Abstract
Bronchiectasis is a congenital or acquired irreversible dilatation of the bronchial airways under the ICD-11 classification code CA24.1,2 Recurrent infection, inflammation or obstructive pressure causes focal or diffuse destruction of the bronchial wall which is responsible for the chronic cough with purulent expectoration and haemoptysis.3 It is responsible for the significant loss of lung function and considerable morbidity and mortality.4 Multiple etiological factors require respective investigation and management according to the underlying cause. It is a heterogeneous andchronic disease that has acute exacerbations which require special care.5 In the past few years, the incidence and prevalence of bronchiectasis have increased worldwide, possibly due to advances in imaging techniques and disease awareness, leading to increased socioeconomic burden and healthcare costs. In homoeopathy, treatment is highly individualized, and remedies are chosen based on the patient’s unique symptoms, emotional state, and overall health. Homoeopathic remedies may be suggested to support the respiratory system, relieve symptoms, and enhance overall health.
Keywords: Bronchiectasis, Clinical updates, Homoeopathy.
Introduction
Bronchiectasis is a common structural endpoint which occurs due to epigenetic factors like genetic susceptibility, malnutrition, infection, poor hygiene, smoking and lack of physical exercise. It leads to lack of physical ability to active exercise and lung function which results in cumulative intensification of the disease and results in depression and anxiety in patients with bronchiectasis. Presentation is typical chronic productive cough with dyspnoea and wheezing. Radiographic features may include dilatation and thickening of airways withscattered and irregular opacities. Evaluation of the bronchiectasis patients include clinical history, genetic analysis, radiographic study and detection of the pathogens. Exclusion of Cystic fibrosis is necessary to outline the treatment procedure. Lung spirometry is an important tool to find out the lung parameters and co
existence of any other obstructive pulmonary diseases. Complication may include right sided heart failure, amyloidosis, secondary visceral abscess.
Epidemiology
The incidence of bronchiectasis has been increasing globally in recent years. It may affect any age group but usually affects children in pre antibiotic period. Women and elderly individuals are more affected. In tuberculosis-prevalent areas, it more frequently occurs as a sequela of granulomatous infection. Bronchiectasis resulting from MAC (Mycobacterium avium-intracellular complex)
infection affects nonsmoking women >50 years of age. Mortality increased with increasing age from 0.5% among patients aged 18–40 years to 23.5% in patients aged >80 years. Malnutrition in certain areas predisposes to immune dysfunction and may develop pathogenesis. Recent studies suggest thatthere might be a new bronchiectasis endophenotype of patients with sensitization to multiple environmental allergens. Bronchiectasis may co-exist with COPD.6
Etiology
Bronchiectasis may have congenital or acquired causes. Acquired causes may have infective or non infective origins. Lungsinvolved may be focal or diffusive manner depending on the underlying factor. •Congenital causes include Cystic fibrosis: A common genetic cause of congenital bronchiectasis that affects chloride ion transport, Williams-Campbell syndrome: A rare formof bronchiectasis that
results from a lack of cartilage in the airways, Mounier-Kuhn syndrome: A rare condition that causes dilation of the trachea and segmental bronchi, Swyer-James syndrome: A developmental disturbance that can lead to bronchiectasis, Kartagener’s syndrome: Also known as “immotile cilia” syndrome, this condition is characterized by bronchiectasis, sinusitis, dextrocardia, and complete visceral
transposition, Primary ciliary dyskinesia: A rare disorder that causes immotility of cilia, alpha 1 antitrypsindeficiency: cause lung and liver damage and ARHGEF1 gene associated with idiopathic bronchiectasis and immunodeficiencies with antibody defects.FOXJ1 gene associated with bronchiectasis in an autosomal dominant inheritance pattern.
⮚ Focal causes include compression by adjacent lymphadenopathy or parenchymal tumourmass, an airway tumour or aspirated foreign body, a scarred/stenotic airway, or bronchial atresia from congenital underdevelopment of the airway.
⮚ Diffuse causes may include an underlying systemic or infectious disease process. Infective causes may include severe infection in infancy from whooping cough or measles.Primary tuberculosis in children. Tuberculous and non-tuberculous mycobacterial infection most commonly the Mycobacterium avium-intracellular complex (MAC). Infection by Pseudomonas aeruginosa, Haemophilus influenza, Streptococcus pneumoniae, and Staphylococcus aureus are commonly identified. Chronic infection with Pseudomonas is a marker for disease severity, frequent exacerbation, accelerated course, and rapid decline inlung function. Other causes of lung abscess and suppurative pneumonia.
⮚ Non-infective causes may include oesophageal motility disorders like those in scleroderma. Immunodeficiency (congenital or acquired hypogammaglobulinemia, selective IgA IgG IgM subclass deficiencies, HIV infection, lymphoma, plasma cell myeloma, leukaemia bronchiolitis obliterans after lung transplantation. Autoimmune or rheumatologic causes (rheumatoid arthritis, Sjögren’s syndrome, inflammatory bowel disease); immune-mediated disease (allergic bronchopulmonary aspergillosis), Recurrent aspiration, Miscellaneous (yellow nail syndrome, traction bronchiectasis from post-radiation fibrosis or idiopathic pulmonary fibrosis).
Pathogenesis
Cole’s vicious cycle hypothesis illustrates that airway dysfunction, inflammation, infection and structural damage are linked together. This multifactor activity stresses the complex relationship between the components of the cycle. This may explain the susceptibility to infection and poor mucociliary clearance result in microbial colonization of the bronchial tree. Focal bronchiectasis may
occur from the accumulation of pus beyond the obstructive pathology. The cavities formed are lined by granulation tissue, squamous epithelium or normal ciliated epithelium. Inflammatory findings may be present on the deeper layer of the bronchial wall and hypertrophic changes in bronchial arteries. It is responsible for thickened and dilated bronchi with mucus plugs in the airways followed by atelectasisand focal consolidation.
Clinical features
Chronic daily persistent cough with copious and purulent cough. Increased sputum volume from infective exacerbations may be accompanied by halitosis, fever, malaise and anorexia. Pleuritic pain due to pleuritic infection or segmental collapse from retained secretions. Haemoptysis with streaks of blood may increase in quantity of blood by acute exacerbation or massive due to pulmonary artery embolism. Weakness, anorexia, and breathlessness may cause general debility and weight loss. Physicalfindings frequently include crackles and wheezing on lung auscultation. Clubbing may be present.
Investigation
CBC and immunoglobulin quantification studies (IgA IgM IgG). Quantitative Sweat Test (>60mEq/L) for and genetic analysis for CFTR gene in case of cystic fibrosis. Nasal FeNO (Fractional Exhaled NitricOxide) sample for screening of ciliary dysfunction, electron microscopy guided brush biopsy and genetic testing for the same. Sputum culture for microorganisms such as bacteria, non-tuberculous mycobacteria, and fungi. Immediate hypersensitivity test Aspergillus antigen and elevated serum IgE for ABPA. Autoimmune serological tests, for rheumatic diseases. Pulmonary function test for obstructive lung diseases. HRCT is diagnostic and may show a “tram track” or “end ring” appearance, which is the hallmark of the disease. Bronchoscopy to evaluate haemoptysis.
Management and Treatment
Aim to treat individuals: Preventing chest infections (exacerbations), during which symptoms get worse, treating symptoms, improving quality of life, and stopping the condition from getting worse.
Antibiotic treatment: it should be guided by sputum culture. If the specific bacterial pathogen is not identified, then empiric oral antibiotic therapy for 10-14 days may follow. Acute exacerbated conditions may be treated with antibiotics, airway clearance and inhaled bronchodilators. Preventive for recurrent exacerbation may be effective by macrolide therapy for 6-12 months. Chest
physiotherapy and Bronchial hygiene: daily physiotherapy for drainage of excess bronchial secretion. It preventsrecurrence. Active cycle of breathing technique: the affected lobe in the uppermostposition, deep breathing followed by forced expiratory manoeuvres, which helps to move the secretions of dilated bronchi towards the trachea, from where it is cleared by vigorous coughing. Handled flutter valve device is used for this by a minimum of 5-10 mins twice daily.
Anti-inflammatory is effective for reduced dyspnoea and sputum production and may treated withinhaled glucocorticoids. Patients with ABPA may benefit from antifungal therapies.
Percutaneous embolism of the bronchial circulation may be performed for massive and recurrent haemoptysis.
Surgery is performed for resection of focal suppuration and in some advanced cases, lungtransplantation is performed.
Differential Diagnosis
| Name of Disease | Suggestive features |
| COPD | • History of smoking.
• Slow, progressive onset. • Exertional dyspnea, may also have nightly onset. • Cough with symptoms of allergy. |
| Congestive Cardiac Failure | • Fine basilar crackles on auscultation
• Chest pain with palpitation. • Pedal oedema. • Urging for frequent urination mainly at night. |
| Tuberculosis | • Nightly onset of fever.
• Progressive weight loss and weakness. • Progressive cough with blood-tinged sputum. • High local prevalence. |
| Kartagener Syndrome | • Classical triad:
Sinus inversus- Bronchiectasis-Chronic sinusitis • Nasal congestion and polyp. • In male, it may cause infertility. |
| Pneumonia | • High fever with chilliness followed by sweating. • Rapid shallow breathing with dyspnea.
• Sharp chest pain, worse while coughing or deep breathing. • Nausea, vomiting with loss of appetite and weakness. |
Table 1: Showing Differential diagnosis
Miasmatic Approach
In treating bronchiectasis, a chronic respiratory condition, homoeopaths might explore the miasmatic layer of the disease to prescribe remedies that address the root causes, not just the symptoms. Bronchiectasis or any
disease cannot be specified under any miasm. It is the patient’s constitution, diatheses, temperament, Miasmatic dyscrasia, accessory circumstances ( in terms of epigenetics and environmental influences in the
present context), susceptibility etc. will be deciding factors. What type of symptomatology will be presenting in one individual at a given period will depend on those individual factors. Such as in Bronchiectasis the symptoms may vary from:
– little infection to Infective changes
– Sac formation with permanent dilation of bronchioles
– massive destructive pathology with massive haemorrhage and excessive sputum production
– developing constitutional symptoms etc.
The person with multi-miasmatic dyspraxia having any predominant miasm and the symptoms of the disease will appear in the individual based on his/ her predominant miasmatic dyspraxia at any given period. All other factors will influence the said disease in the individual. Bronchiectasis often involves a cycle of infections, airway inflammation, and mucus accumulation, which could be associated with one or more of the following miasms:
- Psora: (Deficiency -Connection to Bronchiectasis) Psora is often linked to conditions involving immune system deficiencies or susceptibility to infections. Since bronchiectasis involves recurrent infections and an ongoing struggle with airway inflammation, a person with a psoric miasm might be predisposed to such chronic respiratory issues. Psoric symptoms may remain confined to minimal infective changes in functional level without any massive destruction.
- Sycosis (Chronic Inflammation -Connection to Bronchiectasis): The sycotic miasm involves conditions of chronic inflammation and excessive tissue growth. In bronchiectasis, this could relate to the thickening of airway walls, recurrent infections, or excessive mucus production. It could also be linked to a tendency for the body to form excessive inflammatory responses.
- Syphilitic Miasm (Destructive Process-Connection to Bronchiectasis): Syphilitic miasm is considered more destructive and associated with the degeneration of tissues, which could manifest in the scarring and irreversible damage that occurs in bronchiectasis. Hemoptysis may be massive This miasm might play a role in cases of advanced bronchiectasis, where lung tissue has been severely affected by repeated cycles of infection and inflammation.
A disease is a combination of multiple signs and symptoms, and all these can be classified under miasmatic classification. So, being a Homoeopath if we can diagnose the human in his / her environment with the individual’s constitution then it will be easy to assume the appearance of the diseases with its predominant symptomatology in that person in that period of time.
Homoeopathic Therapeutics
Acetic Acid: Hoarse, hissing respiration; difficult breathing cough when inhaling. Membranous croup. Irritation of trachea and bronchial tubes.7
Allium Sativa: Constant rattling of mucus in bronchi. Cough in the morning after leaving the bedroom, with mucous expectoration, which is tenacious and difficult to raise. Sensitive to cold air. Dilated bronchi, with fetid expectoration. Darting pain in the chest.
Alumina: Cough soon after waking in the morning. Hoarse, aphonia, tickling in larynx; wheezing,rattling respiration. Cough on talking or singing, in the morning. Chest feels constricted.
Ammon Carb: Cough every morning at about three o’clock, with dyspnoea, palpitation, burning in chest; worse ascending. Chest feels tired. Emphysema. Much oppression in breathing; worse after any effort, and entering a warm room, or ascending even a few steps. Asthenic Pneumonia. Slow labored, stertorous breathing; bubbling sound. Winter catarrh, with slimy sputum and specks of blood.
Antim Tart: Great rattling of mucus, but very little is expected. Velvety feeling in the chest. Rapid,short, difficult breathing; seems as if he would suffocate; must sit up. Emphysema of the aged. Coughing and gaping consecutively. Bronchial tubes overloaded with mucus. Cough excited byeating, with pain in chest and larynx.
Bacillinum: Catarrhal dyspnoea. Humid asthma. Bubbling rales and mucopurulent expectoration.
Calcarean Carb: Extreme dyspnoea. Expectoration only during the day; thick, yellow, sour mucus. Bloody expectoration; with a sour sensation in the chest. Suffocating spells; tightness, burning and soreness in chest; worse going upstairs or slightest ascent, must sit down. Sharp pains in the chest from before backwards. Chest very sensitive to touch, percussion, or pressure. Longing for fresh air.
Scanty, salty expectoration.
Crotalus H.: Cough, with bloody expectoration. Tickling from a dry spot in the larynx.
Dioscorea: Tight feeling all along the sternum. The chest does not seem to expand on breathing. Short winded.
Eucalyptus: Expectoration white, thick mucus. Bronchitis in the aged. Bronchorrhea. Profuse expectoration of offensive mucous. Irritative cough. Whooping- cough in rachitic children. Fetidform of bronchitis, bronchial dilatation and emphysema.
[single medicine in synthesis repertory: chest-bronchiectasis-old people]8
Hepar Sulph Calcareum: Cough excited whenever any part of the body gets cold or uncovered, orfrom eating anything cold. Croup with loose, rattling cough; worse in the morning. Choking cough. Rattling, croaking cough; suffocative attacks; has to rise and bend head backwards.
Kali Bi: Profuse, yellow expectoration, very glutinous and sticky, coming out in long, stringy, and very tenacious mass.
Kali Carb: Cutting pain in chest; worse lying on the right side. Expectation scanty and tenacious but increasing in the morning and after eating; aggravated right lower chest and lying on painful side. Expectation must be swallowed; cheesy taste; copious, offensive, lump. Coldness of chest.Tendency to tuberculosis; constant cold taking; better in a warm climate.
Kreosote: After every cough, copious, purulent expectoration. Haemoptysis; periodic attacks. Sternum feels pressed in.
Lycopodium: Expectorations grey, thick, bloody, purulent, salty. Night cough, tickling as from Sulphur fumes. Catarrh of the chest in infants seems full of mucus rattling. Neglected pneumonia, with great dyspnoea, flaying of alae nasal and presence of mucous rales.
Medorrhinum: Much oppression of breathing. Hoarse while reading. Pain and sorenessthrough chestand mammae. Incessant, dry, night cough. Asthma. Incipient consumption. The larynx feels sore. Dyspnoea; cannot exhale. Cough better lying on stomach.
Phosphorus: Tightness across chest; great weight on chest. Sharp stitches in chest; respiration quickened, oppressed. Much heat in the chest. Pneumonia, with oppression; worse, lying on the left side.The whole body trembles, with cough. Sputa rusty, blood coloured, or purulent. Tuberculosis is in tall, rapidly growing young people.
[single medicine in synthesis repertory: chest-bronchiectasis-chronic]
Psorinum: Cough with expectoration of green mucus, nearly like matter; especially in the morning when waking and in the evening when lying down, with nausea; it sticks firmly, and he can only expectoration with difficulty. Expectoration of blood with hot sensation in chest; yellowish green. Chronic blennorrhoea of lungs, threatening physics.9
Pulsatilla: loose cough in the morning, with copious mucous expectoration. Pressure upon the chest and soreness. Expectations are bland, thick, bitter, and greenish. Short breath, anxiety, and palpitation when lying on the left side. Smothering sensation on lying down.
Silicea: Colds fail to yield; sputum persistently muco- purulent and profuse. Slow recovery after pneumonia. Cough and sore throat, with expectoration of little granules like shot, which, when broken, smell very offensive. Cough with expectoration in the day, bloody or purulent. Stitches in the chest through to the back. Violent cough when lying down, with thick, yellow lumpy Expectoration; suppurative stage of expectoration.
Stannum: Mucus expelled by forcible cough. Cough excited by laughing, singing, talking; worse lying on the right side. During the day, with copious green, sweetish, expectoration. Chest feels sore. My chest feelsweak; I can hardly talk. Influenza cough from noon to midnight with scanty expectoration. Respirationis short and oppressive; stitches in the left side when breathing and lying on the same side. Phthisis mucosa.
Sulphur: Loose cough; worse talking, morning, greenish, purulent, sweetish expectoration. Much rattling of mucus. Chest feels heavy; stitches, with heart, feeling too large and palpitating. Pleuriticexudations.
Tuberculinum: Enlarged tonsils. Hard, dry cough during sleep. Expectation thick, easy; profuse bronchorrhea. Shortness of breath. The sensation of suffocation, even with plenty of fresh air. Longs for cold air. Bronchopneumonia in children. Hard, hacking cough, profuse sweating and loss of weight, rales all over the chest. Deposits begin in the apex of the lung.
Conclusion
In homeopathic treatment, individualization is key, meaning the remedy chosen would depend on the patient’s specific symptoms, personality, and medical history. Homeopaths typically use a detailed interview process to determine the most appropriate remedy, which is why the treatment can vary greatly between individuals. The approach is holistic, looking at not just the physical symptoms but also the emotional and psychological factors that may influence health. Even the prognosis part also can be predicted with the advantage of an individualistic approach. The modern-day concept of personalized medicine or precision medicine also depends on these individualistic factors which is the foundation of precision medicine.
Homoeopathy may provide complementary symptom relief and supportive treatment for individuals with bronchiectasis, particularly in improving overall health, reducing inflammation, and addressing recurrent infections.
References
- Harrison TR, Loscalzo. Fauci. Kasper. Hauser. Longo. Jameson. Harrison’s principles of internal medicine. 21st ed. New York, NY: McGraw-Hill; 2022. VOL 2. Peptic Ulcer Disease and Related Disorders. p.2173
- Penman ID, Ralston SH, Strachan MWJ, Hobson R, editors. Davidson’s principles and practice of medicine. 24th ed. London, England: Elsevier Health Sciences; 2022. Gastroenterology. p.509 3. Papadakis M, Rabow M, McQuaid K, Gandhi M. Current medical diagnosis and treatment 2025. 64th ed. Pulmonary Disorders, p.265
- Bird K, Memon J. Bronchiectasis. [Updated 2023 May 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan.
- Flume PA, Chalmers JD, Olivier KN. Advances in bronchiectasis: genotyping, genetics, microbiome, and disease heterogeneity. Lancet. 2018 Sep 8;392(10150):880-890. doi: 10.1016/S0140-6736(18)31767-7. PMID: 30215383; PMCID: PMC6173801.
- Mcshane P, Naureckas E, Tino G, Strek M.E., Concise Clinical Review: Non-Cystic Fibrosis Bronchiectasis, ResearchGate. 2013 Jul; 188(6) DOI:10.1164/rccm.201303-0411CI 7. Boericke O.E., Boericke W. Pocket Manual of Homoeopathic Materia Medica $ Repertory. B. Jain, India, 2013 p.6
- Schroyens F, Sherr J. Synthesis: Repertorium Homeopathicum Syntheticum: the source repertory. India: B. Jain Publishers (P) Ltd; 2016. p.1250
- Herring C. The Guiding Symptoms of our Materia Medica. Volume 9. B Jain, New Delhi, 2024
