BRONCHIAL ASTHMA is a chronic reversible inflammatory destructive disease of the airways characterised by recurrent paroxysmal attacks of dyspnoea chiefly expiratory in nature accompanied by wheeze which may subside spontaneously or with treatment.
AETIOLOGY AND PATHOGENESIS
Asthmatic patients are having a hyper-reacting bronchial tree and numbers of factors may produce obstruction; namely, spasm of the bronchial smooth muscle, oedema of the bronchial mucosa, and presence of mucus in the bronchial lumen, Bronchoconstriction may be due to various factors, known and unknown. Known substances are Histamine, SRS-A (slow reacting substance of Anaphylaxis), Platelet activating factor (PAF), Eosinophil chemotactic factor of Anaphylaxis (ECF-A), Bradykinin, Prostaglandins, 5-HT and other unidentified substances liberated from the mast cells. The factors responsible for releasing these mediators are allergy, infection, exercise, psychological factors, change of temperature and humidity, smoking etc.
Allergens may be inhaled or ingested. Inhaled allergens are house dusts, pollens, dander, kapok and feathers. The antigen in the house dust is derived from feathers, mite, dermatophagoides which live in bedding and mattresses and fungus like A. Fumigatus. Ingested allergens include various substances such as egg, fish, crab, chocolate, aspirin, penicillin, iodide etc. This type of allergic asthma develops in atopic individuals mediated by antibodies. These antibodies belong to a type of immunoglobulin called IgE this is called Type I hypersensitivity reaction. The antigen- antibody reaction causes degranulation of the mast cells which release pharmacologically active substances producing bronchiolar spasm and obstruction. Adenyl cyclase and cyclic adenosine monophosphate are involved in mast cell reaction. After inhalation of enzymes of B. subtilis used in manufacture of washing powders there will be bronchiolar spasm. Similarly cedar wood workers may also develop cedar dust asthma. Air-borne pollution of the environment produces so-called “Tokyo-Yokohma” or “New Orleans” asthma. Meat wrapper’s asthma, Baker’s asthma, wood worker’s asthma are other examples. Asthma may al so develop by Type III hypersensitivity mechanism mediated by IgG…..|BRONCHIAL ASTHMA
Infection of the bronchial mucosa causes airway obstruction due to oedema of the mucosa and overproduction of mucus. Apart from this, bacterial antigen may produce an allergic response. Streptococcus pneumoniae, H. influenzae and viruses are responsible for infection. Asthma in children and middle aged people are mainly due to this…..
It may precipitate asthma or may worsen the asthmatic state. This is called exercise inducted asthma.
Various psychological factors particularly emotional stress may precipitate an attack.
Temperature and humidity
Changing temperature and humidity may cause obstruction to the airways in the asthmatic subjects.
Cigarette smoking also causes airway obstruction.
Attack usually starts in the late hours of the night or in the early hours of the morning. Onset is sudden and may be preceded by a feeling of tightness of the chest.Patient becomes very much dyspnoeic and feels as if there is less air in the room. He rushes to the window, opens it and pants for breath. After sometimes he coughs and brings out a little phlegm and gradually the attack subsides within an hour or so.
General survey: Facies is anxious, decubitus-patient sits upright or in stooping forward posture, accessory muscles of respiration are very much prominent, expiratory wheeze is present (which can be heard from a long distance), central cyanosis may be present, respiration rate is hurried 25-40 per minute, expiration is prolonged and laboured, pulse rate is rapid, BP shows systolic elevation of pressure. Temperature is usually normal. Sweating is present.
Chest is held in a state of full inspiration but as the diaphragmatic function is preserved the lower ribs normally move outward. During inspiration the skin over the chest is sucked inside. Vocal fremitus is slightly increased unless there is pre-existent emphysema. Expiratory rhonchial fremitus is present. Apex beat may not be palpable due to overinflation of the air vesicles and hurried respiration. Percussion shows hyper-resonant note. Normal variation of dullness due to diaphragmatic movement is 1lost. Auscultation reveals breath sound to be vesicular with prolonged expiration, vocal resonance is slightly increased and adventitious sounds include plenty of wheezing rhonchi and few crepitations. Wheezing rhonchi are the cardinal finding in Asthma though not diagnostic of this condition. Wheezing is polyphasic and though heard in both phases of respiration yet they are more prevalent during expiratory phase.
Status asthmaticus (Acute severe asthma)
It is a state of series of asthmatic attacks without any remission in between which makes the patient exhausted and incapacitated and if not treated urgently may lead to a fatal outcome
Severe asthma is diagnosed by the following features:
inability to speak with one breath.
Restlessness and anxiety.
Presence of large amount of bronchial secretion.
Prominent Central cyanosis.
Pulse rate more than 130 per minute.
Diminished level of consciousness.
Severe hyperinflation of the chest.
Markedly diminished breath sound with practically absence of rhonchi. In between Attacks The paroxysmal character of the attack is lost. There is breathlessness only during effort. Cough and expectoration are present but less. A low grade wheeze is always present. Recurrent respiratory infection precipitates the attack and gradually chronic asthmatic bronchitis develops. In the long run patient becomes a respiratory cripple due to development of emphysema. Examination reveals barrel-shaped chest with moist sounds and rhonchi.
Blood: Slight eosinophilia is present but the absolute count is less than 1000/mm3. Other blood changes are elevated IgE (Asthma is uncommon in subjects of low IgE) and rarely elevated SGOT, SGPT, LDH, CPK, OTC and ADH.
Sputum shows eosinophils, Charcot-Leyden crystals, Curschmann’s spirals and Laennec’s pearls and Creola’s bodies apart from the infective agents.
X-ray of chest shows overinflation of lungs in acute attack but may show emphysematous changes in late stages.
Pulmonary function tests: The degree of airway obstruction can be measured by FEV, and FEV,/FVC ratio both of which are reduced and improves after use of bronchodilators. The diffusing capacity is usually normal.
Blood gas analysis shows diminished PaO, and raised PaCO2 in status asthmaticus but normal in mild attacks. In earlier states respiratory alkalosis is present but in severe late stages respiratory acidosis results.
Skin tests: By prick test hypersensitivity reaction to various antigens can be obtained.
ECG shows normal features except Tachycardia. But sometimes P. pulmonale, Right axis or RBBB pattern may be observed.
Bronchial provocative test with methadolin or histamine may be of help in presence of uncertain diagnosis. COMPLICATIONS Status asthmaticus. Secondary infection Bronchitis, Tuberculosis. Emphysema of lungs. Right heart failure in late stages called chronic cor pulmonale. Bronchiectasis. Pneumothorax, pneumomediastinum. DIFFERENTIAL DIAGNOSIS Cardiac asthma See left ventricular failure. Chronic bronchitis History of cough for a long time with sputum and late development of wheeze and breathlessness are present. Family history is absent. Symptom free phase in childhood is present. Middle aged smokers are usually victims of it. Obstruction of trachea and bronchus Inspiratory dyspnoea, sucking of supraclavicular fossae and lower intercostal spaces, prolonged and laboured inspiration and stridor (absence of wheeze) are the main findings present. Uraemic asthma Features of uraemia are present. Recent development of symptoms are the distinguishing features. Hyperventilation with Kussmaul’s air hunger and Cheyne-Stokes breathing are seen Bronchopneuтопia High temperature, toxaemia and dyspnoea of recent onset are the main features. No past history is present. Tropical eosinophilia Young age, dominant cough particularly embarrassing at night, characteristic blood picture are the main findings. Allergic aspergillosis It is a form of pulmonary eosinophilia with combined Type I and III hypersensitivity reaction caused by Aspergillus fumigatus. There are episodic wheeze, breathlessness and migratory pulmonary infiltration. Sputum and bronchial casts contain A. fumigatus. Skin test is positive and precipitins to the fungus are present in blood. Blood eosinophilia is more than 0.5 x 109/L Pulmonary embolism Sudden onset of breathlessness with severe chest pain and rusty sputum but no prominent wheeze or rhonchi are seen. ECG and X-ray of chest are characteristic. Past history of wheeze is absent. Carcinoid syndrome and Endobronchial sarcoid. They are very rare diseases to be differentiated. TREATMENT During Attack
Rest in bed propped up position on a back rest or sitting up in a chair or inclined on a cardiac table.
Oxygen inhalation 4-6 litres per minute usually by mask method.
Inhaled sympathomimetics, e.g., Salbutamol (Albuterol), Biotolterol and Terbutaline may be given every 4-6 hours. One to two inhalations are usually sufficient. In acute exacerbation nebulizer is the best option.
When inhaled sympathomimetics cannot be used, Adrenaline (1 1000) 0.2-0.5 cc subcutaneously very slowly may be given (Hurst’s method) and repeated after 2 hours. It is contraindicated in cases of Hypertension and coronary arterial disease; so blood pressure should always be checked up before administering Adrenaline.
If Adrenaline is contraindicated then Aminophylline 0.24 gm in 10 cc solution IV may be given very slowly.
Steroids: Beclomethasone dipropionate (Becoride) by MDI can be given (42 ug/puff) 2 to 4 puffs every 6-12 hours. The mouth is to be washed with water after each use to prevent candidiasis. Spacer devices are also helpful to prevent candidiasis. Triamcinolone acetonide by MDI with spacer (100 ug/puff) 2-4 puffs every 6-8 hours or Flunisolide or Fluticasone or Budesonide by MDI (250 ug/ puff) 2-4 puffs every 12 hours may be used. In severe cases steroids may be given by IV route (see below).
Antibiotics: Empirical antibiotic therapy with Amoxycillin 500 mg every 8 hours orally; Tetracycline 250-500 mg every 6 hours by mouth or Trimethoprim- sulphamethoxazole 160/800 mg every 12 hourly for 7 days may be given. In status Asthmaticus
Salbutamol inhalation by nebulization.
Subcutaneous Adrenaline 0.2 to 0.3 cc of 1 1000 dilution or Terbutaline 0.25 mg may be used in young or middle aged patients who are unable to use aerosol nebulization.
Corticosteroids: When sympathomimetics fail to respond, steroids are used. Hydrocortisone 4 mg/kg or Methyl prednisolone 1-2 mg/kg to start with and repeated every 6 hours.
Antimicrobial therapy as before.
Oxygen inhalation as before.
Dehydration should be corrected by plenty of fluids given orally or parenterally.
Patient should be hospitalised if any one of the following features are seen: (a) No response to the above regime. (b) Persistently low PEFR (1less than 30%-40% of the predicted value or less than 200 litres/min). (c) Respiratory acidosis. (d) ECG abnormality including supraventricular arrhythmias, conduction disturbances or ventricular Ectopics. (e) Pneumothorax/Pneumomediastinum. (f) Respiratory failure. (g) Respiratory infections. (h) Past history of Status Asthmaticus. (i) Past history of respiratory failure.
Ventillatory assistance may be indicated if: (a) PaO2 is below 50 mm of Hg. (b) PaCO2 is above 44 mm of Hg. (c) FEV, and PEFR less than 10 % of the predicted value. (d) Marked exhaustion. (e) Patient becomes semicomatose. In between Attacks
Inhaled sympathomimetics as given above are recommended now-a-days and oral route is best avoided.
Theophylline and Aminophylline are sometimes used but of limited use now-a-days for their toxicity. When used their plasma level should remain in between 10-20 mg/cc.