Transcript Slide 1

ALOK SINHA
Department of Medicine
Manipal College of Medical Sciences
Pokhara, Nepal
Capillary endothelium
alveolar
epithelium
• Serious disease characterised by damage to
alveolar epithelium & capillary endothelium
resulting in alveolar oedema with high protein
fluid
• It results from increased alveolar capillary
permeability
• NOT CARDIOGENIC IN ORIGIN
severe end of a spectrum of acute lung
injury due to many different insults.
Essentially it is diffuse alveolar injury
Acute, persistent, lung inflammation
Increased vascular permeability
Bilateral and extensive infiltrates (seen in the CXR)
Very poor oxygenation despite PEEP
Not due to clinical left ventricular failure –
associated with a wedge pressure of over
18 mmHg (non-cardiogenic)
Most commonly seen on the ICU where
about 10% of such patients will have
ARDS
PCWP
Normal: 8-12mmHg
International criteria
1. Acute onset of symptoms
2. PaO2 : FIO2 (fraction of inspired oxygen) – 200
mm Hg or less
For Example normal PaO2 = 100, FiO2 = 20% or 1/5 so the above ratio =
100/1/5 = 500 mm Hg
3. Bilateral infiltrates on CXRs
4. Pulmonary arterial wedge pressure of 18
mm Hg or less (or no clinical signs of left atrial
hypertension)
Increased alveolar-arterial (A-a) gradient
A
a
What is this situation ?
1. Acute onset of symptoms
2. PaO2 : FIO2: between 300 to 200 mm Hg
3. Bilateral infiltrates on CXRs
4. Pulmonary arterial wedge pressure of 18
mm Hg or less or no clinical signs of left
atrial hypertension
• Acute lung injury (ALI)
Mild
ALI
ARDS
Pathogenesis of ARDS
Inflammatory damage to the alveoli
– by locally produced pro-inflammatory mediators
– remotely produced and arriving via
pulmonary artery
Through inhalation (eg gastric contents)
 Increased pulmonary capillary permeability fluid and protein leakage into the alveolar
spaces with pulmonary infiltrates
 Alveolar surfactant is diluted with loss of its
stabilizing effect, resulting in diffuse alveolar
collapse and stiff lungs. This leads to:
1. Gross impairment of V/Q matching with shunting
causing arterial hypoxia
– usually enough remaining functioning alveoli to
maintain CO2 clearance- Normal CO2
– Pulmonary hypertension will develop secondary to
the hypoxia (helpful – counters V/Q matching)
2.Reduced compliance (stiff lungs), due to loss of
functioning alveoli
alveolar collapse, filled with fluid and protein
 hyperinflation of remaining alveoli to their limits of
distension
3. Decrease transfer of gases in alveoli

Causes of mediator release leading to ARDS
Sepsis/pneumonia
Gastric aspiration
Major trauma
Smoke/ gas inhalation
Acute pancreatitis
Drug toxicity - tricyclic antidepressants, opiates, cocaine, aspirin
Fat emboli
Direct effects of large amounts of necrotic tissue
(secondary risk factors)
alcoholism
cigarette smoking
Less common causes
Near drowning
Following upper airway obstruction: mechanism unclear
Acute form of Interstitial Pneumonia: Also known as acute
Hamman-Rich syndrome
Post-bone marrow transplant as bone marrow
recovers
Amniotic embolism
Massive haemorrhage
Multiple transfusions
DIC
Massive burns
Head injury
– Raised ICP
– Intracranial bleed
Cardio-pulmonary
bypass
Acute liver failure
Course of ARDS
Phase 1 - early period of alveolar damage and
hypoxaemia with pulmonary infiltration
Phase 2 -develops after a week as pulmonary
infiltrates resolve
– associated with an increase in
type II pneumocytes (surfactant producers)
Myofibroblasts
collagen formation
Phase 3 -if the patient survives, is the
fibrotic stage that leaves the lung with
– Cysts
– deranged micro-architecture
– fibrosis on histology
leading to Cor Pulmonale
ARDS should be considered in any patient with
a predisposing risk factor
develops severe hypoxaemia
stiff lungs
widespread diffuse pulmonary infiltrate
Approximately 1 to 2 days following the clinical
presentation of the precipitating cause
 Rapidly worsening dyspnoea
 Dry cough
 Hypoxaemia
 Coarse crackles in the chest
DIFFERENTIALS
Aspiration Pneumonia
Congestive Heart Failure
Pneumonia Atypical Bacterial Pneumonia
Pneumocystis Carinii
Pneumonia Viral
To exclude other more specifically treatable
conditions
Left ventricular failure excluded
– on clinical grounds
– by echocardiography
– wedge pressure measurement <18 mmHg.
Diffuse alveolar haemorrhage can occur in
Goodpasture's, Leptospirosis
Oher clinical features of these disorders will be present
Some pulmonary infections
– Mycobacteria
– Legionella
– PCP
– viral pneumonia
may mimic ARDS & lavage fluid may reveal these
Occasionally cancer and lymphangitis
carcinomatosa can also mimic ARDS
– will show on a lung biopsy
CXR
ABG (consider arterial line as regular samples
may be required)
CBC,LFTs, coagulation profile, and CRP
Septic screen (culture blood, urine, sputum)
ECG
Consider drug screen
Amylase if history suggestive
Pulmonary artery catheter to measure
– PCWP
– cardiac output
– mixed venous oxygen saturation
– calculation of haemodynamic parameters
Other investigations if appropriate
– CT chest
– Broncho alveolar lavage for microbiology &
cell count (?eosinophils)
Treat the precipitating cause
Provide best supportive care with adequate
oxygenation
I.V. fluids –
– to be used judiciously
– Can increase pulmonary oedema
Inotrope and/or vasopressor support is
commonly required and the choice of agent is
– dobutamine
– dopamine
– epinephrine, norepinepherine
Patients invariably require higher oxygen
concentrations (non-rebreather masks with
reservoir FiO2 ~60- 80%) or CPAP
Consider transfer to HDU/ICU
Different oxygen delivery systems
Nasal canula
Non re breather masks
Indications for mechanical ventilation
– Inadequate oxygenation (PaO2 <60mm
(8kPa) on FiO2 >0.6 or 60%)
– Rising or elevated PaCO2 (> 45 mm or 6kPa)
– Clinical signs of incipient
respiratory/cardiovascular failure
Mechanical ventilation with PEEP -almost
always required to maintain oxygenation, with
high inflation pressures
Is this the meaning of
PEEP ?
PEEP: required to counter atelectasis
High inflation pressures may worsen
ARDS directly (micro-barotrauma)
– try to maintain plateau pressures <30 mmHg
Special ventilation techniques have
been tried to reduce the high inflation
pressures resulting from the stiff lungs (low
compliance)
 Using low tidal volumes to reduce inflation
pressures (6 ml/kg ideal body weight compared
to 12 ml/kg) reduces mortality by 10%
 This results in
Reduced minute ventilation
Rise in PaCO2 – permissive hypercapnia
• Inverse ratio ventilation
• may improve oxygenation, but pCO2 may
rise further
• Prone positioning
• improves oxygenation in ~70% of patients
with ARDS
• Inhaled pulmonary vasodilators (nitric oxide,
nebulized prostacyclin):
• may improve oxygenation
Extracorporeal oxygenation/CO2 removal will
buy time and allow the lung to recover, but
these techniques are very expensive and it is
difficult to demonstrate any long-term benefit
High-dose steroids –
– some evidence of overall improved survival
– later use possibly beneficial if nosocomial
infection rates are not increased
Cardiovascular support
Most patients haemodynamically compromised
due to
– underlying condition
– ventilatory management
Benefit from fluid resuscitation. This may risk
worsening capillary leak in the lung and
compromise oxygenation/ventilation. Aim for a
low-normal intravascular volume whilst
maintaining cardiac index and mean arterial
pressure
Management of other associated conditions
• Renal failure
• Enteral feeding
• Coagulopathy -severe/DIC may be present expert
advice should be sought
• Sepsis
empiric antibiotics guided by possible pathogens, and
following an appropriate sensitivity tests Antibiotics
should be modified or discontinued in light of
microbiological results
High ventilation pressures lead to barotrauma:
– pneumothorax
– surgical emphysema
– pneumomediastinum
– Nosocomial infections
Non-specific problems of
– venous thromboembolism
– GI haemorrhage
– inadequate nutrition
Prognosis
has improved over the last 20 years due to
improvements in supportive care of
– Early deaths due to the precipitating condition
– later deaths to complications
Over half the patients will survive with varying
residual lung damage, pulmonary function tests
often show only minor restrictive abnormalities
Future developments
The optimal level of PEEP is difficult to
predict.
– Inadequate PEEP allows more atelectasis
– too high PEEP contributes to overdistension of
remaining alveoli and further barotrauma
Ways to estimate the best PEEP are under
investigation
Liquid ventilation with perfluorocarbons has
been tried
Nitric oxide (NO) has been tried with clear
improvements in oxygenation but very little
effect on survival
Inhaled prostacyclin: is unconvincing
bilateral patchy opacities in mostly the middle and lower lung zones
Normal size heart
No pleural effusion
.
It appears he is ticking ‘n’
alive