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ORIGINAL ARTICLE
Year : 2006  |  Volume : 23  |  Issue : 3  |  Page : 109-114 Table of Contents   

Patterns in follow up of chronic airway obstruction


Retired Prof. Respiratiory Medicine, KEM Hospital, Mumbai 400012., India

Correspondence Address:
S R Kamat
B - 2 Dattaguru CHS, Deonar, Mumbai 400088.
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-2113.44402

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   Abstract 

Over 5 years from 2000 to 2004 a consecutive series of 420 cases of obstructive airway disease were studied with full history, spirometry, chest radiograph, and other relevant investigations. Several were followed and reassessed: 58.1 % were males - of these 42.1 % were smokers. Sixty percent (252) belonged to age above 40 years; 200 cases revealed clinical history of upto 5 years:

  1. 9.3% had a family history of asthma.
  2. 55.5% showed some changes in chest radiograph
  3. 52.6% had a daily chest symptoms
  4. Chronic cough was seen in 59.5% and paroxysmal dyspnoea in 38.9%
  5. Clinically asthma was labelled in 43.8% and COPD in 56.2%
  6. On follow up 45.6% showed an improvement while 34.1 % deteriorated.
  7. Mainly management was oral theophyllin (93.1 %), beta stimulant inhalers (81.2%). During exacerbations 94.1 % were given antibiotics and 24-29 % had steroids.
  8. A history of hospitalization was seen in 51.9%: 4 died, 4 had IPPR and 8 had malignancies mainly in Lung.
  9. 50.2% had hypertension, 26.1% ischemia and 10.8% a prior lung tuberculosis
  10. 11.2% Showed diabetes.
  11. FVC, FEV 1 , AND VE50 could assess the degree of functinol disability: asthmatics showed a larger bronchoreversibility.
  12. In many, distinction from asthma to COPD was not easy and mainly clinical.

Keywords: Asthma, COPD, Spirometry.


How to cite this article:
Kamat S R. Patterns in follow up of chronic airway obstruction. Lung India 2006;23:109-14

How to cite this URL:
Kamat S R. Patterns in follow up of chronic airway obstruction. Lung India [serial online] 2006 [cited 2021 Jan 20];23:109-14. Available from: https://www.lungindia.com/text.asp?2006/23/3/109/44402


   Introduction Top


With increasing urbanization, widespread prevalence of tobacco smoking, air pollution and occupational exposure to various chemicals in developing world, the prevalence of obstructive airway disease is rising rapidly [1] . Poor congested housing with indoor cooking fuel smoke and acute lung infection - treated inadequately, in children and old persons are important factors in countries like India .[2]

Despite large research in epidemiology and pulmonary functions, diagnosis of obstructive airway disease has remained mainly clinical. In U.S.A, it is the fourth leading cause of death. [1]

Chronic bronchitis / emphysema (COPD) manifests as chronic cough, sputum, variable dyspnoea with exacerbations as acute bronchospasm, lung infection, hypoxemia and later cardiac failure. An earlier classification, described this syndrome as simple bronchitis, subclassified as mucoid, frothy, purulent and with airway spasm [3] . Pulmonary function in early stages could be normal: but it later reveals reduced FEV 1 /FVC% ratio and progressive decline particularly in FEV 1 can be used to grade its severity.

It is not always possible to distinguish COPD from asthma. Many treat the former as poorly responsive asthma [4] . The latter is reckoned to start at an early age, with a positive family history and presenting as episodic cough, chest tightness, wheezing and dyspnoea, triggered by exposure to cold weather, viral (adeno/RSV) infections, exposure to allergenic animal/plant/chemical/fungal products or stress. The attacks may be worse at late night/mornings, with associated acute wheezing and anoxemia. There may be history of long remission with normal lung function and stable asymptomatic status. There is, in clinically symptomatic phase, a large improvement in lung functions after bronchodilator aerosol. [5]

There are theoretical differences between asthma and COPD. While in former there is airway hyperactivity to histamine / leucotriene, eosinophilic inflammation and degranulation of mast cells. In COPD, there may be neutrophilic inflammation macrophage excess with mucus secretion, parenchymal destruction (mediated by TNF, IL 8 , LTB 4 ) with goblet cell hyperplasia. The response to steroids and bronchodilator aerosol may be distinct [6] But about 1020% cases may overlap: some think separation in many may be difficult [7],[8] .

We may have been following cases of airway obstructive disease, exclusive of other primary lung pathology and are presenting a series of consecutive 420 patients seen and followed from year 2000 to 2004. All were personally seen several times and evaluated with lung function and relevant investigations.


   Material and Methods Top


During regular pulmonary clinic practice those who were clinically fitting into the spectrum of obstructive airway disease were included in this effort. Each case was personally seen by the author, a detailed history was taken which included occupation, smoking history (no female smokers), family history, duration of chest symptoms, any history of remission and allergy.

Any associated other diseases were evaluated. All subjects had a chest radiograph, blood counts and other indicated investigations; in older subjects, diabetes (post prandial glucose of 140/90mm or above), ischemic heart (electrocardiographic changes of abnormal Q wave, ST elevation with episodic acute chest pain or ST segment depression each 2mm+, in specified leads) were investigated.

A case of obstructive airway syndrome was labelled as bronchial asthma if the person suffered from paroxysmal breathlessness with wheezing and variable history of symptom free interval; cough with sticky sputum may be present mainly during exacerbations which in later period may become frequent. A person with COPD should have a history of chronic productive cough, extending to 3 months or more with seasonal variation at early stages. Later there is variable paroxysmal and exacerbations dyspnoea. During exacerbations he may present with increased quantity of thick, purulent sputum: Progressively there may be greater functional disability leading to right heart failure.

Usually several follow up assessments were done. At each visit, full lung function, spirometry, airway resistance with post bronchodilator (salbutamol + ipratropium aerosol by electric nebuliser) lung function were done. In serious cases SaO 2 or blood gas measurements were also carried out. We have opted to present analyses by splitting parameter into categories so as to discover patterns as seen in clinical practice in Mumbai.


   Results Top


Over 5 year period we examined 420 cases with obstructive airway syndrome. With seasonal changes in monsoon and winter there were somewhat greater exacerbations. Basal parameters are shown in [Table 1]. There were 58.1% males. As our practice, consists of adult subjects, only 9.8% were upto 20 years age. The other age groups were evenly distributed. Almost one half-revealed a short history of upto 5 years, while 35% had symptom lasting over 10 years.

There were no smokers in females; only 42.1 % males were tobacco smokers. A family history of asthma was revealed in 39 (9.3%) patients; only siblings, parents, uncle, aunt were included for this aspect.

There was no great preponderance of eosinophilia in our group (22 had eosinophil count over 500/ cu ml) In only 44.5% chest radiographs were normal. In many there were nonspecific linear or cystic scars; in few there were old tuberculous residual scars. Gastro - oesophageal reflux symptoms were seen in 27.4%.

Clinical details are shown in [Table 2]. Thus 202 (48.1%) had a history of frequent (more than 4/year) upper respiratory infections. In a majority, daily symptoms of cough/ dyspnoea were present. In 31.2% there were monthly exacerbations while in 16.2% exacerbations occurred less often. Cough was paroxysmal with attacks in 40.5%; In 74.3% sputum was scanty (mainly in attacks - upto 30ml/day) Only in 18 cases, sputum quantity was large.

In 38.9% dyspnoea was complained during exacerbations only; it was severe (gr IV -V by British MRC criteria) in 17.9%. Exertional dyspnoea to mild degree ( gr II - III) was seen in 43.2% cases.

In 43.8% as per standard criteria one would diagnose asthma while in 56.2% COPD (in form of chronic productive cough and exertional dyspnoea ) was reckoned to be the diagnosis. In 51.9% there was a history of hospitalization - suggesting the extent of disability.

The extent of progress on follow up and the type of drug treatment: are shown in [Table 3]. We could not get any follow up assessment in 55 (13.0%) cases. Despite treatment, clinical status was unchanged in 7.2%, improved in 45.6% and deteriorated in 34.1%. Of these 4 died under care in hospital and 4 had to put on IPPR, due to serious respiratory acidosis.

Though most patients were ambulatory, 94.1% were given antibiotics during acute exacerbations, many times by family physicians. For the usual maintenance treatment, oral theophylline was given in 93.1%; inhalers in form of MDI or dry powder with betastimulant/ ipratropium were routinely used for relief in 81.2%. In 29.3% (123 cases) steroid inhalers were regularly used; There was a history of oral steroid intake as a short course in 99 (23.6%) cases. In 41.9% cases parenteral (mainly intramuscular) theophylline was the usual treatment for relief of acute attack. The hospitalized cases, were mainly managed by parenteral theophylline, steroids alongwith bronchodilator nebulisation. In few cases, nebulised steroid was administered.

All associated illnesses are detailed in [Table 4]. As 60% of our patients were older than 40 years it is as expected, than 50.2% showed high blood pressure (140/90 mmHg either by history, treatment or clinical measurement).

There was evidence of ischemia by ECG, clinical history or echocardiography in 26.1% cases. In comparison diabetes (post lunch blood glucose > 130 mg) was seen in 11.2% cases. A history of treatment as pulmonary tuberculosis was present in 10.8%, but active disease was seen uncommonly. There were 8 cases of cancer (in 3 lung, one breast and 4 abdomen). Allergic aspergillosis was suspected in 4 cases with 2 having aspergilloma. A History of allergic skin rashes was uncommon (3.8%): Symptoms HIV/AIDS were present in 5 patients.

The results for lung function are shown in [Table 5]. A large proportion revealed abnormal functions; upto one - half showed large response to salbutamol + ipratropium nebulisation.

For airway resistance measured in 280 cases, 70.4% showed an improvement after nebulisation. We have chosen to present the data by arbitrary division of disability as without age, sex, height standardization, absolute values would be misleading.

There were no real differences between behaviour of asthma and COPD for functional behaviour. Mainly clinical severity at the time of assessment decided the irreversibility. But when percentage changes in FEV 1 is categorized [Table 6], in COPD there is greater tendency of smaller improvement: in asthmatics there is a larger tendency for improvement above 20%. In cases, during a follow-up, these responses were changeable. But it may stated that asthmatics tend to have a greater reversibility.


   Discussion Top


The results obtained in our series show that in many cases, it is difficult to discriminate between the two presentations of asthma and COPD. Our study group had only 40% cases below age 40 years and 48% had a history of illness upto 5 years. The importance of family history of asthma and blood eosinophilia seemed small. In a large proportion chest radiograph showed some abnormalities: while in 10.8% there was evidence of tuberculosis earlier, active disease was rare. On the other hand, cystic lung as primary change with a presentation like obstructive airway disease was seen in 14 cases.

In our group, exacerbations were mainly associated (in 48%) with upper respiratory colds: chest symptoms were seen daily in 52.6% with many suffering from chronic cough with small quantity of sputum daily. Many asthmatics had some exertional breathlessness, suggesting inadequate control. This is corroborated by a large (52%) incidence of hospital admission at some time.

In our series in 87%, we have been able to have a follow up: 45.6% showed an improvement. It is revealing that the major therapeutic history was antibiotic (94%), oral theophyllin (93%) and to a lesser degree beta stimulant pocket inhalers (81%) In contrast, steroid aerosol (29%) and oral steroids (24%) were less frequently used. For relief of acute attacks parenteral theophylline was preferred in 42%.

Our series stresses the need of looking for other diseases, particularly blood pressure, cardiac ischemia, tuberculosis and diabetes.

For detecting bronchodilator response FVC, FEV 1 , VE50 were important but PEF and VE75 were less useful. While airway resistance values were in abnormal range in 88%, the extent of improvement was not quantitatively accurate. Asthmatics showed a tendency for large improvement but generally discrimination from COPD was difficult in a majority on the basis of lung function.

The debate on differences between bronchial asthma and chronic bronchitis will go on. But our series indicate how difficult it is to label correctly in many cases and on individual points. Airway hyper reactivity, tobacco smoking, air pollution and recurrent respiratory infections, allergy, genetic and psychologic factors have been implicated in aetiology and discrimination. But their role in an individual patient is variable. Certainly in our COPD cases, smoking is not the only factor in majority. The role of hyper reactivity as studied by graded histamine aerosol studies has been shown not to separate the two. [9]

A recent paper on GOLD workshop has summarized the picture of COPD [10] . Perhaps in COPD, the role of mucolytics and antibiotics seems greater and that of steroids smaller. But in our practice situation, these difference seem small. In comparison, British guidelines appear less distinct [11] , as also the European position [12].

The role of allergy is considered large in asthma by many. In our present data, we have had a history of cutaneous rashes in 3.8%. We have earlier shown that while these may be a factor in some, this is not a useful procedure in most patients of this syndrome [13],[14] . The factor of bronchoreversibility and airway inflammation have been studied by Chhabra and Bhatnagar [15] and perng et al [16] . These result also indicate the difficulty of assigning their importance in a case.

In our series, this factor of degree of bronchoversibility could not be used to compartmentalize cases. In recent long term follow up of 3099 of asthma cases [17] , it was shown that active asthmatics have a several times higher risk for chronic bronchitis/ emphysema. Thus in 20 year follow up, active asthmatics had 10 times higher risk for chronic bronchitis, 17 times for emphysema and 12.5 for COPD [17] .

While anoxic respiratory failure may be commoner in acute status asthmaticus in COPD cases may show greater prevalence of CO 2 retention and a need for ventilator therapy [19] ; even for diurnal variation in lung function, the differences are relative [20] . In conclusion it seems that while these syndromes are theoretically different, the course in many patients over a long time, does not allow separation and therapeutic approach also seems not too different.

 
   References Top

1.Hurd S. The impact of COPD on Lung health: world wide: epidemiology and incidence. Chest 2000 : 117: 1-4S (Suppl. Feb 2000).  Back to cited text no. 1    
2.Kamat SR Warrier NVU, Shah et al. Clinical and functional patterns in chronic airway obstruction in Bombay: Their correlation with bronchoreversibility and annual changes in spriomentric functions. Lung India 1990: 8: 84-93.  Back to cited text no. 2    
3.Bates DV. The fate of chronic bronchitis. Am. Rev. Resp. Dis. 1973: 108: 1043-1065.  Back to cited text no. 3    
4.Barnes PJ. Mechanisms in COPD: differences from asthma. Chest: 2000: 117: 10-14S (Suppl. Feb 2000).  Back to cited text no. 4    
5.Kamat SR. Problem of COPD: aetiopathology, management and differentiation from bronchial asthma, Lung India 2001: 19: 18-21.  Back to cited text no. 5    
6.Ogilive AG. Asthma: a study in prognosis of 1000 patients. Thorax 1962: 17: 183-189.  Back to cited text no. 6    
7.Oppenheimer EA, Rigatto M and Fletcher CM. Airway obstruction before and after isoprenaline, histamine and prednisolone in patients with chronic obstructive bronchitis. Lancet: 1968:1:552-557.  Back to cited text no. 7    
8.Petty TL, Pierson DI, Dick NP, Hudson LD. And Walker SH. Follow up - evalution of prevalence study of chronic bronchitis and chronic airway obstruction. Am.Rev. Resp. Dis. 1976: 114: 881-890.  Back to cited text no. 8    
9.Rupwate RU. Kolhatkar VP, Parmar DM. Shah SV. Mahashur AA. And Kamat SR, Histamine sensitivity does not separate asthma from chronic bronchitis. Lung India 1990 : 8.15-18.  Back to cited text no. 9    
10.Pauwels RA, Buist AS. Calverley PM, Jenkins CR. Hurd SS. The GOLD Scientific committee: Global strategy for the diagnosis, management and prevention of COPD: NHLBI / WHO: Global initiative for COPD ( GOLD) Workshop summary, Am. J. Resp. Crit. Care Med 2001:163:1256-1276.  Back to cited text no. 10    
11.COPD; national guidelines on management of COPD in adults in primary and secondary care. Thorax 2004: 59: Supplement 1.  Back to cited text no. 11    
12.Celi BR. MacNee W and committee members: standards for the diagnosis and treatment of patients with COPD: A summary of the ATS/ERS: Position paper: Eur Resp. J: 2004: 23: 932- 946.  Back to cited text no. 12    
13.Telang JV. Mahashur AA, Shah SP, Kamat SR. Experience with intradermal antigenic tests and immunotherapy in bronchial asthma. j.Assoc. Phys. Ind 1986: 24: 189-190.  Back to cited text no. 13    
14.Rupwate RU, Potdar PV, Kamat SR, comparison of allergic markers and airway hyperreactivity in bronchial asthma and chronic bronchitis.Lung India 1990 : 8: 19-22.  Back to cited text no. 14    
15.Chhabra SK, Bhatnagar S. comparison of bronchodilator responsiveness in asthma and COPD. Ind. J.Chest Dis, allied Sc. 2002: 44: 91-97.  Back to cited text no. 15    
16.Perng DW, Huang HY, Chen HM, Lee YC, Perng RP. Characteristics of airway inflammation and bronchoreversibility in COPD. Chest 2004: 126:375-381.  Back to cited text no. 16    
17.Silva GE, Sherril DL. Guerra, Barbee RA, Asthma as a risk factor for COPD in a longitudinal study, Chest 2004: 126: 56-65.  Back to cited text no. 17    
18.Shah SP, Mahashur AA. Kamat SR. Blood gas behaviour in status ashtmaticus. j. Assoc. Phys. Ind 1984 : 32: 851-854.  Back to cited text no. 18    
19.Kamat SR, Shobha Heera, Potdar PV, Shah SV, Bhambure MN, and Mahashur AA, Bombay experience in intensive respiratory care over 6 years, j. Postgrad. Med. 1989 : 35: 123- 134.  Back to cited text no. 19    
20.Patil JD, Rupwate RU, Kolhatkar VP, Potdar PV and Kamat SR, comparison of diurnal and circadian variations in normal, bronchial asthmatics and chronic bronchitis, Lung India 1989: 7: 107-112.  Back to cited text no. 20    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]



 

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