COPD: Differential Diagnosis

Maria Luisa Martinez Ortiz1 and Josep Morera1,2
1Servei de Pneumologia, Hospital Universitario Germans Trias i Pujol
2CIBER Enfermedades Respiratorias-CIberes, Barcelona
Spain
1. Introduction
Chronic obstructive pulmonary disease (COPD) is a high prevalent and impact socioeconomic
disease. Although, cigarette smoking clearly fulfils all criteria to be classified as the etiology of
COPD (Hill´s criteria), the latest version of GOLD does not include this concept clearly,
therefore half century of main documents has been culminated and they has never mentioned
in the definition, tobacco or cigarette smoking as cause of COPD. American Thoracic Society
and European Respiratory Society (ATS / ERS) in the definition of COPD include the phrase
“primarily caused by cigarette smoking”. Nevertheless, the next page smoking changes from
the category of “cause” to simply a “risk factor”; in fact, smoking is included in table 2 as a risk
factor under the column of “exposures”, together with socioeconomic status, environmental
pollution, disease in childhood, or diet, among other. A reason for not to refer to cigarette
smoking as aetiology is that only 15% of smokers are susceptible to COPD, a concept wrongly
attributed to Fletcher. Although not all subjects exposed to cigarette smoking develop COPD
does not preclude such exposure is the cause, just as not all people infected with
Mycobacterium tuberculosis develop Tuberculosis, but there is no doubt about the etiologic role
of mycobacteria. Another reason for nor establish smoking to the category of etiological factor
in COPD is the existence of COPD in non-smokers.
Therefore, when the aetiology is not part of the definition of the disease, it is usually
replaced by a clinical description and the definition based on clinical findings are very poor,
so a new definition of COPD is needed to ensure a more valid an accurate way to manage
this worldwide condition.
In the Table 1 shows some of the criteria that different societies, guidelines and
organizations have been used to diagnose COPD.
Actually COPD is defined as postbronchodilator FEV1/FVC ratio < 70%. Threshold of
FEV1/FVC <70% is agedependent and will probably lead to a significant degree of
overdiagnosis of COPD in the elderly and underdiagnose young adults. GOLD guidelines
recommend that using the lower limit of normal (LLN) values for FEV1/FVC is a way to
minimize the misclassification. But use LLN we also overdiagnose healthy subjects.
Although use post-bronchodilator FEV1/FVC ratio <0.70 simplify the diagnosis of COPD,
some pulmonologists, ever more, consider a diagnosis of COPD can not be based only on
spirometry parameters; it is important to include the presence of respiratory symptoms and
exposure to risk factors.
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Society Year Criteria
ECCS 1983 FEV1/VC or FEV1/ FVC<LLN
ATS 1987 FEV1/ FVC<0.75
ATS 1991 FEV1/ FVC<LLN
ECCS/ERS 1993 FEV1/VC or FEV1/ FVC<LLN
ERS 1995 FEV1/VC <88% predicted (men) or 89% (woman)
BTS 1997 FEV1/FVC <0.70 and FEV1<80% predicted
NLHEP 2000 FEV1/FVC or FEV1/ FEV6/<LLN and FEV1<LLN
GOLD 2007 FEV1/FVC<0.70 postbronchodilator
NICE 2004 FEV1/FVC <0.70 and FEV1<80% predicted
ATS/ERS 2004 FEV1/FVC<0.70 postbronchodilator
ATS/ERS 2005 FEV1/VC <LLN
ATS: American thoracic Society; BTS: British Thoracic Society; VC: Vital capacity; ECCS: European
Community for Coal and Steel; ERS: European Respiratory Society; FEV1/ /FVC: ratio of forced
expiratory volume in 1s to forced vital capacity; GOLD: Global Initiative for chronic obstructive lung
disease; LLN: lower limit of normal (LLN); NICE: National Institute for health and clinical excellence;
NLHEP: National Lung Health Education Program.
Table 1. Spirometry criteria to COPD in some guidelines Society
There are many diseases or processes that show a FEV1 / FVC post-bronchodilator < 70%,
these processes constitute the great chapter of what we call "disease" COPD.
Although nosological or semantically, definition of COPD as a syndrome is questionable,
recently the term has come to be considered by other authors. Table 2 outlines a long list
(not exhaustive) of entities that may be associated with airflow obstruction syndrome or
COPD. Most of them are common such as pneumoconiosis and other occupational diseases,
Airway obstruction in pulmonary tuberculosis, some clinical forms of asthma, etc and other
less common such as lymphangioleiomyomatosis, Bronchiolitis obliterans associated with
consumption of Sauropus androgynus among others. This chapter will show a list of
differential diagnosis, as complete as possible and some clues for the recognition of these
processes vs COPD.
2. Smoking COPD
In 1950, smoking was established as a cause of COPD (chronic bronchitis and emphysema)
and Fletcher and Peto corroborated its natural history. The relationship between smoking
and COPD, probably influenced by genetic determinants poorly understood, is primarily a
dose-effect relationship as demonstrated in multiple studies.
Findings have proven smoking cessation disrupts the natural history of COPD, but there are
authors who have more controversial opinions about it and assert that in many cases,
inflammation persists despite smoking cessation. The perpetuation of inflammation may be
related to other factors, bacterial colonization has been proposed.
In the past, it was considered that only 15% of smokers were likely to develop COPD, when
in fact it is known that this percentage is near 50% if they survive long enough. This
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COPD: Differential Diagnosis
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COPD from smoking
COPD from alpha 1 antitrypsin deficiency
COPD in non smokers
Chronic Asthma (perennial)
Aging
Sequelae of tuberculosis
Mitral stenosis
Cardiac failure
Anorexia nervosa
Cystic fibrosis in adult
Bronchiectasis
Ambiental exposure (biomass smoke)
Marihuana smoking
Sequelae accidental exposure (ammoniac)
Occupational exposure
 coal miners
 pulmonary silicosis
 byssinosis
 pig farmers
 cabinetmakers
Others
Endovenous exposure (heroin, cocain)
Digestive exposure
 (Sauropus androgynus)
Bronchiolitis
 Bronchiolitis obliterans
 Diffuse panbronchiolitis
 Obliterative bronchiolitis in microwave
popcorn plant workers
 bronchiolitis by rheumatoid arthritis
 Others
Sjogren syndrome
Inflamatory bowel disease
Wegener syndrome
Sarcoidosis
Extrinsic allergic alveolitis
 Chronic
Eosinophilic granuloma
Lymphangioleiomyomatosis
Neurofibromatosis
Tuberous sclerosis
Birt-Hogg-Dubé syndrome
Scleroderma
HIV
AIDS (Pneumocistis jiroveci)
Placental transmogrification
Paraneoplasic Pemphigus
Fabry disease
Salla disease
Amyloidosis
Ligth chain deposition disease
Relapsing polychondritis
Tracheobronchomalacia
Tracheobronchopathia achondropasia
Ehler Danlos syndrome
Tracheal stenosis
Cord vocal paralysis
Relapsing Polichondritis
Traqueal neoplasia
Papilomatosis tracheobronchopathia multiple
Others
Table 2. Causes of COPD syndrome
percentage of susceptibility increases if others methods, better than simple spirometry, have
been used to detect COPD.
Although transfer of carbon monoxide (DLCO) and computed tomography (CT) with high
resolution have demonstrated useful in early diagnosis of emphysema, they are underused.
Disadvantages for Chest CT and other imaging techniques are expensive and irradiation
exposure.
3. Alpha-1-antitrypsin deficiency
There are excellent reviews about alpha 1 antitrypsin deficiency (AATD). AATD is associated
with impaired pulmonary antiproteasas defenses leading to unopposed protease activity.
ATTD is the best model of COPD and emphysema. The clinical course is accelerated mainly by
the smoking, but also by air pollution, and phenotype well-known. Some cases are diagnosed
as asthma or bronchiectasis for clinical manifestations. Others may be diagnosed by
hepatologists if the first manifestation is liver findings. In recent years, the characteristics in
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subjects over 60 years of age have been described. It is important the determination of the
DLCO for evaluation of its prognosis and outcome, not only spirometry.
Heterozygous individuals have a higher susceptibility to develop COPD in the presence of
smoking or cigarrete exposure, and should be detected for a better affiliation of the
syndrome. Therefore, measurement of alpha-1-antitrypsin should be practiced at least once
in all patients with chronic airflow obstruction.
4. COPD syndrome by tuberculosis
Although Tuberculosis is considered as precursor in pulmonary specialty, airflow
obstruction in pulmonary tuberculosis has been just considered few years ago. (Figure 1). In
1971, Snider et al had described Obstructive airway disease and pulmonary tuberculosis,
and PLATINO study in Latin America has been updated this. In an environment where
tuberculosis is or was common, the sequelae of tuberculosis are a major cause of chronic
airflow obstruction in individuals who have never been smokers. Airway obstruction in
pulmonary tuberculosis:
 do not correlate with the degree of the affected area, could coexist even if area of
damage is small
 is presented in patients with treated pulmonary tuberculosis even healthy subjects
 is unusual progresses and
 is irreversible to bronchodilator.
5. Asthma chronic non-reversible perennial
Problems in the differential diagnosis of bronchial asthma not reversible and COPD are well
known.
It is accepted that 30% of asthmatic patients are smokers, and this variant of overlap syndrome
has been well described by various authors. There is evidence that smokers with asthma are
more resistant to treatment. The natural history of patients with COPD asthmic syndrome
involves a fast loss of FEV1; they have a decreased life expectancy, though this aspect is not
well known because many studies included as non-smokers and former smokers.
6. Aging
In the population over 80 or more years old, up to 50% of individuals may have a
FEV1/FVC <70%. Although some analogies between COPD and elderly have already been
highlighted, further studies are required. Hence tables with normal spirometric values for
the elderly have just been available recently. Nevertheless, the presence of a FEV1/FVC
<70% is clinical data that should not be neglected, because there has been a marker of
reduced life expectancy, even in old age.
7. Heart disease
Classically, the chronic forms of valvular heart disease could present with airflow
obstruction and / or reduction in DLCO. The decrease in the incidence of rheumatic fever
and development of new cardiac diagnostic methods avoid this situation as a common
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Fig. 1. A 55-year old woman, nonsmoker, was seen as outpatient in a check-up, a spirometry
revealed the presence of obstructive patterns. A diagnosis of Pulmonary Tuberculosis had
been made 25 year ago and antituberculosis treatment was completed. Diagnosis: sequelae
of tuberculosis.
problem of differential diagnosis. The comorbidity of COPD and heart failure caused by
smoking, metabolic syndrome, the syndrome of obstructive sleep apnea and aging, could
hinder the diagnosis of COPD exacerbation vs heart failure. However, measurement of the
natriuretic peptide can help in the differential diagnosis. Once patients have been discharged
from hospital, they should be required to filial the impact of both processes. Studio ergometer
should be made in outpatients in stable phase, although this is done in rare occasions.
8. No smoking COPD and antitissular antibody
To date, Birringer et al have perhaps been the only ones who have been systematically
studied COPD in nonsmokers. Four hundred consecutive patients who visited for 2 years,
Birringer found that 25% of them were smokers. Once discarded asthmatics, patients with
bronchiectasis and a small subgroup with sputum eosinophilia, they were probably nonreversible
asthma, a small percentage of 4% had common characteristics: they were
preferably female, with age over 50 years, often with a history of Hashimoto's thyroiditis
and / or antithyroid antibodies and / or antitissular antibodies or other features of
autoimmune disease. Therefore, the measurement of antithyroid antibodies should be
included in patients with features similar.
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9. COPD from exposure to biomass smoke
It is considered that the population at risk of inhaling smoke from biomass could reach 3000
million people worldwide, mostly female. Anatopatology, COPD from inhalation of smoke
from biomass has been becoming well known, has important similarities with COPD from
smoking, but also significant differences.
Although its natural evolution is not well known yet, COPD from exposure to biomass
smoke has some features in common with COPD from smoking. Romieu et al designed a
study with methodology of trial in a group of Mexican women was divided into two
groups: the control group cooking with the traditional open fire and the treatment group
cooking with Patsari stove. After 6 years, confirmed a dramatic difference in the evolution of
FEV1: the control group decline 62 ml FEV1 per year, while the intervention group only lost
half. Orozco et al demonstrated that COPD in Spain by exposure to biomass smoke should
be considered especially in older women from rural areas.
The impact of this disease is usually not epidemiologically relevant in developed countries,
although some cases have been identified in countries as the United States, for example, in New
Mexico, USA reported that 26% of subjects had been exposed to smoke from biomass fuel.
10. Other disease
Bronchiectasis, cystic fibrosis, bronchiolitis and alveolitis extrinsic allergic are disease or
syndromes very often manifested with chronic airflow obstruction, as well as occupational
exposures. Occupational exposures, in particular, are syndromes that constantly
incorporating new disease. An example would be an extrinsic allergic alveolitis called hot
tub, which is related to recreational activities whit contact hot water, as in water parks.
Mycobacterium avium could have a main role.
Paradoxically, until recently it discussed the evidence that pneumoconiosis of miners could
be the cause of pulmonary emphysema in the absence of smoking, which is currently
shown. Other occupational exposure disease is obliterative bronchiolitis in microwave
popcorn plant workers. It was observed when the additives to provide flavor was replaced.
The patients had a very aggressive clinical course.
Another microepidemic is bronchiolitis obliterans associated with sauropus androgynus, it
also led to an extremely aggressive bronchiolitis and is not by respiratory exposure. The
intention to lose weight was the reason of ingestion of extract of Sauropus androgynus.
Recently, CT scan has shown that patients with anorexia nervosa could be associated with
emphysema. This observation was already known in the Nazi death camps. However, there is
not evidence that emphysema cause by anorexia nervosa has airflow obstruction.
Patients infected with the human immunodeficiency virus (HIV) may have some respiratory
disorders including pulmonary emphysema with airflow obstruction. It is accepted that the
combination of smoking and inflammatory reactions caused by HIV accelerates the
presentation of emphysema in 10 to 20 years. Recently it has tended to take an important
role to Pneumocystis jiroveci in the obstruction of patients with HIV, but even this pathogen
has been isolated in patients with COPD from smoking.
The eosinophilic granuloma, lymphangioleiomyomatosis (figure 2), histiocytosis X, tuberous
sclerosis syndrome, Birt-Hogg-Dubé and deposition disease heavy chains are some orphan
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Fig. 2. A 36-year old woman was seen in pneumology clinic because of dyspnea. She had a
5-pack-year history of smoking but had stopped smoking 4 year earlier CT: thin-walled
cystic. Pulmonary function testing reveals an obstructive pattern. Lung biopsy:
Lymphangioleiomyomatosis.
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diseases, most of them genetic disease, they can cause airflow obstruction and pulmonary
emphysema.
In half the cases, a rare disease such as vasculitis with urticaria and hypocomplementemia
syndrome could present with severe emphysema. Its mechanism is could be local
inactivation of alpha-1-antitrypsin.
Systemic diseases such as rheumatoid arthritis, lupus erythematosus, diffuse scleroderma,
polymyositis and mixed connective tissue disease can cause bronchiolitis at some point in its
evolution. Söjgren syndrome can provide images similar in CT of emphysema and
additionally present with airflow obstruction.
Although, Sarcoidosis in advanced stages is present as pulmonary fibrosis, in the initial
and/or mild stages is present as mild obstruction because hyperresponsiveness or
involvement of the bronchial mucosa.
The connective tissue diseases such as Marfan syndrome and Ehlers-Danlos syndrome,
among others, may present with lesions of emphysema, usually paraseptal. Simultaneously,
may present with tracheobronchomegaly and hipercolapsabilidad tracheobronchial. CT and
test of forced expiration have increased the diagnosis of bronchial hipercolapsabilidad. It
probably is one of the main causes of airway obstruction in healthy people.
Likewise, tracheal tumors, the Wegener, vocal cord paralysis and vocal cord dysfunction
also cause of airflow obstruction.
11. Special situations
Parentage of a patient with obstruction initially suffered from asthma and who
subsequently becomes a smoker can be a clinical problem almost insoluble.
The combination of smoking and disease interstitial chronic or pulmonary fibrosis has been
highlighted in several recent publications. A recent epidemiological study in area
cardiology, MESA study, performing CT lung, indicates that this match will be anecdotal in
the future.
Respiratory bronchiolitis with interstitial respiratory disease (RB / ILD) is another example
of interstitial and bronchial disease secondary to smoking. Some patients who do not meet
the criteria for COPD are patients with severe by accelerating their natural evolution.
(Figure 3)
12. Comorbidity and differential diagnosis
Comorbidity in COPD is controversial. In fact, it has been so exaggerated to name as chronic
inflammatory syndrome, including in the same process other systemic manifestations. It is
much more common that the vascular comorbidity in patients with COPD due to chronic
exposure to tobacco that systemic inflammation secondary to COPD. Table 3 lists the
mechanisms of comorbidity and Table 4 summarizes the comorbidities of COPD.
Introduce comorbidity in the differential diagnosis have done difficult in many cases the
appropriate affiliation to the patient. In a smoker of 65 years with a cumulative consumption
of 40 pack / year comes to a vascular surgeon for a pulsatile abdominal mass is likely to
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Fig. 3. High resolution computerized tomography (HRCT) of the same patient. A) Presence
of paraseptal emphysema and subpleural bullae (white arrowheads) and centrilobular
emphysema (arrows) in both upper lobes. B) Reticular interstitial disease with intralobular
thickening and images of subpleural honeycombing and traction bronchiectasis (black
arrowheads) C) Reticular interstitial disease in middle and right lower lobes, with
interlobular septal thickening, subpleural honeycombing and traction bronchiectasis. D)
Coronal reconstruction in the posterior regions of both lungs: Bilateral paraseptal
emphysema (white arrowheads) and reticular interstitial disease and honeycombing in right
lower lobe. (Used with permission MD Portillo)
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Systemic features of cigarette smoking
Systemic features of COPD
Comorbidity of COPD
Extrapulmonary feature of COPD
Table 3. Mechanisms underlying the comorbidity of COPD
Respiratory
 Bronchopulmonary carcinoma
 Pulmonary arterial hypertension
 Bronchiectasis
 Pneumonia
 Pneumocystis pneumonia
 Obstructive sleep apnea
 Invasive aspergillosis
 Others
Cardiovascular
 Coronary disease
 Auricular fibrillation
 Cardiac failure
 Carotid stenosis
 Arritmia
 Aneurysm of thoracoabdominal aorta
 Cor pulmonale
 Others
Neuropsychic
 Depressive disorder
 Ictus
 Lacunar infart
 Anxiety disorders
 Orthostatic hypotension
 Intracranial hypertension
 Cognitive impairment
 Others
Digestive
 Gastroesophageal reflux
 Malabsorption
 Helicobacter pylori infection
 Others
Endocrine
 Diabetes
 Hypogonadism
 Others
Systemic
 Cachexia
 Myopathia
 Anemia
 Osteoporosis
 Polycythemia
 Facial wrinkles
 Hypercoagulable state
 Others
Others
 Rhinitis
 Cataracts
 Inguinal hernia
 Nephrotic syndrome
 Periodontal disease, etc
Table 4. Comorbidity of COPD
delay the practice of spirometry. Recently, Remy-Jardin et al have made an interesting
proposal to TC (dual-energy) for the simultaneous evaluation of pulmonary and vascular
damage smoking.
13. When should we suspect that COPD is not secondary to tobacco?
An example, a female patient over 70 who had lived much of her life in a rural area, who
had never smoked, presents with cough, expectoration and airway obstruction would be a
candidate that her disease was secondary to exposure biomass. We cannot be in accordance
with a diagnosis of COPD in individuals who had smoked fewer than 10 packs / year,
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unless they had simultaneous deficiency of alpha-1-antitrypsin disease. In obvious cases of
airway obstruction in people younger than 40 years, it is unusual that this was secondary to
smoking. If the annual decline of FEV1 was greater than 75 ml, an additional cause should
be suspected. A familial aggregation might suggest cystic fibrosis in adults. The coexistence
of joint, skin or ophthalmic symptoms, mucosal dryness and thyroid disease should alert us
about other causes of COPD. Bronchiectasis, mostly in women, with Micobacterium avium
complex is associated with low body mass index. Finally, laboral and hobbies history should
be complete in the first interview in pneumologic specialty. Table 5 shows signs and
symptoms to help to exclude COPD.
History of smoking <10 pack-year
Onset before 40 years old
Decline of FEV1 >75 mL per year
Autoimmune or collagenous disease
Ambiental exposure
Systemic symptoms
Progression of the obstruction years after smoking cessation
Table 5. Signs and symptoms to help to exclude COPD
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Chronic Obstructive Pulmonary Disease - Current Concepts and
Practice
Edited by Dr. Kian-Chung Ong
ISBN 978-953-51-0163-5
Hard cover, 474 pages
Publisher InTech
Published online 02, March, 2012
Published in print edition March, 2012
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In order to correctly reference this scholarly work, feel free to copy and paste the following:
Maria Luisa Martinez Ortiz and Josep Morera (2012). COPD: Differential Diagnosis, Chronic Obstructive
Pulmonary Disease - Current Concepts and Practice, Dr. Kian-Chung Ong (Ed.), ISBN: 978-953-51-0163-5,
InTech, Available from: http://www.intechopen.com/books/chronic-obstructive-pulmonary-disease-currentconcepts-
and-practice/copd-differential-diagnosis