Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs.
ARDS symptoms include: shortness of breath, tachypnea and cyanosis.
ARDS is a constellation of conditions that shares features of non-cardiogenic pulmonary edema, typically mediated by diffuse alveolar-capillary permeability and inflammation, resulting in impaired gas exchange severe enough to threaten life.
ARDS arises from condition, such as trauma, massive blood transfusion, septic shock, or pneumonia.
Despite medical improvements, the average mortality rate is still 40% in hospitalized patients.
A decreased quality of life is common in survivors.
Usual onset of the process is within a week.
Patients may experience chest pain or chest pressure.
Diagnosis:
Adults: PaO2/FiO2 ratio of less than 300 mm Hg. despite a positive end-expiratory pressure (PEEP) of more than 5 cm H2O.
Children: oxygenation index > 4.
Differential diagnosis:
Heart failure
35 to 90 % risk of death.
Frequency 3 million per year, globally.
Causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration.
The underlying mechanism involves diffuse injury to cells which form the barrier of the alveoli of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction in the regulation of blood clotting.
ARDS is a form of fluid accumulation in the lungs not explained by heart failure.
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 in capillaries in the lungs.
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 of more than 5 cm H2O.
Diagnosis: require a history of known insult to have happened within 7 days of the syndrome.
ARDS signs and symptoms may include: shortness of breath, fast breathing, and hypoxemia due to abnormal ventilation, muscle fatigue and general weakness, low blood pressure, a dry, hacking cough, and fever.
The diagnostic criteria for acute hypoxemic respiratory failure is:
PaO2 < 60 mmHg on room air measured by ABG, or SpO2 < 91% on room air measured by pulse oximetry, or
P/F ratio < 300 on oxygen
Cardiogenic pulmonary edema, as cause, must be ruled out.
Its primary management involves mechanical ventilation together with treatments directed at the underlying cause.
Ventilation strategies include using low volumes and low pressures.
ARDS is associated with a death rate between 35 and 50%.
ARDS affects more than 3 million people a year, worldwide.
ARDS can affect people of all ages.
Signs and symptoms often begin within two hours of an inciting event.
ARDS may take as long as 1–3 days to manifest, but 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, muscle fatigue and general weakness, low blood pressure, a dry, hacking cough, and fever.
Complications of ARDS:
Pulmonary: barotrauma, pulmonary embolism, pulmonary fibrosis, ventilator-associated pneumonia (VAP).
Gastrointestinal: bleeding, dysmotility, pneumoperitoneum, bacterial translocation
Neurological: hypoxic brain damage
Cardiac: abnormal heart rhythms, myocardial dysfunction
Kidney: acute kidney failure, fluid retention
Mechanical: vascular injury,
Pneumothorax from placement of pulmonary artery catheter, tracheal injury/stenosis from intubation and endotracheal tube.
Nutritional: malnutrition,electrolyte abnormalities
Atelectasis
Blood clots formed by inactivity
Weakness in muscles that are used for breathing.
Stress ulcers
Mental health and depression.
Failure of multiple organs
Pulmonary hypertension because of the restriction of the blood vessel due to inflammation of the mechanical ventilation
Direct causes of ARDS include, pneumonia, bacterial and viral, aspiration, inhalational lung injury, lung contusion, chest trauma, and near-drowning.
Indirect causes of ARDS include: sepsis, shock, pancreatitis, trauma, cardiopulmonary bypass, transfusion related lung injury, burns, increased intracranial pressure, and large volumes of fluid used during post-trauma resuscitation.
Common findings in ARDS include atelectasis and low levels of oxygen in the blood (hypoxemia).
The pathological findings with ARDS includE: pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage.
Diffuse alveolar damage is the most commonly associated pathology with ARDS.
Diffuse alveolar damage refers to diffuse inflammation of lung tissue.
It is a non-pulmonary edema.
The initiating/triggering insult results in the release of chemokines and other inflammatory mediators secreted by local epithelial and endothelial cells.
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.
Common findings in ARDS include: atelectasis and hypoxemia.
Neutrophils and some T-lymphocytes quickly migrate to the inflamed lung tissue and amplify the phenomenon.
There is diffuse alveolar damage and hyaline membrane formation in alveolar walls.
Clinically the syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage.
Diffuse alveolar damage (DAD) pathology most commonly associated with ARDS.
Diffuse alveolar damage is characterized by a diffuse inflammation of lung tissue.
Local epithelial and endothelial cells are triggered to release chemical signals and other inflammatory mediators.
Neutrophils and T-lymphocytes migrate into the inflamed lung tissue and contribute in the amplification of the phenomenon.
Histological findings involve diffuse alveolar damage and hyaline membrane formation in alveolar walls.
DIAGNOSTIC criteria for ARDS have changed over time as understanding of the pathophysiology has evolved.
Grades of ARDS severity relate to the degree of decrease in the oxygen content of the blood.
According to the Berlin definition, adult ARDS is characterized by the following:
as an acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue, with hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance.
Key components of Berlin definition:
acute, meaning onset over 1 week or less, bilateral opacities consistent with pulmonary edema must be present and may be detected on CT or chest radiograph.
PF ratio <300mmHg with a minimum of 5 cmH20 PEEP (or CPAP).
must not be fully explained by cardiac failure or fluid overload.
An echocardiogram should be performed in most cases if there is no clear cause such as trauma or sepsis.
Severity
ARDS is categorized as being mild, moderate, or severe.
ARDS Severity PaO2/FiO2 Mortality
Mild 200 – 300 27%
Moderate 100 – 200 32%
Severe < 100 45%
Use of vasopressors at the time of diagnosis of ARDS is associated with a much higher mortality regardless of the PF ratio.
Berlin Definition had a sensitivity of 89% and specificity of 63% to identify ARDS, based on autopsies of 356 patients with clinical criteria for ARDS using evidence of diffuse alveolar damage as the gold standard, 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, decreased PaO2/FiO2 ratio.
The onset of signs and symptoms of ARDS often begin within two hours of an inciting event.
But, signs and symptomshave been known to take as long as 1–3 days;
Radiographic findings of fluid accumulation affecting both lungs and unrelated to increased cardiopulmonary vascular pressure may be suggestive of ARDS.
Ultrasound findings suggestive of ARDS include the following:
Anterior subpleural consolidations,
Pleural line abnormalities,
Nonhomogeneous distribution of B-lines.
Acute respiratory distress syndrome is usually treated with mechanical ventilation delivered through endotracheal intubation, or by tracheostomy when prolonged ventilation (≥2 weeks) is necessary.
The goal of mechanical ventilation is to maintain acceptable gas exchange to meet the body’s metabolic demands and to minimize its adverse effects.
The role of non-invasive ventilation is limited to the very early period of the disease or to prevent worsening respiratory distress in individuals who are at risk of developing ARDS.
Treatment of the underlying cause of ARDS is crucial.
Appropriate antibiotic therapy is started as soon as culture results are available, or if infection is suspected.
PEEP (positive end-expiratory pressure, keeps alveoli open.
The mean airway pressure promotes recruitment and opening of easily collapsible alveoli and predicts hemodynamic effects.
High tidal volumes can overstretch alveoli resulting in volutrauma.
Clinical trials show 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.
Regardless of plateau pressure, individuals with ARDS fare better with low tidal volumes.
No particular ventilator mode is known to improve mortality in acute respiratory distress syndrome.
Some prefer airway pressure release ventilation when treating ARDS.
APRV ventilation decreases 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, 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.
Positive end-expiratory pressure (PEEP) is used in ventilated people with ARDS to improve oxygenation.
In ARDS, there are three populations of alveoli:
normal alveoli that are always inflated and engaging in gas exchange,
flooded alveoli which can never, be used for gas exchange,
atelectatic or partially flooded alveoli that can be recruited to participate in gas exchange with ventilatory regimens.
The recruitable alveoli can be recruited with minimal PEEP, and others can only be recruited with high levels of PEEP.
Some alveoli can only be opened with higher airway pressures than are needed to keep them open, hence PEEP is increased to very high levels for seconds to minutes before dropping the PEEP to a lower level.
High PEEP necessarily increases mean airway pressure and alveolar pressure, which can damage normal alveoli by overdistension.
In patients with ARDS lung recruitment maneuvers and PEEP titration is associated with high rates of barotrauma and pneumothorax and increased mortality.
Repositioning into the prone position may improve oxygenation by relieving atelectasis and improving perfusion.
Early in the treatment of severe ARDS, the prone position confers a mortality benefit of 26% compared to supine ventilation.
Pulmonary function and outcome are better in people with ARDS who lose weight or whose pulmonary wedge pressure was lowered by diuresis or fluid restriction.
It is uncertain whether or not treatment with corticosteroids improves overall survival.
Corticosteroids may increase the number of ventilator-free days during the first 28 days of hospitalization.
Extracorporeal membrane oxygenation (ECMO) is mechanically applied prolonged cardiopulmonary support.
There are two types of ECMO.
Venovenous ECMO provides respiratory support.
Venoarterial which provides respiratory and hemodynamic support.
People with ARDS who do not require cardiac support typically undergo venovenous ECMO.
Patients referred to an ECMO center demonstrated significantly increased survival compared to conventional management (63% to 47%).
No evidence showing that treatments with exogenous surfactants, statins, beta-blockers or n-acetylcysteine decreases early mortality, late all-cause mortality, duration of mechanical ventilation, or number of ventilator-free days.
Prognosis of ARDS is poor, with mortality rates of approximately 40%.
ARDS complications in survivors: exercise limitation, physical and psychological sequelae, and decreased physical quality of life.
The annual rate of ARDS is generally 13–23 people per 100,000 in the general population.
ARDS is more common in people who are mechanically ventilated with acute lung injury (ALI) occurring 16% of ventilated people.
Worldwide, severe sepsis is the most common trigger causing ARDS.
Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients and may be either causes or complications of ARDS.
Complications of ARDS:
barotrauma
pulmonary embolism (PE),
pulmonary fibrosis,
ventilator-associated pneumonia (VAP)
Gastrointestinal: bleeding,
dysmotility,
pneumoperitoneum, bacterial translocation
hypoxic brain damage
abnormal heart rhythms,
myocardial dysfunction
acute kidney failure,
fluid retention
vascular injury, pneumothorax (by placing pulmonary artery catheter)
tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube)
Malnutrition (catabolic state),
electrolyte abnormalities
Atelectasis
Failure of multiple organs
Pulmonary hypertension or increase in blood pressure.
ARDS triggers additionally include: mechanical ventilation, sepsis, pneumonia, drowning, circulatory shock, aspiration, trauma, pulmonary contusion, major surgery, massive blood transfusions, smoke inhalation, drug reaction or overdose, fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy.
The majority of patients with all these conditions do not develop ARDS.
Alcohol excess increases the risk of ARDS.
Elevated abdominal pressure of any cause is also probably a risk factor for the development of ARDS.
ARDS is the severe form of acute lung injury (ALI), and of transfusion-related acute lung injury (TRALI), though there are other causes.
Recombinant human IFN beta-1a drug, showed an 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS.
The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced.
Aspirin and ascorbic acid have not been found to be useful.
Major treatment recommendations for non-into bed patients with acute hypoxic respiratory failure, not due to cardiogenic, pulmonary edema, or chronic lung disease, the use of high flow nasal oxygen versus conventional oxygen therapy to reduce the risk of intubation.
For intubated patients with ARDS the use of low total volume ventilation of 4 to 8 mL per kilogram predicted body weight versus larger total volumes to reduce mortality.
Prolonged high pressure recruitment maneuvers or brief high pressure recruitment maneuvers should not be used.
For intubated patients with moderate to severe ARDS the use of the prone position to reduce mortality is recommended.
Continuous infusions of neuromuscular blockade to reduce mortality should not routinely be used.
Extracorporeal membrane oxygenation should be considered in patients who meet criteria.
Oxygen-enriched air has a higher FIO2 than 0.21; up to 1.00 which means 100% oxygen.
FIO2 is typically maintained below 0.5 even with mechanical ventilation, to avoid oxygen toxicity, but there are applications when up to 100% is routinely used.
The Berlin definition requires a minimum positive end expiratory pressure (PEEP) of 5 cmH
2O for consideration of the PaO
2/FiO2 ratio.
Imaging criteria for diagnosis of ARDS:
Radiographic findings of fluid accumulation 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:
Subpleural consolidations
Absence or reduction of lung sliding
Areas of normal parenchyma
Irregular thickened fragmented pleural lines
B-lines, a characteristic ultrasound finding suggestive of fluid accumulation in the lungs
Acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit (ICU).
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.
The goal of mechanical ventilation is to maintain acceptable gas exchange to meet the body’s metabolic demands and to minimize its adverse effects.
PEEP-positive end-expiratory pressure, to keep alveoli open. mean airway pressure promoting opening of easily collapsible alveoli and plateau pressure to predict alveolar overdistention are used.
Clinical trials show 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 rise in blood carbon dioxide levels and collapse of alveoli because of their inherent tendency to increase shunting within the lung.
A shunt is a perfusion without ventilation within a lung region.
No particular ventilator mode is known to improve mortality in acute respiratory distress syndrome (ARDS).
Airway pressure release ventilation (APRV) when treating ARDS has documented advantages to 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, 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.
The use of APRV may reduce this time significantly.
Positive end-expiratory pressure (PEEP) is used in mechanically ventilated people with ARDS to improve oxygenation.
The recruitable alveoli represent a population, some of which can be recruited with minimal PEEP, and others can only be recruited with high levels of PEEP.
PEEP can be harmful; high PEEP necessarily increases mean airway pressure and alveolar pressure, which can damage normal alveoli by overdistension resulting in diffuse alveolar damage.
Repositioning into the prone, face down, position might improve oxygenation by relieving atelectasis and improving perfusion.
If this is done early in the treatment of severe ARDS, it confers a mortality benefit of 26% compared to supine ventilation.
Several studies have shown that pulmonary function and outcome are better in people with ARDS who lost weight or whose pulmonary wedge pressure was lowered by diuresis or fluid restriction.
It is uncertain whether or not treatment with corticosteroids improves overall survival.
Corticosteroids may increase the number of ventilator-free days during the first 28 days of hospitalization.
Inhaled nitric oxide (NO) selectively widens the lung’s arteries which allows for more blood flow to open alveoli for gas exchange, but there is no evidence that inhaled nitric oxide decreases morbidity and mortality in people with ARDS.
Furthermore, nitric oxide may cause kidney damage and is not recommended as therapy for ARDS regardless of severity.
Extracorporeal membrane oxygenation (ECMO) is prolonged cardiopulmonary support.
There are two types of ECMO: Venovenous which provides respiratory support and venoarterial which provides respiratory and hemodynamic support.
People with ARDS who do not require cardiac support typically undergo venovenous ECMO.
Multiple studies have shown the effectiveness of ECMO in acute respiratory failure.
The CESAR (Conventional ventilatory support versus Extracorporeal membrane oxygenation for Severe Acute Respiratory failure) trial demonstrated ECMO significantly increased survival compared to conventional management (63% to 47%).
There is no evidence treatments with exogenous surfactants, statins, beta-blockers or n-acetylcysteine decreases early mortality, late all-cause mortality, duration of mechanical ventilation, or number of ventilator-free days with ARDS.
The overall prognosis of ARDS is poor: mortality rates of approximately 40% exist.
ARDS sequelae include: exercise limitation, physical and psychological abnormalities, decreased physical quality of life.
ARDS sequelae are more common in people who are mechanically ventilated with acute lung injury occurring 16% of ventilated people.
Severe sepsis is the most common trigger causing ARDS.
Other triggers for ARDS include: mechanical ventilation, sepsis, pneumonia, drowning, circulatory shock, aspiration, trauma, especially pulmonary contusion, major surgery, massive blood transfusions,smoke inhalation, drug reaction or overdose, fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy: the majority of patients with all these conditions do not develop ARDS.
The most common triggers for ARDS are pneumonia and sepsis.
Pneumonia is present in up to 60% of patients and may be either a cause or complication of ARDS.
Alcohol excess increases the risk of ARDS.
Elevated intraabdominal pressure is probably a risk factor for the development of ARDS, particularly during mechanical ventilation.
The definition required the following criteria to be met:
acute onset, persistent dyspnea
bilateral infiltrates on chest radiograph consistent with pulmonary edema
hypoxemia
absence of left atrial hypertension
pulmonary artery wedge pressure < 18 mmHg, obtained by pulmonary artery catheterization
Arterial blood gas analysis and chest X-ray were required for formal diagnosis.
A classification of ARDS by severity: mild, moderate, or severe according to arterial oxygen saturation.
ARDS is the severe form of acute lung injury (ALI), and of transfusion-related acute lung injury (TRALI), though there are other causes.