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- Acad Pathol
- v.7; Jan-Dec 2020
Educational Case: Asthma: Clinical Features and Morphologic Findings
1 Department of Pathology, The University of Chicago, IL, USA
Urooba nadeem, aliya n. husain.
The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040 . 1
Objective: RS4.4: Asthma . Compare and contrast the clinicopathological features and causes of asthma and describe the morphologic changes and consequences that result in airflow obstruction.
Competency 2: Organ System Pathology; Topic: Respiratory System (RS); Learning Goal 4: Obstructive Diseases of the Lung.
A 13-year-old male presents to the emergency department with acute onset of breathlessness. He has had recurrent, episodic attacks of wheezing, cough, dyspnea, itchy red eyes, nasal discharge, stuffiness, and occasional chest tightness for past 2 years. Initially, his symptoms were relieved by short-acting β-blocker, albuterol. However, the frequency and the severity of the symptoms have increased for the past 1 month with the patient waking up with these symptoms. He has a history of eczema. His family history is significant for asthma in his mother.
Physical examination reveals respiratory rate of 22/min and diffuse wheezing all over the lung fields. Pulmonary function test (PFT) shows FEV1/FVC (forced expiratory volume at 1 second [FEV1]/forced ventilatory capacity [FVC]) of 0.65. Forced expiratory volume at 1 second is 60% of predictive and post-bronchodilator therapy the FEV1 increases to 74% of predictive. Chest X-ray is normal.
What is the diagnosis based on clinical findings and pulmonary function test.
Clinical presentation (recurrent, episodic attacks of wheezing, cough, dyspnea, itchy red eyes, nasal discharge, stuffiness, and chest tightness), and PFT findings (FEV1/FVC of 0.65, FEV1 is 60% of predictive and post-bronchodilator therapy the FEV1 increases to 74% of predictive) are consistent with the diagnosis of asthma. Diagnosis of asthma can be confirmed if the evidence of airway obstruction is seen on PFT, especially if it is reversible with a bronchodilator as seen in our case.
What Type of Lung Disease Is Asthma, and What Are Other Diseases in That Category?
Obstructive diseases of lung are characterized by an increased airflow resistance due to partial or complete obstruction of airway at any level from the trachea to the respiratory bronchioles. In contrast, restrictive diseases show reduced lung parenchymal expansion leading to decreased total lung capacity. Obstructive pulmonary diseases can be distinguished from restrictive diseases based on pulmonary function tests. Obstructive disorders show decreased maximal airflow rates during forced expiration, usually expressed as the FEV1 over the FVC. Obstructive pulmonary diseases generally show a FEV1/FVC ratio of less than 0.7 contrasting with restrictive diseases that are characterized by a proportionate reduction in both total lung capacity and FEV1, resulting in normal FEV1/FVC ratio.
Asthma, emphysema, chronic bronchitis, and bronchiectasis are common obstructive lung diseases. Each has distinct clinical and pathologic characteristics ( Table 1 ). 2 Emphysema and chronic bronchitis are frequently grouped as chronic obstructive pulmonary disease (COPD), as the majority of patients share features of both. Also, both entities are triggered by cigarette smoking. Asthma can be distinguished from COPD by the presence of reversible bronchospasm.
Types of Obstructive Pulmonary Disease.
What Are the Differential Diagnoses Based on Clinical Findings?
Cystic fibrosis and noncystic fibrosis bronchiectasis.
Both cystic fibrosis (CF) and diffuse non-CF bronchiectasis present with chronic cough and abundant sputum production that is atypical for an asthmatic child. Furthermore, recurrent chest infections are seen in CF patients from a very young age. Patients with non-CF bronchiectasis frequently report productive cough with sputum expectoration, respiratory distress, growth retardation, and night sweats.
Primary ciliary dyskinesia
Primary ciliary dyskinesia (PCD) commonly involves lower airways. It may present as chronic asthma which is usually unresponsive to maintenance therapy. Patients with unexplained respiratory distress at birth and recurrent upper and lower respiratory infections should be screened for PCD.
Protracted bacterial bronchitis
It presents as chronic cough (lasting ≥ 4 weeks) not responding to asthma treatment and require a prolonged (minimum of 2 weeks) course of antibiotic treatment.
Airway foreign body
The sudden onset of respiratory symptoms is more suggestive of an accidental foreign body aspiration than a sudden onset of asthma. It is more common in young children. The patient may present with choking, persistent cough, unilateral and monophonic wheeze, and respiratory distress.
Vocal cord dysfunction
It is characterized by inappropriate adduction of the vocal cords during inspiration induced by exercise, psychological stress, or local irritation like reflux. It frequently coexists with asthma but is unresponsive to bronchodilator therapy. Patients present with breathlessness, intermittent aphonia or dysphonia, choking sensation, chest tightness or pain, difficulty swallowing, and throat clearing. Direct visualization of the vocal cords by endoscopy is the gold standard for the diagnosis. Abnormal shape of the inspiratory loop is seen on spirometry consistent with a variable extrathoracic obstruction.
Bronchiolitis obliterans occurs secondary to viral and mycoplasma pneumonia infections. It frequently presents as persistent wheezing, rather than paroxysmal symptoms. Computed tomography scan shows a characteristic mosaic pattern and air trapping.
What Is Asthma?
Asthma is a chronic, episodic, inflammatory disorder of the airways associated with bronchoconstriction and airflow limitation that is at least partly reversible, either spontaneously or with treatment. The hallmarks of the disease are as follows 2 :
- ○ Increased airway responsiveness resulting in episodic bronchoconstriction
- ○ Inflammation of the bronchial walls
- ○ Increased mucus secretion
How Does It Present Clinically?
Patients with asthma present with dyspnea, cough, and wheezing due to sudden episodes of bronchospasm. 2 According to the latest National Asthma Education and Prevention Program guidelines, correctly diagnosing asthma is important by establishing the following 3 :
- ○ Episodic symptoms of airflow obstruction or airway hyperresponsiveness
- ○ Airflow obstruction or symptoms are at least partially reversible
- ○ Exclusion of alternative diagnoses.
What Is Acute Severe Asthma (Formerly Known as Status Asthmaticus)?
It is defined as a state of unrelieved attacks of asthma, formerly known as status asthmaticus. It is rare and may prove to be fatal. Usually, it is seen in patients with a long history of severe asthma. Patients may be asymptomatic between episodes. 2
What Are the Risk Factors of Asthma?
Certain factors contribute to the development of airway hyper-reactivity, leading to asthma. These are given as follows 2 :
- ○ Environmental allergens
- ○ Exercise, hyperventilation
- ○ Viral respiratory infections
- ○ Exposure to cold
- ○ Aspirin or nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity
- ○ Inhaled air pollutants such as smoking, sulfur dioxide, ozone, and nitrogen dioxide. Occupational exposure including fumes (epoxy resins, plastics), organic and chemical dusts (wood, cotton, platinum), gases (toluene), or other chemicals (formaldehyde, penicillin products)
What Are the Different Types of Asthma?
Asthma is classified as atopic or non-atopic based on presence or absence of an evidence of allergen sensitization. It may also be categorized according to the triggers that lead to bronchoconstriction. Table 2 shows various types of asthma. 2
Types of Asthma.
Abbreviations: IgE, immunoglobulin E; NSAIDs, nonsteroidal anti-inflammatory drugs.
What Is the Pathogenesis of Asthma?
Asthma results from an interplay between genetic factors, environmental factors, and immune response. Airway inflammation forms the core pathophysiologic mechanism. The pathogenesis of asthma is depicted in Figure 1 . Atopic asthma is characterized by a TH2 and immunoglobulin E (IgE) response to allergens in genetically predisposed individuals. The asthma related genetic polymorphisms possibly influence immune process. Some of the genetic associations are described below 2 :
- ○ Chromosome 5q has a susceptibility locus for asthma close to the gene cluster encoding the cytokines IL-3, IL-4, IL-5, IL-9, and IL-13 and IL-4 receptor among which IL13 gene polymorphisms have the strongest and most consistent association.
- ○ Alleles of class II HLA are associated with production of IgE antibodies against some antigens, like ragweed pollen.
- ○ ADAM33 (a metalloproteinase) gene polymorphisms may be related to increased proliferation of bronchial smooth muscle cells and fibroblasts.
- ○ β2-adrenergic receptor gene variants are linked to differential in vivo airway hyper-responsiveness and in vitro response to β-agonist stimulation.
- ○ IL-4 receptor gene variants are linked to elevated total serum IgE, atopy, and asthma.
Pathogenesis of asthma.
What Are the Morphologic Changes Seen in Asthma?
In patients with severe asthma, the lungs appear overinflated showing atelectatic areas. The most prominent gross finding includes airways (bronchi and bronchioles) occluded by thick, tenacious mucus plugs. 2
A characteristic microscopic finding is Curschmann Spiral ( Figure 2 ) seen in sputum or bronchoalveolar lavage samples of asthma patients. It is the result of mucus plugs extruding from subepithelial mucous gland or bronchioles. Numerous eosinophils with Charcot-Leyden crystals ( composed of an eosinophil protein called galectin-10) are also present. 2 There are other typical microscopic findings of asthma, collectively known as “airway remodeling” that result in airway obstruction, which include ( Figures 3 – 5 ) 2 :
Curschmann spiral (1000×).
Sub-basement membrane fibrosis and submucosal eosinophilic infiltration (×200 magnification).
Squamous metaplasia, sub-basement membrane fibrosis and intraepithelial and submucosal eosinophilic infiltration (×400 magnification).
Goblet cell hyperplasia and smooth muscle hypertrophy (×100 magnification).
- ○ Airway wall thickening
- ○ Subbasement membrane fibrosis (due to type I and III collagen deposition)
- ○ Increase in vascularity and squamous metaplasia
- ○ An increase in the size of the submucosal glands and number of airway goblet cells
- ○ Hypertrophy and/or hyperplasia of the bronchial wall muscle
What Causes Airflow Obstruction in Asthma?
Airflow obstruction is a result of the following changes in asthma 4 :
- Acute bronchoconstriction due to IgE dependent release of mediators (early asthmatic response)
- Airway edema associated with allergen challenge that occurs 6 to 24 hours later (late asthmatic response)
- Exudation of serum proteins and cellular debris resulting in chronic mucus plug formation
- Airway remodeling resulting from structural changes due to chronic inflammation that impacts the extent of airway obstruction reversibility
Airway obstruction leads to increased airflow resistance and expiratory flow rate reduction. These changes result in reduced air expulsion and may lead to hyperinflation of the lung. This overdistention helps preserve airway patency, thus improving expiratory flow. However, it also increases the work of breathing by altering pulmonary mechanics.
- Asthma results in reversible bronchoconstriction due to hyper-responsiveness of the airway to various stimuli.
- Atopic asthma is the result of an immunologic reaction to environmental allergens and is characterized by acute-phase (immediate) and late-phase reactions.
- Nonatopic asthma has less clear triggers but some viral infections and inhaled air pollutants are known to cause it.
- Almost all subtypes of asthma show eosinophils as key inflammatory cells but other inflammatory cells, for example, mast cells, neutrophils, and T lymphocytes can also be found.
- The irreversible component is the result of extensive airway remodeling (sub-basement membrane fibrosis, bronchial glands hypertrophy, and hyperplasia of smooth muscle).
Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.
- Case Report
- Open Access
- Published: 16 December 2008
Bronchial carcinoid in a 39-year-old man treated for bronchial asthma: a case report
- Justyna Emeryk 1 ,
- Elżbieta Czekajska-Chehab 2 ,
- Elżbieta Korobowicz 1 ,
- Marta Korbel 3 ,
- Irena Węgrzyn-Szkutnik 1 &
- Janusz Milanowski 1
Cases Journal volume 2 , Article number: 7414 ( 2008 ) Cite this article
A case study of 39-year old man with persistent wheezing, episodes of haemoptysis and dry cough unsuccessfully treated with inhaled beta2-agonists and steroids for about 10 months. Chest radiograph revealed a disproportion in dimensions between both lungs, with the left one being smaller than the right one. Spirometry demonstrated a restrictive pattern. During bronchoscopy, a polypoid endobronchial tumor, localized in the left main bronchus, completely occluding its lumen, was found. The tumor was diagnosed as carcinoid. In this case, due to the lack of characteristic symptoms, diagnosis of carcinoid was delayed. Patients unsuccessfully treated for bronchial asthma or chronic obstructive pulmonary disease should undergo bronchoscopic examination.
A 39-year-old white man, working as a house builder, was admitted to our pulmonary ward in August 2007 with an eleven-month history of persistent wheezing, heard not only during auscultation but also by patient himself. This wheezing had no correlation with physical exertion. He also reported a few episodes of haemoptysis within last 7 months and dry cough for about a month. Patient's weight was 81.5 kg, his height was 180 cm. Except from nodular goitre (in euthyreosis), the patient reported no other complaints or diseases in his medical history. His family history was not clinically significant. He had a 10 pack-years smoking history, until the age of 31 when he stopped smoking. He drank alcohol occasionally. His symptoms were unsuccessfully treated with inhaled β 2 -agonists and steroids for about 10 months. Apart from these medications, he took no other drugs. On auscultation, there were wheezes in upper fields of both lungs. The chest radiograph (figure 1 ) showed a disproportion in dimensions and vascular markings between both lungs- the left one was significantly smaller and had decreased vascular markings in comparison to the right one- these findings might be the expression of left lung hypoplasia. The heart silhouette was discretely displaced to the left side.
Chest radiograph performed at admission to the hospital .
Spirometry performed during hospitalization in our clinic showed a restrictive pattern (figure 2 ) with forced expiratory volume in one second (FEV 1 ) of 59% predicted and forced vital capacity (FVC) of 66% predicted. The FEV 1 /FVC ratio was 70% predicted.
Flow-volume curve showing a restrictive pattern performed at admission to the hospital .
Bronchoscopy was performed, revealing a polypoid endobronchial tumor, localized in the left main bronchus (2 cm from tracheal bifurcation), completely occluding its lumen. The tumor was biopsied and the specimen was sent to histological examination which gave the diagnosis of bronchial carcinoid.
Thoracic computed tomography showed a polypoid mass in the left main bronchus with a diameter of about 20 mm. The tumor showed very high enhancement after contrast medium administration: from 9 HU (Hounsfield units) (figure 3a ) to 119 HU in arterial phase (figure 3b ) and 47 HU in parenchymal phase (figure 3c ), which is characteristic for carcinoid.
High enhancement of the tumor (arrow) after contrast medium administration: on the left- before administration of contrast medium, in the middle-after administration; arterial phase, on the right-parenchymal phase .
Hilar and mediastinal nodes were not enlarged. In virtual bronchoscopy, as well as in transparent reconstruction of the airways, a total occlusion of the left main bronchus by the tumor could be observed (Figure 4 and 5 ).
Total occlusion of the left main bronchus by the tumor (arrow) .
Amputation of the left main bronchus by the tumor (arrow) .
The patient was transferred to thoracic surgery ward for surgical treatment. He underwent left pulmonectomy and histopathological analysis of post-operative material confirmed the diagnosis of bronchial carcinoid. There were no complications during post-operative period and the patient was discharged from hospital 10 days after the operation. Then, the patient went abroad and was lost for follow-up until May 2008. On control visit in May, he was in very good condition, presenting no signs of pulmonary disease. On physical examination, except from diminished breath sounds and dullness to percussion over left lung (due to pulmonectomy and consequent pleural fluid accumulation) no abnormalities were found. In control computed tomography there were no signs of recurrence of the disease.
Pulmonary carcinoids comprise 1-2% of all lung tumors. They may develop in many locations in the body but most often, they are found in small intestine (26%), respiratory system (25%) and appendix (19%) [ 1 ].
Carcinoid tumors are classified as typical or atypical according to histopathological criteria. This division has a strict extrapolation to survival rates: in case of typical pulmonary carcinoids 5-year survival rate is over 90%, in atypical ones- it is within the range of 40-60% [ 2 ].
The following symptoms are observed most often in patients with carcinoid localized in respiratory system: haemoptysis, cough, recurrent pulmonary infections, fever, chest discomfort, unilateral wheezing and shortness of breath [ 3 ].
Due to the lack of characteristic symptoms, diagnosis of pulmonary carcinoid is delayed and patients are often misdiagnosed with asthma or chronic obstructive pulmonary disease. According to three studies, there is an average delay of, respectively, 19, 13 and 10 months from the first symptoms to the final diagnosis of carcinoid [ 4 – 6 ]. Although general prognosis for patients with this neoplasm is quite favorable, it is obvious that the earlier diagnosis is made, the chances for radical treatment increase.
As the majority of pulmonary carcinoids (70%) are located in the main or lobar bronchi [ 7 ], they are within the reach of a bronchoscope. According to British Thoracic Society, flexible bronchoscopy is a safe procedure and there are no controlled studies concerning the factors disqualifying a patient from it [ 8 ]. Bronchoscopy cannot replace computed tomography, these both procedures are complementary, but to be able to orientate the treatment and prognosis, we have to know the histopathological diagnosis and the specimens for examination can be easily and safely provided by bronchoscopy.
This case is a good example of misdiagnosis of the disease. Extended clinical diagnosis, including computed tomography and bronchoscopy, should be considered in all cases of bronchial asthma or chronic obstructive pulmonary disease which do not respond to standard treatment.
"Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal."
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Authors and affiliations.
Chair and Department of Pulmonology, Oncology and Allergology, Medical University of Lublin, Jaczewski Street 8, 20-950, Lublin, Poland
Justyna Emeryk, Elżbieta Korobowicz, Irena Węgrzyn-Szkutnik & Janusz Milanowski
First Department of Radiology, Medical University of Lublin, Jaczewski Street 8, 20-950, Lublin, Poland
Chair and Department of Clinical Pathomorphology, Medical University of Lublin, Jaczewski Street 8, 20-950, Lublin, Poland
You can also search for this author in PubMed Google Scholar
Correspondence to Justyna Emeryk .
The authors declare that they have no competing interests.
JE performed acquisition of data, review of literature and wrote the paper. ECC performed computed tomography imagings and prepared virtual bronchoscopy reconstructions. EK performed histopathological examination of the tumour. MK was responsible for patient care, follow-up and data collection. IWS was responsible for patient care and drafting of paper. JM performed acquisition of data, revised the manuscript and provided general support as the head of department. All authors read and approved the final manuscript.
Microscopic imaging of bronchial carcinoid (hematoxylin and eosin staining) .
Immunohistochemical staining positive for chromogranine A .
Immunohistochemical staining positive for synaptophysin .
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Authors’ original file for figure 1
Authors’ original file for figure 2, authors’ original file for figure 3, authors’ original file for figure 4, authors’ original file for figure 5, authors’ original file for figure 6, authors’ original file for figure 7, authors’ original file for figure 8, authors’ original file for figure 9, rights and permissions.
This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Cite this article.
Emeryk, J., Czekajska-Chehab, E., Korobowicz, E. et al. Bronchial carcinoid in a 39-year-old man treated for bronchial asthma: a case report. Cases Journal 2 , 7414 (2008). https://doi.org/10.1186/1757-1626-2-7414
Received : 19 November 2008
Accepted : 16 December 2008
Published : 16 December 2008
DOI : https://doi.org/10.1186/1757-1626-2-7414
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- Chronic Obstructive Pulmonary Disease
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- Restrictive Pattern
- Left Main Bronchus
- British Thoracic Society
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- 1. BY 09408103 3-04-2014 CASE STUDY ON ASTHMA
- 2. A 48 yrs old female patient was admitted in the hospital with C/O breathlesness severe for the past one day Chest tightness Cough with expectoration HISTORY OF PRESENT ILLNESS Breathlessness since 7days Cough with expectoration since 7days PAST MEDICAL HISTORY Nil
- 3. PHYSICAL EXAMINATION Patient is conscious,oriented,dyspenic O/E Temp-98.6F Pulse-120 beats/min BP-90/70mmHg RR-25 breaths/min SYSTEMIC EXAMINATION CVS-S1S2+ RS-Wheeze+ CNS-NFND+ P/A-Soft
- 4. LAB INVESTIGATIONS Hb 16.0(↑) 12-15.5g/dl RBC 5.6*×10ᶺ 6(↑)/UL 4.2-5.4×10ᶺ6/UL ESR 25(↑) 5-15mm/hr TOTAL WBC 15.00×10ᶺ9/L(↑) 4.0-11.0×10ᶺ9/L DC N-71 L-23 E-10(↑) 1-6%
- 5. OTHER TESTS Spirometry IMPRESSION 62% of FEV1 was detected DIAGNOSIS Acute exacerbations of Asthma
- 6. DRUG DOSE ROA FREQUENCY DURATION T.UNICONTINE (Theophylline) 1 tab PO BD 5days INJ.AUGMENTIN (Amoxicillin+clavul anicacid) 1.2gm IV BD 3days T.MONTAK LC (Monteleukast+ Levocetirizine) 4 mg+2.5 mg PO BD 5days NEB.IPRAVENT (Ipratropium bromide) 1resp PN TDS 5days T.LYCOLUT (MV,Ca,Fe+FA) 1tab PO OD 5days T.MAHACEF (Cefixime) 200mg PO BD 2days
- 7. CRITICAL ANALYSIS OF PRESCRIPTION MEDICATION ERRORS No medication errors were found DRUG INTERACTIONS Theophylline↔Food(Caeffine containing food)- May increase the serum concentrations of theophylline PHARMACIST INTERVENTION Patient was advised to avoid co-administration of theophylline with caeffine containing foods ..like coffee
- 8. PATIENT COUNSELLING REGARDING DISEASE ASTHMA- is a common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm Symptoms include wheezing, cough, chest tightness, and shortness of breath.
- 9. REGARDING DRUGS Full course of antibiotics should be taken Don’t miss any dose Avoid taking theophylline with caeffine Any seizures ,nausea ,coughing up of blood etc if seen are side effects of theophylline and if she experienced it should be stopped While inhaling ipratropium bromide, it should be prevented from going into eyes,since it can cause irritation and blurred vision. After inhalation the patient should clean her mouth to avoid throat irritation and dry mouth.
- 10. REGARDING LIFE STYLE MODIFICATION Avoid vigorous exercises,and cool places since can cause asthma. Plenty of water should be taken since they keep body’s cells functioning properly, and helps keep the mucus in the airways loose. Eight glasses of water a day is recommended.
- 11. Healthy food choices include: adding more fruits and vegetables,avoid spicy and cold food, fried items as they can cause cough. When you feel out of breath, or become tired, stop what you’re doing and sit down. Rest helps to keep your airways relaxed, and allows you to breathe easier. Exercises like morning walk and yoga should be done regularly as they can improve breathing. Avoid getting in contact with substances like dust,flowers,animal,cigarette smoke,fog etc.
- 12. SOAP NOTES S A 48 year old female patient was admitted in hospital with complaints of breathlesness,cough,chest tightness O On examination patient was dyspenic and pulse rate,Hb,RBC,TWBC,Eosinophills were found to abnormal.Spirometry was done and found to have 62% FEV1 A Based on the above findings and spirometry test, the patient was assessed to have Acute exacerbations of asthma P Patient was treated with Bronchodilators,antibiotics,leukotriene inhibitors and vitamin supplements.
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Case Study: Managing Severe Asthma in an Adult
—he follows his treatment plan, but this 40-year-old male athlete has asthma that is not well-controlled. what’s the next step.
By Kirstin Bass, MD, PhD Reviewed by Michael E. Wechsler, MD, MMSc
This case presents a patient with poorly controlled asthma that remains refractory to treatment despite use of standard-of-care therapeutic options. For patients such as this, one needs to embark on an extensive work-up to confirm the diagnosis, assess for comorbidities, and finally, to consider different therapeutic options.
Case presentation and patient history
Mr. T is a 40-year-old recreational athlete with a medical history significant for asthma, for which he has been using an albuterol rescue inhaler approximately 3 times per week for the past year. During this time, he has also been waking up with asthma symptoms approximately twice a month, and has had three unscheduled asthma visits for mild flares. Based on the National Asthma Education and Prevention Program guidelines , Mr. T has asthma that is not well controlled. 1
As a result of these symptoms, spirometry was performed revealing a forced expiratory volume in the first second (FEV1) of 78% predicted. Mr. T then was prescribed treatment with a low-dose corticosteroid, fluticasone 44 mcg at two puffs twice per day. However, he remained symptomatic and continued to use his rescue inhaler 3 times per week. Therefore, he was switched to a combination inhaled steroid and long-acting beta-agonist (LABA) (fluticasone propionate 250 mcg and salmeterol 50 mcg, one puff twice a day) by his primary care doctor.
Initial pulmonary assessment Even with this step up in his medication, Mr. T continued to be symptomatic and require rescue inhaler use. Therefore, he was referred to a pulmonologist, who performed the initial work-up shown here:
- Spirometry, pre-albuterol: FEV1 79%, post-albuterol: 12% improvement
- Methacholine challenge: PC 20 : 1.0 mg/mL
- Chest X-ray: Within normal limits
Continued pulmonary assessment His dose of inhaled corticosteroid (ICS) and LABA was increased to fluticasone 500 mcg/salmeterol 50 mcg, one puff twice daily. However, he continued to have symptoms and returned to the pulmonologist for further work-up, shown here:
- Chest computed tomography (CT): Normal lung parenchyma with no scarring or bronchiectasis
- Sinus CT: Mild mucosal thickening
- Complete blood count (CBC): Within normal limits, white blood cells (WBC) 10.0 K/mcL, 3% eosinophils
- Immunoglobulin E (IgE): 25 IU/mL
- Allergy-skin test: Positive for dust, trees
- Exhaled NO: Fractional exhaled nitric oxide (FeNO) 53 parts per billion (pbb)
Assessment for comorbidities contributing to asthma symptoms After this work-up, tiotropium was added to his medication regimen. However, he remained symptomatic and had two more flares over the next 3 months. He was assessed for comorbid conditions that might be affecting his symptoms, and results showed:
- Esophagram/barium swallow: Negative
- Esophageal manometry: Negative
- Esophageal impedance: Within normal limits
- ECG: Within normal limits
- Genetic testing: Negative for cystic fibrosis, alpha1 anti-trypsin deficiency
The ear, nose, and throat specialist to whom he was referred recommended only nasal inhaled steroids for his mild sinus disease and noted that he had a normal vocal cord evaluation.
Following this extensive work-up that transpired over the course of a year, Mr. T continued to have symptoms. He returned to the pulmonologist to discuss further treatment options for his refractory asthma.
Diagnosis Mr. T has refractory asthma. Work-up for this condition should include consideration of other causes for the symptoms, including allergies, gastroesophageal reflux disease, cardiac disease, sinus disease, vocal cord dysfunction, or genetic diseases, such as cystic fibrosis or alpha1 antitrypsin deficiency, as was performed for Mr. T by his pulmonary team.
Treatment options When a patient has refractory asthma, treatment options to consider include anticholinergics (tiotropium, aclidinium), leukotriene modifiers (montelukast, zafirlukast), theophylline, anti-immunoglobulin E (IgE) antibody therapy with omalizumab, antibiotics, bronchial thermoplasty, or enrollment in a clinical trial evaluating the use of agents that modulate the cell signaling and immunologic responses seen in asthma.
Treatment outcome Mr. T underwent bronchial thermoplasty for his asthma. One year after the procedure, he reports feeling great. He has not taken systemic steroids for the past year, and his asthma remains controlled on a moderate dose of ICS and a LABA. He has also been able to resume exercising on a regular basis.
Approximately 10% to 15% of asthma patients have severe asthma refractory to the commonly available medications. 2 One key aspect of care for this patient population is a careful workup to exclude other comorbidities that could be contributing to their symptoms. Following this, there are several treatment options to consider, as in recent years there have been several advances in the development of asthma therapeutics. 2
Treatment options for refractory asthma There are a number of currently approved therapies for severe, refractory asthma. In addition to therapy with ICS or combination therapies with ICS and LABAs, leukotriene antagonists have good efficacy in asthma, especially in patients with prominent allergic or exercise symptoms. 2 The anticholinergics, such as tiotropium, which was approved for asthma in 2015, enhance bronchodilation and are useful adjuncts to ICS. 3-5 Omalizumab is a monoclonal antibody against IgE recommended for use in severe treatment-refractory allergic asthma in patients with atopy. 2 A nonmedication therapeutic option to consider is bronchial thermoplasty, a bronchoscopic procedure that uses thermal energy to disrupt bronchial smooth muscle. 6,7
Personalizing treatment for each patient It is important to personalize treatment based on individual characteristics or phenotypes that predict the patient's likely response to treatment, as well as the patient's preferences and practical issues, such as adherence and cost. 8
In this case, tiotropium had already been added to Mr. T's medications and his symptoms continued. Although addition of a leukotriene modifier was an option for him, he did not wish to add another medication to his care regimen. Omalizumab was not added partly for this reason, and also because of his low IgE level. As his bronchoscopy was negative, it was determined that a course of antibiotics would not be an effective treatment option for this patient. While vitamin D insufficiency has been associated with adverse outcomes in asthma, T's vitamin D level was tested and found to be sufficient.
We discussed the possibility of Mr. T's enrollment in a clinical trial. However, because this did not guarantee placement within a treatment arm and thus there was the possibility of receiving placebo, he opted to undergo bronchial thermoplasty.
Bronchial thermoplasty Bronchial thermoplasty is effective for many patients with severe persistent asthma, such as Mr. T. This procedure may provide additional benefits to, but does not replace, standard asthma medications. During the procedure, thermal energy is delivered to the airways via a bronchoscope to reduce excess airway smooth muscle and limit its ability to constrict the airways. It is an outpatient procedure performed over three sessions by a trained physician. 9
The effects of bronchial thermoplasty have been studied in several trials. The first large-scale multicenter randomized controlled study was the Asthma Intervention Research (AIR) Trial , which enrolled patients with moderate to severe asthma. 10 In this trial, patients who underwent the procedure had a significant improvement in asthma symptoms as measured by symptom-free days and scores on asthma control and quality of life questionnaires, as well as reductions in mild exacerbations and increases in morning peak expiratory flow. 10 Shortly after the AIR trial, the Research in Severe Asthma (RISA) trial was conducted to evaluate bronchial thermoplasty in patients with more severe, symptomatic asthma. 11 In this population, bronchial thermoplasty resulted in a transient worsening of asthma symptoms, with a higher rate of hospitalizations during the treatment period. 11 Hospitalization rate equalized between the treatment and control groups in the posttreatment period, however, and the treatment group showed significant improvements in rescue medication use, prebronchodilator forced expiratory volume in the first second (FEV1) % predicted, and asthma control questionnaire scores. 11
The AIR-2 trial followed, which was a multicenter, randomized, double-blind, sham-controlled study of 288 patients with severe asthma. 6 Similar to the RISA trial, patients in the treatment arm of this trial experienced an increase in adverse respiratory effects during the treatment period, the most common being airway irritation (including wheezing, chest discomfort, cough, and chest pain) and upper respiratory tract infections. 6
The majority of adverse effects occurred within 1 day of the procedure and resolved within 7 days. 6 In this study, bronchial thermoplasty was found to significantly improve quality of life, as well as reduce the rate of severe exacerbations by 32%. 6 Patients who underwent the procedure also reported fewer adverse respiratory effects, fewer days lost from work, school, or other activities due to asthma, and an 84% risk reduction in emergency department visits. 6
Long-term (5-year) follow-up studies have been conducted for patients in both the AIR and the AIR-2 trials. In patients who underwent bronchial thermoplasty in either study, the rate of adverse respiratory effects remained stable in years 2 to 5 following the procedure, with no increase in hospitalizations or emergency department visits. 7,12 Additionally, FEV1 remained stable throughout the 5-year follow-up period. 7,12 This finding was maintained in patients enrolled in the AIR-2 trial despite decreased use of daily ICS. 7
Bronchial thermoplasty is an important addition to the asthma treatment armamentarium. 7 This treatment is currently approved for individuals with severe persistent asthma who remain uncontrolled despite the use of an ICS and LABA. Several clinical trials with long-term follow-up have now demonstrated its safety and ability to improve quality of life in patients with severe asthma, such as Mr. T.
Severe asthma can be a challenge to manage. Patients with this condition require an extensive workup, but there are several treatments currently available to help manage these patients, and new treatments are continuing to emerge. Managing severe asthma thus requires knowledge of the options available as well as consideration of a patient's personal situation-both in terms of disease phenotype and individual preference. In this case, the patient expressed a strong desire to not add any additional medications to his asthma regimen, which explained the rationale for choosing to treat with bronchial thermoplasty. Personalized treatment necessitates exploring which of the available or emerging options is best for each individual patient.
Published: April 16, 2018
- 1. National Asthma Education and Prevention Program: Asthma Care Quick Reference.
- 2. Olin JT, Wechsler ME. Asthma: pathogenesis and novel drugs for treatment. BMJ . 2014;349:g5517.
- 3. Boehringer Ingelheim. Asthma: U.S. FDA approves new indication for SPIRIVA Respimat [press release]. September 16, 2015.
- 4. Peters SP, Kunselman SJ, Icitovic N, et al. Tiotropium bromide step-up therapy for adults with uncontrolled asthma. N Engl J Med . 2010;363:1715-1726.
- 5. Kerstjens HA, Engel M, Dahl R. Tiotropium in asthma poorly controlled with standard combination therapy. N Engl J Med . 2012;367:1198-1207.
- 6. Castro M, Rubin AS, Laviolette M, et al. Effectiveness and safety of bronchial thermoplasty in the treatment of severe asthma: a multicenter, randomized, double-blind, sham-controlled clinical trial. Am J Respir Crit Care Med . 2010;181:116-124.
- 7. Wechsler ME, Laviolette M, Rubin AS, et al. Bronchial thermoplasty: long-term safety and effectiveness in patients with severe persistent asthma. J Allergy Clin Immunol . 2013;132:1295-1302.
- 8. Global Initiative for Asthma: Pocket Guide for Asthma Management and Prevention (for Adults and Children Older than 5 Years).
- 10. Cox G, Thomson NC, Rubin AS, et al. Asthma control during the year after bronchial thermoplasty. N Engl J Med . 2007;356:1327-1337.
- 11. Pavord ID, Cox G, Thomson NC, et al. Safety and efficacy of bronchial thermoplasty in symptomatic, severe asthma. Am J Respir Crit Care Med . 2007;176:1185-1191.
- 12. Thomson NC, Rubin AS, Niven RM, et al. Long-term (5 year) safety of bronchial thermoplasty: Asthma Intervention Research (AIR) trial. BMC Pulm Med . 2011;11:8.
Treatable traits and future exacerbation risk in severe asthma, baker’s asthma, the long-term trajectory of mild asthma, age, gender, & systemic corticosteroid comorbidities, ask the expert: william busse, md, challenges the current definition of the atopic march, considering the curveballs in asthma treatment, do mucus plugs play a bigger role in chronic severe asthma than previously thought, an emerging subtype of copd is associated with early respiratory disease.
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A review of the exposure history for the 12-year-old reveals that:
- The family has a long-haired cat that stays in the house,
- The patient develops nasal congestion and chest tightness when playing with the pet,
- The central heating furnace filters have not been cleaned in the last year,
- Wall-to-wall carpet is present throughout the house,
- The home has a wood-burning fireplace, which is occasionally used,
- The shower areas of the bathrooms have some mold, and
- Both parents smoke cigarettes indoors, but do not smoke in the children’s rooms.
In addition, the patient’s mother states that:
- She vacuums regularly,
- She has not seen any insects in the house, and
- The basement is not damp.
The patient with asthma symptoms underwent peak flow testing in your office. The results demonstrated a 24% increase in peak expiratory flow rate (PEFR) after administration of a short-acting B2-agonist bronchodilator. The patient is diagnosed with mild persistent asthma.
Anti-inflammatory therapy consisting of a corticosteroid metered-dose inhaler (MDI) for daily use and a short-acting B2-agonist MDI for symptomatic relief is given to the patient; she is instructed on use of the MDIs with the spacer. The patient uses the spacer in front of you to demonstrate that she understands its proper use. You explain that it might take 7 days or more for the corticosteroid inhaler to be effective. You also explain that the goal is to control the asthma with the corticosteroid inhaler and decrease use of the short-acting B2-agonist for rare breakthrough of acute asthma symptoms. A return visit in 2 to 3 weeks is scheduled.
You tell the mother:
- Both parents should stop smoking or, at a minimum, not smoke in the house or the car.
- Clean or replace the furnace filter on a regular basis.
- The cat should not be indoors.
- Remove the wall-to-wall carpeting from the patient’s bedroom (and preferably the whole house if feasible).
- Encase mattresses and pillows in sealed plastic covers.
- Wash all bedding materials in hot water (>130º F [>55º C]) to kill dust mites.
- Water heaters in homes with young children are frequently set at or below 120º F (50º C) to avoid scalding. Suggest that the mother turn the water heater up for short periods to provide the necessary water temperature for washing bedding and area rugs.
A few weeks later, the father brings his daughter in for her follow-up assessment. The child’s cough has subsided and she is able to sleep through the night. The child has been using the short-acting B2-agonist and corticosteroid inhaler as directed. For the last week, she has not required additional use of the short-acting B2-agonist. The father relates that his daughter has been more active lately and plays soccer without episodes of shortness of breath. Auscultation of the lungs reveals that both fields are clear without wheezes. You decide to maintain the current medication treatment regimen. The father has an audible wheeze and an intermittent cough. He is wearing his factory work clothes and you smell a strong chemical odor coming from him. You reiterate that both parents should stop smoking.
- Case Studies in Environmental Medicine
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- Pediatric Environmental Health Training
- Patient Education
- Community Education
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