1 / 63

1 st described 1967 ( Ashbaugh et al) Incidence 1.5 -7.5/ 100000 population

1 st described 1967 ( Ashbaugh et al) Incidence 1.5 -7.5/ 100000 population 28 day mortality 25 – 30% 1 Diagnosis clinical. Differential diagnosis LVF Fluid overload Mitral stenosis Lymphangitis carcinomatosis Interstitial lung disease. Alveolar Damage. Hypoxic Vasoconstriction.

blade
Télécharger la présentation

1 st described 1967 ( Ashbaugh et al) Incidence 1.5 -7.5/ 100000 population

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. 1st described 1967 (Ashbaugh et al) • Incidence 1.5 -7.5/ 100000 population • 28 day mortality 25 – 30%1 • Diagnosis clinical

  2. Differentialdiagnosis • LVF • Fluid overload • Mitral stenosis • Lymphangitiscarcinomatosis • Interstitial lung disease

  3. Alveolar Damage Hypoxic Vasoconstriction Capillary Damage ↑Dead Space Leakage Oedema Fluid Hypoxia ↓Thoracic Compliance Inflammatory Cellular Infiltrates Atelectasis V/Q Mismatch

  4. LongTerm • Chronic Respiratory Disease • Muscle Fatigue • Muscle Wasting • Weakness

  5. Symptoms and Signs +• Rapid onset of profound dyspnea, usually 12–48 hours after the initiating event • Labored breathing and tachypnea, with crackles on examination • Marked hypoxemia refractory to supplemental oxygen • Multiple-organ failure is seen in many patients

  6. DifferentialDiagnosis Because ARDS is a syndrome, theconcept of differentialdiagnosisappliesonly in consideringtheprecipitatingillnessorinjury • Cardiogenic (hydrostatic) pulmonaryedema • Pneumonia • Aspiration • Diffusealveolarhemorrhage • Acuteinterstitialpneumonitis • Acuteeosinophilicpneumonia • Acutehypersensitivitypneumonitis • Cryptogenicorganizingpneumonia • Pulmonarycontusion • Drug-inducedlungdisease

  7. Diagnosis Laboratory Tests • Tests to identify the systemic or pulmonary causes of ARDS are indicated Imaging Studies Chest radiograph shows diffuse or patchy bilateral opacities that rapidly become confluent Air bronchograms are seen in 80% of cases Features of heart failure (pleural effusions, cardiomegaly, venous engorgement in upper lung zones, indistinct blood vessels) are absent Diagnostic Procedures When indicated to exclude cardiogenic pulmonary edema, pulmonary artery catheterization will demonstrate pulmonary arterial wedge pressures ≤ 18 mm Hg

  8. Noninvasive sampling • Trakeobronchialaspiration • mini-bronkoalveolarlavage Mikroskobik analiz (Gram boyaması , sitoloji ) Mikrobiyolojik kültür • Can be diagnosticforpnomonia , cancer , inflamatuarconditions

  9. Fleksiblbronkoskopi • Mikroskobik analiz ve mikrobiyolojik kültür • Noninvaziv tetkikler başarısız ise • Noninvaziv örnekleme mümkün olmuyor ise • Havayollarında kırmızı taze kan, BAL sıvısında eritrosit artışı, hemosiderin-laden makrofajlar : diffüzalveolarhemoraji • BAL sıvısında eozinofil sayısında artış : idiyopatik akut eozinofilikpnomoni • Yiyecek partikülleri : aspirasyonpnomonisi

  10. Ekokardiyografi • Klinik ve BNP ile kardiyojenikpulmoner ödem tanısı dışlanamazsa transtorasik eko kullanılır Şiddetli aort yada mitral kapak disfonksiyonu Şiddetli diastolikdisfonksiyon Sol ventrikül EF de belirgin azalma • Kardiyojenikpulmoner ödemi destekler • Bazı ARDS tetikleyicileri ( septik şok ) şiddetli kardiyomyopatiye yol açabilir ve ARDS ile birlikte bulunabilir [1,2]. 1 BouhemadB, CritCareMed 2009; 37:441. 2 LandesbergG, EurHeart J 2012; 33:895.

  11. Akciğer biyopsisi • Akut hipoksemik solunum yetersizliğinin diğer nedenleri dışlanamıyorsa cerrahi biyopsinin yeri vardır [1,2]. • Majorkomplikasyon oranı %7 dir. Biyopsiye atfedilen ölüm yoktur. Komplikasyon oranı % 39 olmasına rağmen çoğu tolere edilmektedir (persistan hava kaçağı). • Biyopsi sonucuna göre hastaların % 60 ına spesifik tedavi yapmak mümkün olmuştur. % 37 hastada gereksiz tedaviler kesilmiştir. • Hedefev yönelik tedavi ve prognoz öngörüsü bakımından biyopsi gereklidir. Örnekler: • Kriptojenik organize pnomoni • Akut fungalinfeksiyon • Kronik interstisyen akciğer hastalşığı, vaskülitin alevlenmesi • Dissemine kanser Patel SR, Chest2004; 125:197. Papazian L, Anesthesiology 1998; 88:935.

  12. DIFFERENTIAL DIAGNOSIS  Cardiogenic pulmonary edema • is usually due to left ventricular systolic or diastolic dysfunction • may also be due to fluid overload, severe hypertension, renal artery stenosis, or severe renal disease. • Its presentation is nearly identical to ARDS • exceptthere may be evidence of cardiac dysfunction (S3 or S4 gallop, new or changed murmur), • elevated right-sided filling pressures (elevated jugular venous pressure), • related radiographic abnormalities (pulmonary venous congestion, Kerley B lines, cardiomegaly, and pleural effusions). Distinguishing cardiogenic pulmonary edema from ARDS can be aided by • measurementof a BNP • echocardiography, • right heart catheterization.

  13. An acute exacerbation of idiopathic pulmonary fibrosis or other chronic interstitial lung diseases • Like ARDS, the pathological findings are dominated by diffuse alveolar damage, but the prognosis is substantially worse. • This diagnostic possibility is easily overlooked in patients whose underlying interstitial lung disease is unknown or mild or moderate in severity. • The diagnosis is suggested by careful review of previous chest radiographic images, by discovery of subpleuralreticulocytic changes intermixed with alveolar opacities on a chest CT scan obtained shortly after onset of ARDS, or by surgical lung biopsy

  14. Diffuse alveolar hemorrhage • May be associated with a large, otherwise unexplained drop in the hemoglobin concentration and hematocrit. • While hemoptysis may be minimal or absent, bronchoscopy often reveals frothy bloody secretions throughout the airways and invariably detects an increasing amount of red blood cells in serial bronchoalveolar lavage specimens. • The recovery of hemosiderin-laden macrophages from bronchoalveolar lavage fluid is strongly suggestive of diffuse alveolar hemorrhage.

  15. Idiopathic acute eosinophilic pneumonia (IAEP) Occursin previously healthy individuals and is characterized by cough, fever, dyspnea, and sometimes chest pain. Bronchoalveolarlavage specimens always contain a large number of eosinophils, typically 35 to 55 percent of all recovered cells . Peripheral eosinophil may or may not be present

  16. Cryptogenic organizing pneumonia (COP) • often mimics community-acquired pneumonia with an onset that is heralded by a flu-like illness with fever, malaise, fatigue, and cough. • The most common features a persistent nonproductive cough, dyspnea with exertion, and weight loss. • BAL usually contains a smaller proportion of macrophages and higher proportions of lymphocytes, neutrophils, and eosinophils than healthy patients. • This "mixed pattern" of increased cellularity is thought to be characteristic of COP. • The diagnosis is made by ruling out infectious causes of pneumonia and documenting typical pathologic changes in tissue obtained by open lung biopsy.

  17. Acute interstitial pneumonia (Hamman-Rich syndrome) • is a rare and fulminant form of diffuse lung injury that has a presentation similar to ARDS. • Many people consider acute interstitial pneumonia a subset of idiopathic ARDS since its clinical manifestations are similar and both demonstrate diffuse alveolar damage on histopathology. • The distinguishing characteristic is that ARDS is often associated with a known risk factor, whereas acute interstitial pneumonia is not.

  18. Cancer • can disseminate through the lungs so rapidly that the ensuing respiratory failure may be mistaken for ARDS. • This is most often due to lymphoma or acute leukemia, but lymphangitic spread of solid tumors occasionally behaves this way. • Cytological preparation of bronchoscopic specimens (eg, brushings, lavage) may reveal malignant cells.

  19. Treatment Medications • Medications directed at the underlying cause of ARDS are indicated • Intravascular volume should be maintained at the lowest level required to maintain adequate cardiac output • Diuretics may be needed to reduce pulmonary capillary wedge pressure and improve oxygenation • Cardiac output that falls when PEEP is used may be improved by reducing the level of PEEP or by the judicious use of inotropic drugs (eg, norepinephrine) • Achieving supranormal oxygen delivery through the use of inotropes and blood transfusion is not clinically useful and may be harmful • Sedatives, analgesics, and antipyretics may be used to decrease oxygen consumption • Systemic corticosteroids have not been shown to reliably improve outcomes

  20. Therapeutic Procedures • Intubation and mechanical ventilation are usually required to treat hypoxemia • Use the lowest levels of PEEP and Fio2 needed to maintain Pao2 > 55 mm Hg (7.13 kPa) or the Sao2 above 88% • Mechanical ventilation with small tidal volumes (6 mL/kg of ideal body weight) has been shown to reduce mortality by 10% in a multicenter trial • PEEP may be increased as long as cardiac output and oxygen delivery are not impaired and pulmonary pressures are not excessive • Prone positioning may improve oxygenation in selected patients

More Related