1 / 34

ARDS

30/07/2000. DR.T.M.K- ARDS. 2. DIAGNOSTIC CRITERIA. ARDSAcutePaO2/Fio2<200 mmHgBilateral interstitialor alveolar infiltratesPcwp <15-18 mmHg. ALIAcute<300 mm HgSamesame. 30/07/2000. DR.T.M.K- ARDS. 3. Clinical diagnosis. RapidWithin 12 to 48 hr of the predisposing eventAwake patients be

mura
Download Presentation

ARDS

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. ARDS DR. T. MOHAN KUMAR, MD, AB, DPPR, FCCP CHIEF & SENIOR CONSULTANT, DEPARTMENT OF PULMONOLOGY & CRITICAL CARE, SRI RAMAKRISHNA HOSPITAL, COIMBATORE ARDS IS A CLINICAL SYNDROME CHARACTERIZED BY ACUTE RESPIRATOR DISTRESS,REFRACTORY HYPOXEMIA,DECREASED RESPIRATORY SYSTEM COMPLIANCE AND DIFFUSE PULMONARY INFILTRATESON THE CHEST RADIOGRAPHARDS IS A CLINICAL SYNDROME CHARACTERIZED BY ACUTE RESPIRATOR DISTRESS,REFRACTORY HYPOXEMIA,DECREASED RESPIRATORY SYSTEM COMPLIANCE AND DIFFUSE PULMONARY INFILTRATESON THE CHEST RADIOGRAPH

    2. 30/07/2000 DR.T.M.K- ARDS 2 DIAGNOSTIC CRITERIA ARDS Acute PaO2/Fio2<200 mmHg Bilateral interstitial or alveolar infiltrates Pcwp <15-18 mmHg ALI Acute <300 mm Hg Same same

    3. 30/07/2000 DR.T.M.K- ARDS 3 Clinical diagnosis Rapid Within 12 to 48 hr of the predisposing event Awake patients become anxious,agitated & dyspnoeic Dyspnoea on exertion proceeding to severe when hypoxemia intervenes Stiffening of lung leads to increase work of breathing,small tidal volumes,rapid respiratory rate Initially respiratory alkalosis Respiratory failure

    4. 30/07/2000 DR.T.M.K- ARDS 4 Clinical disorders associated with ARDS Direct lung injury Aspiration of gastric contents Pulmonary contusion Toxic gas inhalation Near drowning Diffuse pulmonary infection Indirect lung injury Severe sepsis Major trauma Hypertransfusion Acute pancreatitis Drug overdose Reperfusion injury Post cardiac bypass/lung transplants

    5. 30/07/2000 DR.T.M.K- ARDS 5 Clinical disorders associated with ARDS FREQUENT CAUSES SEPSIS BACTEREMIA WITHOUT SEPSIS SYNDROME 4% SEVERE SEPSIS/SEPSIS SYNDROME 35-45% MAJOR TRAUMA MULTIPLE BONE FRACTURES 5-10% PULMONARY CONTUSION 17-22% HYPERTRANSFUSION 5-36% ASPIRATION OF GASTRIC CONTENTS 22-36%

    6. 30/07/2000 DR.T.M.K- ARDS 6 CLINICAL MANIFESTATIONS ARDS occurs in the setting of acute severe illness Clinical manifestations may vary Sepsis and trauma most important Multiple organ failure Atelectasis and fluid filled lungs Hypoxemia/dyspnoea Fever /leukocytosis

    7. 30/07/2000 DR.T.M.K- ARDS 7 Laboratory studies To date no lab findings pathognomonic of ARDS X-ray chest shows bilateral infiltrates consistent with pulmonary edema, may be mild or dense, interstitial or alveolar, patchy or confluent ABG shows hypoxemia with respiratory alkalosis. In late stages hypoxemia, acidosis, hypercarbia may be seen.

    8. 30/07/2000 DR.T.M.K- ARDS 8 Leukocytosis/Leukopenia/anemia are common Renal function abnormalities/or liver function Von willebrands factor or complement in serum may be high Acute phase reactants like ceruloplasmin or cytokine (TNF,IL-1,IL-6,IL-8) may be high.

    9. 30/07/2000 DR.T.M.K- ARDS 9 BRONCHOALVEOLAR LAVAGE Inflammatory mediators like cytokines, reactive oxygen species, leukotrienes & activated complement fragments are found in the fluid Cellular analysis shows more than 60% of neutrophils. As ARDS resolves neutrophils are replaced with alveolar macrophages. Another interesting finding is the presence of a marker of pulmonary fibrosis called procollagen peptide III (PCPIII) and this correlates with mortality. Presence of more eosinophils suggest eosinophilic pneumonia, high lymphocyte counts may be seen in hypersensitivity pneumonitis, sarcoidosis, BOOP, or other acute forms of interstitial lung disease.

    10. 30/07/2000 DR.T.M.K- ARDS 10 Differential diagnosis Infectious causes Bacteria - Gm neg & pos , mycobacteriae, mycoplasma, rickettsia, chlamydia Viruses- CMV, RSV, hanta virus, adeno virus, influenza virus Fungi- H.capsulatum, C.immitis parasites- pneumocytis carinii, toxoplasma gondii

    11. 30/07/2000 DR.T.M.K- ARDS 11 Differential Diagnosis Non infectious causes CCF Drugs & toxins (paraquat, aspirin, heroin, narcotics, toxic gas, tricyclic anti depressants, acute radiation pneumonitis) Idiopathic (esinophilic pneumonia, Acute interstitial pneumonitis, BOOP, sarcoidosis, rapidly involving idiopathic pulmonary fibrosis) Immunologic (acute lupus pneumonitis, Good Pastures syndrome, hypersensitivity pneumonitis) Metabolic (alveolar proteinosis) Miscellaneous (fat embolism, neuro/high altitude pulmonary oedema) Neoplastic (leukemic infiltration, lymphoma)

    12. 30/07/2000 DR.T.M.K- ARDS 12 Therapy -goals Treatment of the underlying precipitating event Cardio-respiratory support Specific therapies targeted at the lung injury Supportive therapies

    13. Respiratory Support

    14. 30/07/2000 DR.T.M.K- ARDS 14 Spontaneously Breathing Patient In the early stages of ARDS the hypoxia may be corrected by 40 to 60% inspired oxygen with CPAP Peak inspiratory flow rates of >= 70ltrs / min require a tight-fitting face mask with a large reservoir bag or a high flow generator If the patient is well oxygenated on <= 60 % inspired oxygen and apparently stable without CO2 retention and apparently stable, then ward monitoring may be feasible but close observation( 15 to 30 Min), continuous oximetry, and regular blood gases are required

More Related