A R D S

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A R D S

• Jhansi Nalamati MD FCCP
• Asst. Prof. Of Medicine, AECOM
• BRONX NY

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Definition

• Acute Respiratory Distress Syndrome
• First described in 1967 in Lancet as Adult
  Respiratory Distress Syndrome by Asbaugh et.al.
• 12 pts. had developed acute respiratory distress,
  cyanosis , diffuse pulmonary infiltrates
  decreased lung compliance and was refractory to
  Oxygen therapy
• Also called as wet lung, shock lung and Da
  Nang lung

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Incidence

• Crude estimates of 78.9/100,000 person years
• In patient mortality 38.5
• 190,600 cases/year in the US with 74,500 deaths
  and 3.6 million hospital days

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ARDS and ALI (Acute Lung Injury) in 1992

• Defined by American European Consensus
• Acute Lung Injury is an umbrella term for
  Hypoxemia Respiratory Failure , a severe version
  of which is ARDS.
• Bilateral Infiltrates
• PCWPlt 18mm Hg
• PaO2/FiO2lt 300 ALI
• PaO2/FiO2lt200 ARDS

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ALI/ARDS ( Addl. Features)

• Bilateral widespread infiltrates on CXR
• Airway collapse ( low lung Volumes)
• Surfactant deficiency
• Reduced lung compliance

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Etiology

• Direct insult to the lungs- bacterial, viral,
  fungal agents, lung contusion, Fat embolism
• Systemic medical and surgical conditions- trauma,
  shock, sepsis, burns, pancreatitis
• Noxious agents- exposure to smoke , aspiration

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PATHOPHYSIOLOGY

• Altered Pulmonary Capillary Permeability
  secondary to endothelial injury
• Altered alveolar diffusion capacity
• Increased intrapulmonary shunt
• Degree of epithelial injury can predict outcome

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Patho-physiology(contd.)

• Loss of epithelial integrity and injury to type
  II alveolar cells can disrupt fluid transport
  thereby leading to impairing the removal of fluid
  from alveolar space
• Injury to type II pneumocytes can reduce the
  production of surfactant which leads to worsening
  atelectasis and gas exchange

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Histo-pathological phases

• 1) Exudative Phase 1-3 days- diffuse alveolar
  damage ( DAD) with majority of type I pneumocyte
  necrosis, diffuse microvascular injury and influx
  of inflammatory cells and proteinaceous fluid
  into the interstitium

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Fibroproliferative phase

• Day 3-7- repair manifested by type I pneumocyte
  hyperplasia and proliferation of fibroblasts

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Treatment of ARDS

• Corner stone of treatment is to keep PaO2 gt60mm
  Hg, without causing injury to lung with excessive
  O2 or excessive TV ( FiO2 lt 60 and TV of 6ml/kg)
• Plateau pressure should not exceed 30mmHg and
  minimal TV should be at least 4ml/kg (
  irrespective of MAP or plateau pressure)
• Avoid Volutrauma and Barotrauma

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ATS recommendations

• Minimize O2 toxicity
• Recruit alveoli
• Minimize high airway pressures
• Prevent atelectasis
• Use sedation and paralysis judiciously

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Tx of ARDS/ALI

• SUPPORTIVE CARE
• SUPPORTIVE CARE
• SUPPORTIVE CARE

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Low Tidal Volume Ventilation with or without High
PEEP

• Minimizes the amount of phasic stretch of lung
  units in inspiration to prevent VILI( Ventilator
  Induced Lung Injury)
• Proven to be effective in an NIH coordinated
  multi center trial( NEJM ), patients ventilated
  with TV of 6ml/kg had a 22 reduction in
  mortality compared to patients ventilated with TV
  of 10-12ml/kg

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Open Lung approach

• Attempts to optimize lung mechanics and minimize
  phasic damage by strategically placing PEEP above
  Pflex.
• Quasi- Static Volume Pressure curve- the lungs
  are said to be most compliant between the lower
  inflection point and the upper inflection point,
  beyond which over distension occurs

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PCV( Pressure Controlled ventilation)

• Better gas distribution than volume control
  ventilation by avoiding over distension of low
  complaint units
• Plateau pressure not to exceed 30mm of Hg
• Reverse IE Ratio

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APRV ( Airway pressure release ventilation)

• Sets pressure high and pressure low and time high
  and time low
• Patient can spontaneously breathe within these
  limits, minimizing sedation requirements
• Unclear what is the PEEP ( ? Pressure high, ?
  Pressure low, ? Mean)

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HFV ( High frequency ventilation)

• Reduces barotrauma and improves VQ mismatch
• Potential complications- inspication of mucus,
  airway damage due to high gas velocities and over
  distension causing alveolar injury and worsening
  ALI

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Tx ( contd.)

• Prone Positioning
• Permissive Hypercapnia ( potential complications
  include pulmonary vasoconstriction, pulmonary
  HTN, proarrhythmic effects, cerebral
  vasodilatation, increasing ICP)
• Prophylactic Bil. chest tubes

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Inhaled Nitric Oxide

• Improves oxygenation and decreases Pulmonary
  Vascular Resistance
• Dose varies from 1.25 to 40ppm
• NO clear benefit in limited randomized controlled
  trials
• Needs to be given for days to weeks
• Sensitization can occur
• Can cause renal dysfunction, immunosuppression,
  potentially mutagenic , can cause
  methhemoglobinemia and NO2 concentration

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Steroids in ARDS

• Controversial
• Cytokines decline over the first week in
  survivors of ARDS, but persist in non survivors

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Steroid regimen( Prednisone)

• 2mg/kg day 1-14
• 1mgkg day 15-21
• 0.5mg/kg day 22-28
• 0.25mg/kg day 29-30
• 0.125mg/kg day 31-32
• Not to be started before 7days of ALI or
  admission or beyond 28days of ALI or admission

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Novel therapies for ARDS

• Albuterol
• Salmetrol
• Surfactant
• Pentoxyfylline
• Cyclooxygenase inhibitors
• Antioxidants
• TNF antibodies infusion
• PAF inhibitors and receptor antagonists
• Antiproteases

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Cause of death

• Underlying cause
• Secondary complications- sepsis from ventilator
  associated pneumonia, GI bleed, multi organ
  failure

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Management of secondary effects

• Judicious use of sedation and neuromuscular
  blockade
• Hemodynamic management
• Nutritional support
• Glucose control
• Nosocomial pneumonia prevention and Tx
• GI and DVT prophylaxis

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Nosocomial Pneumonia

• 60 of pts with ARDS in 30days
• Can occur as early as 10days
• Prevention strategies include-continuous
  subglottic aspiration of secretions, selective GI
  tract decontamination ( does not prevent
  pseudomonas) elevation of head 30 degrees, mouth
  care, avoiding vent. Circuit changes or clearing
  the condensate

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Nosocomial pneumonia (contd.)

• Closed suction is of no benefit
• Avoid unnecessary antibiotics
• No use of antibiotic or silver impregnated ETT
  tubes