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INTERNAL MEDICINE ASSIGNEMENT 7a BY DR. SCOTT NEFF
DC DABCO MSOM MPS DABFE FABFE FFABS FAABT
BEATING CHRONIC OBSTRUCTIVE PULMONARY DISEASE THROUGH MEDICAL
INFORMATION MASTERY AND POEMs
INTRO INTO COPD
Diagnosis:
T he
fourth leading cause of death in the United States is Chronic
obstructive pulmonary disease (COPD), affecting approximately 16 million
Americans each year. About 100,000 deaths per year are directly
attributable to COPD, and it is a contributing factor to many more.
Almost 90 percent of COPD is associated with smoking tobacco affecting
at least 15 percent of those. Obviously, because more men smoke tobacco
then women, they are affected more often.
COPD occurs predominantly in
individuals older than 40 years.
COPD has been
recently defined by the National Heart, Lung, and Blood Institute and
the World Health Organization due to increasing concern. They formed
the Global Initiative for Chronic Obstructive Lung Disease (GOLD). In
their 2001 report, Global strategy for the Diagnosis, Management and
Prevention of COPD they define a new classification system for COPD that
places less emphasis on the distinction between chronic bronchitis and
emphysema than the previous statements. The GOD report was also
endorsed by the American Thoracic Society which defines COPD as “a
disease state characterized by airflow limitation that is not fully
reversible. The airflow limitation is usually both progressive and
associated with an abnormal inflammatory response of the lungs to
noxious particles or gases.”
Patients typically have symptoms of both chronic bronchitis and
emphysema, but the classic triad also includes asthma. Most of the time
COPD is secondary to tobacco abuse, although cystic fibrosis, alpha-1
antitrypsin deficiency, bronchiectasis, and some rare forms of bullous
lung diseases may be causes as well.
Pathophysiology:
COPD is a mixture of 3 separate disease processes that together form the
complete clinical and pathophysiological picture. These processes are
chronic bronchitis, emphysema and, to a lesser extent, asthma. Each case
of COPD is unique in the blend of processes; however, 2 main types of
the disease are recognized which follow:
Chronic bronchitis
I n
this type, chronic bronchitis plays the major role. Chronic bronchitis
is defined by excessive mucus production with airway obstruction and
notable hyperplasia of mucus-producing glands.
Damage
to the endothelium impairs the mucociliary response that clears bacteria
and mucus. Inflammation and secretions provide the obstructive component
of chronic bronchitis. In contrast to emphysema, chronic bronchitis is
associated with a relatively undamaged pulmonary capillary bed.
Emphysema is present to a variable degree but usually is centrilobular
rather than panlobular. The body responds by decreasing ventilation and
increasing cardiac output. This V/Q mismatch results in rapid
circulation in a poorly ventilated lung, leading to hypoxemia and
polycythemia.
Eventually, hypercapnia and respiratory acidosis develop, leading to
pulmonary artery vasoconstriction and Cor Pulmonale. With the ensuing
hypoxemia, polycythemia, and increased CO2 retention, these
patients have signs of right heart failure and are known as "blue
bloaters."
Emphysema
T he
second major type is that in which emphysema is the primary underlying
process. Emphysema is defined by destruction of airways distal to the
terminal bronchiole.
Physiology of emphysema involves gradual destruction of alveolar septae
and of the pulmonary capillary bed, leading to decreased ability to
oxygenate blood. The body compensates with lowered cardiac output and
hyperventilation. This V/Q mismatch results in relatively limited blood
flow through a fairly well oxygenated lung with normal blood gases and
pressures in the lung, in contrast to the situation in blue bloaters.
Because of low cardiac output, however, the rest of the body suffers
from tissue hypoxia and pulmonary cachexia. Eventually, these patients
develop muscle wasting and weight loss and are identified as "pink
puffers."
Initial Evaluation:
In
general, the vast majority of COPD cases are the direct result of
tobacco abuse. While other causes are known, such as alpha-1 antitrypsin
deficiency, cystic fibrosis, air pollution, occupational exposure (e.g.,
firefighters), and bronchiectasis, this is a disease process that is
somewhat unique in its direct correlation to human activities.
Most
often the consideration for COPD is in patients over age 50 that have
dyspnea on exertion, chronic cough, and a history of significant smoking
of more than 30 pack-years. Breathing difficulty has often been
described as an inability to get enough air or as “air hunger,” with a
sensation that breathing requires more effort than normal. Often
patients describe wheezing or tightness in the chest. A familial
history of severe early-onset emphysema increases the possibilities of
alpha1 antitrypsin deficiency.
Finally, smokers over age 50 are also at risk for coronary artery
disease and lung cancer, which can yield similar symptoms and thus, it,
is imperative to query the patient about chest pain, palpitations,
hemoptysis, or weight loss, which would point to these conditions. Many
patients can point to occupational exposure to a variety of dusts and
chemicals as the cause for both obstructive and restrictive lung
disease, so an occupations history is mandatory rather than permissive.
Patients with COPD present with a combination of signs and symptoms of
chronic bronchitis, emphysema, and asthma. Symptoms include worsening
dyspnea, progressive exercise intolerance, and alteration in mental
status. In addition, some important clinical and historical differences
can exist between the types of COPD.
In the
chronic bronchitis group, “key” symptoms include the following:
-
Productive cough, with progression over time to intermittent dyspnea
-
Frequent and recurrent pulmonary infections
-
Progressive cardiac/respiratory failure over time, with edema and
weight gain
I n
the emphysema group, the history is somewhat different and may include
the following set of ‘key” symptoms:
-
A long history of progressive dyspnea with late onset of
nonproductive cough
-
Occasional mucopurulent relapses
-
Eventual cachexia and respiratory failure
Physical Examination:
Depending on the type of
COPD, physical examination may vary as follows:
Chronic
bronchitis or the blue bloaters.
-
Patients may be obese.
-
Frequent cough and expectoration are typical.
-
Use of accessory muscles of respiration is common.
-
Coarse rhonchi and wheezing may be heard on auscultation.
-
Patients may have signs of right heart failure (ie, Cor Pulmonale),
such as edema and cyanosis.
-
Because they share many of the same physical signs, COPD may be
difficult to distinguish from CHF. One crude bedside test for
distinguishing COPD from CHF is peak expiratory flow. If patients
blow 150-200 mL or less, they are probably having a COPD
exacerbation; higher flows indicate a probable CHF exacerbation.
Emphysema or the pink puffers.
-
Patients may be very thin with a barrel chest.
-
They typically have little or no cough or expectoration.
-
Breathing may be assisted by pursed lips and use of accessory
respiratory muscles; they may adopt the tripod sitting position.
-
The chest may be hyperresonant, and wheezing may be heard; heart
sounds are very distant.
-
Overall appearance is more like classic COPD exacerbation.
Screening
Examination for COPD:
F orced
expiratory time is a useful screening test for COPD (and asthma). To
perform this test, have the patient take a deep breath and then exhale
as hard and long as possible, listening with a stethoscope placed over
the trachea in the suprasternal notch until the last moment that sounds
are audible. A result of more than 6 seconds has a sensitivity of 75%
to 92% in detecting obstructive disease, but a specificity of only 43%
to75%.
Sensitively can be increased up to 98% by using a cutoff value of 4
seconds, making this a useful screening maneuver, but only half of the
patients identified will actually have obstructive airway disease.
Always evaluate the
suspected COPD patients for evidence of smoking related cardiovascular
disease, such as carotid bruits, fine end-inspiratory rales, abdominal
bruits, peripheral edema, and decreased peripheral pulses. The
oropharynx should be examined carefully for tobacco induced cancers.
Lab
Studies:
Arterial blood gas
-
Arterial blood gas (ABG) analysis provides the best clues as to
acuteness and severity.
-
In general, renal compensation occurs even in chronic CO2
retainers (ie, bronchitis); thus, pH usually is near normal.
-
Generally, consider any pH below 7.3 a sign of acute respiratory
compromise.
Serum chemistry
-
These patients tend to retain sodium.
-
Diuretics, beta-adrenergic agonists, and theophylline act to lower
potassium levels; thus, serum potassium should be monitored
carefully.
-
Beta-adrenergic agonists also increase renal excretion of serum
calcium and magnesium, which may be important in the presence of
hypokalemia.
CBC - Polycythemia
Imaging
Studies:
Chest x-ray
-
Chronic bronchitis is associated with increased bronchovascular
markings and cardiomegaly.
-
Emphysema is associated with a small heart, hyperinflation, flat
hemi diaphragms, and possible bullous changes.
Other
Tests:
Pulse oximetry
-
Pulse oximetry does not offer as much information as ABG.
-
When combined with clinical observation, this test can be a powerful
tool for instant feedback on the patient's status.
Electrocardiogram
-
The presence of underlying cardiac disease is highly likely.
-
Establish that hypoxia is not resulting in ischemia.
-
Establish that the underlying cause of respiratory difficulty is not
cardiac in nature.
Pulmonary function tests
-
Decreased forced expiratory volume in 1 second (FEV1)
with concomitant reduction in FEV1/forced vital capacity
(FVC) ratio
-
Poor/absent reversibility with bronchodilators
-
FVC normal or reduced
-
Normal or increased total lung capacity (TLC)
-
Increased residual volume (RV)
-
Normal or reduced diffusing capacity
Treatment:
T he cornerstone
of COPD prevention and care is avoidance of smoking. Early recognition
and treatment of small airway disease in people, who smoke, combined
with smoking cessation, may prevent progression of the disease. All
smoking must stop. If your patient is smoking then it is imperative to
help them to stop smoking, both to improve current function and to slow
the deterioration of FEV1. Either physician advocacy and/or referral to
smoking cessation programs are extremely valuable. The utility of
nicotine patches, gum, or spray and bupropion (Zyban) increases the
success of cessation labors.
Ipratropium
bromide by metered dose inhaler (MDI) is used today for patients with
continual or frequent symptoms. A combined MDI containing ipratropium
and Albuterol (Combivent) for patients using both medications.
Salmeterol (Serevent, a long acing beta 2 agonist), oral theophylline
(With theophylline the serum level should be 5 to 12 mg/dL to minimize
adverse effects such as nausea, palpitations, insomnia, tremor and
seizures.), or sustained release oral Albuterol is added for more
resistant cases.
Adverse effects
due to corticosteroids have eliminated recommendation albeit COPD
patients have a significant improvement when these agents have been
used. Thus, if stage II-B or III COPD has corticosteroid utility,
performing PFTs and a symptoms assessment and a 6 to 12 week trial of
medication, and then repeating the assessment to maximize clinical
response has proven useful.
Intravenous
replacement therapy with alpha1-protease inhibitor (Prelisting) is given
once per week for severe AAT deficiency. If the patient has stopped
smoking this care will stabilize the condition.
In severe COPD
cases, continuous low-flow oxygen, non-invasive ventilation, or
intubation may be needed. Surgery to remove parts of the disease lung
has been shown to be helpful for some patients with COPD.
Specifically, the mainstays of therapy for acute exacerbations of
COPD are oxygen, bronchodilators, and definitive airway management.
Review:
Oxygen Discussion:
·
Adequate oxygen should be
given to relieve hypoxia. With administration of oxygen, PO2
and PCO2 rise but not in proportion to the very minor changes
in respiratory drive.
·
The need for intubation
can be established quickly at the bedside by asking the patient hold the
nebulizer in his or her hand. If the patient becomes so sleepy that the
nebulizer starts to fall away, the patient should be intubated
regardless of PCO2 level. The cause of increased CO2
production is not decreased respiratory drive but probably reversal of
hypoxic arterial vasoconstriction in areas of less-ventilated lung
tissue, which increases the extent of ventilation/perfusion defects and
thus CO2. "Stated another way, there is probably no single
value for arterial PCO2, pH, or PO2 that by itself
constitutes and indication or [intermittent positive pressure
ventilation (IPPV)]".
·
Occasionally, large
increases in CO2 can lead to deterioration of mental status,
causing stupor and obtundation. In such cases, decreasing O2
delivery is the wrong action. The CO2 narcosis inhibits
respiratory drive to the point that decreasing O2 delivery
leads only to worsening of hypoxia. The correct action is immediate
intubation and oxygenation.
·
Supply the patient with
enough oxygen to maintain a near normal saturation (above 90%) and do
not be concerned about oxygen supplementation leading to clinical
deterioration. If the patient's condition is that tenuous, intubation
most likely is needed anyway.
Bronchodilator
·
In the prehospital
setting, administer only beta-agonist nebulizer therapy, which should be
given as needed.
·
If necessary and
available, continuous positive airway pressure (CPAP) may be used.
·
Of course, in times of
respiratory failure, patients may need intubation in the field.
Emergency Department Care:
In addition to oxygen, proper
care may comprise bronchodilators, antibiotics, magnesium, CPAP or
biphasic positive airway pressure (BiPAP), Heliox (ie, mixture of helium
and oxygen), theophyline, corticosteroids, Terbutaline and antibiotics
as well as definitive airway management via intubation. All of these
should be considered in the context of the individual patient's
condition.
Terbutaline can be considered for
patients with such significant exacerbations that they are not moving
enough air to take full advantage of nebulizer therapy.
The greatest single problem that persists in this area is the under
dosing of beta agonists and the non utilization of anticholinergics.
Although only a small subset of patients respond to beta agonists, a
reasonable dose approaches continuous nebulization, as is seen in
current asthma treatment. Anticholinergics seem to have an important role in the acute treatment
of COPD exacerbations.
The use of antibiotics is still controversial. These patients are almost
uniformly heavily colonized with
Haemophilus influenzae, streptococcal pneumonia, and others;
however, researchers have not proven these organisms to be the cause of
the exacerbation. In fact, viruses are thought to be the instigating
factor in as many as half of the cases. In addition, the particular
antibiotic chosen seems to have much less effect on outcome than the
particular host factors of the patient. Although some meta-analyses have
suggested statistically significant improvement in outcome in those
patients who receive empiric antibiotic coverage, the lack of quality
studies and power leaves the subject open for debate. If antibiotics are
given, the choice should provide coverage against pneumococcus,
H influenzae,
Legionella species, and
gram-negative enterics.
ER
Bronchodilators
--
These agents act to decrease muscle tone in both small and large airways
in the lungs, thus increasing ventilation. Category includes
subcutaneous medications, beta-adrenergic agonists, methylxanthines, and
anticholinergics. Note that only 10-15% of all patients with COPD have a
true reversible (ie, bronchospastic) component; however, because
predicting response is impossible on presentation, all patients should
be treated with aggressive bronchodilator therapy.
Chronic Evaluation:
Smoking education
is the most important fact in the care of COPD. Further , in order to
facilitate a superior collaborative partnership with the physician, the
patient needs to demonstrate the proper use of inhalers, home management
of medications, avoidance or respiratory irritations, and how and when
to contact the patients physician. Pulmonary rehabilitation programs,
exercise programs tailored to the severity of disease, can improve the
patient’s functional status, exercise tolerance, and the symptoms of
breathlessness. A well informed patient able to take charge of their
health care team, will maintain the proper re-evaluation program, to
ensure proper recording of disease and progress or success, as well as
to maintain the most up to date cutting edge medical knowledge and care
for the maintenance of a wonderful and carefree life.
Medical Text
References:
- Dailey RH:
Chronic obstructive pulmonary disease. In: Rosen P, et al, eds.
Emergency Medicine Concepts and Clinical Practice. 3rd ed.
Mosby-Year Book Inc; 1992:1093-1111
- Andreoli
Thomas E et al, Cecil Essentials of Medicine, 4th
Saunders, pages 145-150.
- Kasper Dennis
L et al, Harrison’s Principles of Internal Medicine, 16th
edition, Mc Graw Hill, pages 1547-1554
- Beers, Mark H
et al, The Merc Manual of Diagnosis and Therapy, 17th
Edition, Merck Research Laboratories, pages 568-582
- Sloane, Philip
D et al, Essentials of Family Medicine, 4th Edition,
Lippincott-Williams & Wilkins, pages 730-732
- Siedman JC: Chronic obstructive pulmonary disease. In: Tintinalli J,
et al, eds. Emergency Medicine: A Comprehensive Study Guide.
McGraw-Hill Com; 1992: 298-302.
- Brunton
Laurence L et al, Goodman & Gilman’s The Pharmacological Basis of
Therapeutics, 11th edition, Mcgraw-Hill, pages 431-453
- Ibid, pages
253-254
- Ibid,
1608-1609
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By Scott David Neff for INTERNAL MEDICINE
DECEMBER 19th, 2010
"The most acceptable service to God is doing
good to man" Ben
Franklin |
