Bronchial Asthma and Its Homoeopathic Treatment

Dr. Ashokkumar Dantkale

INTRODUCTION:

Bronchial asthma is a chronic inflammatory disease of airways, characterized by increased responsiveness of tracheo-bronchial tree to a multiplicity of stimuli, resulting in symptoms of wheeze, cough, chest tightness, and dyspnoea.

3 characteristics:-

?Airflow limitation � Reversible spontaneously with or without tt.

?Air way hyper responsiveness to a wide range of stimuli � eg.cold air, exercise etc.

?Inflammation of the bronchi � with eosinophils, T lymphocytes, mast cells + plasma exudation, oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage.

Prevalence: Increasing in the 2nd decade of life (10-15% of population)

Classification:

Extrinsic

�Definite external cause

�Young patient

�History of eczema

�FH of asthma, eczema, hay fever

�Attacks related to specific antigens

�Intermittent attacks

�a/c attacks, self-limiting

�Occasional polyps

�Skin test +ve

�IgE raised

�Prognosis favorable

Intrinsic

�No causative agent can be identified

�Adults > 35 years

�No h /o eczema in childhood

�No FH

�Attacks related to infection/ exercise

�Persistent asthma

�More fulminant , severe

�Nasal polyps common

�Skin test �ve

�Normal/ low IgE

�Poor prognosis

Etiology & Pathogenesis:

�Atopy and Allergy

�Genetic & environmental factors affect IgE levels

�Airway responsiveness � greater the degree of hyperactivity more persistent the symptoms, greater the need for treatment.

Precipitating factors:

  • Occupational sensitisers � �isocyanates, acid unhydrides etc bond chemically to epithelial cells to activate them. Atopic persons develop occupational asthma more rapidly than non- atopic individuals.
  • Cold air and exercise
  • Atmospheric pollution, irritant dust vapours and fumes
  • Diet � milk, egg, nuts, chocolate, shell fish etc.
  • Drugs
  • Infections
  • Smoking
  • Anxiety, psychosomatic factors

Allergen induced asthma – 4 types of reaction

�Immediate asthma � airflow limitation begins within minutes of contact with allergen; reaches its max. in 15-20 mts, subsides in 1 hr.

�Late phase reaction � more prolonged and sustained attack of airflow limitation response poor to bronchodilators

�Dual reaction � combination of early reaction followed by late reaction

�Recurrent asthmatic reaction � continuing episodes of asthma on subsequent days.

PATHOGENESIS:

Pathogenesis involves a number of cells , mediators , nerves and vascular leakage that can be activated by several different mechanisms of which exposure to allergens is the most important.The inhalation of allergen in a sensitized atopic asthmatic patient results in a two phase broncho constrictor response. The inhaled allergen rapidly interacts with mucosal mast cells via an IgE dependent mechanism, resulting in mediators such as histamines and cysteinyl leukotrienes which leads to broncho constriction. A full spectrum of inflammatory cells however are involved in the perpetuation of chronic inflammatory reactions in the bronchial wall which characterizes asthma. T lymphocytes are present in increased numbers in asthmatic airways and have an important roll in regulation of inflammatory response.They are programmed to release inflammatory cytokines amongst which IL4 andIL5 are of importance. since they both recruit eosinophils to the airways delay apoptosis of these cells. Eosinophils present in increased numbers in the airway. These cells release bioactive lipid mediators and radicals etc. No; of airway macrophages also increased. Epithelial shedding is commonly observed in biopsies. Micro vascular leakage is also seen and this results in plasma exudation into lumen of airways, contributing to mucous plugging, decresed mucociliary clearance, release of kinines and complement fragments and oedema of airway wall which facilitates epithelial stripping. As a result the asthmatic airway wall is thickened by oedema, cellular infiltration, increased smooth muscle mass and hypertrophy of mucus secreting glands. With increasing severity and chronicity of the disease remodelling of airway occures, leading to fibrosis of airway wall, and narrowing and reduced response to bronchodilators

CLINICAL FEATURES:

Typical symptoms of asthma comprises

-Wheeze

-Breathlessness

-Cough

-Sensation of chest tightness

Patients with episodic asthma are usually asymptomatic between exacerbations,which occur during viral respiratory tract infections or after exposure to allergens.This pattern is commonly seen in children or young adults who are atopic.In other patients the clinical pattern is of persistent asthma with chronic wheeze and breathlessness.this pattern is common in older patients with adult onset asthma who are non atopic and typifies intrinsic asthma.

Typically there is a diurnal pattern of symptoms <morning.

�Symptoms of cough wheeze often disturb sleep and the term nocturnal asthma emphasizes this.

�Cough may be dominant symptoms and lack of wheeze or breathlessness may lead to a delay in making the diagnosis of so called cough variant asthma. All of these clinical terms are useful in emphasizing characteristic features of asthma particular to each patient and high light the fact that asthma is not a static disease but a broad dynamic syndrome.

ACUTE SEVERE ASTHMA:

�This term replaced status asthmaticus as a description life threatening attack of asthma.

�Patients are extremely distressed, using accessory muscles of respiration.and are hyperinflated and tachypnoeic.

�Respiratory symptoms are accompanied with tachycardia, pulsus paradoxus and sweating. In very severe asthma central cyanosis may occur and air flow may have become so restrictive that rhonchi are no longer produced.

�Presence of a silent chest and bradycardia in such a patient is an omnious sign.

INVESTIGATIONS:

�Diagnosis of asthma made by clinical history + demonstration of variable airflow obstruction which may classically seen as morning dipping of PEF.

�Reversibility � There is greater than 15% improvement in FEV1 or PEFR following inhalation of bronchodilator.

Exercise test � This is used in diagnosis of asthma in children.

�Histamine or Methacholine bronchial provocation test

�Chest X-Ray test- Hypertranslusency in chronic severe disease

�Skin test � Skin prick test to identify extrinsic causes.

�Blood & sputum test – Increase of eosinophils

MANAGEMENT:

Asthma is extremely common and causes considerable morbidity.

�The aims of treatment are

  • To abolish symptoms.
  • To restore normal or best possible long term airway function.
  • To reduce risk of severe attacks.
  • To enable normal growth to occur in children
  • To minimize absences from school or employment. This involves the patient & family education about asthma.
  • Avoidance of identified causes where possible
  • Patient & family participation in treatment.
  • Rapid identification of extrinsic causes of asthma their removal wherever possible

DIFFERENTIAL DIAGNOSIS:

  1. Tropical Eosinophilia
  2. Acute bronchitis
  3. ChronicBronchitisEmphysema syndrome
  4. Emphysema
  5. Left sided heart failure
  6. Metabolic acidosis
  7. Air way obstruction
  8. Psychogenic dyspnoea

HOMOEOPATHIC TREATMENT: It offers both preventive and curative medicines for Bronchial Asthma. Homoeo medicines improve the disease resisting capacity of the body and in vitality. Homoeopathy treatment is not in accordance with the nosological term but with the symptoms presented by the individual. In Homoeopathy we treat the cause and not the effects of the disease. We give medicine to who is suffering, rather than what he is suffering. In Homoeopathic Science we have to treat the individual in diseases.

Asthma is one of the distressing ailments which are not easy to cure. After using palliative medicines to overcome an acute attack, one should resort to constitutional treatment in order to give permanent relief to the patient.

The main constitutional medicines are:
1. Tuberculinum
2. Thuja
3. Natrum Sulph
4. Medorrhinum
5. Syphilinum

The above medicines are to be given inter-currently in potency not below 200. No other medicine is to be given for 2 – 3 days before and after. If any of the above medicines have the desired effect, further drugging of the patient should be avoided. Further, in Asthma the diet plays a very vital role. Thus, the use of white flour, eggs, white sugar, meat, fish, milk, curd and puddings should be avoided.

THERAPEUTICS:

  • ANTI ARS: Emphysema and excessive dyspnoea and cough. Much mucous secretion <eating and lying down.
  • ANTI TART: Rattling of mucous but little expectorated; Oedema impending paralysis of lungs.Dyspnoea and cough >lying down on right side; >by eructation.
  • ARS ALB: Asthma < after midnight; Burning in chest. Wheezing respiration. Suffocative catarrh.
  • ARS IOD:Hay fever ,sneezing/c nasal catarrh., dry stopped up nostrils with hacking cough
  • ARALIA: Asthma on lying down at night. With spasmodic cough < after first sleep with tickling in throat. Constriction in throat.
  • ASPIDOSPERMA: Uremic dyspnoea. Want of breath during exertion. Cardiac asthma.
  • BLATTA: Asthma associated with bronchitis. Stout and corpulent patients Cough with dyspnoea.
  • CARBO VEG: Asthma associated with blue skin. Wheezing and rattling of mucous in chest. Hoarseness <evening. Breath cold. Must be fanned.
  • CALC ARS: Dyspnoea with feeble heart. Chilliness.
  • COCA: Spasmodic asthma. Want of breath, short breath in aged athlets and alcoholic users.
  • GRINDELIA: Cannot breath while lying down. Bronchorrhoa with tough whitish, mucous expectoration. Sibilant rales.
  • IPECAC: Dyspnoea with constriction in chest. Asthma. Cough incessant and violent with every breath. With nausea. Child stiff and blue in face.
  • LOBELIA: dyspnoea with constriction of chest, <exertion >rapid walking. Asthma attacks with weakness, felt in pit of stomach and preceded by prickling all over.
  • KALI CARB: Dry hard cough < at 3 a.m. Coldness of chest. Wheezing. Leaning forward relieves chest symptoms.
  • EUCALYPTUS: Asthma with dyspnoea and palpitation. Moist asthma. Expectoration thick white mucous.
  • NAT SULPH: Dyspnoea in damp weather. Humid asthma. Rattling in chest. <4-5a.m. Asthma in children.
  • NAPHTHALINE: Spasmodic asthma. Dyspnoea and sighing inspiration. Hay fever.
  • POTHOS: Asthma >by stool. Dyspnoea with chest pain.
  • PSORINUM: Asthma with dyspnoea. <sitting up >lying down and keeping arms spread wide apart. Weakness of chest.
  • SAMBUCUS: Miller�s asthma. Child awakes suddenly. Turns blue, sits up. Cannot expire. Paroxysmal suffocative cough coming on about midnight.
  • SULPHUR: Dyspnoea in middle of night >sitting up. Much rattling of mucous. Wants windows open. Oppression as of a load in chest.
  • MEDORRHINUM: Dyspnoea cannot exhale. >lying of stomach. Dry, night cough.
  • VISCUM: Asthma connected with rheumatism or gout. Suffocation while lying on left side. Spasmodic cough
  • KALI IOD: Dyspnoea on ascending with pain in heart. Cough <morning. Expectoration greenish.
  • SILICEA: Stone-cutters asthma.
  • THUJA: Asthma in children. Dry hacking cough in afternoon.

NOTE: Any information given above is not intended to be taken as a replacement for medical advice. Therefore, it is very important that the patients should avoid self-treatment and rather consult qualified Homoeopath and take the treatment under his proper guidance and advice.

�In Homoeopathy We Treat the Diseased Individual not the disease in an individual�.

BY:

Dr. Ashokkumar Dantkale� MD (Hom)

Assistant Professor

Govt. Homoeo Medical College,Bangalore-79.

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