ARDS septicaemia by mikeholy

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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
DIAGNOSTIC CRITERIA
ARDS                            ALI
  Acute                               Acute
  PaO2/Fio2<200                       <300 mm Hg
  mmHg
  Bilateral interstitial              Same
or alveolar infiltrates
  Pcwp <15-18                         same
  mmHg

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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          Indirect lung injury
 Aspiration of gastric      Severe sepsis
  contents                   Major trauma
 Pulmonary contusion        Hypertransfusion

 Toxic gas inhalation       Acute pancreatitis
                             Drug overdose
 Near drowning
                             Reperfusion injury
 Diffuse pulmonary
                             Post cardiac
  infection
                              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 willebrand’s 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
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 >= 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 <= 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 < 8k Pa
  on FiO2 >= 0.6)
 Rising or elevated PaCO2(>= 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:



30/07/2000          DR.T.M.K- ARDS            Contd.. 16
   Start with FiO2 = 1.0, tidal volume 6 to 10 ml
    per Kg, PEEP <= 5 cm H2O and inspiratory
    flow rates ~ 60 L / min. Subsequent
    adjustments are done to try to achieve
    arterial oxygen sats. of > 90% with FiO2 <
    0.6 and peak airway pressures < 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 (I:E
   ratio) of between 1:1 and 4:1 may be tried.

                                             Contd..
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   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 < 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
   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




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                                                             22
   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
   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
   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 (> 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             GI   bleed(Stress Ulcer)
     (Haemothorax)
     Aspiration(Eg NG             Septicaemia
     feed)
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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

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