Post on 07-May-2015
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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)GUIDE - DR.SHIV.S.SHARMA
- DR.Y. JAMRACANDIDATE-DR.SARATH MENON.R
Intensive care unit,Dept.Internal Medicine
MGM MEDICAL COLLEGE & M Y HOSPITAL,INDORE
OUTLINE
Definition Clinical history Pathophysiology Diagnosis Management
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
CXR – WHAT’S DIAGNOSIS ?
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)
Acute PaO2/FiO2 < 200 B/l interstitial
/alveolar infiltrates PCWP <18mmHg
Acute < 300mmHg Same
Same
ARDS ALI
ARDS DIAGNOSTIC CRITERIA
Acute Onset
Predisposing Condition
Bilateral Infiltrates
PaO2/FiO2 ≤ 200 mm Hg
Pulmonary capillary Wedge Pressure ≤ 18 mm Hg or no clinical evidence increase in LA pressure.
ARDS CAUSES Direct Lung Injury: a) Pneumonia b) pulmonary contusion c) near drowning d) inhalation injury f) aspiration of gastric contents
ARDS CAUSES Indirect lung injury
a) sepsis b) severe trauma w/ shock, hypoperfusion c) acute pancreatitis d) transfusion of multp blood
products
PATHOPHYSIOLOGY
Diffuse alveolar damage Lung capillaries damage Inflammatory cells Alveolar edema Severe hypoxemia Decreased lung compliance & atelectasis Pulmonary hypertension
NATURAL HISTORY OF ARDS
3 phases - exudative (0-7 d) - proliferative ( 7-21 d)
- fibrotic ( > 21 days)
HISTOLOGIC FINDINGS
Typical histological findings in ARDS alveolar inflammation,
thickened septal from protein leak (pink), congestion and decreased alveolar volume
www.burnsurgery.com/.../pulmonary/part3/sec4.htm
←Normal Lung Histology—large alveolar volumes, septal spaces very thin, no cellular congestion.
Hyaline Protein in air spaces
Cellular Congestion
CLINICAL HISTORY
Acute Critically ill Rapid –tachypnoea,dyspnoea,hypoxia Within in 12-48 hr of precipitating event Initial respiratory alkalosis Respiratory failure
LAB INVESTIGATIONS
Routine blood counts RFT CXR ABG CT chest BNP 2D Echo BAL PCWP
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
Bilateral infiltrates predominately in lung bases. Kerley B’s. Cardiomegaly.
Diffuse Bilateral patchy infiltrates homogenously distributed throughout the lungs. No Kerley B’s.
CARDIOGENIC V/S NON CARDIOGENIC EDEMA
Patchy infiltrates in bases
Effusions + Kerley B lines + Cardiomegaly + Pulmonary vascular
redistribuition Excess fluid in alveoli
Homogenous pluffy shadows
Effusions – Kerley B lines – Cardiomegaly – No pulm.vascular
redistribuition Protein,inflammatory
cells,fluid
cardiogenic Non-cardiogenic
ARDS
early late
Cardiogenic Non-Cardiogenic
No septal thickening. Diffuse alveolar infiltrates. Atelectasis of dependent lobes usually seen .
Septal thickening. More severe in lung bases.
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 VENTILATION
The Aims are to increase PaO2 while
minimizing the risk of further lung injury
(ventilator induced lung injury)
ARDSNETVENTILATOR PROTOCOL
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 FOR ARDS THERAPY
TREATMENT
MECHANICAL VENTILATION
Low tidal volumeMinimize LAFPHigh PEEPProne positionRecruitment maneuversHigh frequency
ventilation Glucocorticoids Sufactant
replacement,inhaled NO,others
RECOMMENDATIONS
A B CCC D DD
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.
PEEPSetting 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
Inverse ratio ventilation - reduce peak airway pressure - I: E – 1:1 & 4:1 - severe hypoxemic resp.failure Permissive hypercapnea - controlled hypoventilation - PaCO2 upto 55mmhg - pH upto 7.25 Proning
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
TREATMENT OF SEPSIS
Empirical antibiotics Culture sensitivity & change antibiotics Avoid nephrotoxic drug Enteral feeding
OTHER TREATMENT MODALITIES
NO Ketoconazole Albuterol Pentoxyphylline NSAIDS N-acetyl cysteine
PROGNOSIS
Mortality ranges-26 %-44% Risk factors- - advanced age - CKD,CLD - Chronic immunosuppression - chronic alcohol abuse ARDS from direct lung injury has double
mortality
REFERENCES
Harrison’s text book of medicine-18th edition ARDS Network clinical trials - www.ardsnet.org ARDS Foundation - www.ardsusa.org
THANK U….