Sierra Acai Company
Sierra Acai Company
Open 7 Days a Week
MonaVie Independent Distributor
Distributor Training
Shop Online
Enroll Now
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
Friends
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
16-September-2008 16:15:15 - respiratory distress syndrome ARDS redirects here. For other uses, see ARD. Acute respiratory distress syndrome Classification and external resources Chest x-ray of patient with ARDS ICD-10 J80. ICD-9 518.5, 518.82 DiseasesDB 892 MedlinePlus 000103 eMedicine med/70 MeSH 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. 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 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. Contents 1 Definition 1.1 Historical background 1.2 Consensus after 1967 and 1994 2 Patient presentation and diagnosis 3 Pathophysiology 3.1 Inflammation 3.2 Mechanical stress 3.3 Progression 4 Treatment 4.1 General 4.2 Mechanical ventilation 4.3 APRV Airway Pressure Release Ventilation and ARDS / ALI 4.4 Positive end-expiratory pressure 4.5 Prone position 4.6 Fluid management 4.7 Corticosteroids 4.8 Nitric oxide 4.9 Surfactant therapy 5 Complications 6 Epidemiology 7 References 7.1 Further reading 8 External links Definition Historical background Acute respiratory distress syndrome was first described in 1967 by Ashbaugh et al.12 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.13 It had two advantages: 1 it recognizes that severity of pulmonary injury varies, 2 it is simple to use.4 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:13 Acute onset Bilateral infiltrates on chest radiograph Pulmonary artery wedge pressure 18 mmHg obtained by pulmonary artery catheterization, if this information is available; if unavailable, then lack of clinical evidence of left ventricular failure suffices if PaO2:FiO2 300 mmHg acute lung injury ALI is considered to be present if PaO2:FiO2 200 mmHg acute respiratory distress syndrome ARDS is considered to be present Patient presentation and diagnosis ARDS can occur within 24 to 48 hours of an injury or attack of acute illness. In such a case the patient usually presents with shortness of breath, tachypnea, and symptoms related to the underlying cause, i.e. shock. ARDS is classically associated with hypoxemia, petechiae in the axillae and neurologic abnomalities such as mental confusion.1 Long term illnesses can also trigger it, eg malaria. The ARDS may then occur sometime after the onset of a particularly acute case of the infection. See xray of malarial ARDS. An arterial blood gas analysis and chest X-ray allow formal diagnosis by inference using the aforementioned criteria. Although severe hypoxemia is generally included, the appropriate threshold defining abnormal PaO2 has never been systematically studied. Any cardiogenic cause of pulmonary edema should be excluded. This can be done by placing a pulmonary artery catheter for measuring the pulmonary artery wedge pressure. However, this is not necessary and is now rarely done as abundant evidence has emerged demonstrating that the use of pulmonary artery catheters does not lead to improved patient outcomes in critical illness including ARDS. Plain Chest X-rays are sufficient to document bilateral alveolar infiltrates in the majority of cases. While CT scanning leads to more accurate images of the pulmonary parenchyma in ARDS, it has little utility in the clinical management of patients with ARDS, and remains largely a research tool. Pathophysiology A pathohistological image of ARDS. A pathohistological image of ARDS. ARDS is characterized by a diffuse inflammation of lung parenchyma. The triggering insult to the parenchyma usually results in an initial release of cytokines and other inflammatory mediators, secreted by local epithelial and endothelial cells. Neutrophils and some T-lymphocytes quickly migrate into the inflamed lung parynchema and contribute in the amplification of the phenomenon. Typical histological presentation involves diffuse alveolar damage and hyaline membrane formation in alveolar walls. Although the triggering mechanisms are not completely understood, recent research has examined the role of inflammation and mechanical stress. Inflammation Inflammation alone, as in sepsis, causes endothelial dysfunction, fluid extravasation from the capillaries and impaired drainage of fluid from the lungs. Dysfunction of type II pulmonary epithelial cells may also be present, with a concomitant reduction in surfactant production. Elevated inspired oxygen concentration often becomes necessary at this stage, and they may facilitate a 'respiratory burst' in immune cells. In a secondary phase, endothelial dysfunction causes cells and inflammatory exudate to enter the alveoli. This pulmonary edema increases the thickness of the alveolo-capillary space, increasing the distance the oxygen must diffuse to reach blood. This impairs gas exchange leading to hypoxia, increases the work of breathing, eventually induces fibrosis of the airspace. Moreover, edema and decreased surfactant production by type II pneumocytes may cause whole alveoli to collapse, or to completely flood. This loss of aeration contributes further to the right-to-left shunt in ARDS. As the alveoli contain progressively less gas, more blood flows through them without being oxygenated resulting in massive intrapulmonary shunting. Collapsed alveoli and small bronchi do not allow gas exchange. It is not uncommon to see patients with a PaO2 of 60 mmHg 8.0 kPa despite mechanical ventilation with 100% inspired oxygen. The loss of aeration may follow different patterns according to the nature of the underlying disease, and other factors. In pneumonia-induced ARDS, for example, large, more commonly causes relatively compact areas of alveolar infiltrates. These are usually distributed to the lower lobes, in their posterior segments, and they roughly correspond to the initial infected area. In sepsis or trauma-induced ARDS, 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 important changes in lung mechanical properties. These alterations are fundamental in the process of inflammation amplification and progression to ARDS in mechanically ventilated patients. Mechanical stress Mechanical ventilation is an essential part of the treatment of ARDS. As loss of aeration and the underlying disease progress, the work of breathing WOB eventually grows to a level incompatible with life. Thus, mechanical ventilation is initiated to relieve respiratory muscles of their work, and to protect the usually obtunded patient's airways. However, mechanical ventilation may constitute a risk factor for the development, or the worsening, of ARDS.1 Aside from the infectious complications arising from invasive ventilation with tracheal intubation, positive-pressure ventilation directly alters lung mechanics during ARDS. The result is higher mortality, i.e. through baro-trauma, when these techniques are used.1 In 1998, Amato et al published a paper showing substantial improvement in the outcome of patients ventilated with lower tidal volumes Vt 6 mL·kg-1.15 This result was confirmed in a 2000 study sponsored by the NIH.6 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 Pl generated by the ventilator or, better, its cyclical variations. The better outcome obtained in patients ventilated with lower Vt may be interpreted as a beneficial effect of the lower Pl. Transpulmonary pressure, is an indirect function of the Vt setting on the ventilator, and only trial patients with plateau pressures a surrogate for the actual Pl were less than 32 cmH2O 3.1 kPa had improved survival. The way Pl 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 Pl at the same Vt, 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 are 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 Pl/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 is not removed, the amount of inflammatory mediators released by the lungs in ARDS may result in a systemic inflammatory response syndrome or sepsis if there is lung infection.1 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 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. Mechanical ventilation Further information: Pressure Regulated Volume Control 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. 7 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. 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 Vt may cause hypercapnia and atelectasis.1 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 APRVis 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.citation needed 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 is 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' i.e., 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 Pl 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 Vt. Intrinsic PEEP iPEEP, or auto-PEEP, is not 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 is true, it is 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.81 Fluid management Several studies have shown that pulmonary function and outcome are better in patients that lost weight or wedge pressure was lowered by diuresis or fluid restriction.1 Corticosteroids A Meduri et al study has found significant improvement in ARDS using modest doses of corticosteroids. This is probably because of a suppression of ongoing inflammation during the fibroproliferative phase of ARDS. The initial regimen consists of methylprednisolone 2 mg/kg daily. After 3-5 days a response must be apparent. In 1-2 weeks the dose can be tapered to methylprednisolone 0.5-1.0 mg daily. Patients with ARDS do not benefit from high-dose corticosteroids.91 The recent NIH-sponsored ARDSnet LAZARUS study of corticosteroids for ARDS demonstrated that they are 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 is not known whether this combination is useful.1 Surfactant therapy To date no prospective controlled clinical trial has shown a significant mortality benefit of exogenous surfactant in ARDS.1 Complications Since ARDS is an extremely serious condition which requires invasive forms of therapy it is not without risk. Complications to be considered are:1 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 1.5-13.5 people per 100,000 in the general population.citation needed 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. The mortality rate varies from 30% to 60%.citation needed 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 enrollment criteria. Observational studies generally report 50%-60% mortality.citation needed References ^ a b c d e f g h i j k l m n o Irwin RS, Rippe JM 2003. Irwin and Rippe's Intensive Care Medicine, 5th ed., Lippincott Williams Wilkins. ISBN 0-7817-3548-3. ^ Ashbaugh D, Bigelow D, Petty T, Levine B 1967. Acute respiratory distress in adults. Lancet 2 7511: 319-23. doi:10.1016/S0140-67366790168-7. PMID 4143721. ^ a b Bernard G, Artigas A, Brigham K, Carlet J, Falke K, Hudson L, Lamy M, Legall J, Morris A, Spragg R 1994. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 149 3 Pt 1: 818-24. PMID 7509706. ^ Ware L, Matthay M 2000. The acute respiratory distress syndrome. N Engl J Med 342 18: 1334-49. doi:10.1056/NEJM200005043421806. PMID 10793167. ^ Amato M, Barbas C, Medeiros D, Magaldi R, Schettino G, Lorenzi-Filho G, Kairalla R, Deheinzelin D, Munoz C, Oliveira R, Takagaki T, Carvalho C 1998. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 338 6: 347-54. doi:10.1056/NEJM199802053380602. PMID 9449727. ^ MacIntyre N 2000. Mechanical ventilation strategies for lung protection. Semin Respir Crit Care Med 21 3: 215-22. doi:10.1055/s-2000-9850. PMID 16088734. ^ Malhotra A 2007. Low-tidal-volume ventilation in the acute respiratory distress syndrome. N Engl J Med 357 11: 1113-20. doi:10.1056/NEJMct074213. PMID 17855672. ^ Gattinoni L, Tognoni G, Pesenti A, Taccone P, Mascheroni D, Labarta V, Malacrida R, Di Giulio P, Fumagalli R, Pelosi P, Brazzi L, Latini R 2001. Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J Med 345 8: 568-73. doi:10.1056/NEJMoa010043. PMID 11529210. ^ Meduri G, Tolley E, Chrousos G, Stentz F 2002. Prolonged methylprednisolone treatment suppresses systemic inflammation in patients with unresolving acute respiratory distress syndrome: evidence for inadequate endogenous glucocorticoid secretion and inflammation-induced immune cell resistance to glucocorticoids. Am J Respir Crit Care Med 165 7: 983-91. PMID 11934726. Further reading Marino, Paul L. 1998. The ICU book. Baltimore: Williams Wilkins. ISBN 0-683-05565-8. Martin GS, Moss M, Wheeler AP, Mealer M, Morris JA, Bernard GR 2005. A randomized, controlled trial of furosemide with or without albumin in hypoproteinemic patients with acute lung injury. Crit. Care Med. 33 8: 1681-7. PMID 16096441. Jackson WL, Shorr AF 2005. Blood transfusion and the development of acute respiratory distress syndrome: more evidence that blood transfusion in the intensive care unit may not be benign. Crit. Care Med. 33 6: 1420-1. PMID 15942365. External links Acute Respiratory Distress Syndrome - May 1, 2002 - American Family Physician Basic Chest X-Ray Review Antioxidant status in patients with acute respiratory distress syndrome. ARDSNet - the NIH / NHLBI ARDS Network ARDS Support Center - information and support for patients with ARDS and their loved ones ARDS Foundation - a charitable organization offers support to families/victims of Acute Respiratory Distress Syndrome v d e Pathology of respiratory system J, 460-519, respiratory diseases Upper RT including URTIs, Common cold Head sinuses: Sinusitis nose: Rhinitis Vasomotor rhinitis, Atrophic rhinitis, Hay fever - Nasal polyp - Deviated septum tonsil: Tonsillitis - Adenoid hypertrophy - Peritonsillar abscess Neck pharynx: Pharyngitis Strep throat larynx: Laryngitis - Croup - Laryngospasm - vocal folds: Vocal fold nodule - epiglottis: Epiglottitis trachea: Tracheitis - Tracheal stenosis Lower RT/lung disease including LRTIs Pneumonia Viral - Bacterial/Atypical pneumonia Mycoplasma - Fungal pneumonia Pneumocystis pneumonia - Parasitic pneumonia - Bronchopneumonia - Chemical pneumonia Mendelson's syndrome Bronchial/ obstructive Acute: Bronchitis Acute, Chronic - Bronchiolitis Chronic: Emphysema - COPD - Asthma Status asthmaticus - Diffuse panbronchiolitis - Bronchiectasis Interstitial/ restrictive External agents/ occupational lung disease Pneumoconiosis Asbestosis, Baritosis, Bauxite fibrosis, Berylliosis, Caplan's syndrome, Chalicosis, Coalworker's pneumoconiosis, Siderosis, Silicosis, Byssinosis Hypersensitivity pneumonitis Bagassosis, Bird fancier's lung, Farmer's lung Other ARDS - Pulmonary edema - Löffler's syndrome/Eosinophilic pneumonia - Respiratory hypersensitivity Allergic bronchopulmonary aspergillosis Hamman-Rich syndrome - Idiopathic pulmonary fibrosis Obstructive or restrictive Atelectasis - Bronchiolitis obliterans Pleural cavity/mediastinum Suppuration Empyema - Lung abscess Pleural disease/pleural effusion Hemothorax - Pneumothorax - Hemopneumothorax - Hydrothorax - Pleurisy Mediastinal disease Mediastinal emphysema - Mediastinitis Other/general Respiratory failure - Influenza - SARS - Idiopathic pulmonary haemosiderosis see also congenital, neoplasia Retrieved from http://en..org/wiki/Acute_respiratory_distress_syndrome Categories: Causes of death | Intensive care medicine | Pulmonology | SyndromesHidden categories: All articles with statements | Articles with statements since May 2008 | Articles with statements since June 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Català Deutsch Español Français Nederlands Polski Português Suomi Svenska 中文 This page was last modified on 13 August 2008, at 04:20
39 Reasons to Drink Acai Juice Every Day
What is MonaVie - Watch the 8-minute video
Discovering MonaVie Video
The Power of You Video
Effects of MonaVie Active on Antioxidant Capacity in Humans
Log into your Wholesale MonaVie Account
So many of us do not eat a balanced diet, get enough sleep, have too much stress, or are impacted with toxins and pollutants. Drinking 2 ounces of MonaVie twice a day will help your body detoxify as well as build your immune system. Its the smartest thing you can do for yourself, so start today. Buying MonaVie through our company guarantees you support 7 days a week and, if you would like to share MonaVie with your family and friends we will guide you from start to finish.
1. Click on Enroll Now (30 - 55% off retail price)
2. Pay $39 for your Wholesale ID number.
3. NO minimum order required.
4. MonaVie is delivered to your door in 3 to 5 days.