Ards kumar

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Ards kumar

  1. 1. ARDS DR. T. MOHAN KUMAR, MD, AB, DPPR, FCCP CHIEF & SENIOR CONSULTANT, DEPARTMENT OF PULMONOLOGY & CRITICAL CARE, SRI RAMAKRISHNA HOSPITAL, COIMBATORE
  2. 2. DIAGNOSTIC CRITERIA ARDS ALI Acute Acute PaO2/Fio2<200 <300 mm Hg mmHg Bilateral interstitial Same or alveolar infiltrates Pcwp <15-18 same mmHg 30/07/2000 DR.T.M.K- ARDS 2
  3. 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 30/07/2000 DR.T.M.K- ARDS 3
  4. 4. Clinical disorders associated with ARDS Direct lung injury Indirect lung injury  Aspiration of gastric  Severe sepsis contents  Major trauma  Pulmonary contusion  Hypertransfusion  Toxic gas inhalation  Acute pancreatitis  Drug overdose  Near drowning  Reperfusion injury  Diffuse pulmonary  Post cardiac infection bypass/lung transplants 30/07/2000 DR.T.M.K- ARDS 4
  5. 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% 30/07/2000 DR.T.M.K- ARDS 5
  6. 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 30/07/2000 DR.T.M.K- ARDS 6
  7. 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. 30/07/2000 DR.T.M.K- ARDS 7
  8. 8. Leukocytosis/Leukopenia/anemia are common Renal function abnormalities/or liver function Von willebrand’s 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. 30/07/2000 DR.T.M.K- ARDS 8
  9. 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. 30/07/2000 DR.T.M.K- ARDS 9
  10. 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 30/07/2000 DR.T.M.K- ARDS 10
  11. 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) 30/07/2000 DR.T.M.K- ARDS 11
  12. 12. Therapy -goals Treatment of the underlying precipitating event Cardio-respiratory support Specific therapies targeted at the lung injury Supportive therapies 30/07/2000 DR.T.M.K- ARDS 12
  13. 13. Respiratory Support
  14. 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 Contd.. 30/07/2000 DR.T.M.K- ARDS 14
  15. 15. Indications for mechanical ventilation  Inadequate Oxygenation(PaO2 < 8k Pa on FiO2 >= 0.6)  Rising or elevated PaCO2(>= 6k Pa)  Clinical signs of incipient respiratory failure 30/07/2000 DR.T.M.K- ARDS 15
  16. 16. Mechanical Ventilation The Aims are to increase PaO2 while minimizing the risk of further lung injury (Oxygen toxicity, Barotrauma). This is the realm of the IRCU Physician: seek specialist advice early to prevent complications. The general principles are the following: 30/07/2000 DR.T.M.K- ARDS Contd.. 16
  17. 17.  Start with FiO2 = 1.0, tidal volume 6 to 10 ml per Kg, PEEP <= 5 cm H2O and inspiratory flow rates ~ 60 L / min. Subsequent adjustments are done to try to achieve arterial oxygen sats. of > 90% with FiO2 < 0.6 and peak airway pressures < 40 to 45 cm H20  Controlled Mandatory Ventilation (CMV) with sedation and neuromuscular blockade (to try to suppress the respiratory drive and reduce respiratory muscle oxygen requirement.) 30/07/2000 DR.T.M.K- ARDS 17
  18. 18. PEEP improves PaO2 in most patients and allows reduction of FiO2. Increase by 2 to 5 cm H2O increments every 20 min watching for hemodynamic deterioration (due to impaired venous return and decreased cardiac out put). Optimal PEEP is usually 10 to 15 cm H2O Inverse Ratio Ventilation may decrease peek inflation pressures and thus Barotrauma. Inspiratory time : Expiratory time ratio (I:E ratio) of between 1:1 and 4:1 may be tried. Contd.. 30/07/2000 DR.T.M.K- ARDS 18
  19. 19. The ventilatory rate required to clear CO2 and normalize pH is commonly high (20 to 25 breaths / min). However this may result in unacceptable airway pressures. Another strategy is’ permissive hypercapnoea’ which as the name suggests is controlled hypoventilation. PaCO2 up to 13 kPa is generally well tolerated; acidosis (pH < 7.25) may be treated with intravenous bicarbonate 30/07/2000 DR.T.M.K- ARDS 19
  20. 20.  Changing the patients position (lateral decubitus or prone instead of supine) can improve oxygenation by improving perfusion of aerated portion of lung. Consider this in patients with non uniform or predominantly posterior and lower lobe infiltrates  Inhaled nitric oxide (18 ppm) reduces pulmonary artery pressures, intra pulmonary shunting and improves oxygenation while not affecting mean arterial pressure or cardiac output. However studies showing an effect on mortality are awaited.  Newer methods such as high frequency jet ventilation, extra corporeal gas exchange (CO2 removal +- Oxygenation) and intravascular oxygenation devices (IVOX) may be of use but are currently not widely available. 30/07/2000 DR.T.M.K- ARDS 20
  21. 21. Cardiovascular Support
  22. 22.  Invasive monitoring is mandatory(Arterial line, PA catheter (Swan-Ganz) to measure cardiac outputs and if available, continuous mixed venous oxygen saturation)  In order to minimize pulmonary oedema, aim to keep PCWP low (8 to 10 mm Hg) and support the circulation with inotropes if necessary  The role of colloids and albumin is relatively minor: the increased capillary permeability allows these molecules to equilibrate with the alveolar fluid with little increase in net plasma oncotic pressure 30/07/2000 DR.T.M.K- ARDS Contd.. 22
  23. 23.  Renal failure is common and may require haemofiltration to achieve a negative fluid balance and normalize blood chemistry.  Oxygen consumption (VO2) in patients with ARDS appears to be delivery dependent. The current trend is to aim for target levels of oxygen delivery (DO2 = Cardiac Index(HbXSao2X1.34)X10) as guided by tissue perfusion (clinically and serum lactate, pHi from a gastric tonometer). DO2 may be increased by blood transfusion, inotropes and vasodilators including prostacyclin). 30/07/2000 DR.T.M.K- ARDS 23
  24. 24.  Selection of appropriate inotropes and vasodilators can only be made by repeated measurements of haemodynamic parameters and calculating DO2 and VO2 while evaluating the effects of the various agents  Nutritional support must be chosen to try to avoid fluid overload. Lipid metabolism produces marginally less CO2 than dextrose metabolism and thus favourably affects the respiratory quotient but there is controversy as to whether lipid can exacerbate lung injury 30/07/2000 DR.T.M.K- ARDS 24
  25. 25. Treatment of Sepsis
  26. 26. Fever, Neutrophil leukocytosis and raised inflammatory markers (CRP) are common in patients with ARDS and do not always imply sepsis. However sepsis is common precipitant of ARDS A trial of empirical antibiotics guided by possible pathogens should be given early. Eg Cefotaxime. This may be modified in light of the results of appropriate cultures. Avoid nephrotoxic antibiotics. Enteral feeding seems to carry a lower risk of sepsis than parenteral feeding and helps maintain the integrity of the gut mucosa. Ileus is common in multi-organ failure, so entral feeding may not be possible. 30/07/2000 DR.T.M.K- ARDS 26
  27. 27. Minimizing lung injury and treating the cause
  28. 28. Look for a precipitant In general prevention (example of aspiration of gastric acid) is more effective than trying to treat ARDS. However there are no effective measures for prophylaxis in patients at risk ( Eg from Trauma) Steroids : there is no benefit from treatment early in the disease. Treatment later (> 7 to 14 days from onset) especially in patients with peripheral blood eosinophilia or eosinophils in bronchoalveolar lavage, improves prognosis 30/07/2000 DR.T.M.K- ARDS 28
  29. 29. Give 2 to 4 mg / Kg prednisolone or equivalent: the duration depends on the clinical response( 1 to 3 weeks) Other therapies such as inhaled nitric oxide , exogenous surfactant, antioxidants (acetylcysteine), ketoconazole, NSAIDs, Pentoxifylline and anticytokine antibodies are still under investigation 30/07/2000 DR.T.M.K- ARDS 29
  30. 30. Causes of Sudden deterioration in ARDS Respiratory Cardiovascular Pneumothorax Arrhythmia Bronchial plugging Cardiac tamponade Displaced ET tube Myocardial infarction Pleural effusion GI bleed(Stress Ulcer) (Haemothorax) Aspiration(Eg NG Septicaemia feed) 30/07/2000 DR.T.M.K- ARDS 30
  31. 31. Completed trials  Reducing lung stretching  Lisophyllin  Corticosteroids in late ARDS  ALVEOLI study 30/07/2000 DR.T.M.K- ARDS 31
  32. 32. Completed trials -II  Fluids and catheters treatment trial (FACTT)  Low tidal volume versus high tidal volume ventilation  Ketoconazole  Role of MODS 30/07/2000 DR.T.M.K- ARDS 32
  33. 33. WHAT IS NEW? ALI & Gene transfer New approaches to enhancing lung edema clearance Nitric oxide donors New treatment for altered pulmonary vascular permeability Inflammatory & cytokine networks in ARDS 30/07/2000 DR.T.M.K- ARDS 33
  34. 34. What is new Use of surfactant therapy Liquid ventilation in ALI CPAP trial 30/07/2000 DR.T.M.K- ARDS 34

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