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!
