الفهرس 
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Abstract
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are both defined by the acute onset of bilateral infiltrates consistent with pulmonary edema, but without evidence of elevated left atrial pressure. The severity of the hypoxemia distinguishes ARDS from ALI, being in ALI an arterial oxygen tension to fraction of inspired oxygen ratio (PaO2/FiO2) of 201 to 300 mmHg, while ARDS PaO2/FiO2 of ≤200 mmHg
The initial courses of ALI and ARDS are characterized by pulmonary abnormalities that typically develop within 48 hours of the inciting event and rapidly worsen. These include dyspnea, tachypnea, and hypoxemia. Physical examination usually reveals tachycardia, cyanosis, tachypnea, and diffuse rales, while arterial blood gases usually detect an acute respiratory alkalosis, hypoxemia, and an elevated alveolar-arterial oxygen gradient. The initial chest radiograph typically has bilateral, fluffy alveolar infiltrates with prominent air bronchograms. Mechanical ventilation is almost universally required.
Following the initial period, most patients with ALI and ARDS exhibit better oxygenation and decreasing alveolar infiltrates on the chest radiograph. However, some have persistent interstitial infiltrates and ventilator-dependence.
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ALI and ARDS are diagnoses of exclusion. Cardiogenic pulmonary edema and other causes of acute hypoxemic respiratory failure with bilateral infiltrates (eg, pneumonia, diffuse alveolar hemorrhage) must be excluded before the diagnosis of ALI or ARDS is made.
Healthy lungs regulate the movement of fluid to maintain a small amount of interstitial fluid and dry alveoli. In patients with ALI or ARDS, this regulation is interrupted by lung injury, causing excess fluid in both the interstitium and alveoli. Consequences include impaired gas exchange, decreased compliance, and increased pulmonary arterial pressure.
Management of acute respiratory distress syndrome (ARDS) is supportive, aimed at improving gas exchange and preventing complications while the underlying disease that precipitated ARDS is treated. Potential ARDS-specific therapies have been studied; however, they have not been shown to improve clinical outcome and, thus, cannot be recommended for routine care.
Key components of supportive care include intelligent use of sedatives and neuromuscular blockade, careful hemodynamic management, nutritional support, control of blood glucose, evaluation and treatment of nosocomial pneumonia, and
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prophylaxis against deep vein thrombosis (DVT) and gastrointestinal (GI) bleeding.
Protective ventilatory strategy by adopting a low tidal volume, high PEEP with a limit (≤30 cm H2O) on static end-inspiratory airway pressure (plateau pressure) offers improved oxygenation, increased ventilator-free days.
Until now no final or definite protocols for fluid management in ALI and ARDS in ICU is established and whether we use libral or conservative strategies or both and when we can use them but several and many studies tried hardly to reach the best for the patient, and the following are the most impressing and the most effective in this field;
Early goal-directed Therapy which concluded that early therapy provided at the earliest stages of severe sepsis and septic shock, though accounting for only a brief period in comparison with the overall hospital stay, has significant short-term and long-term benefits. These benefits arise from the early identification of patients at high risk for cardiovascular collapse and from early therapeutic intervention to restore a balance between oxygen delivery and oxygen demand ,So Early goal-directed cardiovascular resuscitation decreases mortality in patients with septic shock.
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Another promising study done by Wiedmann et al showing that Fluid management with the goal to obtain zero fluid balance in ARDS patients without shock or renal failure significantly improving the prognosis of ARDS patients .
On the other hand ,more recent study confirmed that patients with hemodynamic failure must receive early and adapted fluid resuscitation . Liberal and conservative fluid strategies are therefore complementary and should ideally follow each other in time in the same patient whose hemodynamic state progressively stabilizes .
At present, albumin treatment does not appear to be justi-fied for limitation of pulmonary edema and respiratory morbidity. Finally, the resorption of alveolar edema occurs through an active mechanism, which can be pharmacologically upregluated. In this sense, the use of beta-2 agonists may be beneficial, but further studies are neded to confirm preliminary promising results.