April 29th COPD exacerbation, If you don't know, now you know

Our super star resident haifa talked about management of COPD exacerbation.

Please refer to previous article on approach to shortness of breath.

Firstly, on medicine you may have realized we don’t see many patients presenting with a new diagnosis of COPD. Often there is a previous diagnosis. It's crucial toconsider how that diagnosis was made.

Similarly when he hear “heart failure” we wonder about a recent echo, history of MI, leg edema, previous exacerbations, have they seen a cardiologist before, etc. So should the same be with COPD.

Also to consider ruling out other things that may change management such as… is this really asthma they’ve had a child or new adult onset asthma which may make us suspicious for vasculitis, bronchiectasis?

Diagnosis of COPD:

1.    symptoms compatible with it: SOB at rest, or exertion, cough +/- sputum, limitation of activity.

2.    Gold standard test to diagnose copd would be pulmonary function tests looking for an FEV1/FVC ratio <0.7 plus FEV1 <80% predicted with an incomplete response to short acting beta agonist (remember asthma involves >12% and 200mL improvement in FEV1 with bronchodilator)

3.    Absence of alternative explanation

A chest x ray is gernally part of standard of care

What about alpha one anti-trypsin?

- Consider in patients <45 years of age with COPD

- Predominance in the basilar areas of the lungs (as opposed to typical copd which is more in apices)

- minimal smoking history or no smoking history

- family history of early onset COPD or a family history of alpha one anti-trypsin deficiency.

To clarify, probably he most important thing we can do is counselling on smoking session (for asthma and copd). But in regards to pharmacologic treatment, considering an anticholinergic would be first line after ventolin for COPD, as oppose to inhaled steroids for asthma (this is commonly tested on exams).

So when someone with known COPD comes in with worsening shortness of breath, we consider this being an acute exacerbation. We’d expect worsening shortness of breath, wheeze, and productive cough. We would also want to know about infectious symptoms (fevers, chills, decrease po intake, N/V/D), medication adherence, lifestyle/environment (dust pollutants, cold air), CHF/pulm edema, ACS, pneumothorax, and post op related.

*note - ~25% of patients with COPD also have underlying CHF, have a low threshold for an echo when unable to explain decline in breathing.

Some physical exam findings we expect:

Early on: normal +/- prolonged expiration or wheezes on forced exhalation

With increased severity of obstruction: hyperinflation signs

·       Increased resonance on percussion (hyper-resonance): SN 32%, SP 94%, LR+ 4.8

·       Barrel Chest (increased AP diameter): SN 10%, SP 99%, LR+ 10

·       Decreased Cardiac Dullness on Percussion: SN 13%, SP 99%, LR+10

·       Match Test: requires patients to extinguish a lighted match held 10 cm from the open mouth. Failure to accomplish this is associated with a higher likelihood of airflow limitation. SN 61%, SP 91%, LR + 7.1

·       Sub-xiphoid cardiac impulse: SN 8%, SP 98%, LR+4.6

·       Pulsus Paradoxus (>15 mm Hg): SN 45%, SP 88%, LR+ 3.7

·       FEV1>9 seconds LR+ 4.8

·       Maximum laryngeal height <4cm; the distance measured between the top of the thyroid cartilage to the suprasternal notch at end of expiration: LR+ 2.8

End-Stage: may adopt positions to relieve dyspnea

o   Lean forward with arms outstretched and weight supported on palms or elbows

o   Accessory respiratory muscles (anterior scalene, SCM)

o   Expiration through pursed lips

o   Paradoxical retraction of lower interspaces during inspiration (Hoover’s sign)

o   Cyanosis;

o   Asterixis (4-6 beats/minute) due to hypercapnia

o   Cor pulmonale (elevated JVP, tender enlarged liver)—increased intra-thoracic pressure

o   Clubbing-NOT TYPICAL! (it is associated with ILD, Lung CA, bronchiectasis)

The Winnipeg criteria develop in the 80’s is used to decide if patient with COPD exacerbation are candidates for antibiotic therapy.

1.    increase sputum production

2.    increase purulence of sputum

3.    increase dyspnea

2 out of 3 makes the patient a candidate for antibiotic therapy in addition to steroids.

Acute Management:

Consider DDx: CHF, PE, Pneumoia, Aspiration, Metabolic, etc

Optimize lung function

1.OXYGEN & IV Access: supplemental O2 (target SpO2 88-92%); reduce pulm artery vasoconstriction, improve cardiac output

-Venture mask: preferred, to permit precise delivery of FiO2; can use nasal prong delivery for feeds

-Inability to correct hypoxemia with low dose FiO2: consider PE, CHF, ARDS, pulmonary edema, Acute Interstitial Pneumonia (AIP), severe CAP

-Re-assess frequently

2. GOALS of CARE: Discuss, as you may need NIPPV or Intubation/ICU management

3. MEDICAL MANAGEMENT:

o   INH SA BRONCHODILATORS (Beta-agonists & anti-cholinergics)

o   Ventolin: 2.5 mg NEB INH q1-4h PRN OR 4-8 puff by MDI with spacer q1-4h (while awake) prn

o   Atrovent: 500 mcg NEB q4h prn; 2 puff (18 mcg/puff MDI) with spacer q4h (while awake) prn

o   MDI vs NEB: during AECOPD, NEB may be easier to use

NOTE: in RCTs, NEBs are no more effective than MDI (when used properly!)

o   STEROIDS: decrease Length of Stay (0.5-2 days) & reduce treatment failure

o   Oral: rapid absorption, complete bioavailability, equally efficacious to IV

o   REDUCE TRIAL: compared 40 mg PO daily x 5 days vs 14 days—extending treatment duration did NOT reduce risk of recurrent exacerbation. We often give 50 mg daily as that’s how the pills come.

o   ANTIBIOTICS: indicated (i.e. Cefuroxime, Azithromycin, Levofloxaxin); some meta-analysis data suggest that Abx reduce treatment failure among inpatients, shorten LOS, and reduce mortality

o   MUCOACTIVE AGENTS: little evidence to support N-acetylcysteine

4. NON PHARMACOLOGICAL

o   Chest Physiotherapy: many techniques have NOT been shown to be beneficial…

5. MECHANICAL VENTILATION (NIPPV) - mortality benefit and decrease risk of intubation

-Trial may be needed in patients with AECOPD

-Indications: pH<7.3, RR>25, use of accessory muscles, hypoxemic *(must be alert, no facial trauma, no UBIG/Aspiration risk/copious secretions, HD instability, etc)

-R/A frequently and if no improvement in 30 min-1 h, move to intubation if goals of care allow

6. DVT Prophylaxis!

7. LT MANAGEMENT & FOLLOW UP

o   Education: Symptoms of AECOPD

o   Smoking cessation

o   Vaccinations: pneumovax, annual influenza vaccine

o   Exercise tolerance/rehabilitation

o   Review of puffer technique

o   Review of triggers

o   Treat other contributing illnesses or conditions (dysphagia, aspiration-SLP, GERD, etc)

o   Screen: Follow up with PFTs, 6 minute walk test, monitor BMI* (better outcome with less in patient admissions with overweight or normal weight)

o   LA agents: i.e. LA anti-cholinergic (Spiriva), LABA + ICS (Symbicort-budesonide & formoterol; 2 puff BID), SABA prn

o   Home O2 assessment with specific delivery of O2

·      PaO2< 55 mg Hg, or <60 mm Hg with cor pulmonale or Hct>56

People often quote a trial in 2006 in annals of internal medicine showing that 25% of unexplained COPD exacerbation, were screen to show pulmonary embolus. The three highest associations were history of DVT/PE, known malignancy, and a pCO2 5 mmHg below their baseline.  Thus if a patient is short of breath, wheezy, and is getting relief with ventolin, may hold of on that CTPA. D-dimer in this situation is tricky as it is generally designed for the outpatient setting and in the setting of inflammation (pneumonia) may be elevated.

Just as with cardiology, cardio rehab for patients post MI or severe CHF is ideal, so is the same with COPD with and is recommended with an FEV1 <50%, has not been shown to have mortality benefit but to improve quality of life. 

Please post questions or comments here to shake things up!