Allen RP, Albertson TE. Pressure controlled inverse ratio ventilation in severe adult respiratory failure. Chest 1988; 94(4):755-762. (4) Lewandowski K. Permissive hypercapnia in ARDS: just do it? Intensive Care Med 1996; 22(3):179-181.

Acute Lung Injury How do I treat severe hypoxia?


A number of adjunct therapies are available, none have proven effective. Prone positioning and inhaled nitric oxide are the most commonly used. It is uncertain what the lowest safe PaO2 is. Profound hypoxia will lead to death. In this situation it is necessary to oxygenate the patient at all costs if this means increasing the FiO2, tidal volume or peak pressure, then so be it. Often neuromuscular blocking agents are required to improve patientventilator interaction, and increase chest wall compliance. It is my practice to assume mucus plugging and derecruitment until otherwise proven. The therapy involves aggressive suctioning with or without bronchoscopy, followed by recruitment maneuvers. There are many different methods of performing this: e.g. switch off the control breaths, and gradually increase the CPAP level to 10cmH2O above the peak airway pressure, and hold it there for 30 to 40 seconds. Multiple methods of lung recruitment have been described (1-3). The efficacy and safety of recruitment maneuvers has not been established. Another method of improving oxygenation is to alter the alveolar gas content. This is achieved by washing carbon dioxide out of the anatomical dead space by insufflating oxygen at the level of the carina during expiration. When the next breath is delivered this dead space gas is the first to arrive into the alveoli. This process, tracheal gas insufflation (TGI) can be performed by placing a catheter at the level of the catheter and delivering a flow of gas. The catheter can be inside or outside the endotracheal tube (outside is better as it does not increase airways resistance). The problem with this technique is in the application: the easiest method is continuous gas flow at 2 to 5 liters per minute. Unfortunately, this will significantly increase end inspiratory volumes, even in pressure control ventilation. Care must be taken that the patient does not develop large amounts of auto-PEEP. In addition, there are a number of unproven adjunct therapies available, which

may,

at

least

in

the

short

term,

improve

oxygenation:

1. Turn the patient prone this improves ventilation-perfusion matching, although the exact mechanism is unknown (4). 2. Administer inhaled nitric oxide this is a local vasodilator, which dilates up the capillaries around the well-ventilated alveoli, potentially improving ventilation-perfusion matching(5;6). Due to the high cost of administering this agent, nebulized prostacyclin has been used as an alternative.

3. Add almitrine which enhances hypoxic pulmonary vasoconstriction, and may reduce right to left shunt (7). This agent is not available in the USA; phenylephrine can be used instead. 4. High frequency oscillation full tidal volume ventilation, with no cyclic opening and closing of lung units. Experience with this mode has been very good in pediatric and neonatal practice; there is little published data in adults. 5. Tracheal gas insufflation - 2 or more litres of oxgen are delivered into the major bronchi in expiration to wash out dead space gas. 6. Partial liquid ventilation (PLV) with perfuocarbons, which carry oxygen. This very attractive proposition of liquid PEEP has been underutilized, due to lack of availability. The FRC is filled with the liquid, and the patient ventilated above it. PLV has the added advantage of lavaging the airways and removing cellular debris (7;8). Although of academic interest, this strategy is not currently available. 6. Extracorporeal membrane oxygenation: the patient is put on an extracorporeal circuit and oxygenated by a type of heart-lung bypass machine: there is little evidence of efficacy in adults (9). Although none of these techniques have been shown to improve outcome, when a patient is severely hypoxemic many physicians feel that their backs are to the wall, and there is little alternative but to go down the road of adjunct therapy.

Acute Lung Injury The open lung approach


Current ventilation strategies involve using low tidal volumes with or without high levels of PEEP. The open lung approach attempts to optimize lung mechanics and minimize phasic damage by strategically placing PEEP above Pflex. Two modern approaches to ventilating patients with acute lung injury are the open lung approach and the low tidal volume approach. These are not mutually exclusive. The premise of both is that phasic opening and closing of injured lung units causes further injury to lung tissue and can worsen the lung injury. The low tidal volume approach involves minimizing the amount of phasic stretch of lung units in inspiration, to prevent ventilator induced lung injury. This technique has been proven to be effective: in a landmark NIH coordinated multicenter trial, patients ventilated with tidal volumes of 2-6ml/kg had a 22% reduction in mortality than patients ventilated with tidal volumes of 10-12ml/kg (1). The open lung approach takes a slightly different tack: it is believed that reinflating collapsed lung units also causes lung injury and cytokine release. By stenting the airways open at end expiration, using PEEP, it may be possible to reduce these shearing injuries. There has been a preliminary trial by Amato and colleagues (2), demonstrating the efficacy of this technique. This group painstakingly constructed pressure volume curves on each patient to determine Pflex (the lower inflection point on the pressure volume curve), and applied PEEP just above this level. The patients invariably receive a higher than conventional PEEP level, with lower tidal volumes. Critics of this technique have suggested that plotting pressure volume curves is difficult, that Pflex often is impossible to find, and that overdistension of less diseased tissues may occur. As a consequence of this controversy, the NIH is currently performing the Alveoli trial, which randomizes patients into two groups, low and high PEEP in patients on low tidal volume strategies (the trial is now complete an the early indications is that there was no difference in outcomes with this approach). It is important to note that while Amato and most other "open lung" practitioners performed recruitment maneuvers (moderate to high pressures are applied to the airway intermittently to re-open collapsed alveoli), this was not a part of the Alveoli study.

Above: Quasi Static volume pressure curve of an injured lung: the lungs are said to be most compliant between the lower inflection point of the curve and the upper inflection point, beyond which overdistension takes place.

Acute Lung Injury Pressure controlled ventilation


The advantages of using pressure controlled ventilaton in acute lung injury (ALI): 1) Gas Distribution: acute lung injury is a heterogeneous disease process. Lung units are affected differently by disease. Some are effectively normal, some have low compliance, some have normal compliance but long time constants. Others are not involved in gas exchange. In volume ventilation, gas is preferentially delivered to more compliant lung units, causing overdistension and poor mixing. In pressure control, there is better distribution of gas to these differing lung units.

In the cartoon above, see, on the left side an injured lung segment: this contains normal alveoli (A1), non compliant alveoli (A2 e.g. consolidation) and alveoli with long time constants due, in this case, to proximal obstruction - such as a mucus plug or bronchial constriction. When a volume breath is delivered (with constant flow pattern) the gas passes down the path of least resistance into the most compliant alveoli - so there is relative overdistension of A1, A2 is inflated as expected, and A3 does not have time to inflate before the ventilator cycles off.

In the second cartoon, a pressure controlled breath is delivered. In this case there is better distribution of gas - because A1 will not overdistend to the same extent as before, and there is sufficient time for A3 to inflate. Gas Distribution the main reason for using pressure control ventilation (along with variable flow in the spontaneously breathing patient. The same effect can actually be achieved in volume control - using low peak flow rates, decelerating flow patterns and an inspiratory pause. However this requires a considerable amount of skill to apply than using pressure control. The major drawbacks of pressure control is changing tidal volume in relation to 1. changes in lung compliance, and 2. auto-PEEP. 2) Control of mean airway pressure: it is possible to increase the mean airway pressure, by varying the inspiratory time, without increasing the peak or plateau pressure. This facilitates maintaining oxygenation within a pressure limit, without overstretching the alveoli. However, if the prolongation of inspiration causes auto-PEEP, this advantage is lost. The remedy is to reduce the respiratory rate initially, and then to reduce the I:E. This concept, inverse ratio ventilation, is a key part of the open lung approach to ARDS and is the basis of some modern pressure controlled modes - BiLEVEL/APRV.

TELL ME MORE ABOUT PRESSURE CONTROL VENTILATION CLICK HERE TO LEARN MORE ABOUT PRESSURE CONTROL VENTILATION STRATEGY

Copyright Patrick Neligan 2001-2002

Acute Lung Injury Ventilator Induced Lung Injury


Ventilator induced lung injury is caused by volutrauma and excessive use of oxygen. Ventilator induced lung injury occurs when the lung is directly damaged by the action of mechanical ventilation. It is not a new concept. Macroscopic injuries associated with the ventilation of patients with ARDS have been described for decades: pneumothorax, pneumomediastinum, pneumoperitoneum, associated with alveolar rupture from overdistension. The term historically applied to this situation was barotrauma. This word expressed the tendency towards alveolar overdistension when high inspiratory pressures are applied. However the paradigm has shifted somewhat in recent years away from pressure induced to volume induced lung injury volutrauma. This term recognizes that alveolar overdistension is more likely to occur as a result of excessive volume, than excessive pressure. There is a considerable body of animal evidence to support this claim. A number of researchers have demonstrated that applying the same airway pressure in a volume limited animal (their chests were bound to prevent expansion), causes considerably less lung damage than when volume is not

limited. If the alveoli cannot overdistend, then they are unlikely to become damaged (1). Moreover, if normal lungs are exposed to tidal volumes of 1015ml/kg, there is parenchymal inflammation, increased vascular permeability, accumulation of fluid in the lung and alveolar space and atelectasis. These findings are very similar to what is seen in ALI. So if high tidal volumes injure the lung, then in patients ventilated in this way with ALI, repair of the lungs will be slowed and resolution may not take place. We know, empathically, that if you inflate a balloon excessively, it bursts. Alveoli will burst if excessive volumes inflate them. However, there is more to ventilator induced lung injury than just overdistension. It is believed that the phasic opening an closing of lung units causes release of cytokines and reinforcement and amplification of the local and systemic inflammatory response (2). Limiting the extent of volume expansion certainly curtails this, as may the prevention of phasic opening and closing of lung units keeping the lungs open with PEEP. Undoubtedly, the best way to heal an injury is to rest it, and this is also true of the lungs(3). The less the lungs are forced to expand-collapse, the less likely a lung injury is. The ultimate question therefore is should we be moving towards full tidal volume ventilation (i.e. the lungs are not permitted to deflate at all). This can be achieved using high frequency oscillation. The other notable source of lung injury is, of course, oxygen. High FiO2 can cause lung injury by two effective mechanisms the first is the formation of oxygen free radicals which are cytotoxic, the second is the problem of absorption atelectasis as the FiO2 increases, the alveoli that are well ventilated rapidly empty of oxygen along the concentration gradient (into the blood), their volume falls and they are vulnerable to collapse. It was the obsession with controlling the FiO2 that led physicians to develop the high tidal volume strategies of the 1970s and 1980s, which we have since discovered cause lung injury in their own right. However, it appears that an FiO2 of greater than 50% should be considered toxic (4). For patients with acute lung injury, the ventilation strategy is thus low tidal volumes with a relatively fast rate, with or without more generous PEEP has heretofore been given. For the patient who does not have ALI, there is little evidence that any particular ventilation strategy has any advantage. In all cases, keeping the FiO2 below 50% is appropriate where possible.

Acute Lung Injury What is the role of steroids?


Steroids may have a role in chronic ARDS in patients, without infection, with high O2 requirements days to weeks into the disease process. Acute lung injury is an inflammatory disease. We know that circulating cytokines decline in survivors over the first week, and persist in non survivors (1). At this time, the disease appears to take on a life of its own, and begins to involve lobules previously unaffected, and cause fibroproliferation in

already injured lung units. A series of studies utilizing glucocorticoids to prevent progression of inflammation in early ARDS have had very disappointing outcomes. Certainly immunosupression in the presence of infection can be expected to worsen outcomes. Conversely, there appears to be a small body of data supporting the use of steroids in the treatment of chronic persistent ARDS. Meduri and colleagues (2) have looked at the single hit model of persistent lung inflammation and postulated that ongoing inflammation due to host defense response was responsible for poor outcomes. Their study of 24 patients (it was originally powered for 100, but was cut short by the supervisory committee) demonstrated statistically significant improvement in outcomes, both in terms of lung injury scores and mortality figures. The results await confirmation by a multicenter trial, being conducted by the NIH-ARDS network. Below is a protocol for steroids in late ARDS, based on the Meduri paper (2):

The patient must have no demonstrable infection, broncho-alveolar lavage may be necessary to confirm this. This includes undrained abscesses, disseminated fungal infection and septic shock. Steroids should not be started less than 7 days, or more than 28 days, from admission. The patient should not have a history of gastric ulceration of active gastrointestinal bleeding. Patients with burns requiring skin grafting, pregnant patients, AIDS, and those in whom life support is expected to be withdrawn, are unsuitable. The patient should have evidence of ALI and require an FiO2 >/= 50% The steroid regimen: Loading dose 2mg/kg Then 2mg/kg/day from day 1 to 14 Then 1mg/kg/day from day 15 to 21 Then 0.5mg/kg/day from day 22 to 28 Then 0.25mg/kg/day on days 29 and 30 Finally 0.125mg/kg on days 31 and 32.

Patients should be meticulously screened for evidence of lower respiratory tract infection, by performing protected lavage every 3 to 4 days (while the patient is ventilated), and line sepsis (lines should be changed at regular intervals in immunosuppressed patients like this)

Acute Lung Injury Key Points

ALI is a diffuse heterogeneous lung injury characterized by hypoxemia, non cardiogenic pulmonary edema, low lung compliance and widespread capillary leakage. ALI is caused by any stimulus of local or systemic inflammation, principally sepsis. Acute Lung Injury (ALI) & Acute Respiratory Distress Syndrome (ARDS) are defined as:

Bilateral pulmonary infiltrates on chest x-ray Pulmonary Capillary Wedge Pressure <18mmHg PaO2/FiO2* <300 = ALI PaO2/FiO2 <200 = ARDS

Primary ALI is caused by a direct injury to the lung (e.g. pneumonia). Secondary ALI is caused by an indirect insult (e.g. pancreatitis). There are two stages the acute phase characterized by disruption of the alveolar-capillary interface, leakage of protein rich fluid into the interstitium and alveolar space and extensive release of cytokines and migration of neutrophils. A later reparative phase is characterized by fibroproliferation, and organization of lung tissue. The patient has low lung volumes, atelectasis, loss of compliance, ventilation-perfusion mismatch (increased deadspace) and right to left shunt. Clinical features are - severe dyspnea, tachypnea and resistant hypoxemia. There are two diagnoses to be made: the syndrome of Acute Lung Injury and the underlying cause. ALI is a clinical diagnosis. There are probably two forms of ALI primary ALI, caused by a direct injury to the lung, and secondary ALI, caused by an indirect injury to the lung. The cornerstone of treatment is to keep the PaO2 >60mmHg, without causing injury to the lungs with excessive O2 or volutrauma. Pressure control ventilation is more versatile than volume control: but a volume limited strategy should be used. A number of adjunct therapies are available, none have proven effective. Of these, inhaled nitric oxide and prone positioning are most frequently used. Current ventilation strategies involve using low tidal volumes with or without high levels of PEEP. The open lung approach attempts to optimize lung mechanics and minimize phasic damage by strategically placing PEEP above Pflex. Ventilator induced lung injury is caused by volutrauma and excessive use of oxygen. Steroids may have a role in chronic ARDS in patients, without infection, with high O2 requirements days to weeks into the disease process.