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Corticosteroids in ARDS

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A syndrome of acute and persistent lung inflammation with increased ... obliteration of normal lung architecture, diffuse fibrosis, cyst formation. Treatment ... – PowerPoint PPT presentation

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Title: Corticosteroids in ARDS


1
Corticosteroids in ARDS
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2
Acute lung injury(ALI)
  • Definition
  • A syndrome of acute and persistent lung
    inflammation with increased vascular permeability
  • Clinical features
  • 1. Bilateral radiographic infiltrates
  • 2. PaO2/FiO2 201-300mmHg
  • 3. No clinical evidence for an elevated left
    atrial pressure (pulmonary capillary wedge
    pressure ? 18 mmHg)

3
Acute Respiratory Distress Syndrome
  • Definition
  • Same as ALI except worse hypoxia
  • Acute in onset
  • Clinical features
  • 1. Bilateral radiographic infiltrates
  • 2. PaO2/FiO2 less than 200
  • 3. No clinical evidence for an elevated left
    atrial pressure (pulmonary capillary wedge
    pressure ? 18 mmHg)

4
Epidemiology
  • ALI
  • Age-adjusted incidence 86 per 100,000
  • In-hospital mortality 39
  • ARDS
  • Age-adjusted incidence 64 per 100,000
  • In-hospital mortality 41
  • Overall mortality 25-58

5
Causes predisposing conditions
6
Pathophysiology - Baseline
  • 3 mechanisms keep
  • normal lung from
  • alveolar edema
  • 1. Intravascular protein
  • 2. Interstitial lymphatics
  • 3. Tight junctions between
  • alveolar epithelial cells

7
Pathophysiology - Injury
  • Pro-inflammatory cytokines(ex.TNF, IL-1, IL-6,
    IL-8)
  • Neutrophils recruited, activated, release toxic
    mediators
  • Damage capillary endothelium and alveolar
    epithelium
  • Normal barriers lost

8
Pathophysiology - Consequence
  • Impair gas exchange
  • increase physiologic dead space
  • Decrease lung compliance
  • due to stiffness of poorly or nonaerated lung
  • Pulmonary hypertension
  • occur in up to 25 ARDS patients
  • acute cor pulmonale is rare

9
Pathologic stages
  • Exudative stage diffuse alveolar damage
  • Proliferative stage
  • resolution of pulmonary edema and
    proliferation of type II alveolar cells, squamous
    metaplasia, myofibroblasts infiltration, early
    collagen deposition
  • Fibrotic stage
  • obliteration of normal lung architecture,
    diffuse fibrosis, cyst formation

10
Treatment
  • Supportive care
  • sedatives and neuromuscular blockade
  • hemodynamic management
  • nutritional support
  • control of blood glucose
  • treatment of nosocomial pneumonia
  • ventilator
  • prophylaxis against deep venous thrombosis and
    gastrointestinal bleeding
  • Novel therapy
  • beta agonist
  • surfactant
  • inhaled vasodilator
  • ECMO
  • anti-inflammatory
  • anti-oxidant

11
ARDS
  • Ongoing inflammation, parenchymal-cell
    proliferation, disordered deposition of collagen
  • May be responsive to corticosteroid?

12
Related Studies
  • 4 trials of high-dose, short-course for early
    ARDS failed to show survival improvement
  • Small case series suggest benefit of
    moderate-dose in persistent ARDS
  • A 24-patients trial moderate-dose improve lung
    function and survival for ARDS 7 or more days

13
Related studies
  • High-dose increase the risk of secondary
    infections?
  • Hyperglycemia, poor wound healing, psychosis,
    pancreatitis, prolonged muscle weakness, impaired
    function status

14
NHLBI ARDS Clinical Trials Network
  • 180 patients from 1997 to 2003
  • 7 to 28 days after onset of ARDS
  • PaO2FIO2 less than 200
  • Protocol of methylprednisolone given
  • 1. Single dose of 2mg/kg predicted BW
  • 2. 0.5mg/kg Q6H for 14 days
  • 3. 0.5mg/kg Q12H for 7 days
  • 4. Tapering

15
Results
  • No difference in 60-day or 180-day hospital
    mortality rate, in days in ICU or hospitalization
  • Steroid group had more ventilator-free days, more
    improvement in PaO2FiO2, improved compliance,
    higher serum glucose level, lower suspected or
    probable pneumonia

16
Discussion
  • Routinely use of steroids in ARDS patient is NOT
    supported
  • Increased mortality rate if Initiation 2 or more
    weeks after onset of ARDS
  • Improve cardiopulmonary physiology, increase
    ventilator-free days, ICU-free days, and
    shock-free days
  • Not increase infection, but may increase risk of
    neuromyopathy

17
Apply in our patient
18
4B1 06-1 ?X?
  • 86-year-old man
  • 1. RUL adenocarcinoma, status post VATS RUL
    lobectomy and LN dissection
  • 2. Pneumonia with septic shock
  • 3. hematuria
  • 4. BPH s/p TURP

19
SICU course
  • Increase infiltration of bil. lung
  • Fail to wean
  • 3/6 sputum culture
  • 1. Pseudomonas aeruginosa 3
  • 2. Neisseria species 3
  • 3. Viridans streptococci 3
  • 3/14
  • 1. O2 desaturation, unstable hemodynamic status
  • 2. FiO2 100, SaO2 lower than 80. On VA ECMO

20
ARDS
  • 3/4 PaO2/FiO2 94.7/40 236.75
  • 3/5 PaO2/FiO2 75.3/40 188.25

21
Steroid, timing and dosage
  • Body weight 74kg
  • 3/14 Solu-Cortef 50mg stat
  • 3/15 Solu-Medro 40mg Q8H
  • 3/23 Solu-Medro 40mg Q12H
  • Protocol of methylprednisolone given
  • 1. Single dose of 2mg/kg predicted BW
  • 2. 0.5mg/kg Q6H for 14 days
  • 3. 0.5mg/kg Q12H for 7 days
  • 4. Tapering

22
The Final Chapter
  • 3/29
  • Hypoglycemia
  • Asystole, recover after bosmin injection
  • 3/30
  • Asystole again
  • Family decided to hold ECMO support.
  • Passed away at 1057am
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