Friday, April 4, 2014

COPD

And so today finally I have passed one of my hated exams in my medical student life...

I would think everybody should know about COPD. Smoking is the strongest risk factor for COPD, and global pollution now makes our lungs sicker !!

COPD ( chronic obstructive pulmonary disorder ) actually refers to two conditions - bronchitis ( the blue bloater ) and emphysema ( the pink puffer ) - of course this is just textbook stuff, real life patient doesn't always present classically

Blue bloater - remember bronchitis causes mucus secretion and bronchial inflammation ( which causes it to be edematous and closing the airway ), causing V/Q mismatch and cyanosis ( blue ). And because there is obstruction, CO2 cannot go out ( bloater part )

Pink puffer - emphysema destroys your alveoli together with your capillaries, therefore no V/Q mismatch will happen although ventilation and perfusion both decrease ( pink ). As a result of decreased O2 delivery to capillaries of lung, patient will hyperventilate ( puffer part )

More important than these are:
1) Asthmatic patients can decompensate into COPD
2) COPD is not a local process, it's a systemic inflammatory state
3) Emphysema in young patients should make you consider alpha-1 antitrypsin deficiency - PiZZ homozygous form

Important things to note are:
1) GOLD classification of COPD 
- COPD is diagnosed when FEV1/FVC < 70% 
- Remember FEV1 is used to stage the disease
  • FEV1 > 80% - mild
  • FEV1 between 50-80% - moderate
  • FEV1 between 30-50% - severe
  • FEV1 < 30% or < 50% with resp.failure - very severe
2) Tx options differ according to different stages
  • For all stages, SABA is given prn
  • For moderate COPD, long acting bronchodilators ( LABA alone or with LAMA - adding together gives addictive effect as they act on different receptors ) are given together with pulmonary rehab
  • For severe COPD, inhaled corticosteroid is added
  • For very severe COPD, consider O2 therapy and surgical lung reduction
Indications for Long Term O2 Therapy ( LTOT ) are:
1) PaCO2 < 7.3 kPa ( for easy remember < 7 kPa ) / 55mmHg ( if you are reading US sources )
2) If PaCO2 is between 7.3-8 kPa ( 55-59 mmHg ), consider if patient having secondary polycythaemia ( Hct > 45% ) and cor pulmonale



3) What improves Mortality? Remember SOFA
  • Smoking cessation ( of course !!! - for me it's the MOST important non-medical treatment )
  • Oxygen therapy
  • Flu vaccination
  • Antibiotics during acute exacerbation
AECOPD ( acute exacerbation of COPD )
Risk factor for severe form AECOPD includes:
1) Previously severe exacerbation : Has previously been admitted to ICU due to severe AECOPD/ near fatal episode
2) use of steroids : patient just starts to use ( indicates at least stage 3 COPD )/ patient never uses it ( decompensation/worsening of COPD )/ patient stops it due to side effects ( COPD is irreversible so once you use it you cannot stop it )

Precipitant for AECOPD is commonly infections ( resp.infections esp )

What to do in AECOPD?
U can remember by this mnemonic AECOPD ( not in order of tx )
A - Antibiotics if suggestive
E - Extra help ( NPPV )
C - Corticosteroids ( oral/IV form has delayed onset of 6 hrs so inhaled form initially may help )
O - Oxygen
P - Pneumococcal and flu vaccination ( done afterwards )
D - Dilators ( SABA prn )

Generally, the order of tx will be 
1) Assess ABC - normally B will be the problem , O2 or NPPV
2) IV access and  VBG/ABG
3) Bronchodilators for better air entrance and symptomatic relief + oral/IV corticosteroids started ( inhaled corticosteroids can also be given )
4) CXR and sputum C & S after patient has stabilized, antibiotics if needed

There are a few criteria to start antibiotic therapy in AECOPD ( known as Anthonisen Classification )
1) Increased sputum purulence
2) Increased sputum volume
3) Worsening of dyspnea

If 3 are satisfied, abx should be started, if 2 are satisfied, abx recommended if purulence is included, abx is NOT recommended if there is only 1 satisfied

Basically, there are 3 groups of microorganisms causing AECOPD
1) Group A - the usual gram positive bacteria causing CAP and viral causes
  • Beta lactams are DOC
2) Group B - the above bacteria but with resistance + gram negative Enterobacteriaceae
  • Beta-lactams + beta-lactamase inhibitors are DOC
  • Macrolides and resp.fluoroquinolones as alternative
3) Group C - PSA 
  • Need 2 anti-pseudomonal antibiotics
RFs for severe course of AECOPD includes SEAP
1) Severe COPD
2) Exacerbation is frequent
3) Antibiotics in 3 months ( more risk of abx resistant m/o )
4) Presence of comorbids ( naturally, a CHF patient with AECOPD is more difficult to treat )

These are some of the studies which i think is important to know
- It proves that corticosteroids for 5 days in AECOPD is enough ( REDUCE trial )
- It somehow shows the efficacy of nebulized corticosteroids in AECOPD
- It proves the utility of systemic corticosteroids in AECOPD






Summary



References



Optimizing antibiotic selection in treating COPD exacerbations 
Attiya Siddigi and Sanjay Sethi
Int J Chron Obstruct Pulmon Dis. Mar 2008; 3(1): 31–44
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2528209/


COPD (Chronic Obstructive Pulmonary Disease): What people should Know about COPD http://www.daynightclinic.com/COPD.aspx


Short-term vs conventional glucocorticoid therapy in acute exacerbations of chronic obstructive pulmonary disease: the REDUCE randomized clinical trial.
Leuppi JD1, Schuetz P, Bingisser R, Bodmer M, Briel M, Drescher T, Duerring U, Henzen C, Leibbrandt Y, Maier S, Miedinger D, Müller B, Scherr A, Schindler C, Stoeckli R, Viatte S, von Garnier C, Tamm M, Rutishauser J.
JAMA. 2013 Jun 5;309(21):2223-31
http://www.ncbi.nlm.nih.gov/pubmed/23695200

Steroids in acute exacerbations of chronic obstructive pulmonary disease: are nebulized and systemic forms comparable?
Gunen H1, Mirici A, Meral M, Akgün M.
Curr Opin Pulm Med. 2009 Mar;15(2):133-7
http://www.ncbi.nlm.nih.gov/pubmed/19532028

Optimizing antibiotic selection in treating COPD exacerbations

Systemic corticosteroids in chronic obstructive pulmonary disease: an overview of Cochrane systematic reviews.
Wood-Baker R1, Walters J, Walters EH.
Respir Med. 2007 Mar;101(3):371-7. Epub 2006 Sep 7
http://www.ncbi.nlm.nih.gov/pubmed/16962307


8 comments:

  1. great work!!! is better to include also the indications of long oxygen therapy.. I have been quizzed abt that before

    ReplyDelete
  2. Thanks. Actually if u see below there is indication for long term O2 - chronic resp. failure ( i,e in very severe COPD not responding to even ICS )

    ReplyDelete
  3. Offer LTOT to patients with a pO2 of < 7.3 kPa or to those with a PO2 of 7.3 - 8 kPa and one of the
    following:
    -Secondary polycythaemia
    -Nocturnal hypoxaemia
    -Peripheral oedema
    ABG should be measured when clinically stable and on 2 occasions at least 3 weeks apart (pO2 should rise with treatment above 8 kPa without unacceptable hypercapnia)

    ReplyDelete
  4. Good read Ryan. What does LAMA stands for ? And there is a typo for the table under the summary section 'SABA prn'. Do you mind adding a short section for ddx between bronchial asthma and COPD ? For eg. using bronchodilator test. Thank you :)

    ReplyDelete
  5. Thanks Jun Ting, sorry for the typo
    Well COPD vs asthma, ok i will add it here
    - Asthma is reversible, and COPD is irreversible, so patient will have a baseline dyspnea
    - Asthma is seldom associated with smoking, but COPD is ( ask pts how long he smokes? how many packs )
    - Asthmatic patient will normally give u a hx of atopy, but COPD patient will not
    - Asthmatic patient normally has a positive family Hx of atopy/ asthma, but COPD is an acquired disorder
    - Coughing with sputum favours COPD than asthma
    - For Dx, as asthma is reversible, a metacholine challenge test / exercise tolerance test can be used
    - In metacholine challenge test, metacholine as cholinergic agonist dilates the airway resulting in > 12% improvement from baseline FEV1 ( for simplicity rmb > 10% improvement and u got the dx )

    LAMA stands for long acting muscarinic antagonist eg tiotropium

    ReplyDelete
  6. But remember asthmatic patient can deteriorate into COPD if not managed properly, as prolonged inflammation can eventually destructs ur small airways and lung tissues

    ReplyDelete