acute respiratory distress syndrome acute respiratory distress syndrome acute respiratory distress syndrome (ards) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). for those who survive, a decreased quality of life is common. acute respiratory distress syndromeother namesrespiratory distress syndrome (rds), adult respiratory distress syndrome, shock lung, wet lungchest x-ray.specialtycritical care medicinesymptomsshortness of breath, rapid breathing, bluish skin coloration, chest pain, loss of speechcomplicationsblood clots, collapsed lung (pneumothorax), infections, scarring (pulmonary fibrosis)usual onsetwithin a weekdiagnostic methodadults: pao2/fio2 ratio of less than 300 mm hgchildren: oxygenation index > 4differential diagnosisheart failuretreatmentmechanical ventilation, ecmoprognosis35 to 90 % risk of deathfrequency3 million per year causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration. the underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body's regulation of blood clotting. in effect, ards impairs the lungs' ability to exchange oxygen and carbon dioxide. adult diagnosis is based on a pao2/fio2 ratio (ratio of partial pressure arterial oxygen and fraction of inspired oxygen) of less than 300 mm hg despite a positive end-expiratory pressure (peep) of more than 5 cm h2o. cardiogenic pulmonary edema, as the cause, must be excluded. the primary treatment involves mechanical ventilation together with treatments directed at the underlying cause. ventilation strategies include using low volumes and low pressures. if oxygenation remains insufficient, lung recruitment maneuvers and neuromuscular blockers may be used. if these are insufficient, extracorporeal membrane oxygenation (ecmo) may be an option. the syndrome is associated with a death rate between 35 and 50%. globally, ards affects more than 3 million people a year. the condition was first described in 1967. although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ards from "infant respiratory distress syndrome" in newborns, the international consensus is that "acute respiratory distress syndrome" is the best term because ards can affect people of all ages. there are separate diagnostic criteria for children and those in areas of the world with fewer resources. signs and symptoms the signs and symptoms of ards often begin within two hours of an inciting event, but have been known to take as long as 1–3 days; diagnostic criteria require a known insult to have happened within 7 days of the syndrome. signs and symptoms may include shortness of breath, fast breathing, and a low oxygen level in the blood due to abnormal ventilation. other common symptoms include muscle fatigue and general weakness, low blood pressure, a dry, hacking cough, and fever. complications complications may include the following: lungs: barotrauma (volutrauma), pulmonary embolism (pe), pulmonary fibrosis, ventilator-associated pneumonia (vap) gastrointestinal: bleeding (ulcer), dysmotility, pneumoperitoneum, bacterial translocation neurological: hypoxic brain damage cardiac: abnormal heart rhythms, myocardial dysfunction kidney: acute kidney failure, positive fluid balance mechanical: vascular injury, pneumothorax (by placing pulmonary artery catheter), tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube) nutritional: malnutrition (catabolic state), electrolyte abnormalities other complications that are typically associated with ards include: atelectasis: small air pockets within the lung collapse complications that arise from treatment in a hospital: blood clots formed by lying down for long periods of time, weakness in muscles that are used for breathing, stress ulcers, and issues with mental health and depression. failure of multiple organs pulmonary hypertension or increase in blood pressure in the main artery from the heart to the lungs. this complication typically occurs due to the restriction of the blood vessel due to inflammation of the mechanical ventilation causes there are direct and indirect causes of ards depending whether the lungs are initially affected. direct causes include pneumonia (including bacterial and viral), aspiration, inhalational lung injury, lung contusion, chest trauma, and near-drowning. indirect causes include sepsis, shock, pancreatitis, trauma (e.g. fat embolism), cardiopulmonary bypass, trali, burns, increased intracranial pressure. fewer cases of ards are linked to large volumes of fluid used during post-trauma resuscitation. pathophysiology main article: pathophysiology of acute respiratory distress syndrome micrograph of diffuse alveolar damage, the histologic correlate of ards. h&e stain. ards is a form of fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). it is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. additional common findings in ards include partial collapse of the lungs (atelectasis) and low levels of oxygen in the blood (hypoxemia). the clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (dad). of these, the pathology most commonly associated with ards is dad, which is characterized by a diffuse inflammation of lung tissue. the triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells. neutrophils and some t-lymphocytes quickly migrate into the inflamed lung tissue and contribute in the amplification of the phenomenon. the typical histological presentation involves diffuse alveolar damage and hyaline membrane formation in alveolar walls. although the triggering mechanisms are not completely understood, recent research has examined the role of inflammation and mechanical stress. one research group has reported that broncho-alveolar lavage fluid in later-stage ards often contains trichomonads, in an amoeboid form (i.e. lacking their characteristic flagellum) which makes them difficult to identify under the microscope. diagnosis a chest x-ray of transfusion-related acute lung injury (left) which led to ards. right is a normal x-ray before the injury. diagnostic criteria diagnostic criteria for ards have changed over time as understanding of the pathophysiology has evolved. the international consensus criteria for ards were most recently updated in 2012 and are known as the "berlin definition". in addition to generally broadening the diagnostic thresholds, other notable changes from the prior 1994 consensus criteria include discouraging the term "acute lung injury," and defining grades of ards severity according to degree of decrease in the oxygen content of the blood. according to the 2012 berlin definition, adult ards is characterized by the following: lung injury of acute onset, within 1 week of an apparent clinical insult and with the progression of respiratory symptoms bilateral opacities on chest imaging (chest radiograph or ct) not explained by other lung pathology (e.g. effusion, lobar/lung collapse, or nodules) respiratory failure not explained by heart failure or volume overload decreased pao2/fio2 ratio (a decreased pao2/fio2 ratio indicates reduced arterial oxygenation from the available inhaled gas): mild ards: 201 – 300 mmhg (≤ 39.9 kpa) moderate ards: 101 – 200 mmhg (≤ 26.6 kpa) severe ards: ≤ 100 mmhg (≤ 13.3 kpa) the berlin definition requires a minimum positive end expiratory pressure (peep) of 5 cmh2o for consideration of the pao2/fio2 ratio. this degree of peep may be delivered noninvasively with cpap to diagnose mild ards. the 2012 "berlin criteria" are a modification of the prior 1994 consensus conference definitions (see history). medical imaging radiologic imaging has long been a criterion for diagnosis of ards. original definitions of ards specified that correlative chest x-ray findings were required for diagnosis, the diagnostic criteria have been expanded over time to accept ct and ultrasound findings as equally contributory. generally, radiographic findings of fluid accumulation (pulmonary edema) affecting both lungs and unrelated to increased cardiopulmonary vascular pressure (such as in heart failure) may be suggestive of ards. ultrasound findings suggestive of ards include the following: anterior subpleural consolidations absence or reduction of lung sliding "spared areas" of normal parenchyma pleural line abnormalities (irregular thickened fragmented pleural line) nonhomogeneous distribution of b-lines (a characteristic ultrasound finding suggestive of fluid accumulation in the lungs) treatment acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit (icu). mechanical ventilation is usually delivered through a rigid tube which enters the oral cavity and is secured in the airway (endotracheal intubation), or by tracheostomy when prolonged ventilation (≥2 weeks) is necessary. the role of non-invasive ventilation is limited to the very early period of the disease or to prevent worsening respiratory distress in individuals with atypical pneumonias, lung bruising, or major surgery patients, who are at risk of developing ards. treatment of the underlying cause is crucial. appropriate antibiotic therapy is started as soon as culture results are available, or if infection is suspected (whichever is earlier). empirical therapy may be appropriate if local microbiological surveillance is efficient. where possible the origin of the infection is removed. when sepsis is diagnosed, appropriate local protocols are followed. mechanical ventilation further information: pressure regulated volume control the overall goal of mechanical ventilation is to maintain acceptable gas exchange to meet the body's metabolic demands and to minimize adverse effects in its application. the parameters peep (positive end-expiratory pressure, to keep alveoli open), mean airway pressure (to promote recruitment (opening) of easily collapsible alveoli and predictor of hemodynamic effects), and plateau pressure (best predictor of alveolar overdistention) are used. previously, mechanical ventilation aimed to achieve 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 clinical trial that showed improved mortality when people with ards were ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg. low tidal volumes (vt) may cause a permitted rise in blood carbon dioxide levels and collapse of alveoli because of their inherent tendency to increase shunting within the lung. physiologic dead space cannot change as it is ventilation without perfusion. a shunt is a perfusion without ventilation within a lung region. 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 h2o 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, individuals with ards fare better with low tidal volumes. airway pressure release ventilation no particular ventilator mode is known to improve mortality in acute respiratory distress syndrome (ards). some practitioners favor airway pressure release ventilation when treating ards. well documented advantages to aprv ventilation include decreased airway pressures, decreased minute ventilation, decreased dead-space ventilation, promotion of spontaneous breathing, almost 24-hour-a-day alveolar recruitment, decreased use of sedation, near elimination of neuromuscular blockade, optimized arterial blood gas results, mechanical restoration of frc (functional residual capacity), a positive effect on cardiac output (due to the negative inflection from the elevated baseline with each spontaneous breath), increased organ and tissue perfusion and potential for increased urine output secondary to increased kidney perfusion. a patient with ards, on average, spends between 8 and 11 days on a mechanical ventilator; aprv may reduce this time significantly and thus may conserve valuable resources. positive end-expiratory pressure positive end-expiratory pressure (peep) is used in mechanically ventilated people with ards to improve oxygenation. in ards, three populations of alveoli can be distinguished. there are normal alveoli that are always inflated and engaging in gas exchange, flooded alveoli which can never, under any ventilatory regime, be used for gas exchange, and atelectatic or partially flooded alveoli that can be "recruited" to participate in gas exchange under certain ventilatory regimens. the recruitable alveoli represent a continuous population, some of which can be recruited with minimal peep, and others can only be recruited with high levels of peep. an additional complication is that some alveoli can only be opened with higher airway pressures than are needed to keep them open, hence the justification for maneuvers where peep is increased to very high levels for seconds to minutes before dropping the peep to a lower level. peep can be harmful; high peep necessarily increases mean airway pressure and alveolar pressure, which can damage normal alveoli by overdistension resulting in dad. a compromise between the beneficial and adverse effects of peep is inevitable. the 'best peep' used to be defined as 'some' cmh2o above the lower inflection point