There are no gold standard radiological, laboratory or pathological tests to diagnosis ALI and ARDS and patients are given the diagnosis based on meeting the criteria agreed in See Table 1. ALI is diagnosed clinically and radiologically by the presence of non-cardiogenic pulmonary oedema and respiratory failure in the critically ill. Chest Radiological Appearance.
Bilateral Pulmonary Infiltrations which may or may not be symmetrical. Pulmonary Wedge Pressure. Incidence of ALI is reported as per , person years. A recent prospective population-based cohort study in a single US county demonstrated a higher incidence around ALI is a multi-factorial process which occurs due to environmental triggers occurring in genetically predisposed individuals, as ALI-inducing events are common, yet only a fraction of those exposed develop the syndrome.
Environmental triggers for developing ALI can be divided into those causing direct and those causing indirect lung injury, with sepsis, either intrapulmonary or extrapulmonary being the commonest cause.
See table 2. Direct Lung Injury. Indirect Lung Injury. Aspiration of gastric contents. Less Common. Pulmonary contusion. High Altitude. Near Drowning. Inhalation Injury. Reperfusion Injury. Severe trauma with shock and multiple transfusions. Disseminated intravascular coagulation. Cardiopulmonary bypass. Drug overdose heroin, barbiturates. Acute pancreatitis. Transfusion of blood products.
At present there is research into the role of genetic factors and how they contribute to susceptibility and prognosis. However possible candidate genes which predispose patients to ALI have been identified and other genes exist which may influence its severity, thus providing targets for research in treatment development.
Secondary factors including chronic alcohol abuse, chronic lung disease and low serum pH may increase risk of developing ALI. It is thought ALI patients follow a similar pathophysiological process independent of the aetiology. This occurs in two phases; acute and resolution, with a possible third fibrotic phase occurring in a proportion of patients. This is characterised by alveolar flooding with protein rich fluid secondary to a loss of integrity of the normal alveolar capillary base, with a heterogeneous pattern of alveolar involvement.
There are two types of alveolar epithelial cells Table 3 , both of which are damaged in ALI, likely via neutrophil mediation, with macrophages secreting pro-inflammatory cytokines, oxidants, proteases, leucotrienes and platelet activating factor.
Type I. Type II. Percentage of cells. Provide lining for alveoli. Replace damaged type I cells by differentiation. Produce surfactant. Transport ions and fluids. Damage to type I alveolar epithelial cells causes disruption to alveolar-capillary barrier integrity and allows lung interstitial fluid, proteins, neutrophils, red blood cells and fibroblasts to leak into the alveoli. Damage to type II cells decreases surfactant production and that produced is of low quality, likely to be inactivated by fluid now in alveoli, which leads to atelectasis.
Additionally there is impaired replacement of type I alveolar epithelial cells and an inability to transport ions and therefore remove fluid from the alveoli. Coagulation abnormalities occur including abnormal fibrinolysis and formation of platelet and fibrin rich thrombi which result in microvascular occlusion, causing intrapulmonary shunting leading to hypoxaemia. Ventilation-perfusion mismatch, secondary to alveolar collapse and flooding, decreases the number of individual alveoli ventilated, which in turn increases alveolar dead space, leading to hypercapnia and respiratory acidosis.
Additionally pulmonary compliance decreases and patients start to hyperventilate in an attempt to compensate the above changes. The release of inflammatory mediators from damaged lung tissue triggers systemic inflammation and systemic inflammatory response syndrome SIRS which may progress to multiple organ failure, a leading cause of death in ARDS patients.
This phase is dependent on repair of alveolar epithelium and clearance of pulmonary oedema and removal of proteins from alveolar space. The type II alveolar epithelial cells proliferate across the alveolar basement membrane and then differentiate into type I cells. Fluid is removed by initial movement of sodium ions out of the alveoli via active transport in type II alveolar epithelial cells, with water then following, down a concentration gradient through channels in the type I alveolar epithelial cells.
Soluble proteins are removed by diffusion and non soluble proteins by endocytosis and transcytosis of type I alveolar epithelial cells and phagocytosis by macrophages. The diagnosis should be considered in all patients with risk factors who present with respiratory failure, as the onset though usually over 12 to 72 hours, can be as rapid as 6 hours in presence of sepsis.
Patients present with acute respiratory failure where hypoxaemia is resistant to oxygen therapy and chest auscultation reveals diffuse, fine crepitations, indistinguishable from pulmonary oedema. This phase usually occurs after around 7 days after onset of ALI, where a resolution of hypoxaemia and improvement in lung compliance is seen. There is persistent impairment of gas exchange and decreased compliance. In severe cases it can progress to pulmonary hypertension through damage to pulmonary capillaries and even severe right heart failure, with the signs and symptoms of this developing over time.
Diagnostic criteria require arterial blood gas analysis to demonstrate the required ratio between the partial pressure of arterial oxygen and fractional inspired oxygen concentration. Although there are no pathognomonic radiographic findings for ALI, features on plain chest radiography include;. The aims of management are to provide good supportive care, maintain oxygenation and to diagnose and treat the underlying cause.
Good supportive care, as for all ICU patients, should include nutritional support with an aim for early enteral feeding, good glycaemic control and deep venous thrombosis and stress ulceration prophylaxis. It is important to identify and treat any underlying infections with antibiotics targeted at culture sensitivities and if unavailable, towards common organisms specific to infection site.
It is not uncommon for ALI patients to die from uncontrolled infection rather than primary respiratory failure. Ventilator associated pneumonia is common in patients with ALI and can be difficult to diagnoses, as ALI radiological findings can mask new consolidation and raised white cell count and pyrexia may already be present.
If suspected this should be treated with appropriate antibiotics, although long term ventilation can cause colonisation which leads to endotracheal aspirate culture results being difficult to interpret.
Although the role of physiotherapy in ALI is unclear, aims of treatment should be similar to those in all ICU patients, including removal of retained secretions and encouragement of active and passive movements, as patients are often bed bound for prolonged periods of time. Traditionally, high volumes were used in an effort to normalize the patient's arterial blood gases.
These large volumes are thought to damage the remaining areas of healthy lung by over-inflation due to the relatively normal compliance of these areas compared with the segments affected by ALI. This more conservative ventilatory strategy is also associated with a significantly lower level of circulating cytokines, the cause of biotrauma, and distant organ damage.
It also prevents atelectrauma caused by the repeated opening and closing of alveoli. Two recent large randomized controlled trials also studied the effect of elevated levels of PEEP and failed to show any reduction in mortality.
Recruitment manoeuvres have been used for many years to improve oxygenation by opening up collapsed alveoli. Notwithstanding recent advances in the monitoring of recruitment manoeuvres using CT and electrical impedance tomography, no study has demonstrated an improvement in survival using these measures.
Despite the many different ventilator modes available, there is no evidence to date to suggest that any method improves survival, provided the above limitations to tidal volume and peak pressure are adhered to. With regard to weaning from mechanical ventilation, no method has been proven to be superior to any other. Owing to the altered capillary permeability in ALI, excessive fluid administration leads to a deterioration in gas exchange.
This is because excess fluid increases the capillary hydrostatic pressure, which in turn causes pulmonary oedema and worsening oxygenation and carbon dioxide elution. On the other hand, the benefits of a more liberal fluid strategy are an increase in cardiac output with a possible improvement in non-pulmonary organ perfusion.
Patients who were in the conservative fluid group had a reduction in duration of ventilation and ICU stay, but no reduction in mortality. Notably, there was no increase in any clinically significant adverse event, including renal failure. On this basis, we would recommend a conservative fluid regime as a low-cost, low-risk intervention that could lead to improvement in clinically important outcomes. Steroids exert an anti-inflammatory effect by inhibiting arachidonic acid metabolism and reducing eosinophil activity.
As ALI is associated with an increase in both serum and bronchoalveolar lavage levels of cytokines and chemokines, it is tempting to think that the anti-inflammatory effects of steroids would be beneficial. For this reason, their use has been investigated as a preventive measure and also a therapeutic one in all phases of the condition. A recent meta-analysis of the use of steroids in the early exudative phase of ALI confirmed that steroids confer no survival benefit.
In the subacute phase, the alveoli are infiltrated by myofibroblasts and collagen deposits. Following a study that showed a significant reduction in this process after the administration of methylprednisolone, 8 the ARDSnet group performed a large multicentre randomized controlled trial using the same trial protocol.
On the basis of these studies, the routine use of methylprednisolone is not recommended in patients with ALI. It improves lung mechanics by increasing compliance and recruitment of atelectatic basal regions in addition to improving clearance of respiratory secretions.
By achieving the same P a o 2 at lower airway pressures, it was postulated that prone positioning might reduce the occurrence of ventilator-induced lung injury.
On this basis, its routine use is not recommended; however, it may be a useful temporary measure in a patient who is critically hypoxic. A recent systematic review of the use of iNO in ALI 11 showed no improvement in clinical outcome, despite a short-lived 24—48 h improvement in oxygenation and a reduction in pulmonary vascular resistance. The recently completed Conventional ventilation vs ECMO in Severe Acute Respiratory failure CESAR trial suggests that the use of ECMO results in improved survival without severe disability with a number needed to treat of 6 and thus may prove to be cost-effective when compared with conventional ventilation.
This study was not published in a peer-reviewed journal at the time this manuscript was written. Current evidence is based on case series and results from these are promising. Uncoupling of respiratory functions allows carbon dioxide clearance while maintaining oxygenation by low-frequency positive pressure ventilation or apnoeic oxygenation, effectively preventing further ventilator-induced injury. The role of physiotherapy in ARDS is uncertain and little evidence exists concerning its use.
Aims of physiotherapy in ARDS are similar to those in most ICU patients—to promote the removal of retained secretions and to encourage active and passive movements in patients who are often bed bound for a long period of time.
Independent factors associated with an increase in mortality include: Although respiratory function is often normal by 12 months after admission to the ICU for patients who survive ALI, long-term sequelae are common. These include neurocognitive impairment, psychological morbidity, and muscle weakness that often delay the return to a normal quality of life and sometimes lead to permanent disability.
Despite recent advances, ALI is still associated with significant morbidity and mortality. Basic management should include good supportive care and treatment of the underlying cause. A conservative fluid management strategy has been shown to reduce duration of mechanical ventilation and ICU stay.
Other measures may be considered in individual cases, but there is insufficient evidence to recommend their widespread use for all patients. Google Scholar. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.
Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Data would also suggest that African-American males with ARDS have a higher mortality rate than males of other racial backgrounds. Similarly, females of African-American race have a higher ARDS mortality rate than females of other racial backgrounds [ 22 ].
Despite the higher percentage of ARDS cases in females, the mortality between female and male patients with ARDS after traumatic injury does not appear to differ [ 38 ].
This data supports the concept of sex hormones, specifically estrogens, having immunologic properties enabling the development of lung injury. For both male and female patients, ARDS increases in incidence with increasing estradiol levels.
Additionally, for both male and female patients, ARDS declines with increasing testosterone levels [ 38 ]. A recent study by the National Institute of Health in the United States brought awareness to a potential treatment variability [ 39 ]. Women received lung protective ventilation less frequently than men. However, after adjustment for height and severity of illness, this difference was no longer detectable. The pro-inflammatory environment of the pulmonary parenchyma in ARDS patients has led some investigators to examine the effects of enteral nutrition enriched with fish oils and borage oils containing high levels of antioxidants.
Early studies suggested a favorable effect on oxygenation, number of ventilator and ICU days, and a lower incidence of new organ failure [ 40 ]. These findings have been disproven by the recent OMEGA study [ 41 ], which was stopped early for futility. Not all patients are able to tolerate enteral feeds after traumatic injury, thus leading some to examine the effects of total parenteral nutrition TPN.
Ventilated trauma patients receiving TPN were retrospectively analyzed over a 6-year period. These data would suggest that the inflammatory modulation properties of the nutritional source be carefully considered in the patient at risk for ARDS.
A number of management strategies relevant to acute lung injury with an emphasis on prevention of further deterioration are discussed below Table 2.
It is common practice to resuscitate the trauma patient in shock with intravenous fluids even at the expense of worsening pulmonary edema. A fluid-conservative management strategy is recommended in the absence of hypotension or vasopressor requirement based on a randomized-controlled trial in medical and surgical ICU patients [ 43 ].
While this study did not measure a lower mortality rate, it also did not increase non-pulmonary organ failure. Instead, fluid restriction shortened the duration of mechanical ventilation and the length of intensive care unit stay. No randomized controlled studies exist that provide sufficient evidence to guide fluid management specific to the trauma population [ 44 ].
Pulmonary contusions can evolve over several days. Therefore, goals in the initial period are to prevent atelectasis and derecruitment as seen in the patient in Figure 3 and 4. Incentive spirometry and patient initiated positive airway pressure therapy have been shown to decrease mechanical ventilator-dependent days, lengths of stay, infectious morbidity, and mortality in awake and cooperative patients with rib fractures assigned to a multidisciplinary pathway [ 45 ].
There is no evidence to draw conclusions on whether recruitment maneuvers independently reduce mortality or length of ventilation in patients with ALI or ARDS [ 46 ]. Of note, NIPPV was combined with a multi-modal analgesia regimen including epidural analgesia, followed by a combination of intravenous patient-controlled analgesia, non-steroidal anti-inflammatory drugs and acetaminophen.
More recently, a small randomized-controlled trial in patients with thoracic trauma came to the same conclusion in regard to the use of NIPPV to avoid intubation [ 48 ]. Patients who develop frank respiratory failure hypoxia, hypercarbia, increased work of breathing should be intubated and mechanically ventilated without inappropriate delay.
Other indications for intubation are the need for airway protection, combativeness, cardiovascular instability, to facilitate imaging and procedures, and anticipated pulmonary deterioration. Following two landmark randomized controlled trials that demonstrated a reduced mortality in patients ventilated with small volumes and low plateau pressures [ 49 , 50 ], small tidal volume ventilation and the use of PEEP has been accepted to maintain alveolar recruitment and oxygenation [ 51 ].
Borges et al. A well-designed trial demonstrated that in patients ventilated with low tidal volumes, higher levels of PEEP in combination with recruitment maneuvers did neither result in a difference in hospital mortality nor in the rate of barotrauma when compared to conventional levels of PEEP [ 53 ]. The optimal level of PEEP is still unknown [ 54 , 55 ]. Patients with unilateral pulmonary contusions can progress to a clinical picture consistent with ARDS without meeting the formal criterion of bilateral infiltrates on chest x-ray for ARDS [ 5 ].
Posttraumatic patients at risk for or who develop ARDS should be ventilated with low tidal volumes according to ARDS Network guidelines as non-traumatized patients are. Airway pressure release ventilation APRV is the continuous administration of positive airway pressure CPAP to achieve recruitment with intermittent airway pressure releases to allow CO 2 clearance. Patients can breathe at any point while remaining at a higher mean airway pressures [ 58 ]. It is similar to inverse ratio pressure control ventilation IRV with the added benefit of spontaneous breathing, and without the degree of sedation or muscle relaxation necessary for IRV [ 59 ].
In a recent trial conducted by Roy et al. Neuromuscular blocking agents have been thought to aid in faster achievement of targeted lung-protective ventilation settings and patient synchrony with the ventilator. Papazian et al. A systematic review of 33 randomized controlled trials came to the conclusion that the evidence to support pharmacological interventions, namely prostaglandin E1, N-acetylcysteine, the early administration of high dose corticosteroids, or surfactant for ALI and ARDS is insufficient [ 62 , 63 ].
Extracorporeal membrane oxygenation ECMO has been used in severe ARDS when the risks of refractory hypoxemia outweigh the risks of this invasive procedure. Although an early NIH study showed a greater volume of blood lost due to systemic coagulation in ECMO patients and no mortality benefit [ 67 ], more recent studies have demonstrated improved survival with ECMO in patients following traumatic injury [ 68 , 69 ].
The availability of heparin-bonded circuitry can negate the need for systemic anticoagulation for several days in patients following injury that in the majority of cases is performed with systemic anticoagulation [ 70 ]. Newer, mobile, and more compact circuits allow for the use of this life-saving intervention in far-forward military locales and during military transport [ 71 ]. Surgical management is controversial despite two level one evidence trials favoring operative fixation [ 72 ].
Tanaka et al. A retrospective study in by Voggenreiter [ 75 ] had suggested that patients with pulmonary contusions did not benefit from surgical fixation as much as patients without pulmonary contusions did. This trend was also observed in a recent retrospective case-controlled study [ 76 ], but did not reach statistical significance.
The controversy is further highlighted by two reports of improved pulmonary function testing results after surgical stabilization of flail chest at the Eastern Association for the Surgery of Trauma annual scientific meeting [ 77 , 78 ]. Large prospective randomized-controlled trials are needed for definite answers to relevant outcome questions.
Acute lung injury and acute respiratory distress syndrome are heterogeneous diseases, the end result of many different types of acute pulmonary injury and with at times overlapping pathogenetic mechanisms [ 79 ]. Although there are several management strategies to improve oxygenation in patients on mechanical ventilation, decisions which therapies to use should be guided by meaningful outcome measures, including reduced duration of mechanical ventilation, length of ICU stay, and mortality [ 80 ].
Many trials examining the potential benefits of interventions have used mechanical ventilation strategies that are recognized as harmful today. Until recently, too many studies have failed to compare their intervention group to controls that reflect the current standard of care and mitigate progression of the lung injury. While we await future trials, we as clinicians can incorporate what has been shown to save lives a decade ago: lung protective ventilation.
Implications for management. Clin Chest Med. Article PubMed Google Scholar. Crit Care Clin. Crit Care Med.
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