Acute respiratory distress syndrome Totally Explained

Everything about Acute Respiratory Distress Syndrome totally explained

| ICD9 =, | ICDO = | Image = AARDS X-ray cropped.jpg | Caption = Chest x-ray of patient with ARDS| OMIM = | MedlinePlus = 000103 | eMedicineSubj = med | eMedicineTopic = 70 | DiseasesDB = 892 | MeshID = D012128 | }}
Acute respiratory distress syndrome (ARDS), also known as respiratory distress syndrome (RDS) or adult respiratory distress syndrome (in contrast with IRDS) is a serious reaction to various forms of injuries to the lung. This is the most important disorder resulting in increased permeability pulmonary edema.
ARDS is a severe lung disease caused by a variety of direct and indirect issues. It is characterized by inflammation of the lung parenchyma leading to impaired gas exchange with concomitant systemic release of inflammatory mediators causing inflammation, hypoxemia and frequently resulting in multiple organ failure. This condition is life threatening and often lethal, usually requiring mechanical ventilation and admission to an intensive care unit. A less severe form is called acute lung injury (ALI).
ARDS formerly most commonly signified adult respiratory distress syndrome to differentiate it from infant respiratory distress syndrome in premature infants. However, as this type of pulmonary edema also occurs in children, ARDS has gradually shifted to mean acute rather than adult. The differences with the typical infant syndrome remain.

Definition

Historical background

Acute respiratory distress syndrome was first described in 1967 by Ashbaugh et al. Initially there was no definition, resulting in controversy over incidence and mortality. In 1988 an expanded definition was proposed which quantified physiologic respiratory impairment.
   In 1994 a new definition was recommended by the American-European Consensus Conference Committee. It had two advantages: 1 it recognizes that severity of pulmonary injury varies, 2 it's simple to use.
   ARDS was defined as the ratio of arterial partial oxygen tension (PaO₂) as fraction of inspired oxygen (FiO₂) below 200 mmHg in the presence of bilateral alveolar infiltrates on the chest x-ray. These infiltrates may appear similar to those of left ventricular failure, but the cardiac silhouette appears normal in ARDS. Also, the pulmonary capillary wedge pressure is normal (less than 18 mmHg) in ARDS, but raised in left ventricular failure.
   A PaO₂/FiO₂ ratio less than 300 mmHg with bilateral infiltrates indicates acute lung injury (ALI). Although formally considered different from ARDS, ALI is usually just a precursor to ARDS.

Consensus after 1967 and 1994

ARDS is characterized by: This result was confirmed in a 2000 study sponsored by the NIH. Although both these studies were widely criticized for several reasons, and although the authors were not the first to experiment lower-volume ventilation, they shed new light on the relationship between mechanical ventilation and ARDS.
   One opinion is that the forces applied to the lung by the ventilator may work as a lever to induce further damage to lung parenchyma. It appears that shear stress at the interface between collapsed and aerated units may result in the breakdown of aerated units, which inflate asymmetrically due to the 'stickiness' of surrounding flooded alveoli. The fewer such interfaces around an alveolus, the lesser the stress.
   Indeed, even relatively low stress forces may induce signal transduction systems at the cellular level, thus inducing the release of inflammatory mediators.
   This form of stress is thought to be applied by the transpulmonary pressure (gradient) (P_l) generated by the ventilator or, better, its cyclical variations. The better outcome obtained in patients ventilated with lower V_t may be interpreted as a beneficial effect of the lower P_l. Transpulmonary pressure, is an indirect function of the V_t setting on the ventilator, and only trial patients with plateau pressures (a surrogate for the actual P_l) were less than 32 cmH₂O (3.1 kPa) had improved survival.
   The way P_l is applied on alveolar surface determines the shear stress to which lung units are exposed. ARDS is characterized by an usually inhomogeneous reduction of the airspace, and thus by a tendency towards higher P_l at the same V_t, and towards higher stress on less diseased units.
   The inhomogeneity of alveoli at different stages of disease is further increased by the gravitational gradient to which they're exposed, and the different perfusion pressures at which blood flows through them. Finally, abdominal pressure exerts an additional pressure on inferoposterior lung segments, favoring compression and collapse of those units.
   The different mechanical properties of alveoli in ARDS may be interpreted as having varying time constants (the product of alveolar compliance × resistance). A long time constant indicates an alveolus which opens slowly during tidal inflation, as a consequence of contrasting pressure around it, or altered water-air interface inside it (loss of surfactant, flooding).
   Slow alveoli are said to be 'kept open' using positive end-expiratory pressure, a feature of modern ventilators which maintains a positive airway pressure throughout the whole respiratory cycle. A higher mean pressure cycle-wide slows the collapse of diseased units, but it has to be weighed against the corresponding elevation in P_l/plateau pressure.
   The prone position also reduces the inhomogeneity in alveolar time constants induced by gravity and edema.

Progression

If the underlying disease or injurious factor isn't removed, the amount of inflammatory mediators released by the lungs in ARDS may result in a systemic inflammatory response syndrome (or sepsis if there's lung infection). The evolution towards shock and/or multiple organ failure follows paths analogous to the pathophysiology of sepsis.
This adds up to the impaired oxygenation, the real mainstay of ARDS, and respiratory acidosis, often caused by the ventilation techniques indicated in ARDS.
The result is a critical illness in which the 'endothelial disease' of severe sepsis/SIRS is worsened by the pulmonary dysfunction, which further impairs oxygen delivery.

Treatment

General

Acute respiratory distress syndrome is usually treated with mechanical ventilation in the Intensive Care Unit. Ventilation is usually delivered through oro-tracheal intubation, or tracheostomy whenever prolonged ventilation (≥2 weeks) is deemed inevitable.
   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).
   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 hasn't 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.

Mechanical ventilation

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 (V_t) of 12-15 ml/kg. 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 landmark trial that showed improved mortality when ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg. Low tidal volumes (V_t) may cause hypercapnia and atelectasis.
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 (as well as other experimental data) demonstrate that there appears to be NO safe upper limit to plateau pressure; that is, regardless of plateau pressure, patients fare better with low tidal volumes (see Hager et al, American Journal of Respiratory and Critical Care Medicine, 2005).

APRV (Airway Pressure Release Ventilation) and ARDS / ALI

Although a particular ventilation mode has yet to be "proven in clinical trials"* more effective than others in treating patients with ARDS, ever increasing empirical evidence and clinical experience is showing that APRV

is the primary mode of choice when ventilating a patient with ARDS or ALI (Acute Lung Injury).
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 and an often positive effect on cardiac output (due to the negative inflection from the elevated baseline with each spontaneous breath).
A patient with ARDS on average spends 8 to 11 days on a mechanical ventilator; APRV may reduce this time significantly.

*This would require a side by side study of APRV and the current ARDSNet protocol. There seems to be little political will, within the medical community, to address the need for this study, in spite of the successes seen with APRV.

Positive end-expiratory pressure

Positive end-expiratory pressure (PEEP) must be used in mechanically-ventilated patients in order to contrast the tendency to collapse of affected alveoli.
   Ideally, a 'perfect' PEEP would match the increased alveolar surface tension, caused by surfactant deficiency and external pressure (edema), thus restoring a normal time constant in all affected units.
   However, because of the cited inherent inhomogeneity, surface tension varies, and so do PEEP requirements for the diseased units. Furthermore, high levels of PEEP may impair venous blood return to the right heart, although the actual impact of PEEP on hemodynamics is still debated.
   The 'best PEEP' used to be defined as 'some' cmH₂O above the lower inflection point (LIP) in the sigmoidal pressure-volume relationship curve of the lung. Recent research has shown that the LIP-point pressure is no better than any pressure above it, as recruitment of collapsed alveoli, and more importantly the overdistension of aerated units, occur throughout the whole inflation. Despite the awkwardness of most procedures used to trace the pressure-volume curve, it's still used by some to define the minimum PEEP to be applied to their patients. Some of the newest ventilators have the ability to automatically plot a pressure-volume curve. The possibility of having an 'instantaneous' tracing trigger might produce renewed interest in this analysis.
   PEEP may also be set empirically. Some authors suggest performing a 'recruiting maneuver' (for example, a short time at a very high continuous positive airway pressure, such as 50 cmH₂O (4.9 kPa), to recruit, or open, collapsed unit with a high distending pressure) and then to increase PEEP to a rather high level before restoring previous ventilation. The final PEEP level should be the one just before the drop in PaO₂ (or peripheral blood oxygen saturation) during a step-down trial.
   PEEP 'stacks up' to P_l during volume-controlled ventilation. At high levels, it may cause significant overdistension of (and injury to) compliant, aerated units, and higher plateau pressures at the same V_t. Intrinsic PEEP (iPEEP), or auto-PEEP, isn't detected during normal ventilation. However, when ventilating at high frequencies, its contribution may be substantial, both in its positive and negative effects. There are 'underground', unproven claims that the Amato and NIH/ARDS Network studies got a positive result because of the high iPEEP levels reached by spontaneously breathing patients in low-volume assist-control ventilation. Whether or not that's true, it's a fact that iPEEP has been measured in very few formal studies on ventilation in ARDS patients, and its entity is largely unknown. Its measurement is recommended in the treatment of ARDS patients, especially when using high-frequency (oscillatory/jet) ventilation.
   A compromise between the beneficial and adverse effects of PEEP is, as usual, inevitable.

Prone position

Distribution of lung infiltrates in acute respiratory distress syndrome is non-uniform. 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. The recent NIH-sponsored ARDSnet LAZARUS study of corticosteroids for ARDS demonstrated that they're not efficacious in ARDS.

Nitric oxide

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. Almitrine bismesylate stimulates chemoreceptors in carotic and aortic bodies. It has been used to potentiate the effect of NO, presumably by potentiating hypoxia-induced pulmonary vasoconstriction. In case of ARDS it isn't known whether this combination is useful.

Surfactant therapy

To date no prospective controlled clinical trial has shown a significant mortality benefit of exogenous surfactant in ARDS.

Complications

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

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

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

Cardiac: arrhythmias, myocardial dysfunction.

Renal: acute renal failure (ARF), 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 deficiency.

Epidemiology

The annual incidence of ARDS is between 1.5 to 13.5 people per 100,000 in the general population. Its incidence in the intensive care unit (ICU), mechanically ventilated population is much higher. Brun-Buisson et al. (2004) reported a prevalence of acute lung injury (ALI) (see below) of 16.1% percent in ventilated patients admitted for more than 4 hours. More than half these patients may develop ARDS. Mechanical ventilation, sepsis, pneumonia, shock, aspiration, trauma (especially pulmonary contusion), major surgery, massive transfusions, smoke inhalation, drug reaction or overdose, fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy may all trigger ARDS. Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients. Pneumonia and sepsis may be either causes or complications of ARDS.
Elevated abdominal pressure of any cause is also probably a risk factor for the development of ARDS, particularly during mechanical ventilation.
Mortality varies from 30% to 60%. Usually, randomized controlled trials in the literature show lower death rates, both in control and treatment patients. This is thought to be due to stricter enrolment criteria. Observational studies generally report 50%-60% mortality.

Further Information

Get more info on 'Acute Respiratory Distress Syndrome'.

External Link Exchanges

Do you know how hard it is to get a link from a large encyclopaedia? Well we're different and will prove it. To get a link from us just add the following HTML to your site on a relevant page:

<a href="http://acute_respiratory_distress_syndrome.totallyexplained.com">Acute respiratory distress syndrome Totally Explained</a>

Then simply click through this link from your web page. Our crawlers will verify your link, extract the title of your web page and instantly add a link back to it. If you like you can remove the words Totally Explained and embed the link in article text.
As long as your link remains in place, we'll keep our link to you right here. Please play fair - our crawlers are watching. Your site must be closely related to this one's topic. Any kind of spamming, dubious practises or removing the link will result in your link from us being dropped and, potentially, your whole site being banned.