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Pulmonary (Restrictive Lung disease (Hamman-Rich syndrome/Acute…

- - - - DDx for clubbing and crepitations: Pulmonary Fibrosis, Bronchiectasis(productive cough, coarse pan-inspiratory +=expiratory crepittaions), lung abscess, mitotic lung conditions
      - Other DDx of ILD: Pulmonary Edema (CCF:No clubbing, evidence of fluid overload, crepitations clear with coughing)
    - - Pharmacological
        
        Trial of steroids( monitor with symptoms, CXR , Lung function test such as spirometry) --> If works, continue steroids, if not use cyclophosphamide or azathioprine
        
        Triple therapy for most secondary ILDs (not for Idiopathic pulmonary fibrosis): Steroids + azathioprine + N-acetylcysteine
        
        Antifibrotic agents: Eg penicillamine which has not been proven to be useful
      - Surgical: Lung transplantation
      - Vaccinations and regular follow up
        
        Influenza, Pneumococcal vaccine
      - Lifestyle changes --> Education and counselling to stop smoking
      - Manage complications
        
        Cause of death usually due to
        
        Lung cancer (increased risk)
        
        Type 2 respiratory failure --> Oxygen therapy
        
        Corpulmonale -diuresis for heart failure
        
        Pneumonia
        
        Polycythemia - venesection if Hematocrit >55%
        
        Possibly due to chronic hypoxemia leading to the release of erythropoietin that leads to polycythemia
      - Good Prognostic factors: Young age, Female, Short duration, Ground glass appearance on the CXR, minimal fibrosis on lung biopsy
      - Gradual clinical course of patients with IPF --> Gradual onset, progressive, median survival from timeof diagnosis is about 3 years
      - Supportive therapy such as O2 supplemtation for patients with significant hyoixemia (Po2 <55mgHg at rest and/or with exercise) and pulmonary rehab
      - Treat underlying cause
        
        Glucocorticosteroids can be highly effective for eosinophilic pneumonias, Cryptogenic organising pneumonia(COP), hypersensitivity pneumonitis (HP), acute radiation pneumonitis and drug induced ILD
        
        But not so effective for IPF
        
        Prednisolone at 0.5-1.0mg/kg per day is commonly given for 4-12 weeks followed by a gradual tapered dose.
  - - - Differ from ARDS as it does not have a cause
    - - Imaging: CXR showing ARDS (fluid in the small air sacs (alveoli) in both lungs). .
        
        Others:Lung biopsy shows organizing diffuse alveolar damage. FBC, blood cultures, and bronchoalveolar lavage.
- - - - ABC—O2 to keep sat >90%, or 88–92% if CO2 retainer,
        IV
      - STEROIDS—prednisone 40–60 mg PO daily 14
        days (tapering dose not necessary in all cases) or
        methylprednisolone 60–125 mg IV daily
        (inpatient)
      - ANTIBIOTICS—give if any two of the following
        criteria are met: " sputum purulence, " dyspnea or
        " sputum volume.
      - BRONCHODILATORS—salbutamol 2.5–5 mg NEB
        q4h ATC + q1h PRN and ipratropium 0.25–0.5 mg
        NEB q4h. Puffers preferable for acute management if
        proper technique used
      - Other considerations include the
        need for non-invasive mechanical ventilation and
        ‘‘at risk’’ for poor outcome (substantial comorbidities,
        severe COPD, frequent exacerbations
        3/year, recent antibiotics within 3 months);
        choices depend on clinical circumstance (levofloxawcin
        500 mg PO daily 7 days, doxycycline 100 mg
        PO BID 7–10 days, amoxicillin 500 mg PO BID 7
        days, cefuroxime 250–500 mg PO BID 10 days, or
        azithromycin 500 mg PO 1 day then 250 mg PO
        daily 4 days)
        MECHANICAL VENTILATION—BIPAP, intubation
        OTHERS—DVT prophylaxis (heparin 5000 U SC BID),
        physiotherapy
    - - Smoking cessation, reducing number of cigarettes have little impact on the course and progression of COPD
      - Bronchodilator
        
        Bronchodilator therapy is central to the management
        of breathlessness. The inhaled route is preferred and
        a number of different agents delivered by a variety of
        devices are available. Choice should be informed by
        patient preference and inhaler assessment. Short-acting
        bronchodilators, such as the β2
        -agonists salbutamol and
        terbutaline, or the anticholinergic, ipratropium bromide,may be used for patients with mild disease. Longer-acting
        bronchodilators, such as the β2
        -agonists salmeterol
        and formoterol, or the anticholinergic tiotropium
        bromide, are more appropriate for patients with moderate
        to severe disease. Significant improvements in
        breathlessness may be reported despite minimal changes
        in FEV
        1
        , probably reflecting improvements in lung emptying
        that reduce dynamic hyperinflation and ease the
        work of breathing.
        Oral bronchodilator therapy may be contemplated
        in patients who cannot use inhaled devices efficiently.
        Theophylline preparations improve breathlessness and
        quality of life, but their use has been limited by sideeffects,
        unpredictable metabolism and drug interactions.
        Bambuterol, a pro-drug of terbutaline, is used on occasion.
        Orally active highly selective phosphodiesterase
        inhibitors are currently under development