MANAGEMENT OF COPD

DR EKWERE M.E
SR,RESP UNIT
UUTH
Learning objectives
Be able to define copd
Be familiar with the aetiology &
pathophysiology
Be familiar with the clinical features
Be able to dfferentiate COPD from
asthma
Be familiar with the investigations and
treatment
outline
Definition
Aetiology/pathogenesis
Clinical features
Diagnosis
Treatment
 DEFINITION OF COPD
Chronic obstructive pulmonary disease (COPD) is a
preventable and treatable disease state
characterized by airflow limitation that is not fully
reversible.
The airflow limitation is usually progressive and is
associated with an abnormal inflammatory response
of the lungs to noxious particles or gases, primarily
caused by cigarette smoking. Although COPD
affects the lungs, it also produce significant
systemic consequences.(GOLD guideline)
aetiology
In developed countries, 95% of cases
are smoking related(>10-20pack years)
Only 10-20% of heavy smokers develop
COPD
pathophysiology
Mucus gland hyperplasia(large airways
especially)
Squamous metaplasia
Loss of cilial function
Chronic inflammation & fibrosis
Emphysema(panacinar, centriacinar and
periacinar)
Thickened pulmonary arteriolar wall and
remodelling
Clinical features
Dyspnoea
Productive cough
Decreased exercise tolerance
Wheeze
COPD is a systemic disease(systemic
effects include osteoporosis,
depression, weight loss, decreased
muscle mass)
Signs
Depends on the severity of the
underlying disease
Raised respiratory rate
Hyperinflated /barrel chest
Prolonged expiratory phase>5 secs,
with pursed lip breathing
Use of accessory muscles of respiration
Quiet breath sounds+/- wheeze
Signs
Quiet heart sounds due to
hyperinflation
Signs of cor pulmonale and CO2
retention(ankle oedema, raised JVP,
warm extremities, plethoric conjunctiva,
bounding pulse, polycythaemia, flapping
tremor if CO2 is acutely raised)
 EXACERBATION

An exacerbation of COPD is an event in the natural

course of the disease characterised

by a change in the patient’s baseline dyspnoea,

cough and/or sputum beyond day-to-day variability,
sufficient to warrant a change in management.
 Disease Trajectory of a Patients with COPD

Symptoms

Exacerbations

Exacerbations
Deterioration
Exacerbations

End of Life
Signs of hyperinflation

barrel shaped chest

decrease chest expansion
Reduced tactile fremitus
loss hepatocardiac dullness
Reduced breath sound and vocal resonance
sitting characteristic tripod position
Tripod position in COPD
patient
Investigations

Aim-
To assist in diagnosis
Help to identify precipitants
To diagnose ungoing complications
Identify co morbidities
For the diagnosis and assessment of
COPD, spirometry is the gold
standard.
Health care workers involved in the
diagnosis and management of COPD
patients should have access to
spirometry.

19
SPIROMETRY
21
MILD OBSTRUCTION

22
CXR

Shows features of hyperinflation-

Hyperlucency,narrowed
mediastinum,flatened diaphragm,can
count more than 9 ribs posterioly and 7
anteriorly
Consolidation
Pneumothorax
Investigation cont

Sputum for microscopy, culture and

sensitivity
FBC –leucocytosis,with neutrophilia
PCV-usually high(chronic hypoxic state)
Pulse oximetry
Arterial blood gases
ABG
Radial artery is used because it is easily accessible,
can be compressed to control bleeding. The syringe
is pre-packaged and contains heparin, to prevent
coagulation
Once the sample is obtained, care is taken to
eliminate visible gas bubbles, as these bubbles can
dissolve into the sample and cause inaccurate
results. The sealed syringe is taken to a
blood gas analyzer.
If the sample cannot be immediately analyzed, it is
chilled in an ice bath in a glass syringe to slow
metabolic processes which can cause inaccuracy.
Analyte Range Interpretation
pH 7.35 - 7.45
The pH indicates if a patient is acidemic
(pH < 7.35 or alkalemic pH > 7.45)

PO2 -9.3-13.3 kPa or 80-100 mmHg .

PCO2- 4.7-6.0 kPa or 35-45 mmHg ] A

high PCO2 (respiratory acidosis)
indicates underventilation, a low PCO2 (
respiratory alkalosis) hyper- or
overventilation.
MANAGEMENT
Goals of the therapy:(ERMIR C)
1. Education
2. Retard the process of airflow
limitation
3. Minimizing airflow limitation
4. Eliminate and prevent infection
5. Correction of complication like
hypoxaemia and Cor pulmonale
6. Rehabilitation
28
Four Components of COPD
Management

1. Assess and monitor

disease
2. Reduce risk factors
3. Manage stable COPD
 Education
 Pharmacologic
 Non-pharmacologic

4. Manage
exacerbations 29
PREVENTIVE COMMENTS
MEASURES
Immunization Vaccination with a flu shot has been shown to result in
52% fewer hospitalization for pneumonia and influenzae in
patient with COPD. Vaccinated patient also have fewer
outpatient for respiratory disease

Smoking ceasation Will retard the growth of COPD as shown from the Lung
health study. Therapy with antidepressant. Bupropion
hydrochloride has also been shown to be effective.
five A’s used to aid a patients in smoking ceasation are:-
Ask: implement an office wide system that routinely
document smoking status.
Advise: encourage all patients who smoke to quit
smoking
Assess: provide motivation for patient to be willing to
quit.
Assist: provide practical counseling.
Arrange: provide short and long-term follow-up to
evaluate therapies.

30
PHARMACOLOGIC
THERAPY
 Therapy at Each Stage of COPD
I: Mild II: Moderate III: Severe IV: Very Severe

 FEV1/FVC < 70%

 FEV1/FVC < 70%  FEV1 < 30%

 FEV1/FVC < 70%
predicted
 FEV1/FVC < 70%
 30% < FEV1 < 50% or FEV1 < 50%
 50% < FEV1 < 80%
predicted predicted plus
 FEV1 > 80% predicted
chronic respiratory
predicted
failure
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Add long term oxygen
if chronic respiratory
failure. Consider
surgical treatments
32
Oxygen therapy
Controlled oxygen therapy
(24% oxygen) should be
given(venturi mask)
The risk of aggravating
hypercapnea is minimal
with controlled oxygen
therapy.
Nasal prongs could be
used at fixed flow-
rates(1L=24%,2L=28%)
Aim for 7.3-
10kPa(saturation 85-
92%)
NASAL CANULA
OXYGEN THERAPY
Oxygen therapy reverses hypoxic
pulmonary vasoconstriction
Relieves right heart strain
Lessens myocardial ischaemia
Improves cardiac output
BEWARE
Oxygen overdose may result in
worsening hypercapnia and acidosis in
those with chronic type 2 respiratory
failure;
Due to suppression of the central
hypoxic drive
CONSIDER ADDITIONAL DIAGNOSIS IF
OXYGENATION DOES NOT IMPROVE
Bronchodilators
Inhaled or nebulised short- acting
bronchodilators(B-agonist and anticholinergic
agent) remain main treatment modalities in
exacerbations(Salbutamol,albuterol,terbutalin
e)
Advantages-
They open the small airways to promote
better emptying of the lungs , thus reducing
dynamic hyperinflation and residual volume
Improve inspiratory capacity and work of
breathing
Use of steroids
Tab prednisolone 30-60mg
IV hydrocortisone200mg 6hrly
Continue oral prednisolone and taper
off
Benefits of steriods

They reduce airway inflammatory markers

Reduces treatment failures(define as death from

any cause,need for intubation, and mechanical
ventilation,readmission ,or intensification of
pharmacological treatment)

They shorten hospital stay and speed up rate of

recovery of PEF and improve FEV1 significantly
within 72hrs

They prolong inter exacerbation period

Antibiotics
Most frequent cause of an exacerbation
is infection about 50% are ass with
bacteria infection

The choice antibiotic should depend on

the local antibiotic policy,guidelines and
resistance pattern

Reasonable choices will include Amino

penicillins and Macrolides, Respiratory
fluoroquinolones(levofloxacin,sparfloxa
cin)
Theophyllines
(Aminophyline)
Phosphodiesterase inhibitors
Cause bronchodilation by increasing the cyclic AMP
and GMP levels.
There is no evidence supporting a role for
theophyllines in exacerbations
It is possible when used intravenously that the
concentrations achieved at the small airways may
lead to some bronchodilation
But the narrow therapeutic range usually result in
side-effects rather than bronchodilation
Mucolytic therapy
Most COPD are associated with excess
mucous production in the airways and
mucuos plugging
Strategies aiming to reduce mucuos viscosity
and thus facilitate mucuos clearance would
seem to be beneficial
However although some evidence that
mucolytic therapy can reduce exacerbations,
There is no data supporting it’s routine use in
exacerbations of COPD
E.g include;bromhexene,
(bisolvon),carbocysteine
Supportive measures
The fluid and electrolyte balance should
be optimised.
Prophylaxis against venous thrombo-
embolism should be given
Optimise nutrition
Patients’ morbidity and mortality can be
assessed using various measurements. This
include FEV1 (see GOLD)

Dyspnea assessed by MRC

Body mass index
Exercise capacity
Arterial blood gases
COPD exacerbation
Quality of life status

44
Discharge Criteria for Patients with Acute Exacerbations
of COPD

 Inhaled β2-agonist therapy is required no more

frequently than every 4 hours

 Patient, if previously ambulatory, is able to walk

across room

 Patient is able to eat and sleep without frequent

awakening by dyspnoea

 Patient has been clinically stable for 12-24 hours

Discharge criteria cont
Arterial blood gases have been stable for 12-24 hours

Patients (or home caregiver) fully understands correct

use of medications

Follow-up and home care arrangements have been

completed
(e.g. visiting nurse, oxygen delivery, meal
provisions)

Patient, family, and physician are confident patient can

manage successfully
 Follow-up Assessment 4-6 Weeks After
Discharge from Hospital for an Acute
Exacerbation of COPD

 Ability to cope in usual environment

 Measurement of FEV1
 Reassessment of inhaler technique
 Understanding of recommended treatment
regimen
 Need for long-term oxygen therapy and/or
home nebulizer (for patients with severe
COPD)
INDICATIONS FOR LTOT
Patients with a PaO2 of less than 7.3kPa
when stable or PaO2 of 7.3 to 8.0kPa
when stable but an additional risk
feature such as secondary
polycythaemia, nocturnal hypoxaemia,
peripheral oedema or pulmonary
hypertension.
Indications cont
Severe airflow obstruction with FEV1 of
less than 30% of predicted.
Cyanosis.
Polycythaemia.
Peripheral oedema.
Elevated jugular venous pressure.
Oxygen saturation less than 92% when
breathing air.
 OXYGEN THERAPY trials

Cumulative percent survival of patients in the Nocturnal Oxygen Therapy Trial (NOTT) and Medical
Research Council (MRC) controlled trials of long-term domiciliary therapy for men aged over 70.
The control subject (. - .) received no oxygen; the NOTT subject (...) received oxygen for 12 hours in
the 24-hour day, including the sleeping hours; MRC O 2 subjects ( ) received oxygen for 15 hours
in the 24 hour day, including the sleeping hours; and continuous oxygen therapy (COT) subjects
(- - -) received oxygen for 24 hours in the 24 hour day (on average, 19 hours). (From Flenley DC:
Long-term oxygen therapy. Chest 87:99-193, 1985).
SUMMARY

COPD is a preventable and

treatable condition. The need for
increased awareness among health
care providers to ensure early
recognition of the disease cannot
be overemphasized. Quality of life
can be improved with appropriate
therapeutic interventions.
THANKS FOR LISTENING
REFERENCES
Global Strategy for the Diagnosis,
Management & Prevention of COPD;
updated 2009
Current Medical Diagnosis &
Treatment;2007
Harrison’s Principles of Medicine, 17th
Edition
Baum-Baum’s Textbook of Pulmonary
Diseases,7th Edition