ARDS

nullARDSARDSDR. T. MOHAN KUMAR, MD, AB, DPPR, FCCP CHIEF & SENIOR CONSULTANT, DEPARTMENT OF PULMONOLOGY & CRITICAL CARE, SRI RAMAKRISHNA HOSPITAL, COIMBATOREDIAGNOSTIC CRITERIADIAGNOSTIC CRITERIAARDS Acute PaO2/Fio2<200 mmHg Bilateral interstitial or alveolar infiltrates Pcwp <15-18 mmHgALI Acute <300 mm Hg Same sameClinical diagnosisClinical diagnosisRapid 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 failureClinical disorders associated with ARDSClinical disorders associated with ARDSDirect 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 Clinical disorders associated with ARDSClinical disorders associated with ARDSFREQUENT 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% CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONSARDS 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 /leukocytosisLaboratory studiesLaboratory studiesTo 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.nullLeukocytosis/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.BRONCHOALVEOLAR LAVAGEBRONCHOALVEOLAR LAVAGEInflammatory 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.Differential diagnosisDifferential diagnosisInfectious 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 gondiiDifferential DiagnosisDifferential DiagnosisNon 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)Therapy -goalsTherapy -goalsTreatment of the underlying precipitating event Cardio-respiratory support Specific therapies targeted at the lung injury Supportive therapiesRespiratory SupportRespiratory SupportSpontaneously Breathing PatientSpontaneously Breathing PatientIn 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 requiredContd..Indications for mechanical ventilationIndications for mechanical ventilation Inadequate Oxygenation(PaO2 < 8k Pa on FiO2 >= 0.6) Rising or elevated PaCO2(>= 6k Pa) Clinical signs of incipient respiratory failure Mechanical VentilationMechanical VentilationThe 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:Contd..nullStart 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.)nullPEEP 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..nullThe 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 nullChanging 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.Cardiovascular SupportCardiovascular SupportnullInvasive 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 pressureContd..nullRenal 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). nullSelection 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 Treatment of SepsisTreatment of SepsisnullFever, 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.Minimizing lung injury and treating the causeMinimizing lung injury and treating the causenullLook 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 prognosisnullGive 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 Causes of Sudden deterioration in ARDSCauses of Sudden deterioration in ARDSCompleted trialsCompleted trialsReducing lung stretching Lisophyllin Corticosteroids in late ARDS ALVEOLI studyCompleted trials -IICompleted trials -IIFluids and catheters treatment trial (FACTT) Low tidal volume versus high tidal volume ventilation Ketoconazole Role of MODS WHAT IS NEW?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 ARDSWhat is newWhat is newUse of surfactant therapy Liquid ventilation in ALI CPAP trial