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BY S F HASHMI
GUIDED BY DR D G MHAISEKAR SIR
22TH FEB 2011
Discovery of the disease
1954 model of the
Engstrom anesthesia / ventilator
had lead to discovery of the disease.
FIRST DESCRIBED
IN 1967 BY Ashbaugh et al
Synonyms:
1. Non-Cardiogenic pulmonary edema
2. Adult hyaline membrane disease
3. Capillary leak syndrome
4. Stiff lung syndrome
5. Shock lung
DEFINITION
The 1994North American - European
Consensus Conference (NAECC) criteria:
• Onset - Acute and persistent
Non-Cardiogenic
Cardiogenic
Protein,
Excess fluid
inflammatory
in alveoli cells, and fluid
accumulation in the alveoli
Due to high pulmonary capillary pressure
Due
(estimated
to highbypermeability
measuring pulmonary
oedema & artery
wedge pressure)
“other” systemic factors NOT elevated
pulmonary capillary pressure
Cardiogenic vs. Non-Cardiogenic Edema
Non-Cardiogenic
Cardiogenic
Patchy
Infiltrates
infiltrates
are more appearing
homogeneous
in the lung bases first
No
Effusions
pleuralmay
effusions
be present
Clinical
No Kerleysigns
B’s and symptoms lag behind radiographic
evidence (i.e. CXR
Radiographic is more
evidence impressive
lags than the
behind clinical degree
signs and of
hypoxemia)
symptoms (i.e. the CXR is unimpressive given the
degree of hypoxemia)
Cardiogenic Non-Cardiogenic
FREQUENT CAUSES
SEPSIS
BACTEREMIA WITHOUT SEPSIS SYNDROME 4%
MAJOR TRAUMA
HYPERTRANSFUSION 5-36%
ASPIRATION OF GASTRIC CONTENTS 22-36%
PATHOLOGICAL STAGES OF ARDS
Recovery
PATHOGENESIS
Decreased ventilation
Impaired diffusion
Reduced perfusion
CLINICAL FEATURES – SYMPTOMS
Dyspnoea
Tachypnoea
Tachycardia
Restlessness
Cyanosis even with supplemental oxygen
( refractory hypoxemia)
DIFFERENTIAL DIAGNOSIS
Cardiogenic pulmonary edema
Diffuse alveolar hemorrhage
Acute pulmonary embolism
Acute eosinophilic pneumonia
Hypersensitivity pneumonitis
Pulmonary alveolar protienosis
Sarcoidosis
Leukemic infiltration
Drug induced pulmonary edema
INVESTIGATIONS
Chest x-ray & CT thorax:
bilateral diffuse alveolar infiltrates more on
the peripheral lung fields.
R/O Cardiogenic edema if there is
* cardiomegaly
* pulmonary artery dilatation
* bat’s wing perihilar distribution
* responding to diuretics
NEONATAL RESPIRATORY DISTRESS SYNDROME
INVESTIGATIONS
Arterial blood gas analysis:
PaO2 range 55 – 60 mm of Hg
Initially respiratory alkalosis later
mixed acidosis
Routine CBC, urea, creatinine, Na, K
Echocardiogram to R/O Cardiogenic
cause.
PAWP < 18mm of Hg ALI / ARDS
INVESTIGATIONS
Bronchoscopy
LUNG BIOPSY
SERUM MARKERS
Von willebrand’s factor or
complement in serum may be
high.
Typical histological
findings in ARDS
alveolar inflammation,
thickened septal from
protein leak (pink),
congestion and decreased
alveolar volume
Advanced age
Extra pulmonary organ dysfunction
Sepsis
HIV
Alcoholism
Active malignancy
Organ transplantation
• PHARMACOLOGICAL TREATMENT 3
• Steroids, vasodilators, surfactant, anti inflammatory
• SUPPORTIVE THERAPY (5P’s)
• Perfusion, Position, Protective lung ventilation,
2
Protocol weaning, Preventing complications
• TREATMENT OF CAUSE 1
• e.g. antibiotics for pneumonia
TREATMENT OF ALI/ARDS
TREATMENT - Ventilation
Goals of ventilation in ARDS are to:
Maintain oxygenation by keeping O2
saturation at 85-90%
Avoiding oxygen toxicity and complication of
mechanical ventilation – decreasing FiO2 to
less than 65% within the 1st 24-48 hours .
Tidal Volume Strategies in ARDS
Airway Trauma
“Stretch”
“Shear”
Ventilator-Induced
Lung Injury
Positive pressure ventilation may injure the lung
via several different mechanisms
Lung inflammation
“BIOTRAUMA”
VILI
Steroids
IN TGI
Stream of fresh air (4 to 8 L/min) insufflated
through – small catheter or through small channel
in wall of ET into lower trachea flushing Co2 laden
gas.
EXTRACORPOREAL MEMBRANE
OXYGENATION
OXYGENATE BLOOD and REMOVE CO2 EXTRACORPORALLY.
TYPES
1) High-flow VENOARTERIAL bypass system.
2) Low-flow VENOVENOUS bypass system.
CRITERIA
Fast entry criteria
PaO2 <50 mmHg for >2 h at FiO2 1.0; PEEP > 5 cmH2O
A) Decrease production .
B) Abnormal composition .
C) Inhibitors of surfactant function .
D) Conversion of large to small surfactant aggregates
E) Alteration/Destruction caused by substances in alveolar
space (plasma, fibrinogen, fibrin, )
IMPAIRED SURFACTANT FN
1) ATELACTASIS / COLLAPSE
2) INCREASE EDEMA FORMATION
SURFACTANT REPLACEMENT.
Improved lungs function , compliance ,
oxygenation.
Surfactant of possible therapeutic use :
Class Origin Example
1. Natural Amniotic Human amniotic fluid
surfactant
2. Modified - Bovine Infasurf, alveofact
Natural BLESS, Survanta
- Procine Curosurf
3. Synthetic Exosurf, ALEC, KL4
Surfactant, Venticute
DOSE
Sufficient dose should reach alveolar environment
TIMING
• As early as possible [<48 hr]
• Little benefit at 3 to 5 days [Fibrosis already set]
ENHANCED RESOLUTION OF ALVEOLAR
EDEMA
Alveolar clearance of edema depends on active
SODIUM TRANSPORT across the alveolar
epithelium
b2 adrenergic stimulation :
1. Salmetrol
2. Dopamine
3. Dobutamine
ENHANCED REPAIR :
Mitogen for type-II pneumatocyte :
1. HEPATOCYTE GROWTH FACTOR
2. KERATINOCYTE GROWTH FACTOR.
COMPLICATIONS ( ACUTE )
ACUTE RESPIRATORY FAILURE