ARDS

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ARDS

• DR. T. MOHAN KUMAR, MD, AB, DPPR, FCCP
• CHIEF SENIOR CONSULTANT,
• DEPARTMENT OF PULMONOLOGY CRITICAL CARE,
• SRI RAMAKRISHNA HOSPITAL,
• COIMBATORE

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DIAGNOSTIC CRITERIA

• ARDS
• Acute
• PaO2/Fio2lt200 mmHg
• Bilateral interstitial
• or alveolar infiltrates
• Pcwp lt15-18 mmHg

• ALI
• Acute
• lt300 mm Hg
• Same
• same

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Clinical diagnosis

• Rapid
• Within 12 to 48 hr of the predisposing event
• Awake patients become anxious,agitated
• dyspnoeic
• Dyspnoea on exertion proceeding to severe when
  hypoxemia intervenes
• Stiffening of lung leads to increase work of
  breathing,small tidal volumes,rapid respiratory
  rate
• Initially respiratory alkalosis
• Respiratory failure

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Clinical disorders associated with ARDS

• Direct lung injury
• Aspiration of gastric contents
• Pulmonary contusion
• Toxic gas inhalation
• Near drowning
• Diffuse pulmonary infection

• Indirect lung injury
• Severe sepsis
• Major trauma
• Hypertransfusion
• Acute pancreatitis
• Drug overdose
• Reperfusion injury
• Post cardiac bypass/lung transplants

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Clinical disorders associated with ARDS

• FREQUENT CAUSES
• SEPSIS
• BACTEREMIA WITHOUT SEPSIS SYNDROME
  4
• SEVERE SEPSIS/SEPSIS SYNDROME
  35-45
• MAJOR TRAUMA
• MULTIPLE BONE FRACTURES
  5-10
• PULMONARY CONTUSION
  17-22
• HYPERTRANSFUSION
  5-36
• ASPIRATION OF GASTRIC CONTENTS
  22-36

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CLINICAL MANIFESTATIONS

• ARDS occurs in the setting of acute severe
  illness
• Clinical manifestations may vary
• Sepsis and trauma most important
• Multiple organ failure
• Atelectasis and fluid filled lungs
• Hypoxemia/dyspnoea
• Fever /leukocytosis

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Laboratory studies

• To date no lab findings pathognomonic of ARDS
• X-ray chest shows bilateral infiltrates
  consistent with pulmonary edema, may be mild or
  dense, interstitial or alveolar, patchy or
  confluent
• ABG shows hypoxemia with respiratory alkalosis.
  In late stages hypoxemia, acidosis, hypercarbia
  may be seen.

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• Leukocytosis/Leukopenia/anemia are common
• Renal function abnormalities/or liver function
• Von willebrands factor or complement in serum
  may be high
• Acute phase reactants like ceruloplasmin or
  cytokine (TNF,IL-1,IL-6,IL-8) may be high.

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BRONCHOALVEOLAR LAVAGE

• Inflammatory mediators like cytokines, reactive
  oxygen species, leukotrienes activated
  complement fragments are found in the fluid
• Cellular analysis shows more than 60 of
  neutrophils.
• As ARDS resolves neutrophils are replaced with
  alveolar macrophages.
• Another interesting finding is the presence of a
  marker of pulmonary fibrosis called procollagen
  peptide III (PCPIII) and this correlates with
  mortality.
• Presence of more eosinophils suggest eosinophilic
  pneumonia, high lymphocyte counts may be seen in
  hypersensitivity pneumonitis, sarcoidosis, BOOP,
  or other acute forms of interstitial lung disease.

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Differential diagnosis

• Infectious causes
• Bacteria - Gm neg pos , mycobacteriae,
  mycoplasma, rickettsia, chlamydia
• Viruses- CMV, RSV, hanta virus, adeno virus,
  influenza virus
• Fungi- H.capsulatum, C.immitis
• parasites- pneumocytis carinii, toxoplasma gondii

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Differential Diagnosis

• Non infectious causes
• CCF
• Drugs toxins (paraquat, aspirin, heroin,
  narcotics, toxic gas, tricyclic anti depressants,
  acute radiation pneumonitis)
• Idiopathic (esinophilic pneumonia, Acute
  interstitial pneumonitis, BOOP, sarcoidosis,
  rapidly involving idiopathic pulmonary fibrosis)
• Immunologic (acute lupus pneumonitis, Good
  Pastures syndrome, hypersensitivity pneumonitis)
• Metabolic (alveolar proteinosis)
• Miscellaneous (fat embolism, neuro/high altitude
  pulmonary oedema)
• Neoplastic (leukemic infiltration, lymphoma)

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Therapy -goals

• Treatment of the underlying precipitating event
• Cardio-respiratory support
• Specific therapies targeted at the lung injury
• Supportive therapies

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Respiratory Support
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Spontaneously Breathing Patient

• In the early stages of ARDS the hypoxia may be
  corrected by 40 to 60 inspired oxygen with CPAP
• Peak inspiratory flow rates of gt 70ltrs / min
  require a tight-fitting face mask with a large
  reservoir bag or a high flow generator
• If the patient is well oxygenated on lt 60
  inspired oxygen and apparently stable without CO2
  retention and apparently stable, then ward
  monitoring may be feasible but close observation(
  15 to 30 Min), continuous oximetry, and regular
  blood gases are required

Contd..
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Indications for mechanical ventilation

• Inadequate Oxygenation(PaO2 lt 8k Pa on FiO2 gt
  0.6)
• Rising or elevated PaCO2(gt 6k Pa)
• Clinical signs of incipient respiratory failure

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Mechanical Ventilation
The Aims are to increase PaO2 while minimizing
the risk of further lung injury (Oxygen toxicity,
Barotrauma). This is the realm of the IRCU
Physician seek specialist advice early to
prevent complications. The general principles are
the following
Contd..
17

• Start with FiO2 1.0, tidal volume 6 to 10 ml
  per Kg, PEEP lt 5 cm H2O and inspiratory flow
  rates 60 L / min. Subsequent adjustments are
  done to try to achieve arterial oxygen sats. of gt
  90 with FiO2 lt 0.6 and peak airway pressures lt
  40 to 45 cm H20
• Controlled Mandatory Ventilation (CMV) with
  sedation and neuromuscular blockade (to try to
  suppress the respiratory drive and reduce
  respiratory muscle oxygen requirement.)

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• PEEP improves PaO2 in most patients and allows
  reduction of FiO2. Increase by 2 to 5 cm H2O
  increments every 20 min watching for hemodynamic
  deterioration (due to impaired venous return and
  decreased cardiac out put). Optimal PEEP is
  usually 10 to 15 cm H2O
• Inverse Ratio Ventilation may decrease peek
  inflation pressures and thus Barotrauma.
  Inspiratory time Expiratory time ratio (IE
  ratio) of between 11 and 41 may be tried.

Contd..
19

• The ventilatory rate required to clear CO2 and
  normalize pH is commonly high (20 to 25 breaths /
  min). However this may result in unacceptable
  airway pressures.
• Another strategy is permissive hypercapnoea
  which as the name suggests is controlled
  hypoventilation. PaCO2 up to 13 kPa is generally
  well tolerated acidosis (pH lt 7.25) may be
  treated with intravenous bicarbonate

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• Changing the patients position (lateral decubitus
  or prone instead of supine) can improve
  oxygenation by improving perfusion of aerated
  portion of lung. Consider this in patients with
  non uniform or predominantly posterior and lower
  lobe infiltrates
• Inhaled nitric oxide (18 ppm) reduces pulmonary
  artery pressures, intra pulmonary shunting and
  improves oxygenation while not affecting mean
  arterial pressure or cardiac output. However
  studies showing an effect on mortality are
  awaited.
• Newer methods such as high frequency jet
  ventilation, extra corporeal gas exchange (CO2
  removal - Oxygenation) and intravascular
  oxygenation devices (IVOX) may be of use but are
  currently not widely available.

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Cardiovascular Support
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• Invasive monitoring is mandatory(Arterial line,
  PA catheter (Swan-Ganz) to measure cardiac
  outputs and if available, continuous mixed venous
  oxygen saturation)
• In order to minimize pulmonary oedema, aim to
  keep PCWP low (8 to 10 mm Hg) and support the
  circulation with inotropes if necessary
• The role of colloids and albumin is relatively
  minor the increased capillary permeability
  allows these molecules to equilibrate with the
  alveolar fluid with little increase in net plasma
  oncotic pressure

Contd..
23

• Renal failure is common and may require
  haemofiltration to achieve a negative fluid
  balance and normalize blood chemistry.
• Oxygen consumption (VO2) in patients with ARDS
  appears to be delivery dependent. The current
  trend is to aim for target levels of oxygen
  delivery (DO2 Cardiac Index(HbXSao2X1.34)X10)
  as guided by tissue perfusion (clinically and
  serum lactate, pHi from a gastric tonometer). DO2
  may be increased by blood transfusion, inotropes
  and vasodilators including prostacyclin).

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• Selection of appropriate inotropes and
  vasodilators can only be made by repeated
  measurements of haemodynamic parameters and
  calculating DO2 and VO2 while evaluating the
  effects of the various agents
• Nutritional support must be chosen to try to
  avoid fluid overload. Lipid metabolism produces
  marginally less CO2 than dextrose metabolism and
  thus favourably affects the respiratory quotient
  but there is controversy as to whether lipid can
  exacerbate lung injury

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Treatment of Sepsis
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• Fever, Neutrophil leukocytosis and raised
  inflammatory markers (CRP) are common in
  patients with ARDS and do not always imply
  sepsis. However sepsis is common precipitant of
  ARDS
• A trial of empirical antibiotics guided by
  possible pathogens should be given early. Eg
  Cefotaxime. This may be modified in light of the
  results of appropriate cultures. Avoid
  nephrotoxic antibiotics.
• Enteral feeding seems to carry a lower risk of
  sepsis than parenteral feeding and helps maintain
  the integrity of the gut mucosa. Ileus is common
  in multi-organ failure, so entral feeding may not
  be possible.

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Minimizing lung injury and treating the cause
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• Look for a precipitant
• In general prevention (example of aspiration of
  gastric acid) is more effective than trying to
  treat ARDS. However there are no effective
  measures for prophylaxis in patients at risk ( Eg
  from Trauma)
• Steroids there is no benefit from treatment
  early in the disease. Treatment later (gt 7
  to 14 days from onset) especially in patients
  with peripheral blood eosinophilia or eosinophils
  in bronchoalveolar lavage, improves prognosis

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• Give 2 to 4 mg / Kg prednisolone or equivalent
  the duration depends on the clinical response( 1
  to 3 weeks)
• Other therapies such as inhaled nitric oxide ,
  exogenous surfactant, antioxidants
  (acetylcysteine), ketoconazole, NSAIDs,
  Pentoxifylline and anticytokine antibodies are
  still under investigation

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Causes of Sudden deterioration in ARDS
Respiratory Cardiovascular
Pneumothorax Arrhythmia
Bronchial plugging Cardiac tamponade
Displaced ET tube Myocardial infarction
Pleural effusion (Haemothorax) GI bleed(Stress Ulcer)
Aspiration(Eg NG feed) Septicaemia
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Completed trials

• Reducing lung stretching
• Lisophyllin
• Corticosteroids in late ARDS
• ALVEOLI study

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Completed trials -II

• Fluids and catheters treatment trial (FACTT)
• Low tidal volume versus high tidal volume
  ventilation
• Ketoconazole
• Role of MODS

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WHAT IS NEW?

• ALI Gene transfer
• New approaches to enhancing lung edema clearance
• Nitric oxide donors
• New treatment for altered pulmonary vascular
  permeability
• Inflammatory cytokine networks in ARDS

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What is new

• Use of surfactant therapy
• Liquid ventilation in ALI
• CPAP trial