Acute respiratory distress syndrome ( ARDS ) is a medical condition that occurs in critically or critically ill patients characterized by extensive inflammation in the lungs. ARDS is not a particular disease; more precisely, it is a clinical condition triggered by pathologies such as trauma, pneumonia, and sepsis.
Characteristics of ARDS are diffuse injury to cells that form the barrier of the lung microscopic air sacs, surfactant dysfunction, activation of the innate immune system response, and clotting and bleeding body regulatory dysfunction. As a result, ARDS damages the lung's ability to exchange oxygen and carbon dioxide with blood across a thin layer of microscopic lung air sacs known as alveoli.
This syndrome is associated with a mortality rate of between 20 and 50%. The risk of death varies according to the severity, age of a person, and the presence of other underlying medical conditions.
Although the term "adult respiratory distress syndrome" has sometimes been used to differentiate ARDS from "infant respiratory syndrome" in newborns, the international consensus is that "acute respiratory distress syndrome" is the best term because ARDS can affect people of all age.
Video Acute respiratory distress syndrome
Signs and symptoms
Signs and symptoms of ARDS often begin within two hours after inciting events, but can occur after 1-3 days. Signs and symptoms may include shortness of breath, rapid breathing, and low oxygen levels in the blood due to abnormal ventilation.
Maps Acute respiratory distress syndrome
Cause
The diffuse compromise of the pulmonary system resulting in ARDS generally occurs in the setting of critical illness. ARDS may be seen in severe pulmonary (pneumonia) or systemic infections (sepsis), subsequent trauma, multiple blood transfusions (TRALI), severe burns, severe pancreatitis (pancreatitis), near drowning or other aspiration events, drug reactions or injuries inhalation. Some cases of ARDS are associated with large volumes of fluids used during post traumatic resuscitation.
Diagnosis
The diagnostic criteria for ARDS have changed over time as understanding of pathophysiology has evolved. The international consensus criteria for ARDS was recently updated in 2012 and is known as the "Berlin definition". In addition to generally extending the diagnostic threshold, other significant changes from previous 1994 consensus criteria include downplaying the term "acute lung injury," and defining the severity of ARDS according to the degree of decreased blood oxygen content.
By definition Berlin 2012, ARDS is indicated by the following:
- acute onset lung injury, within 1 week of clear clinical insults and with respiratory symptoms develop
- bilateral opacities in chest imaging (chest radiograph or CT) are not described by other lung pathologies (eg effusion, lobar/lung collapse, or nodules)
- Respiratory failure is not explained by heart failure or excess volume
- decreases Pa O
2 /Fi O
2 ratio (decreased Pa O
2 /Fi O
2 ratio indicates reduced arterial oxygenation of available inhalation gas):- mild ARDS : 201 - 300 mmHg (<= 39.9 kPa)
- moderate ARDS : 101 - 200 mmHg (<= 26.6 kPa)
- heavy ARDS : <= 100 mmHg (<= 13.3 kPa)
- Note that the Berlin definition requires a minimum positive end-expiratory (PEEP) pressure of 5 cm H
2 O for consideration Pa O
2 /Fi O
2 . This PEEP level can be delivered noninvasively with CPAP to diagnose mild ARDS.
Note that the 2012 Berlin "criterion" is a modification of the previous 1994 consensus conference definition (see history ).
Medical description
Radiological imaging has long been a criterion for the diagnosis of ARDS. While the original definition of ARDS determined that correlative chest X-ray findings are required for diagnosis, the diagnostic criteria have been extended over time to receive CT and ultrasound findings as the same contributor. Generally, radiographic fluid accumulation (pulmonary edema) findings that affect the lung and are not associated with increased cardiopulmonary vascular pressure (as in heart failure) may be suggestive of ARDS. Suggestive ultrasound suggestions of ARDS include the following:
- The anterior subpleural incorporation
- There is no lung reduction or reduction
- "Protected Area" of the normal parenchyma
- Pleural line disorder (irregularly thickened pleural line thickening)
- Distribution of non-homogeneous B-lines (ultrasound findings that indicate fluid accumulation in the lungs)
Pathophysiology
ARDS is a form of fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). This is usually triggered by an acute injury to the lungs that causes flooding of the lung microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional general findings in ARDS include partial pulmonary collapse (atelectasis) and low levels of oxygen in the blood (hypoxemia). Clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrin organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most often associated with ARDS is DAD, which is characterized by diffuse inflammation of lung tissue. The tissue-inducing insults usually result in early release of chemical signals and other inflammatory mediators secreted by local epithelial cells and endothelial cells.
Neutrophils and some T lymphocytes rapidly migrate to the inflamed lung tissue and contribute to the amplification of the phenomenon. Typical histologic presentations involve diffuse alveolar damage and formation of hyaline membranes in alveolar walls. Although the trigger mechanism is not fully understood, recent research has examined the role of inflammation and mechanical stress.
Inflammation
Inflammation, such as those caused by sepsis, causes endothelial cell dysfunction, leakage of fluid from capillaries and damage of fluid drainage from the lungs. Increased inspired oxygen concentrations are often required at this stage, and can facilitate 'respiratory explosions' in immune cells. In the secondary phase, endothelial cell dysfunction causes cells and inflammatory exudates to enter the alveoli. This pulmonary edema increases the thickness of the layer that separates the blood in the capillaries from space in the air sac, which increases the oxygen distance that must diffuse to reach the blood. It damages gas exchange and causes hypoxia, improves respiratory work, and ultimately induces scarring of the air sacs of the lungs.
Loss of aeration may follow different patterns depending on the nature of the underlying disease and other factors. These are usually distributed to the lower lobe of the lung, in their posterior segment, and they roughly correspond to the initial infected area. In sepsis or trauma-induced ARDS, the infiltrates are usually more patchy and diffuse. The posterior and basal segments are always more affected, but the distribution is even less homogeneous. Loss of aeration also causes an important change in the fundamental lung mechanical properties in the process of inflammatory amplification and progression to ARDS in patients with mechanical ventilation.
Mechanical pressure
When the loss of aeration and progression of the underlying disease, eventually the tidal volume grows to levels that are inconsistent with life. Thus, mechanical ventilation begins to lighten the muscles responsible for supporting respiration (respiratory muscle) of their work and to protect the airways of the affected person. However, mechanical ventilation may be a risk factor for the development - or worsening - of ARDS. In addition to infectious complications arising from invasive ventilation with endotracheal intubation, positive pressure ventilation directly alters pulmonary mechanics during ARDS. When this technique is used the result is higher mortality through barotrauma.
In 1998, Amato et al. published a paper showing a substantial increase in the results of a ventilated patient with a lower tidal volume ( V t ) (6 mLÃ, kg -1 ). These results were confirmed in a 2000 study sponsored by NIH. Both studies are widely criticized for several reasons, and the authors were not the first to experiment with lower volume vents, but they improved understanding of the relationship between mechanical ventilation and ARDS.
This form of stress is thought to be applied by the transpulmonary pressure (gradient) ( P l ) produced by the ventilator or, preferably, the cyclical variation. Better results obtained in lower ventilated individuals V t can be interpreted as beneficial effects of lower P l .
The P l method applied to the alveolar surface determines the shear stress at which the alveoli is exposed. ARDS is characterized by a normally heterogeneous reduction of the air space, and thus by a higher upward trend P l at the same time V < sub> t , and towards higher emphasis on less ill units. The heterogeneity of the alveoli at various stages of the disease is increased by the gravity gradient they face and the different perfusion pressures in which blood flows through it.
The different mechanical properties of alveoli in ARDS can be interpreted to have varying time constants - products of alveolar resistance ÃÆ'â € "resistance. The slow alveolus is said to "stay open" using PEEP, a modern ventilator feature that maintains positive air pressure throughout the entire breathing cycle. The higher pressure average cycle slows down the collapse of the sick alveoli, but should be weighed against the corresponding elevation in P l /highland pressure. A newer ventilation approach seeks to maximize average airway pressure due to its ability to "recruit" collapsed alveoli while minimizing the shear stress caused by frequent opening and closing of the aeration unit.
Stress Index
Mechanical ventilation may aggravate the inflammatory response in people with ARDS by inducing alveolar hyperinflation and/or increased shear stress by frequently opening and closing the folded alveoli. The stress index is measured during the mechanical flow flow ventilation of the constant flow volume without changing the base ventilation pattern. Identifies the most stable part of the inspiration flow (F) waveform according to the corresponding portion of the waveform air wave (Paw) waveform in the following power equations:
Paw = a ÃÆ'â € "t b c where the coefficient b - Stress Index - describes the shape of the curve. The Stress Index represents constant compliance if the value is about 1, increased adherence during inspiration if the value is below 1, and compliance decreases if the value is above 1. Ranieri, Grasso, et al. set a strategy guided by the stress index with the following rules:
- Stress index below 0.9, PEEP raised
- Stress Index between 0.9 and 1.1, no changes made
- Stress index above 1.1 PEEP decreases.
Alveolar hyperinflation in patients with focused ventilated ARDS with the ARDSnet protocol is attenuated by a physiological approach to the regulation of PEEP based on the measurement of the stress index.
Progression
If the underlying illness or adverse factor is not removed, the number of inflammatory mediators released by the lung in the ARDS can cause systemic inflammatory response syndrome (SIRS) or sepsis if there is a pulmonary infection. The evolution toward shock or multiple organ dysfunction syndromes follows an analogue path to the pathophysiology of sepsis. This causes oxygenation disorders, which is a major problem of ARDS, as well as respiratory acidosis. Respiratory acidosis in ARDS is often caused by ventilation techniques such as permissive hypercapnia, which attempts to limit ventilator-induced lung injury to ARDS. The result is a critical illness in which 'endothelial disease' from severe sepsis or SIRS is exacerbated by lung dysfunction, which further damages the delivery of oxygen to the cell.
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 entering the oral cavity and secured in the airway (endotracheal intubation), or with tracheostomy when prolonged ventilation (> = 2 weeks) is required. The role of non-invasive ventilation is limited in the early period of disease or to prevent worsening respiratory distress in individuals with atypical pneumonia, bruising of the lungs, or large surgical patients, who are at risk of developing ARDS. The underlying cause treatment is very important. Appropriate antibiotic therapy should be given as soon as microbiological culture results are available, or suspected clinical infection (whichever is earlier). Empirical therapy may be appropriate if local microbiological monitoring is efficient. The origin of the infection, when it can be handled surgically, should be eliminated. When sepsis is diagnosed, appropriate local protocols should be applied.
Mechanical Ventilation
The overall purpose of mechanical ventilation is to maintain an acceptable gas exchange to meet the body's metabolic needs and to minimize adverse effects in its application. PEEP parameters (positive end-expiratory pressure, to keep alveoli open), airway pressure (to promote alveoli recruitment and predictors of the folded hemodynamic effect) and plateau pressure (best predictors of overdistention alveolar) are used.
Previously, mechanical ventilation aims to achieve a tidal volume ( V t ) of 12-15 ml/kg (where weight is the ideal body weight rather than the actual weight). Recent studies have shown that high tidal volumes may extend beyond the alveoli boundary resulting in volutrauma (secondary lung injury). The ARDS Clinical Network, or ARDSNet, completed a clinical trial showing an increase in mortality when people with ARDS were ventilated with a tidal volume of 6 ml/kg compared with traditional 12 ml/kg. Low tidal volumes ( V t ) can cause elevated levels of blood carbon dioxide and alveoli collapse due to their inborn tendency to increase shunting in the lungs. Physiological dead space can not change due to ventilation without perfusion. Shunt is perfusion without ventilation.
Low tidal volume ventilation is the main independent variable associated with decreased mortality in NDSH sponsored ARDSnet trials of tidal volume in ARDS. Plain pressure less than 30 cm H
2 O is a secondary purpose, and subsequent analysis of data from ARDSnet trials and other experimental data suggests that there appears to be no safe upper limit for upland pressure; Regardless of plateau pressure, individuals with ARDS fare better with low tidal volume.
Ventilation of air pressure release
No particular ventilator mode is known to increase mortality in acute respiratory distress syndrome (ARDS).
Some practitioners prefer air-pressure ventilation ventilation when treating ARDS. Well documented benefits for APRV ventilation include decreased airway pressure, decreased ventilation minutes, decreased ventilation of dead spaces, promotion of spontaneous breathing, nearly 24 hours daily alveolar recruitment, decreased sedation use, neuromuscular blockade close removal, optimized arterial blood gas yield, restoration FRC mechanics (functional residual capacity), positive effects on cardiac output (due to negative inflections of baseline increase with each spontaneous breath), increased organ and tissue perfusion and increased potential of increased secondary urine output. renal perfusion.
A patient with ARDS, on average, spends between 8 and 11 days with a mechanical ventilator; APRV can reduce this time significantly and conserve valuable resources.
Positive final expiratory pressure
The positive end-expiratory pressure (PEEP) is used in patients with mechanical ventilation with ARDS to improve oxygenation. In ARDS, three alveoli populations can be distinguished. There is a normal alveolus that is always increasing and involved in gas exchange, the flooded alveoli that can never, under the ventilation regime, be used for gas exchange, and alveoli flooded by alleles or alveolar that can be "recruited" to participate in the gas exchange below certain. ventilation regimen. Recruited alveoli represent sustainable populations, some of which can be recruited with minimal PEEP, and others that can only be recruited with high-level PEEP. An additional complication is that some alveoli can only be opened with higher air pressure than is necessary to keep them open, then a justification for maneuvering where PEEP is increased to a very high level for seconds to minutes before dropping PEEP to a lower level. PEEP can be dangerous; High PEEP always increases the mean airway pressure and alveolar pressure, which can damage the normal alveoli with overdistension resulting in DAD. The compromise between beneficial and detrimental effects of PEEP is inevitable.
'Best PEEP' is used to be defined as 'some' cm H
2 O above the lower inflection point (LIP) in the sigmoidal lung pressure relation curve. Recent research has shown that LIP-point pressure is no better than the overlying pressure, because recruitment of collapsed alveoli - and, more importantly, overdistension of aeration units - occurs across inflation. Despite the awkwardness of most of the procedures used to track the pressure-volume curve, it is still used by some to determine the minimum PEEP to apply to their patients. Some new ventilators can automatically plot the volume-pressure curve.
PEEP can also be arranged empirically. Some authors suggest to do 'maneuver recruitment' - short time at very high continuous positive air pressure, such as 50 cm H
2 (4.9 kPa) - to recruit or open a collapsed unit at high pressure before restoring the previous ventilation. The final PEEP level should be one before the drop in Pa O
2 or peripheral blood oxygen saturation during a step-down test.
Intrinsic PEEP (iPEEP) or auto PEEP - first described by John Marini of St. John's Regional Hospital Paul - is an unacknowledged potential contributor to PEEP on an intubated individual. When ventilated at high frequencies, the contribution can be very large, especially in people with obstructive pulmonary disease such as asthma or chronic obstructive pulmonary disease (COPD). iPEEP has been measured in some formal studies of ventilation in ARDS patients, and its contribution is unknown. Measurements are recommended in the treatment of people who have ARDS, especially when using high-frequency (oscillatory/jet) ventilation.
Prone position
The position of pulmonary infiltrates in acute respiratory distress syndrome is not uniform. Repositioning onto the prone position (facing down) can increase oxygenation by reducing atelectasis and increasing perfusion. If this is done early in the treatment of severe ARDS, it provides death benefits of 26% compared to supine ventilation.
Liquid management
Several studies have shown that lung function and outcomes are better in people with weight loss ARDS or whose pulmonary wedge pressure is lowered by diuresis or fluid restriction.
Corticosteroids
An ARDSnet-sponsored ARDSnet multicenter study on corticosteroids lasting from August 1997 to November 2003 titled LaSRS for ARDS showed that despite improvements in cardiovascular physiology, methylprednisone has no efficacy in the treatment of ARDS.
Nitric oxide
Inhaled nitric oxide (NO) selectively widens the pulmonary artery allowing more blood flow to open the alveoli for gas exchange. Despite evidence of increased oxygenation status, there is no evidence that inhaled nitric oxide decreases morbidity and mortality in people with ARDS. In addition, nitric oxide can cause kidney damage and is not recommended as a therapy for ARDS regardless of its severity.
Surfactant therapy
To date, no prospective controlled clinical trials have demonstrated significant mortality benefits from exogenous surfactants in adult ARDS.
Extracorporeal membrane oxygen
Extracorporeal membrane oxygenation (ECMO) is mechanically applied to prolonged cardiopulmonary support. There are two types of ECMO: Venovenous which provides respiratory and venoarterial support that provide respiratory and haemodynamic support. People with ARDS who do not require cardiac support usually develop ECMO venovenous. Several studies have demonstrated the effectiveness of ECMO in acute respiratory failure. In particular, CESAR (conventional ventilation support versus oxygenation of the Extracorporeal membrane for the failure of Acute Severe Respiration) showed that the group referred to the ECMO center showed significantly improved survival compared with conventional management (63% to 47%).
Complications
Because ARDS is a very serious condition requiring an invasive form of therapy is not without its risks. Complications to be considered include the following:
- Lungs: barotrauma (volutrauma), pulmonary embolism (PE), pulmonary fibrosis, ventilator-related pneumonia (VAP)
- Gastrointestinal: bleeding (ulcers), dysmotility, pneumoperitoneum, bacterial translocation
- Heart: abnormal heart rhythm, myocardial dysfunction
- Kidney: acute renal failure, positive fluid balance
- Mechanical: vascular injury, pneumothorax (by placing a pulmonary artery catheter), tracheal injury/stenosis (due to intubation and/or irritation by endotracheal tube
- Nutrition: malnutrition (catabolic state), electrolyte deficiency. Epidemiology
- acute onset, persistent dyspnea
- bilateral infiltrate on chest x-rays consistent with pulmonary edema
- hypoxemia, defined as Pa O
2 : Fi O
2 & lt; 200 mmHg (26,7 kPa) - no left atrial hypertension (LA)
- pulmonary artery wedge pressure & lt; 18 mmHg (obtained by pulmonary artery catheterization)
- If no LA pressure is measured, there should be no other clinical evidence showing an increase in left heart pressure.
- Respiratory monitoring
- ARDSNet - NDS/NHLBI ARDS Network
- ARDS Support Center - information for patients with ARDS
- ARDS Foundation - charitable organization offering family support/victims of Acute Respiratory Distress Syndrome
- MESENCHYMAL STEM CELLS AND SIGNAL DISTRESS CHANNELS EVER
The annual incidence of ARDS is 13-23 people per 100,000 in the general population. The incidence in the population with mechanical ventilation in the intensive care unit is much higher. According to Brun-Buisson et al (2004), there was an acute lung injury prevalence (ALI) of 16.1% percent in patients who were ventilated for more than 4 hours.
Around the world, severe sepsis is the most common trigger that causes ARDS. Other triggers include mechanical ventilation, sepsis, pneumonia, Gilchrist disease, drowning, circulatory shock, aspiration, trauma - especially lung bruising - major surgery, massive blood transfusion, smoke inhalation, drug reactions or overdose, fat embolism and pulmonary edema reperfusion after lung transplantation or pulmonary embolectomy. However, the majority of these patients with all these conditions did not develop ARDS. It is unclear why some people with the above mentioned factors do not get ARDS and some do it.
Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients and may be the cause or complication of ARDS. Excess alcohol appears to increase the risk of ARDS. Diabetes was initially thought to reduce the risk of ARDS, but this has been shown to be an increased risk of pulmonary edema. The increased stomach pressure of various causes is also a risk factor for the development of ARDS, especially during mechanical ventilation.
Mortality rates vary from 25-40% in centers using the latest ventilation strategies and up to 58% in all centers.
History
Acute respiratory distress syndrome was first described in 1967 by Ashbaugh et al. Initially there was no clear definition, which resulted in controversy over the incidence and death of ARDS.
In 1988, an expanded definition was proposed, which measures physiological respiratory disorders.
1994-American Consensus Conference 1994
In 1994, the new definition was recommended by the American-European Consensus Conference Committee which recognized the variability in the severity of lung injury.
The definitions required for the following criteria must be met:
If Pa O
2 : Fi O
2 & lt; 300 mmHg (40 kPa), then the definition recommends classification as "acute lung injury" (ALI). Note that according to this criterion, arterial and chest x-ray blood analysis is required for formal diagnosis. Limitations of this definition include lack of precise definition of sharpness, nonspecific imaging criteria, lack of precise definition of hypoxemia associated with PEEP (affecting partial pressure of arterial oxygen), Pa O
2 thresholds without systematic data.
definition of Berlin 2012
In 2012, the definition of ARDS in Berlin was made by the European Society of Intensive Care Medicine, and endorsed by the American Thoracic Society and the Society of Critical Care Medicine. This recommendation is an attempt to update the classification criteria to improve clinical utility, and to clarify terminology. In particular, the Berlin guidelines prevent the use of the term "acute lung injury" or ALI, since the term is generally misused to describe milder lung injury rates. Instead, the committee proposes the classification of severity of ARDS as mild, moderate or severe according to arterial oxygen saturation. The Berlin definition represents the current international consensus guidelines for both clinical classification and ARDS research.
Direction of research
There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to help prevent vascular bed leakage. Traumakine (FP-1201-lyo), a recombinant human recombinant IFN beta-1a drug developed by Faron pharmaceuticals, is undergoing international phase III trials after initial open label testing, showing an 81% reduction in 28-day mortality opportunities in patients ICU with ARDS. This drug is known to work by increasing CD73 lung expression and increasing the production of anti-inflammatory adenosine, resulting in leakage of blood vessels and escalation of inflammation is reduced.
See also
References
Further reading
External links
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