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CASE 35 yr old male met with an RTA was admitted in surgery icu developed severe tachpnoea,dyspnoea within 24hrs admission o/e- pulse- 110/mt,bp- 80/50mmHg pallor+ cyanosis + no jvp S1/S2- NL Chest b/l rales present in mid/lower area p/a- soft ,no HSM Abg analysis- O2 sat 50%,pao2-40%,pco2-45% ph – 7.3
ARDS -DEFINITION ARDS is a clinical syndrome of dyspnea of rapid onset,hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. Inflammatory cells and proteinaceous fluid accumulate in the alveolar spaces leading to a decrease in diffusing capacity and hypoxemia.
ALI V/S ARDS ALI is the term used for patients with significant hypoxemia (PaO2/FiO2 ratio of ≤ 300) ARDS is the term used for a subset of ALI patients with severe hypoxemia (PaO2/FiO2 ratio of ≤ 200)
HISTOLOGIC FINDINGS Hyaline Protein in air spaces Cellular Congestion Typical histological findings in ARDSwww.burnsurgery.com/.../pulmonary/part3/sec4.htm alveolar inflammation, thickened septal from protein leak (pink), congestion and decreased alveolar volume ←Normal Lung Histology—large alveolar volumes, septal spaces very thin, no cellular congestion.
CLINICAL HISTORY Acute Critically ill Rapid –tachypnoea,dyspnoea,hypoxia Within in 12-48 hr of precipitating event Initial respiratory alkalosis Respiratory failure
HOW TO DETERMINE ARDS BY CXR Can be difficult to do. Should always try to make the diagnosis in light of the clinical picture. Need to determine Cardiogenic vs. Non-cardiogenic edema.
Cardiogenic Non-Cardiogenic Diffuse Bilateral patchy infiltratesBilateral infiltrates predominately in homogenously distributedlung bases. Kerley B’s. throughout the lungs. No KerleyCardiomegaly. B’s.
CARDIOGENIC V/S NON CARDIOGENIC EDEMA cardiogenic Non-cardiogenic Patchy infiltrates in bases Homogenous pluffy Effusions + shadows Kerley B lines + Effusions – Cardiomegaly + Kerley B lines – Pulmonary vascular Cardiomegaly – redistribuition No pulm.vascular Excess fluid in alveoli redistribuition Protein,inflammatory cells,fluid
Cardiogenic Non-Cardiogenic No septal thickening. DiffuseSeptal thickening. More severe in alveolar infiltrates. Atelectasislung bases. of dependent lobes usually seen .
THERAPY- GOALS Treatment of underlying cause Cardio-pulmonary support Specific therapy targeted at lung injury Supportive therapy.
SPONTANEOUSLY BREATHING PATIENT In the early stages of ARDS the hypoxia may be corrected by 40 to 60% inspired oxygen . If the patient is well oxygenated on <= 60 % inspired oxygen and apparently stable without CO2 retention then ward monitoring may be feasible but close observation( 15 to 30 Min), continuous oximetry, and regular blood gases are required
INDICATION FOR MECHANICAL VENTILATION Inadequate oxygenation ( PaO2- < 60 with FiO2 >=0.6) Rising or elevated PaCO2 ( > 50mmHg) Clinical signs of incipient respiratory failure
MECHANICAL VENTILATIONThe Aims are to increase PaO2 whileminimizing the risk of further lung injury(ventilator induced lung injury)
ARDS NET PROTOCOL -WEANING Spontaneous breathing trial daily PaO2/FiO2-<8/<.4 or <5/ <.5 PaO2/FiO2 less than previous day Systolic BP > 90 without vasopressors No neuromuscular blockade 2 hr trial- with T piece with 1-5cm water CPAP. ABG,RR,SPO2 monitoring If tolerated for 30 mt,consider extubation
EVIDENCE BASED RECOMMENDATIONS FORARDS THERAPYTREATMENT RECOMMENDATIONS MECHANICAL VENTILATIONLow tidal volume AMinimize LAFP BHigh PEEP CProne positionRecruitment maneuvers CHigh frequency ventilation C Glucocorticoids D Sufactant D replacement,inhaled D NO,others
MANAGEMENT: REDUCING VENTILATOR-INDUCED LUNG INJURY Low tidal volume mechanical ventilation In ARDS there is a large amount of poorly compliant (i.e. non-ventilating) lung and a small amount of healthy, compliant lung tissue. Large tidal volume ventilation can lead to over-inflation of the healthy lung tissue resulting in ventilator-induced lung injury of that healthy tissue. PEEP Setting a PEEP prevents further lung injury due to shear forces by keeping airways patent during expiration
ARDS NETWORK CLINICAL TRIALS High TV vs low TV (12ml/kg vs 6ml/kg) - 861 pts - mortality rate 39.2 % vs 31% High PEEP vs low PEEP 13cm H20 vs 8 cm H20 –NO difference Amato etal- optimal PEEP- 15cm H20
OTHER METHODS High flow ventilation ECMO Partial fluid ventilation (PLV)
EXTRA CORPOREAL MEMBRANE OXYGENATION(ECMO)
MANAGEMENT Fluids – - conservative management - normal or low LAFP - reduce icu stay,duration of ventilation Steroids - Meduri et al study - methyprednisolone-2mg/kg & taper to .5-1mg/kg in 1-2wk