ARDS is mostly prevalent in critically ill hospitalized patients. The initial presentation of ARDS includes acute onset of dyspnea, tachypnea, hyperventilation, low oxygen saturation, cyanosis, and anxiety. A cough with frothy sputum may also be seen. The underlying cause will most likely exhibit signs and symptoms as well such as in the cases with pneumonia. Ominous signs are hypotension, tachycardia, confusion, and fatigue which are indicative of inadequate oxygen perfusion of organs. 

Hospitalized patients with ARDS are susceptible to other medical conditions such as pneumonia. Ventilation is also a risk factor for pneumonia. In addition to infection, there are other complications. One of them is pneumothorax, in which ventilated air pressure enters the space around the lungs causing subsequent collapse in one or both. In addition, lung scarring inhibits its ability to expand. Another major and potentially fatal complication is clot formation. Thromboembolism can occur due to prolonged immobility and other pathological mechanisms.

The diagnosis of ARDS is clinical and should be considered in ill patients presenting with acute respiratory failure. The Berlin definition guides the clinician in terms of timing of the onset, chest X-ray findings (opacities not consistent with effusion, atelectasis, or nodules) and oxygenation criteria per the Berlin definition [2].

In addition to the above, a full history and physical is key. The clinician should investigate and ascertain any underlying conditions. One should be highly suspicious for sepsis, which is associated with the highest rate of mortality. Examination of patient involves lung exam and determination of basilar or diffuse rales [11]. Also another critical finding is the requirement of high oxygenation and/or PEEP to maintain saturation greater than 90%. Workup is comprised of the following tests:

1. Arterial blood gas analysis provides values to calculate the PaO2/FIO2 ratio per the Berlin definition.
2. Chest X-ray will show any opacities indicative of pulmonary edema.
3. Brain natriuretic protein (BNP) can determine the etiology of pulmonary edema. BNP<100 picograms/mL suggest non cardiac causes while BNP> 500 picograms/mL are suggestive of cardiac etiology.
4. Echocardiogram is performed to assess cardiac function if BNP and other findings are inconclusive.
5. Pulmonary artery catheterization measures estimation of left ventricular end diastolic pressure. This is used to differentiate cardiogenic versus noncardiogenic etiology of pulmonary edema if BNP levels, echocardiogram and findings from history and physical are inconclusive. This is not a routine procedure. 
6. Other significant laboratory tests include cultures of blood, urine, and sputum to assess for infection. Lipase and liver functions tests are helpful to detect pancreatitis. 
7. Bronchoalveolar lavage (BAL) or endotracheal aspiration provides samples for culture and Gram stain are done to confirm suspected pneumonia [12]. There is a high mortality risk associated with these procedures. Therefore, the risks and benefits have to be weighed.
8. CT of chest is more sensitive than a chest X-ray and is useful in diagnosing pneumonia and underlying lung processes [13].

These patients are admitted to ICU. Treatment is divided into 3 categories: Respiratory support, cardiovascular resuscitation, and other therapies.

Respiratory support: Most patients require ventilation when: PaO2 <8.3kPa (60mm HG) despite using FIO2 60% and PaCO2 >6kPa (45mm HG). Clinicians should be aware that increased tidal volumes coupled with poor lung compliance can further increase lung damage. Lower tidal volumes have been shown to improve survival [10].

Cardiovascular support: Clinicians should remain vigilant while monitoring the cardiovascular status in these ill patients. It is critical to maintain cardiac output and oxygenation. In many cases, drugs such as dobutamine and other vasodilators are beneficial. Fluid resuscitation is carefully monitored as well. Blood transfusions may be warranted. Clinician may consider Swan-Ganz catheter placement for invasive monitoring of cardiac output and pulmonary capillary wedge pressure.

Further therapy depends on underlying diseases. It is critical to treat sepsis and the source if the organism(s) is/are known. In certain cases where organisms are not found on culture, broad spectrum renal safe antibiotics are used.  

Other supportive therapies include prophylactic drugs such as low molecular weight heparin for venous thromboembolism prophylaxis and antacids for gastric ulcer prophylactics. Also nutrition has to be maintained. 

While steroids were commonly used in ARDS patients, their use is no longer recommended. Steroids have been linked to many cases of septicemia and hyperglycemia. Results from the Late Steroid Rescue Study report the increase in the mortality rate with methylprednisolone therapy.

The mortality rate in patients with ARDS is 30 to 50% and increases with severity [2]. Fatality is usually secondary to multiorgan failure [5]. Furthermore, younger age is associated with better prognosis [6]. Residual lung damage may be seen in survivors [7] [8]. Post ARDS residual effects can include neuropathies, joint disorders, chronic pain, and muscle weakness [9].

Mechanical ventilation can cause lung damage and increased mortality. Furthermore, the 2000 ARDS Network Trial shows that lower tidal volumes decrease mortality from 40 to 31% [2]. This research study further demonstrates that tidal volumes at 4-6 mL/kg are protective [10].

The etiology of ARDS is extensive. Underlying diseases serve as risk factors. Sepsis is the most common cause and can be attributed to pulmonary and nonpulmonary etiologies [4]. Direct pulmonary insults such as pneumonia, aspiration of gastric contents, inhalation injury, pulmonary contusion, transfusion-related lung injury, and cardiopulmonary bypass are risk factors for ARDS. Nondirect pulmonary insults such as acute pancreatitis, fat embolism, noncardiogenic shock, disseminated intravascular coagulation, drug overdose, and trauma also place patients at risk for this debilitating pulmonary failure [1]. Other risk factors may include previous lung disease, smoking, obesity, and alcohol abuse.

Due to the usage of varied definitions of ARDS in older research studies, there is an inaccurate estimate regarding the actual incidence of ARDS. However, research emerging from the United States and international regions provide some insight on the incidence.

About 4 decades ago, the National Institute of Health (NIH) estimated that the incidence is 75 cases per 100,000 population. However, the ARDS Study Network suggests that the incidence is actually greater than that. The 2005 study in King County, Washington, using the outdated definition from the 1994 AECC, reports the incidence of ALI as 86.2 per 100,000 population [4]. A further statistical analysis of the data yields an estimate of 190,600 annual cases in the United States of which 74,500 result in death. Furthermore it is estimated that ALI is associated with an annual 3.5 million hospital days [4].

The same study also shows that age is directly proportional to the incidence of ALI. In the 15-19 year old range, the incidence was 16 per 100,000 while it was 306 in the age range of 75 to 84 [4]. As for gender, the incidences are similar with the exception of trauma patients in which females have a higher incidence of ARDS.

The complex pathophysiology of ARDS is not completely clear. The early stages consist of diffuse alveolar damage and increased permeability across the alveolar capillary membrane. Capillary endothelial cells and alveolar pneumocytes (Type I and Type II) undergo necrosis and apoptosis marking an exudative inflammatory process. This involves flooding of alveolar air spaces with edema, neutrophils and activated alveolar macrophages, in addition to mediators such as cytokines and oxidants [1]. The acute onset of alveolar flooding may result in recovery due to active clearance of pulmonary edema or may progress to disease [1].

Type II cell injury and exudative flooding contribute to surfactant dysfunction. This consequently increases alveolar-arterial oxygen gradient and leads to acute hypoxemic respiratory failure. The main features of this phase include respiratory failure, high minute ventilation and low compliant lungs [1].

Severe epithelial injury can cause progression of the inflammatory phase to a fibroproliferative phase. Necrotic type I cells denude the basement membrane thereby allowing fibrin deposition. Histologically, hyaline membranes are observed. This irreversible devastating phase consists of extensive formation or fibrous and collagen deposition [1] [4].

ARDS cannot necessarily be prevented but cessation of smoking and alcohol may help. It is also important for all individuals, especially those as risk, to comply with appropriate immunization recommendations such as flu (annual) and pneumococcal (per guidelines) vaccines. 

Acute respiratory distress syndrome (ARDS) is characterized by rapidly progressive respiratory failure. Individuals with ARDS can develop multiorgan damage and are usually at high risk for mortality [1].

The European Society of Intensive Care Medicine, the American Thoracic Society and the Society of Critical Care Medicine formulated the new criteria for ARDS in 2011. The new updated guidelines, referred to as the Berlin definition, are as follows: [2]

Timing of ARDS: Occurs within one week of clinical risk factor/insult or within one week of new or worsening respiratory condition.
Chest imaging: Bilateral opacities that are not explained by effusions, atelectasis, or nodules.
Etiology of edema: Respiratory failure not due to cardiac etiology or fluid overload.
Oxygenation: Degree of oxygenation determines the severity. 

• Mild: PaO2/FIO2 ≤300 mmHg and >200 mmHg  with PEEP or CPAP ≥5 cmH2O
• Moderate: PaO2/FIO2 ≤200 mmHg and >100mm Hg with PEEP ≥5 cmH2O
• Severe: PaO2/FIO2 ≤100 mmHg with PEEP ≥5 cmH2O

The Berlin definition replaces the previous American -European Consensus Committee (AECC) definition which differentiated ARDS from other varied or lesser forms such as acute lung injury (ALI), noncardiac pulmonary edema, and increased permeability pulmonary edema [2] [3]. This AECC definition presented diagnostic limitations and therefore was updated for accuracy.

Acute respiratory distress Syndrome (ARDS) is a condition in which respiratory failure occurs. The most common cause is sepsis, which is an overwhelming response of the body to an infection. Other causes are acute pancreatitis, fat embolism, aspiration, inhalation injury, acute pancreatitis, disseminated intravascular coagulation, drug overdose, and trauma.

In ARDS, fluid accumulates in the lungs and makes it very difficult to expand and facilitate oxygen exchange. Therefore, there are low oxygen blood levels in the body which can lead to damage of organs. The main common signs and symptoms are shortness of breath, difficulty breathing, fast and shallow breathing, blue colored skin, and other signs showing brain (confusion, lethargy) and heart dysfunction.

In patients with suspected ARDS, a chest X-ray is done to evaluate for any fluid in the lungs. Also, a blood test is done to determine the levels of oxygen. Other laboratory tests may be important to determine the exact cause. Also an ultrasound of the heart may be done to look for any cardiac problems. Individuals with ARDS are likely very ill from other diseases as well. Patients with ARDS are admitted to the intensive care unit for special care. Since the lungs are not working properly and oxygen is low in the body, most patients require mechanical ventilation to help deliver oxygen to the organs. These patients are monitored closely to make sure their heart, lungs, kidneys, and other organs are receiving adequate oxygen. Other treatments are for prevention of blood clots, stomach ulcers and nutritional care.

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