Acute respiratory distress syndrome (ARDS) is a lung problem. It happens when fluid builds up in the lungs, causing breathing failure and low oxygen levels in the blood. ARDS is life-threatening, because it keeps organs like the brain and kidneys from getting the oxygen they need to work.

ARDS is a rapidly developing, life-threatening condition in which the lung is injured to the point where it can't properly do its job of moving air in and out of the blood. ARDS occurs most often in people who are being treated for another serious illness or injury. Most of the time, people who get ARDS are already in the hospital for another reason.

Doctors first recognized the syndrome in 1967, when they came across 12 people who developed sudden breathing problems and rapid lung failure. All of them had similar patchy spots on their chest X-rays.

At first, the condition was called adult respiratory distress syndrome, so people would not confuse it with a similar type of lung distress seen in infants. But because ARDS can also occur in children aged 1 and older, doctors now refer to it as acute respiratory distress syndrome. Acute means sudden or new.

ARDS may also be called acute lung injury, noncardiac pulmonary edema, and increased-permeability pulmonary edema. In the past it was also called stiff lung, wet lung, and shock lung.

According to the National Heart Lung and Blood Institute, about 190,000 people in the U.S. develop ARDS each year. About 40% of people (4 out of 10) who get ARDS don't survive it. That means that 60% of people (6 out of 10) survive.

ARDS can occur when a major injury or extreme inflammation somewhere in the body damages the small blood vessels including those in the lungs. As a result, the lungs are unable to fill with air and can't move enough oxygen into the bloodstream.

The lung damage can be direct or indirect.

Conditions that can directly injure the lungs and possibly lead to ARDS include:

●Breathing in smoke or poisonous chemicals

●Breathing in stomach contents while throwing up (aspiration)

●Near drowning

●Pneumonia

●Severe acute respiratory syndrome (SARS), a lung infection

Conditions that can indirectly injure the lungs and possibly lead to ARDS include:

●Bacterial blood infection (sepsis)

●Drug overdose

●Having many blood transfusions

●Heart-lung bypass

●Infection or irritation of the pancreas (pancreatitis)

●Severe bleeding from a traumatic injury (such as a car accident)

●Severe hit to the chest or head

The conditions that have most commonly been linked to ARDS include sepsis, traumatic injury, and lung infections such as pneumonia. However, it's important to note that not everyone who has these conditions develops ARDS. Doctors are not sure why some people develop ARDS and others do not.

Symptoms of ARDS come on suddenly, usually within hours or days of the event that initially caused injury to the lung.

ARDS is defined by three main signs and symptoms:

●Rapid breathing

●Feeling like you can't get enough air in your lungs

●Low oxygen levels in your blood, which can lead to organ failure and symptoms such as rapid heart rate, abnormal heart rhythms, confusion, and extreme tiredness

Other symptoms can occur, depending on the event that caused the ARDS. For example, if pneumonia is causing the ARDS, symptoms may also include chest pain and fever.

ARDS mostly occurs about 72 hours after the trigger, such as an injury (trauma, burns, aspiration, massive blood transfusion, drug/alcohol abuse) or an acute illness (infectious pneumonia, sepsis, acute pancreatitis).

ARDS is characterized by:

●Acute onset

●Bilateral infiltrates on chest radiograph sparing costophrenic angles

●Pulmonary artery wedge pressure ＜ 18mmHg (obtained by pulmonary artery catheterization), if this information is available; if unavailable, then lack of clinical evidence of left atrial hypertension

●If PaO ₂:FiO ₂ ＜ 300mmHg (40kPa) acute lung injury (ALI) is considered to be present

●If PaO ₂:FiO ₂ ＜ 200mmHg (26.7kPa) acute respiratory distress syndrome (ARDS) is considered to be present

The PaO ₂:FiO ₂ ratios above refer to the gradient between the inspired oxygen level and the oxygen that is present in the blood. The lower the ratio, the less inspired oxygen is getting into the blood, and so the worse the patient's condition — so ARDS represents a more severe progression of disease from ALI by these diagnostic criteria.

Since ARDS is an extremely serious condition which requires invasive forms of therapy it is not without risk. Complications to be considered are:

barotrauma (volutrauma), pulmonary embolism (PE), pulmonary fibrosis, ventilator-associated pneumonia (VAP).

hemorrhage (ulcer), dysmotility, pneumoperitoneum, bacterial translocation.

arrhythmias, myocardial dysfunction.

acute renal failure (ARF), positive fluid balance.

vascular injury, pneumothorax (by placing pulmonary artery catheter), tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube.

malnutrition (catabolic state), electrolyte deficiency.

To summarize and simplify, ARDS is an acute (rapid onset) syndrome (collection of symptoms) that affects the lungs widely and results in a severe oxygenation defect, but is not due to heart failure. ARDS is a medical emergency. The severe loss of oxygen can rapidly lead to death without prompt treatment.

There is no test to definitively diagnose ARDS. The doctor will perform a physical exam and listen to your heart and lungs using a stethoscope. If one has ARDS, the doctor will hear abnormal breathing sounds, such as wheezing or crackles.

If one have low blood oxygen levels, his skin and lips may be a bluish color. An arterial blood gas test is done to check the oxygen level in his blood. Low blood oxygen levels can be a sign of ARDS.

Other tests that are done to help diagnose ARDS include:

●Chest X-ray to check for fluid in the air spaces in your lungs

●Complete blood count and other blood tests to look for signs of infection

●Sputum culture to see if bacteria or fungi are present in a sample of mucus that you coughed up from your lungs

●Lung CT scan to look for fluid in the lungs, signs of pneumonia, or other lung problems

●Heart tests are also done to rule out heart failure as the cause. Heart failure can cause fluid buildup in the lungs

Four main criteria for ARDS:

●Acute onset

●Chest X-Ray: Bilateral diffuse infiltrates of the lungs

●No cardiovascular lesion

●No evidence of left atrial hypertension: PaO ₂/FiO ₂ ratio equal to or less than 200mmHg.

The criteria for diagnosis of Acute Lung Injury (ALI) are similar except that PaO ₂/ FiO ₂ ratio is ＜300mmHg.

To assess the severity of ARDS, the Murray scoring system is used, which takes into account the chest X-ray, the PaO ₂/FiO ₂ ratio, the positive end-expiratory pressure, and lung compliance.

Most people who develop ARDS are very sick and already in the hospital. A person who has ARDS is admitted to the hospital's intensive care unit (ICU). There is no specific treatment for ARDS. The goal is to support breathing and allow the patient's lungs to heal. This involves the use of a breathing machine (mechanical ventilator) and supplemental oxygen. Researchers continue to study new ways to provide patients oxygen. A study by the National Heart Lung and Blood Institute found that smaller puffs of air from a mechanical ventilator lowered the death rate and allowed a patient to be off the machine for more days.

The possibilities of non-invasive ventilation are limited to the very early period of the disease or, better, to prevention in individuals at risk for the development of the disease (atypical pneumonias, pulmonary contusion, major surgery patients).

It's also very important to treat the underlying cause of the ARDS. For example, if there is a bacterial infection, antibiotics will be prescribed. The patient will also be given fluids and nutrients through an IV or feeding tube. The fluid balance will be carefully monitored to make sure fluid does not build up in the lungs.

Treatment of the underlying cause is imperative, as it tends to maintain the ARDS picture.

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. More than 60% ARDS patients experience a (nosocomial) pulmonary infection either before or after the onset of lung injury.

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. It is now debated whether mechanical ventilation is to be considered mere supportive therapy or actual treatment, since it may substantially affect survival.

Survivors of ARDS have an increased risk of lower quality of life, persistent cognitive impairment, depression and posttraumatic stress disorder.

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

Conventional therapy aimed at tidal volumes (Vt) of 12-15 ml/kg. Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma (secondary lung injury). Low tidal volumes (Vt) may cause hypercapnia and atelectasis due to their inherent tendency to increase physiologic shunt. Physiologic dead space cannot change as it is ventilation without perfusion. A shunt is perfusion without ventilation.

It is often said that no particular ventilator mode is known to improve mortality in airway pressure release ventilation (APRV). 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 renal perfusion.

A patient with ARDS, on average, spends between 8 and 11 days on a mechanical ventilator; APRV may reduce this time significantly and conserve valuable resources.

Positive end-expiratory pressure (PEEP) is used in mechanically-ventilated patients with ARDS to improve oxygenation. In ARDS, three populations of alveoli can be distinguished. There are normal alveoli which 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 recruitablealveoli represent a continuous population, some of which can be recruited with minimal PEEP, and others which can only be recruited with high levels of PEEP. An additional complication is that some or perhaps most 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. Finally, PEEP can be harmful. High PEEP necessarily increases mean airway pressure and alveolar pressure. This in turn can damage normal alveoli by overdistension resulting in DAD.

A compromise between the beneficial and adverse effects of PEEP is inevitable.

Distribution of lung infiltrates in acute respiratory distress syndrome is nonuniform. Repositioning into the prone position (face down) might improve oxygenation by relieving atelectasis and improving perfusion. However, although the hypoxemia is overcome there seems to be no effect on overall survival.

Several studies have shown that pulmonary function and outcome are better in patients that lost weight or pulmonary wedge pressure was lowered by diuresis or fluid restriction.

A study has found significant improvement in ARDS using modest doses of corticosteroids. But high dose steroid therapy has no effect on ARDS when given within 24 hours of the onset of illness. This was a study involving a small number of patients in one center. A recent study demonstrated that they are not efficacious in ARDS. The benefit of steroids in late ARDS may be explained by the ability of steroids to promote breakdown and inhibit fibrosis.

Inhaled nitric oxide (NO) potentially acts as selective pulmonary vasodilator. Rapid binding to hemoglobin prevents systemic effects. It should increase perfusion of better ventilated areas. There are no large studies demonstrating positive results. Therefore its use must be considered individually.

The survival rate for people with ARDS has improved in recent years, although doctors aren't sure why. Some people who get ARDS make a full recovery, but others have lasting lung damage and long-term breathing problems.

The following factors have been associated with a poor prognosis:

●Active cancer

●Advanced age

●Bacteria blood infection (sepsis)

●Being African-American

●Long-term alcohol abuse

●Long-term liver disease

●HIV infection

●Multiple organ failure

●Organ transplant

It can take many months or even years to recover from ARDS. Some people are very tired and weak after being on a breathing machine, and still have some shortness of breath after going home from the hospital. Pulmonary rehabilitation is an important part of recovery. Such therapy teaches patients how to exercise their lungs and become active again. Support groups and counseling can also be helpful.

alveoli [æl'viəlai] n.肺泡

atelectasis [,æti'lektəsis] n.肺不张

barotrauma [,bærə'trɔːmə] n.气压伤

bloodstream ['blʌd,striːm] n.血流

crackle ['kræk(ə)l] n.爆裂声

diuresis [,daijʊ(ə)'riːsis] n.利尿

fungi ['fʌŋgai] n.真菌

gastrointestinal [,gæstroin'tɛstinl] adj.胃肠的

hemodynamic [,hɛmodai'næmik] n.血液动力学的

hypoxemia [,haipɑk'simiə] n.血氧不足；低氧血症

parameter [pə'ræmitə] n.参数

permeability [pɜːmiə'biliti] n.渗透性

pneumonia [njuː'məʊniə] n.肺炎

pneumoperitoneum ['njuːmə,peritə'niəm] n.气腹

pneumothorax [,njuːmə(ʊ)'θɔːræks] n.气胸

sepsis ['sepsis] n.败血症

tracheostomy [,treki'ɑstəmi] n.气管造口术

vasodilator [,veizəʊdai'leitə] n.血管舒张药

wheezing [hwiz] n.哮喘，气喘

acute lung injury (ALI) 急性肺损伤

acute renal failure (ARF) 急性肾功能衰竭

acute respiratory distress syndrome (ARDS) 急性呼吸窘迫综合征

airway pressure release ventilation(APRV) 气道压力释放通气

arterial blood gas test 动脉血气分析

costophrenic angles 肋膈角

functional residual capacity(FRC) 功能残气量

mechanical ventilation 机械通气

nitric oxide (NO) 一氧化氮

PaO2:FiO2 ratios 动脉血氧分压（PaO ₂）/吸入氧分数值（FiO ₂）

positive end-expiratory pressure (PEEP) 呼气末正压通气

posttraumatic stress disorder 创伤后应激障碍

pulmonary artery wedge pressure 肺动脉楔压

pulmonary fibrosis 肺纤维化

severe acute respiratory syndrome (SARS) 严重急性呼吸系统综合征；非典型肺炎

sputum culture 痰培养

tidal volumes (Vt) 潮气量

ventilator-associated pneumonia (VAP) 呼吸机相关性肺炎