Acute Respiratory Distress Syndrome

(ARDS) Acute respiratory distress syndrome  is a medical condition occurring in critically ill patients characterized by widespread inflammation in the lungs. ARDS is not a particular disease, rather it is a clinical phenotype which may be triggered by various pathologies such as trauma, pneumonia and sepsis. The hallmark of ARDS is diffuse injury to cells which form the alveolar barrier, surfactant dysfunction, activation of the innate immune response, and abnormal coagulation. In effect, ARDS results in impaired gas exchange within the lungs at the level of the microscopic alveoli.The syndrome is associated with a high mortality rate between 20 and 50%. The mortality rate with ARDS varies widely based on severity, the patient's age, and the presence of other underlying medical conditions.Although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ARDS from "infant respiratory distress syndrome" in neonates, international consensus is that "acute respiratory distress syndrome" is the best moniker because ARDS can affect those of all ages.

Signs and symptoms

The signs and symptoms of ARDS often begin within two hours of an inciting event, but can occur after 1–3 days. Signs and symptoms may include

shortness of breath

fast breathing

 low oxygen level in the blood

       A chest x-ray frequently demonstrates generalized infiltrates or opacities in both lungs, which represent fluid accumulation in the lungs. Other signs and symptoms that occur in people with ARDS may be associated with the underlying disease process. For example, those with ARDS from sepsis may have low blood pressure and fever, while a person with pneumonia may have a cough.

Causes

The predisposing factors of ARDS are numerous and assorted. Common causes of ARDS include

 Sepsis

 Pneumonia

 Trauma

 Multiple blood transfusions

 Babesiosis

 Lng contusion

 Aspiration of stomach contents

 Drug abuse or overdose

         Other causes of ARDS include:-

 Burns

 Pancreatitis

 Near drowning

 The inhalation of chemical irritants such as smoke, phosgene, or chlorine gas

 Some cases of ARDS are linked to large volumes of fluid used during post-trauma resuscitation

Treatment

Acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit (ICU). Mechanical ventilation is usually delivered through orotracheal intubation, or by 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 to prevention in individuals with atypical pneumonias, lung contusion, or major surgery patients, who are at risk of developing ARDS. Treatment of the underlying cause is imperative. 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.

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.

Mechanical ventilation

The overall goal is to maintain acceptable gas exchange and to minimize adverse effects in its application. The parameters 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) are used.

Conventional therapy aimed at tidal volumes (Vt) of 12–15 ml/kg (where the weight is ideal body weight rather than actual weight). Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma (secondary lung injury). The ARDS Clinical Network, or ARDSNet, completed a trial that 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[10] because of their inherent tendency to increase physiologic shunt. Physiologic dead space cannot change as it is ventilation without perfusion. A shunt is perfusion without ventilation.

Low tidal volume ventilation was the primary independent variable associated with reduced mortality in the NIH-sponsored ARDSnet trial of tidal volume in ARDS. Plateau pressure less than 30 cm H

2O was a secondary goal, and subsequent analyses of the data from the ARDSnet trial and other experimental data demonstrate that there appears to be no safe upper limit to plateau pressure; regardless of plateau pressure, patients fare better with low tidal volumes.