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Year : 2018  |  Volume : 6  |  Issue : 1  |  Page : 17-20

A Case of Unexplained Shortness of Breath

Department of General Medicine, Calcutta National Medical College, Kolkata, West Bengal, India

Date of Web Publication3-Jan-2018

Correspondence Address:
Sudip K Majumdar
Department of General Medicine, Calcutta National Medical College, 32, Gorachand Road, Kolkata 700014, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jacp.jacp_16_16

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Unexplained shortness of breath is a challenging problem in clinical medicine. Many a times, the cause remains unexplored. Herein, we report one unusual case in a middle-aged chicken handler who had repeatedly been treated with antitubercular drugs with a diagnosis of pulmonary tuberculosis. However, it was finally recognized as a case of hypersensitivity pneumonitis. This case reminds us of the importance of professional history taking. We are also apprehensive regarding the possibility of a burden of a similar situation in the background of ever-growing slaughter houses running without proper precautions.

Keywords: Chicken handler’s disease, DPLD, hypersensitivity pneumonitis, occupational lung disease, shortness of breath

How to cite this article:
Majumdar SK, Datta S, Biswas T, Mukherjee S. A Case of Unexplained Shortness of Breath. J Assoc Chest Physicians 2018;6:17-20

How to cite this URL:
Majumdar SK, Datta S, Biswas T, Mukherjee S. A Case of Unexplained Shortness of Breath. J Assoc Chest Physicians [serial online] 2018 [cited 2023 Jan 28];6:17-20. Available from: https://www.jacpjournal.org/text.asp?2018/6/1/17/220987

  Introduction Top

Shortness of breath or dyspnea is a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity.[1] It is a common presenting symptom of many causes. Most cases of dyspnea are primarily caused by cardiac or pulmonary diseases; therefore, the differential diagnosis should be expanded to include asthma, chronic obstructive pulmonary disease (COPD), diffuse pulmonary lung disease (DPLD), pulmonary thromboembolism, pulmonary arterial hypertension, metabolic cause, neuromuscular abnormality, hypersensitivity pneumonitis (HP), etc. to explain shortness of breath in an unusual case. The condition of some patients has been inappropriately labeled as psychogenic dyspnea or physical deconditioning when their dyspnea remains unexplained to reach an appropriate clinical diagnosis.

HP or extrinsic allergic alveolitis is a spectrum of interstitial, alveolar, and bronchiolar lung diseases, which result because of immunologically induced inflammation in response to inhalation[2] of a wide variety of materials that may lead to irreversible lung damage. It is not associated with increased serum IgE or eosinophils.[3] The prevalence of HP is variable in different populations due to difference in intensity, frequency, and the duration of inhalation exposure. The population at risk and the season of exposure vary with the type of HP. This is most clearly demonstrated in HP caused by bird exposure such as bird fancier’s disease, chicken handler’s disease,[3] duck fever, and farmer’s lung. There are three main forms of HP: acute, subacute, and chronic forms. Not very surprisingly, chronic HP may often be confused with other diseases as common as chronic bronchitis or as morbid as DPLD that includes idiopathic pulmonary fibrosis (IPF), NonSpecific Interstitial Pneumonia (NSIP), sarcoidosis, and also organic toxic dust syndrome. In the case of acute presentation, it may be confused with respiratory infection. Therefore, making an early diagnosis is of immense importance [Figure 1] and [Figure 2],.
Figure 1: Chest X-ray Postero-anterior (PA) view showing reticulonodular opacity

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Figure 2: HRCT thorax showing reticular opacity with bronchiectatic changes

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  Case Report Top

A 45-year-old male, nonsmoker, presented with a complaint of low-grade fever that lasted a few weeks along with increased shortness of breath for the past 1 week. Fever was low-grade, intermittent in nature and subsided following the use of medications. He also complained of shortness of breath, which gradually progressed for the past 1–2 years and increased over the last few days. At presentation, the severity of shortness of breath was Modified Medical Research Council (mMRC) grade 4. He also complained of having dry cough for the past 9–10 years; however, for the past 1 week, his cough was mucoid in nature. On enquiry, he did not mention any history of weekly variation of cough and breathlessness. In addition, there was no history suggestive of pleuritic type of chest pain, paroxysmal nocturnal dyspnea, hemoptysis, wheeze, epistaxis, and joint pain. He had a history of recurrent hospital admission for the same complaint. He had been treated as a case of sputum negative pulmonary tuberculosis twice in the past. During the previous treatment, he had received Category 2 antitubercular drugs (similar to previously treated cases), which he had completed few months back. He had been working for more than 25 years at a slaughterhouse dealing with chicken.

On examination, he was orthopneic. His accessory muscles of respiration were working. He was admitted with tachypnea (28/min), tachycardia (108 beats/min), blood pressure (BP) around 118/76 mmHg, and cyanosis with SPO2 80%; jugular venous pressure was raised and pulsatile. On auscultation, there was bilateral vesicular breath sound with coarse bilateral late inspiratory crackles along with accentuated P2.

  • On investigating the patient, the following were noted: Hb% − 12.5 g/dL (N − 78%, L − 20%, E − 2%); total lung capacity (TLC) − 14,500/cmm; erythrocyte sedimentation rate (ESR) − 46 in 1st h.
  • liver function test (LFT) was within normal limit.
  • The function of the kidneys was determined by the following: urea − 40 mg/dL; creatinine − 1.1 mg/dl; Na+ − 138 meq/dL; K+ − 4.5 meq/dl.
  • Sputum for acid fast bacilli (AFB) stain and Gram stain was negative.
  • Tests on the blood revealed the following: arterial blood gas (ABG) − pH 7.45; pO2–55 mmHg; pCO2–38 mmHg; HCO3 − 26 mmHg (type 1 respiratory failure).
  • Electrocardiography (ECG) was suggestive of right axis deviation, poor R wave progression, and P pulmonale.
  • Reticular opacity and honeycombing were noted on chest X-ray.
  • high resolution computer tomography (HRCT) scan of the thorax revealed reticulonodular opacity with ground glassing and bronchiectasis.
  • Pulmonary function test (PFT) showed restrictive changes with forced vital capacity (FVC) of 1.48 L (66% of predicted value) and forced expiratory volume in 1second (FEV1) of 0.79 L.
  • 2D echocardiography with color Doppler detected residual volume (RV) dilatation with increased Tricuspid regurgitation (TR) jet velocity and pulmonary arterial systolic pressure (PASP) of 45 mmHg.
  • bronchoalveolar lavage (BAL) fluid study revealed 290 total cells with predominant lymphocytosis (around 56%), moderate neutrophilia, and mild eosinophilia. CD4/CD8 ratio was 0.8.

During hospital stay, he improved gradually. He was diagnosed to be a case of chronic HP or extrinsic allergic alveolitis considering his age-old profession along with pulmonary hypertension, which was secondary to chronic HP. His condition was explained to him and his family members. Thereafter, he was counseled to consider modification in his livelihood. He was treated with antibiotics. He also received oral prednisolone (1 mg/kg BW) for 4 weeks with a plan to taper off on subsequent visits. We also discussed the situation with his employer, who incidentally came to visit him. We advised his employer to consult with occupational health experts for preventive measures to be undertaken for the rest of the workers.

  Discussion Top

A diagnosis of HP was made considering the clinical presentation and radiological evidence. This was further supported by a BAL study in the background of a temporal relationship of exposure to avian antigens with the disease onset. Though our patient did not experience any weekly variation in his respiratory symptoms similar to other persons having occupational health hazards, it was consistent with his exposure pattern.

HP is a pulmonary disease that occurs due to inhalational exposure to a variety of antigens leading to an inflammatory response of the alveoli and small airways.[2] Systemic manifestations such as fever and fatigue can accompany respiratory symptoms. The disease is histologically characterized by a triad of non-necrotizing granulomas, chronic inflammatory changes in the small airways, and diffuse interstitial infiltrates of the chronic inflammatory cells.[4]

Those who are at particular risk include farmers, bird handlers, and industrial workers. Occupational exposure to birds causes HP, as seen in poultry workers’ lung and chicken handler’s disease. The disease is predicted by exposure to antigens derived from feathers, droppings, and serum proteins. Our patient had a chronic course of the disease supported by a history of more than 20 years of exposure to chicken. Therefore, the disease was diagnosed as is a case of chronic HP because of its long duration of symptoms and the subsequent development of pulmonary arterial hypertension (PAH). Ground glass opacity on imaging and leukocytosis can be explained by the underlying acute infectious/inflammatory process on chronic HP.

There are no specific radiological, immunological, or physiological diagnostic tests for HP. Diagnosis is considered based on the following criteria:
  • Major criteria:[5],[6] (1) symptoms compatible with HP, (2) evidence regarding exposure to antigens either by history taking or by the detection of antibody in the serum and/or BAL fluid, (3) finding the symptoms compatible with HP on chest X-ray or a HRCT scan of the thorax, (4) BAL fluid lymphocytosis (if bronchoalveolar lavage performed), (5) histologic changes compatible with HP (if lung biopsy performed), and (6) positive natural history.
  • Minor criteria:[5],[6] (1) basilar crackles, (2) decreased diffusion capacity, and (3) arterial hypoxemia either at rest or with exercise.[5],[6]

The diagnosis of chronic HP requires the fulfillment of more than four major criteria and less than two minor criteria. Our patient met the diagnostic criteria for chronic HP.The recognition and diagnosis of HP is often challenging because of difficulty in identifying a temporal relationship with the offending antigen, and because, often, it mimics other respiratory disorders.

We find this case to be unique because though there are several previous case reports of bird fancier’s disease, farmers’ lung, etc., there are no case reports concerning patients handling chickens at least in this part of the world.

Chicken handler’s disease is a cause of chronic HP, and its prevalence may be high, because in India the poultry industry has made tremendous strides over the past 2–3 decades.[7] The number of people involved in this business is also growing every day along with shift in food habits in our country. Unfortunately, there are no available data regarding the respiratory complaints of those people directly involved to this industry, at least in this part of the country. We have already planned a pilot project to probe the burden of this problem.

  Conclusion Top

Prevention and early diagnostic measures should be undertaken for those who are at risk of developing HP. This requires adequate knowledge, awareness, and understanding by the treating physician. Physicians should be encouraged to take a detailed occupational history of patients presenting with respiratory symptoms, particularly in those with unexplained breathlessness. The case we have discussed herein also tells us about the need for initiatives which should be undertaken by the occupational health expert to cater to this segment of people.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patients has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

American Thoracic Society. Dyspnea: Mechanism, assessment & management. A consensus statement. Am J Respir Crit Care Med 1999;159:321-40.  Back to cited text no. 1
Fink JN. Hypersensitivity pneumonitis. J Allergy Clin Immunol 1984;74:1-10.  Back to cited text no. 2
Kurup VP, Zacharisen MC, Fink JN. Hypersensitivity pneumonitis. Indian J Chest Dis Allied Sci 2006;48:115-28.  Back to cited text no. 3
Coleman A, Colby TV. Histologic diagnosis of extrinsic allergic alveolitis. Am J Surg Pathol 1988;12:514-8.  Back to cited text no. 4
Schuyler M, Cormier Y. The diagnosis of hypersensitivity pneumonitis. Chest 1997;111:534-36.  Back to cited text no. 5
Zacharisen MC, Fink JN. Hypersensitivity pneumonitis. In: Gramer LC, Greenberger PA, editors. Atterson’s Allergic Disease. Philadelphia: Lippincott Williams & Wilkins; 2002. p. 515-27.  Back to cited text no. 6
Mehta R, Nambiar RG, Singh SK, Subrahmanyam S, Ravi C. Livestock Industrialization, Trade & Social Health Environment Impact in Developing Countries: A Case Study of Indian Poultry Sector. Phase 1 project report submitted to IFPRI, May 2002. [Mimeo].  Back to cited text no. 7


  [Figure 1], [Figure 2]


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