Académique Documents
Professionnel Documents
Culture Documents
Department of Medicine
J.L.N. Medical College, Ajmer (Raj.)
REFERANCE
Harrisons Principle of Internal Medicine 17th Edition, 2008.
API of General Medicine 2008. The Washington Manual of Medical Therapeutics 32th edition 2007. Wikipedia Images from various internet sites
Difficulties:
lacks specific criteria
controversy over incidence and mortality
Severe lung injury characterized by noncardiogenic pulmonary edema, decreased lung compliance, refractory hypoxemia
1994 Consensus Definition
Acute onset (<2 weeks) Bilateral infiltrates on chest x-ray PCWP 18mmHg or lack of evidence of left atrial hypertension
Incidence of acute lung injury (ALI): up to 80 cases per 100,000 person-years Incidence of acute respiratory distress syndrome (ARDS): up to 60 cases per 100,000 person-years Approx 10% of ICU beds in US In India study from Mumbai ,respiratory failure due to ARDS occurred in 26% patients with severe malaria ,with a nearly 90% mortality.
Pneumonia (40-50%)
Sepsis (31%) Aspiration (9%)
Trauma (20%)
Pulmonary contusion Multiple fractures
Sepsis
40% of patients with sepsis develop ARDS
Differential diagnosis
Pulmonary edema from left heart failure BOOP or COP Hypersensitivity pneumonitis
EXUDATIVE
PROLIFERATIVE
FIBROTIC
FIBROSIS
DAY
0-7
14
21..
11
In ALI/ARDS damage to either one occurs resulting in increased permeability of the barrier
influx of protein-rich edema fluid into the alveolar space Injury of Type I cells results loss of epithelial integrity and fluid extravasations (edema)
Injury of Type II cells then impairs the removal of the edema fluid
Dysfunction of Type II cells also leads to reduced production and turnover of surfactant which leads to alveolar collapse
If severe injury to epithelium occurs disorganized/insufficient epithelial repair occurs resulting in fibrosis
In addition to inflammatory process, there is evidence that the coagulation system is also involved
Alveolar Filling
Hyaline Membranes
Rapid onset respiratory failure in patient at risk for ARDS Hypoxemia refractory to oxygen Chest x-ray resembles cardiogenic pulmonary edema
Bilateral infiltrates worse in dependent lung zones, effusions Infiltrates may be asymmetric
A representative computed tomographic scan of the chest during the exudative phase of ARDS in which dependent alveolar edema and atelectasis predominate.
Proliferative Phase
With intervention (mechanical ventilation) there is clearance of alveolar fluid
Soluble proteins are removed by diffusion between alveolar epithelial cells
Insoluble proteins are removed by endocytosis and transcytosis through epithelial cells and phagocytosis through macrophages
Type II cells begin to differentiate into Type I cells and reepithelialize denuded alveolar epithelium
After acute phase, some pt will have uncomplicated course and rapid resolution
Impaired gas exhange leading to severe hypoxemia - ventilation-perfusion mismatch, increase in physiologic deadspace
Decreased lung compliance due to the stiffness of poorly or nonaerated lung Pulm HTN 25% of pts, due to hypoxic vasoconstriction, Vascular compression by positive airway compression, airway collapse and lung parenchymal destruction
ARDS Clinical
Chest X-ray:
Bilateral pulmonary infiltrates, diffuse, symmetric or asymmetric, evolve rapidly, with maximal severity within the first 3 days Initially, the infiltrates may have a patchy peripheral distribution but soon progress to diffuse bilateral involvement with ground glass changes or frank alveolar infiltrates For patients who begin to improve and show signs of resolution, improvement in radiographic abnormalities generally occurs over 10-14 days
CXR
During the exudative phase, chest radiographs reveal a progression from diffuse interstitial infiltrates to diffuse, fluffy, alveolar opacities . Although ARDS cannot reliably be distinguished from cardiogenic pulmonary edema on radiologic grounds, patients with ARDS often lack cardiomegaly, pleural effusions, and vascular redistribution. Reticular opacities may ensue, suggesting the development of interstitial fibrosis.
A representative anteroposterior (AP) chest x-ray in the exudative phase of ARDS that shows diffuse interstitial and alveolar infiltrates, which can be difficult to distinguish from left ventricular failure.
ARDS Clinical
Clinical evaluation and routine chest radiography are sufficient in patients with ARDS
More sensitive than plain chest radiography in detecting pulmonary interstitial emphysema, pneumothorax, pleural effusions, cavitations and mediastinal lymphadenopathy CT scanning in ARDS reveals extensive heterogeneity of lung involvement.
CT SCAN SHOWS:
ARDS
ABGs:
Initial respiratory alkalosis acidosis If sepsis, metabolic acidosis initially Hematological Renal Hepatic Cytokines( TNF-L , IL1,1L6,1L8)
ARDS
Hemodynamic monitoring with pulmonary artery catheter. a) helpful in separating cardiogenic from non-cardiogenic PE
Adequate nutrition
Supportive care DVT prophylaxis GI prophylaxis Medications
ARDS Management
Perform objective assessment with arterial blood gas and chest radiograph
Provide supplemental oxygen, monitor saturation and investigate risk factors for ARDS
ARDS
1) Conventional ventilation(invasive ventilation): aim : a) maintain oxygenation and avoid toxicity O2 sat 85%-90% on FiO2 <65% b) avoid complications of mechanical ventilation
PEEP
(8.3-13.2 cmH2O)
Low tidal volume (6ml/kg): inspiratory pressure< 30mm H2O Maintain pH around normal (HCO3) Pressure control ventilation?? Inverse I:E ratio Permissive hypercapnia
Pressur support Pressure regulated volume control ( PaCO2<75mmHg, pH>7.2) (autoPEEP,heavy sedation)
} weaning
ARDS management..
Algorithm for the initial management of ARDS. Clinical trials have provided evidence-based therapeutic goals for a step-wise approach to the early mechanical ventilation, oxygenation, correction of acidosis and diuresis of critically ill patients with ARDS.
Contraindications : Diminished level of consciousness Inadequate cough Vomiting or upper gastrointestinal bleeding Inability to properly fit the mask Poor patient cooperation
Hemodynamic instability
Prone position
ARDS Management
Partial Liquid ventilation Nitric oxide (Inhaled) ECMO (extra corporeal membrane oxygenation) HFOV Lung protective strategies.
Prone position
ARDS Management
Antioxidants
Sedation Fluids ( conservative therapy )
5) Nutrition
6) Surgical care
CONVENTIONAL VENTILATION
o o o o o Oxygen PEEP Inverse I:E ratio Lower tidal volume Ventilation in prone position
PEEP - Benefits
o To prevent end-expiratory collapse and maintain the alveoli open throught respiratory cycle so it.. o Increases transpulmonary distending pressure o Displaces edema fluid into interstitium o Decreases atelectasis o Decrease in right to left shunt o Improved compliance o Improved oxygenation
Prone Position
o o o o o Improved gas exchange More uniform alveolar ventilation Recruitment of atelectasis in dorsal regions Improved postural drainage Redistribution of perfusion away from edematous, dependent regions
Often used to help evaluate for cardiogenic pulmonary edema SUPPORT trial (retrospective study) first raised doubts about utility Two multicenter RCTs confirmed lack of mortality benefit of PA catheters in ARDS (ARDSnet FACTT) Monitoring CVP equally effective, so PAC not recommended in routine management
861 patients randomized to Vt 10-12 mg/kg ideal body weight and plateau pressure 50cmH2O vs. Vt 6-8 mg/kg IBW and plateau pressure 30cm H2O
KEYS
Low tidal volumes 6-8mL/kg ideal body weight
Maintain plateau (end-inspiratory) pressures <30cm H20 Permissive hypercapnia and acidosis
PEEP can improve lung recruitment and decrease end-expiratory alveolar collapse (and therefore right-to-left shunt) Can also decrease venous return, cause hemodynamic compromise, worsen pulmonary edema
ARDSnet PEEP trial of 549 patients show no difference in mortality or days on ventilator with high vs low PEEP
Agents studied:
Corticosteroids Ketoconazole
No benefit demonstrated
Earlier studies showed no benefit to early use steroids, but small study in 1990s showed improved oxygenation and possible mortality benefit in late stage
ARDSnet trial (Late Steroid Rescue Study LaSRS lazarus) of steroids 7+ days out from onset of ARDS 180 patients enrolled, RCT methylprednisolone vs placebo Overall, no mortality benefit
Steroids increased mortality in those with sx >14 days
Ketoconazole
ARDSnet study of 234 patients, ketoconazole did NOT decrease mortality, duration of mechanical ventilation or improve lung function
Surfactant
Multicenter trial, 725 patients with sepsis-induced ARDS, surfactant had no effect on 30-day survival, ICU LOS, duration of mechanical ventilation or physiologic function
ARDS
1) Related to ventilation :
(a) barotrauma
(i) pneumothorax (ii)pneumomediastinal
(b) subglottic stenosis 2) Related to IV lines and catheters : (a) sepsis (b) pneumothorax
3) Nosocomial infection- a significant potential complication 4) Renal failure : frequent complication 5) GI : illeus, stress gastritis 6) Anemia 7) Critical illness myopathy
ARDS
ARDS Prognosis
Advanced age(>75yrs have ~60% mortality vs <45 have~20% mortality Chronic liver disease , cirrhosis & alcohol abuse MOF ,Sepsis Chronic renal disease Chronic immunosuppression Increased APACHE Elevated levels of PCP-III (marker of pulmonary fibrosis in the BAL fluid) Early elevation in dead space
( within 24h of presentation)
Extent of hypoxemia
The level of PEEP used in mechanical ventilation The respiratory compliance
Low tidal volume High PEEP or open lung prone position Recruitment maneuvers
A C C C
Surfactant replacement, inhaled nitric oxide, and other anti-inflammatory therapy (e.g.., ketoconazole,PGE1,NSAIDs)
A-recommended therapy based on strong clinical evidence from randomized clinical trials Brecommended therapy based on supportive but limited clinical data C-indeterminate evidence recommended as alternative therapy D-not recommended based on clinical evidence against efficacy of therapy
ARDS is a clinical syndrome characterized by severe, acute lung injury, inflammation and scarring
Significant cause of ICU admissions, mortality and morbidity