Acute Respiratory Distress Syndrome: Pathophysiology and Therapeutic Options

Abstract

Acute Respiratory Distress Syndrome (ARDS) is a common entity in critical care. ARDS is associated with many diagnoses, including trauma and sepsis, can lead to multiple organ failure and has high mortality. The present article is a narrative review of the literature on ARDS, including ARDS pathophysiology and therapeutic options currently being evaluated or in use in clinical practice. The literature review covers relevant publications until January 2011. Recent developments in the therapeutic approach to ARDS include refinements of mechanical ventilatory support with emphasis on protective lung ventilation using low tidal volumes, increased PEEP with use of recruitment maneuvers to promote reopening of collapsed lung alveoli, prone position as rescue therapy for severe hypoxemia, and high frequency ventilation. Supportive measures in the management of ARDS include attention to fluid balance, restrictive transfusion strategies, and minimization of sedatives and neuromuscular blocking agents. Inhaled bronchodilators such as inhaled nitric oxide and prostaglandins confer short term improvement without proven effect on survival, but are currently used in many centers. Use of corticosteroids is also important, and appropriate timely use may reduce mortality. Finally, extra corporeal oxygenation methods are very useful as rescue therapy in patients with intractable hypoxemia, even though a survival benefit has not, to this date been demonstrated. Despite intense ongoing research on the pathophysiology and treatment of ARDS, mortality remains high. Many pharmacologic and supportive strategies have shown promising results, but data from large randomized clinical trials are needed to fully evaluate the true effectiveness of these therapies.KeywordsARDS; Pathophysiology; Treatment

Analysis of risk factors for and the prognosis of postoperative acute respiratory distress syndrome in patients with Stanford type A aortic dissection

“…Acute respiratory distress syndrome (ARDS) can occur in cases of severe infection, shock, trauma, burns and other diseases following the damage to pulmonary capillary endothelial cells and alveolar epithelial cells (1,2). Currently, most investigators believe that ischemia-reperfusion injury (IRI) and the release of massive amounts of inflammatory mediators during cardiopulmonary bypass (CPB) and circulatory arrest are responsible for ARDS after cardiac surgery (3)(4)(5)(6).…”

A tree-matching algorithm: Application to airways in CT images of subjects with the acute respiratory distress syndrome

“…This syndrome occurs after various aggressions of the lung, e.g., bacteriological or chemical. Mortality is estimated around 40% (Brun-Buisson et al, 2004;Pierrakos et al, 2012) and may be slightly decreasing over the past two decades (Zambon and Vincent, 2008). Its treatment, besides being focused on the main cause of the syndrome, uses mechanical ventilation to support respiration, but inappropriate ventilator settings may aggravate the lung condition (ARDSnet, 2000;Fan et al, 2013).…”

Clinical Reasoning:

“…Physical examination and normal central venous pressure (CVP ϭ 6 cmH 2 O) ruled out the presence of cardiac failure, while bilateral, diffuse, and heterogeneous pattern of interstitialalveolar infiltrates on chest X-ray together with refractory hypoxemia and rigid lungs (PaO 2 /F I O 2 ratio: 71; static compliance: 19 mL/cm) suggested the presence of ARDS. 3 In patients with acute spinal cord injury, ARDS may develop due to neurogenic pulmonary edema (NPE). 4 NPE is a relatively rare form of pulmonary edema developing after a neurologic insult and caused by an increase in pulmonary interstitial and alveolar fluid.…”

“…EEG was normal (only an increase of fast, ␤-rhythms), suggesting the noncortical origin of myoclonus. Initial laboratory findings showed a white blood cell count increase (17,550/ mm 3 ) without shift to the left, elevations of glycemia (3.43 g/dL), creatinine (2.9 mg/dL), serum lactate dehydrogenase (834 IU/mL), and creatine phosphokinase (686 IU/mL), associated with myoglobinuria (Ͼ1 g/L) and metabolic acidosis (pH ϭ 7.22, base excess ϭ Ϫ16). Sustained muscle contraction may result in rhabdomyolysis, myoglobinuria, and lactic acidosis.…”