|Year : 2021 | Volume
| Issue : 2 | Page : 70-74
Recurrent hemoptysis in a patient with bronchial asthma
Vishnu M Sharma, Baseer Ahmmad Walikar
Department of Respiratory Medicine, AJ Institute of Medical Sciences and Research Centre, Mangalore, Karnataka, India
|Date of Submission||10-Feb-2021|
|Date of Decision||07-Apr-2021|
|Date of Acceptance||09-Apr-2021|
|Date of Web Publication||21-Jun-2021|
Dr. Vishnu M Sharma
Department of Respiratory Medicine, AJ Institute of Medical Sciences and Research Centre, Kuntikana, Mangalore, Karnataka
Source of Support: None, Conflict of Interest: None
Hemoptysis is not a common symptom in bronchial asthma. We aim to discuss the approach to a patient with uncontrolled asthma with recurrent hemoptysis in this case-based discussion. Causes in such cases include pulmonary tuberculosis, bronchiectasis, endobronchial lesions, bronchial carcinoid, factitious hemoptysis, allergic bronchopulmonary aspergillosis, granulomatosis with polyangiitis, allergic angiitis (hypersensitivity vasculitis), Churg-Strauss syndrome, and valvular heart disease which can coexist with asthma.
Keywords: Allergic bronchopulmonary aspergillosis, bronchial asthma, differential diagnosis, radiological features, recurrent hemoptysis, serum immunoglobulin E
|How to cite this article:|
Sharma VM, Walikar BA. Recurrent hemoptysis in a patient with bronchial asthma. J Adv Lung Health 2021;1:70-4
| History|| |
A35-year-old female patient was admitted for the evaluation of recurrent hemoptysis. She was a known asthmatic since the last 15 years. She was on a regular inhaled bronchodilator and inhaled glucocorticosteroid since the last 5 years. Since the last 2 years, she had frequent exacerbations once in 2–3 months requiring increase in the dose of medications. During exacerbations, she used to have cough, and scanty hemoptysis which used to subside with symptomatic treatment. She used to receive rescue course of oral steroids in the form of prednisolone 20 mg once daily for 5-7 days during exacerbations. There was no history of fever, weight loss, chest pain, purulent sputum, postural variation for cough and sputum production. She had no history suggestive of allergic rhinitis. She had no symptoms suggestive of gastroesophageal reflux disease. She had no history of palpitations, chest pain or paroxysmal nocturnal dyspnea. No past history of pulmonary tuberculosis.
Question 1: Which of the following is LEAST LIKELY to cause recurrent hemoptysis in this patient?
- Pulmonary tuberculosis
- Mitral stenosis
- Bronchogenic carcinoma
- Factitious hemoptysis.
Answer: D. Bronchogenic carcinoma is least likely in this age group. Patients with bronchial asthma who develop recurrent exacerbations are at higher risk to develop pulmonary tuberculosis as they are usually administered systemic steroids during exacerbation. Long-term use of inhaled Glucocorticosteroids also increase the risk of pulmonary tuberculosis. Patients with long-standing asthma can develop bronchiectasis due to mucous plugging and bronchial obstruction. Mitral stenosis is more common in females, symptoms can be atypical in some patients which can mimic bronchial asthma and may present with hemoptysis and recurrent exacerbation of breathlessness. In some patients, mitral stenosis can coexist with asthma. Factitious hemoptysis is not uncommon in females, can manifest as a symptom of underlying psychological disturbance which may be aggravated by chronic disease like asthma.
Further detailed history was elicited. Her symptoms were characteristic of bronchial asthma. No symptoms suggestive of any psychological stress.
Question 2: Which of the following symptom is NOT suggestive of bronchial asthma?
- Episodic breathlessness relieved with bronchodilators
- Specific precipitating factors
- Progressive breathlessness over a period of time
- Symptom-free interval in between the exacerbations
- Other associated allergic manifestations.
Answer: C. Progressive breathlessness is not a symptom of bronchial asthma. It is suggestive of COPD or asthma COPD overlap. Most often asthma is diagnosed by a carefully taken history. Spirometry will help to confirm the reversible airflow obstruction characteristic of asthma.
| Physical Examination|| |
She was conscious, alert, and cooperative. Higher mental functions were normal. She had no clubbing, no respiratory distress. She had no tachypnea or tachycardia. General physical examination was unremarkable. Respiratory system examination revealed bilateral polyphonic rhonchi. No crepitation. Cardiovascular system examination and other systemic examination were normal.
Question 3: Which of the following is LEAST LIKELY differential diagnosis in this patient in addition to bronchial asthma?
- Slow growing benign endobronchial lesion
- Allergic bronchopulmonary mycosis
- Pulmonary tuberculosis
- Recurrent pulmonary embolism.
Answer: E. This patient has no known risk factors to develop pulmonary embolism. She had no signs of peripheral venous thrombosis. She had no features of pulmonary hypertension on clinical examination. All the other conditions can coexist with asthma and can lead to recurrent hemoptysis. Active pulmonary tuberculosis can sometimes present with recurrent hemoptysis without other systemic symptoms such as fever and weight loss. Other possible causes for hemoptysis in an asthmatic include allergic bronchopulmonary aspergillosis (ABPA), granulomatosis with polyangiitis (Wegener's granulomatosis) allergic angiitis (hypersensitivity vasculitis), and Churg-Strauss syndrome (eosinophilic granulomatosis with polyangiitis).
Question 4: Which of the following is NOT a cause for poor control of symptoms in a patient with asthma?
- Poor adherence to medications
- Poor inhalation technique
- Low body mass index (BMI)
- Continued exposure to triggers
- Psychological stress.
Answer: C. Obesity can lead to poor asthma control. A detailed history should be taken when a patient with asthma has poor control of the disease. This patient was taking medications regularly, her inhaler technique was correct, BMI was 22.4 kg/m2, she had no comorbidities, no specific triggers, or exposure history to allergens. She denied any psychological stress.
| Investigations|| |
Her total white cell count was 14500/cmm and eosinophils were 16%. The absolute eosinophil count was 2320/cmm. Blood sugar, renal function, liver function, thyroid function tests were normal. Serum immunoglobulin E (IgE) was found to be elevated to 2,520 IU/ml. Sputum AFB smear was negative. Sputum gram stain and culture did not show any pathogen.
Question 5: Which is a WRONG statement regarding serum IgE?
- Associated with Type 1 hypersensitivity reaction
- Increases in exposure to allergens
- May be normal in nonallergic asthma
- Anti IgE therapy may be useful in the treatment of asthma
- The level of serum IgE reduces after allergen immunotherapy.
Answer: E. IgE level usually does not change much in patients who receive allergen immunotherapy. Immunotherapy acts by promoting regulatory responses involving regulatory T-cells and IgG-blocking antibodies so as to block the IgE-driven allergic responses in asthma.
Chest X-ray PA view [Figure 1] was taken.
Question 6: What is the MOST LIKELY diagnosis from the chest X-ray?
- Pulmonary tuberculosis
- Bronchogenic carcinoma
- Carcinoid tumor.
Answer: Chest x ray shows the finger in glove sign suggestive of ABPA. This occurs due to bronchial obstruction, where the bronchus distal to the obstruction is dilated with the presence of mucous secretions. This can occur in obstructive causes such as tumor, stricture, or foreign body. Nonobstructive causes include asthma, cystic fibrosis, and ABPA.
A presumptive diagnosis of ABPA was done with the chest x-ray. Further evaluations were done to confirm the diagnosis.
Question 7: Which of the following is NOT useful in the diagnosis of ABPA?
- Serum precipitin test for ABPA
- Skin prick test for Aspergillus
- Serum IgE estimation
- Family history of asthma
- High resolution computed tomography (CT) scan of thorax.
Answer: D. History of asthma in the individual is helpful but family history is not useful for diagnosis of ABPA.
High-resolution CT scan was done [Figure 2].
Question 8: Which of the following high-resolution CT (HRCT) finding is NOT a characteristic feature of ABPA?
- Central bronchiectasis
- High-attenuation mucus
- Centrilobular nodules
- Fleeting shadows
Answer: C. Centrilobular nodules are small 5–10 mm lung nodules seen within secondary pulmonary lobules in HRCT. They space the pleural surface. Centrilobular nodules can occur in a variety of conditions like hypersensitivity pneumonitis, Small airway disease, Infectious airways diseases (endobronchial spread of tuberculosis or nontuberculous mycobacteria, bronchopneumonia). Rare causes include bronchoalveolar carcinoma, pulmonary edema, and vasculitis.
High attenuation mucus has almost 100% specificity for diagnosing ABPA. High attenuation mucus is said to be present if the mucus plug is visually denser than the normal skeletal muscle. HRCT scan chest of our patient showed finger in glove appearance with high attenuation mucus thus confirming the diagnosis of ABPA.
| Diagnostic criteria for Allergic bronchopulmonary aspergillosis|| |
ABPA is found most commonly in atopic patients, or in patients with bronchial asthma or cystic fibrosis.
In the year 1977, Rosenberg et al. proposed the diagnostic criteria for ABPA known as Rosenberg-Patterson Criteria.
(1) Asthma, (2) Presence of fleeting or fixed pulmonary opacities on chest radiograph, (3) Immediate cutaneous hypersensitivity reaction to aspergillus fumigatus, (4) Total serum IgE elevated, more than 1000 IU/mL, (5) Precipitating antibodies against Aspergillus fumigatus, (6) Peripheral blood eosinophilia, (7) Central or proximal bronchiectasis with normal tapering of distal bronchi.
(1) Golden brown sputum plugs in expectorant, (2) Positive sputum culture for Aspergillus species, (3) Late (Arthus-type) skin reactivity to Aspergillus fumigatus.
In 2012, minimum criteria and additional criteria for diagnosis of ABPA were proposed.
(1) Patients with asthma or cystic fibrosis, (2) Worsening lung function, (3) Positive skin prick test with Aspergillus species, (4) Total serum IgE greater than 1000 ng/mL (416 IU/mL), (5) Increased Aspergillus species-specific IgE and IgG antibodies, (6) Infiltrates noted on chest radiography.
(1) Increase in serum eosinophilia when the patient is not on corticosteroids (more than 400 eosinophils/μL), (2) Aspergillus species-specific precipitating antibodies, (3) Central bronchiectasis, (4) Aspergillus species-specific containing mucus plugs.
In 2013, International Society for Human and Animal Mycology Working Group proposed modified criteria as follows.
(1) Asthma, (2) Cystic fibrosis.
Obligatory criteria (both need to be present)
(1) Type I Aspergillus skin test positive (immediate cutaneous hypersensitivity reaction to Aspergillus fumigatus) or elevated IgE levels against Aspergillus fumigatus, (2) Elevated total IgE levels more than 1000 IU/mL (unless all other criteria are met, then total IgE levels can be <1000 IU/mL).
Other criteria (two out of three at least)
(1) Presence of IgG antibodies against Aspergillus fumigatus or precipitating antibodies, (2) Presence of fleeting or fixed pulmonary opacities on chest radiograph consist with ABPA, (3) Eosinophil count more than 500 cells/μL in steroid naïve patient (may be a historical value).
Modified Rosenberg-Patterson diagnostic criteria:
- Episodic bronchial obstruction (asthma)
- Peripheral blood eosinophilia (≥500/mm3)
- Immediate skin reactivity or specific IgE antibody to filamentous fungal antigen
- Precipitating antibodies or IgG antibodies against filamentous fungal antigen
- Elevated serum IgE concentrations (≥417 IU/mL)
- History of pulmonary infiltrates (transient or fixed)
- Central bronchiectasis.
Allergic bronchopulmonary mycosis (ABPM) is caused by colonization of the respiratory tract by various fungi. ABPA entails hypersensitivity to Aspergillus species.
New clinical diagnostic criteria for ABPM in patients without cystic fibrosis:
- Current or previous history of asthma or asthmatic symptoms
- Peripheral blood eosinophilia (≥500 cells/mm3)
- Elevated total serum IgE levels (≥417 IU/mL)
- Immediate cutaneous hypersensitivity or specific IgE for filamentous fungi
- Presence of precipitins or specific IgG for filamentous fungi
- Filamentous fungal growth in sputum cultures or bronchial lavage fluid
- Presence of fungal hyphae in bronchial mucus plugs
- Central bronchiectasis on CT
- Presence of mucus plugs in central bronchi, based on CT/bronchoscopy or mucus plug expectoration history
- High attenuation mucus in the bronchi on CT.
Filamentous fungi in criteria 4–6 should be identical.
Patients that meet 6 or more of these criteria are diagnosed with ABPM.
In addition to the standard asthma medications patient was started on oral prednisolone 0.5 mg/kg/day for 4 weeks. She showed marked improvement in symptoms. The steroid was tapered gradually. Radiological improvement was evident after 3 months [Figure 3]. Chest x-ray after 1 year showed marked resolution [Figure 4]. Her exacerbations, cough, and hemoptysis subsided after starting oral steroids.
| Conclusions|| |
ABPA should be considered as a differential diagnosis in a patient with recurrent exacerbation of asthma and hemoptysis.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Jick SS, Lieberman ES, Rahman MU, Choi HK. Glucocorticoid use, other associated factors, and the risk of tuberculosis. Arthritis Rheum 2006;55:19-26.
Lee CH, Kim K, Hyun MK, Jang EJ, Lee NR, Yim JJ. Use of inhaled corticosteroids and the risk of tuberculosis. Thora×2013;68:1105-13.
Crimi C, Ferri S, Campisi R, Crimi N. The link between asthma and bronchiectasis: State of the art. Respiration 2020;99:463-76.
Raj B, Chawla RK. Fictitious haemoptysis. Indian J Chest Dis Allied Sci 1985;27:190-2.
Antoniu SA. Descriptors of dyspnea in obstructive lung diseases. Multidiscip Respir Med 2010;5:216-9.
Gosavi S, Nadig P, Haran A. Factors contributing towards poor asthma control in patients on regular medication. J Clin Diagn Res 2016;10:OC31-5.
Froidure A, Mouthuy J, Durham SR, Chanez P, Sibille Y, Pilette C. Asthma phenotypes and IgE responses. Eur Respir J 2016;47:304-19.
Agarwal R, Khan A, Garg M, Aggarwal AN, Gupta D. Pictorial essay: Allergic bronchopulmonary aspergillosis. Indian J Radiol Imaging 2011;21:242-52.
] [Full text]
Boitsios G, Bankier AA, Eisenberg RL. Diffuse pulmonary nodules. AJR Am J Roentgenol 2010;194:W354-66.
Agarwal R. High attenuation mucoid impaction in allergic bronchopulmonary aspergillosis. World J Radiol 2010;2:41-3.
Patel AR, Patel AR, Singh S, Singh S, Khawaja I. Diagnosing allergic bronchopulmonary aspergillosis: A review. Cureus 2019;11:e4550.
Rosenberg M, Patterson R, Mintzer R, Cooper BJ, Roberts M, Harris KE. Clinical and immunologic criteria for the diagnosis of allergic bronchopulmonary aspergillosis. Ann Intern Med 1977;86:405-14.
Rodrigues J, Caruthers C, Azmeh R, Dykewicz MS, Slavin RG, Knutsen AP. The spectrum of allergic fungal diseases of the upper and lower airways. Expert Rev Clin Immunol 2016;12:531-50.
Agarwal R, Chakrabarti A, Shah A, Gupta D, Meis JF, Guleria R, et al
. Allergic bronchopulmonary aspergillosis: Review of literature and proposal of new diagnostic and classification criteria. Clin Exp Allergy 2013;43:850-73.
Asano K, Hebisawa A, Ishiguro T, Takayanagi N, Nakamura Y, Suzuki J, et al
. New clinical diagnostic criteria for allergic bronchopulmonary aspergillosis/mycosis and its validation. J Allergy Clin Immunol 2021;147:1261-8.e5.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]