A Case of

Bronchial Asthma

Presented By
Dr. Smitha K. Mohan
II M.D

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 ABOUT THE PATIENT
 Name : Sreekala
 Age : 49
 Sex : Female
 Address : Kowdiar, TVM
 Occupation :Accountant
 O.P no. : 12578
 Date : 20/8/05

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 PRESENTING COMPLAINTS
 Breathing difficulty (2years)
< night
> Sitting up, lying on right side
 Cough (2 years)
From tickling in the throat
Associated with expectoration of whitish
frothy sputum

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 HISTORY OF PRESENTING
COMPLAINTS
 Complaints started 3 yrs ago as recurrent attacks of
sneezing and cough . Sneezing < from dust
exposure. Cough < from exposure to cold air.
Patient used to suffer fom difficulty in breathing
from the least exertion.

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 TREATMENT HISTORY
 When the complaints of sneezing and cough
became severe she sought for treatment from
an allopathic doctor (at SP fort hospital) who
prescribed at first antihistamines. Though the
recurrent attacks of sneezing subsided, the
dyspnoea on exertion worsened. She was
diagnosed with bronchial asthma. He then
prescribed bronchodilatators. She has been
using inhalers since the past 1 ½ yrs.
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 FAMILY HISTORY
 Father – Bronchial asthma
 Mother – Diabetes Mellitus
 Elder brother - Bronchial asthma
 Younger sister - Bronchial asthma

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 MENSTRUAL HISTORY
 Menopause 2 yrs ago

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 OBSTETRIC HISTORY
 G 1 L1 P1 A 0
Normal full term delivery

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 PHYSICAL GENERALS
 FUNCTIONALS
 Appetite – N
 Thirst – Decreased
 Sleep – Decreased due
to complaints
 ELIMINATIONS
 Bowels – Regular
 Urine – Normal
 Sweat - Normal

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 RESPONSE TO

Food & drinks –
Desires warm drinks +++
Desires warm food ++

Desires sweets +++

Aversion fish ++

 Thermal reaction – Hot

Fanning desire
Aversion to covering

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 REGIONALS
 Extremities – Burning of soles at night

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 MENTAL SYMPTOMS
 Easily gets irritated
 Weakness of memory

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 PHYSICAL EXAMINATION
 General examination
 Built- Medium
 Anaemia – no pallor
 Clubbing – absent
 Lymphadenopathy –
absent
 Jaundice – not icteric
 Pulse rate – 70/mt
 Respiratory rate – 22/mt
 B.P – 130/80 mm of Hg www.similima.com 13
 SYSTEMIC EXAMINATION
 INSPECTION
 Shape of the chest – Bilaterally symmetrical
 Movements – Symmetrically diminished movt of chest
 PALPATION
 Pain & tenderness – nil
 Tracheal shift – nil
 Vocal fremitus - Normal
 PERCUSSION
 Note is normal
 AUSCULTATION
 B/L High pitched expiratory rhonchi (sibilant rales)
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 LAB INVESTIGATION
 TC; 8700 cell/mm3
 DC N-55% L-38% E-7%
 ESR-15mm/hr
 HB-10gm%
 RA Factor-negative
 ASO titre- negative

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PRESCRIPTION AND FOLLOW UP
 DATE - 20/8/05
R - SULPHUR 200/ 2d
 DATE - 21/9/05
Relief of complaints; occasional numbness of fingers
R – S.L 3 D; advised patient to stop use of inhaler
 DATE – 18/10/05
Relief of complaints; numbness of fingers persisting
R – Rhus tox 200/ 2 D
Advised the patient to take vitamin supplements
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 FOLLOW UP contd…
 DATE – 3/1/06
Return of attack last night. In the course of 2 ½
months , patient needed to use inhaler only once.
Numbness of fingers relieved
R – Sulphur 1 M /2 D . 2nd dose only when needed
(pnr)

 DATE – 15/6/06
Relief of complaints. No further attacks since
5 months
R – S.L 4 D
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 About Bronchial Asthma
 Chronic inflammatory disease of airways
 Characterized by increased responsiveness of
tracheo-bronchial tree to a multiplicity of stimuli
 Results in symptoms of wheeze, cough, chest
tightness, and dyspnoea < night
 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.
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 Prevalence
Increasing in the 2nd decade of life (10-15% of
population)

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 Classification
Extrinsic Intrinsic / Cryptogenic
 definite external cause
 no causative agent can be
identified
 Young patient  Adults > 35 years
 History of eczema  No h /o eczema in childhood
 FH of asthma, eczema, hay fever  No FH
 Attacks related to specific  Attacks related to infection/
antigens exercise
 Intermittent attacks  Persistent asthma
 a/c attacks, self-limiting  More fulminant , severe
 Occasional polyps  Nasal polyps common
 Skin test +ve  Skin test –ve
 IgE raised  Normal/ low IgE
 Prognosis favourable  Poor prognosis
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 Aetiology & 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 tt
 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
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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 r‘n followed by late r n
 Recurrent asthmatic r n – continuing episodes of asthma on
subsequent days.

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 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 spectrom of
inflamatory cells however are involved in the perpetuation
of chronic inflammatory reactions in the bronchial wall
which characterizes asthma
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 T lymphocytes are present in increased numbers in
asthmatic airways and have an important roll in
regulation of inflammatory response.They are
programed to release inflammatory cytokines
amongst which IL4 andIL5 are of importance.since
they both recruit oesinophils 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.

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 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
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 CLINICAL FEATURES
 Typical symptoms of asthma
comprises
 Wheeze
 Breathlessness

 Cough

 Sensation of chest tightness

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 Patients with episodic asthma are usually
asymptomatic between exacerbations,which
occur during viral rti 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.

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 Typically there is a diurnal pattern of symptoms
<morning. symptoms of cough wheeze often
disturbs sleep and the term nocturnal asthma
emphasizes this.Cough may be dominant symptoms
and lack of wheeze or breathlessness may lead to
adelay in making the diagnosis of so called cough
variant asthma. All of these clinical terms are
useful in emphazising characteristic features of
asthma particular to each patient and high light the
fact that asthma is not a static diseasebut a broad
dynamic syndrome.
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 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.
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 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.

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 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

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 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.

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 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

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 DIFFERENTIAL DIAGNOSIS
 Tropical Eosinophilia - It is an allergic reaction to
helminthic parasites, particularly filarial worm. It
may present with exertional dyspnoea, vague ill
health or asthmatic symptom. Absolute eosinophil
count ranges from 2000-10,000/cmm. In some cases
the WBC count may go as high as 30,000 –
40,000/cmm. Eosinophils may from 70-90% of the
total, all of them are mature.

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 Acute bronchitis - Acute infection of bronchi and
its ramification characterized by cough,
discomfort behind sternum;, scanty expectoration
to start with, later developing productive cough.
Infective agents are viral to start with, later
bacteria such as pneumococcus or H influensae
complicate the picture. Usually disease subsides
in 1-2 weeks.

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  Chronic Bronchitis Emphysema syndrome
 The disease is common in damp cold and
dusty regions. Atmospheric pollution accompanied by
higher incidence of CBES. Emphysema sets in when
airways obstruction progress in c/c bronchitis.
Initially there is cough recurring in winter seasons,
with expectoration of mucoid, tenacious sputum. O/E
chest reveals mild wheeze which disappears as the
patient clears the bronchi by expectoration. With
development of emphysema the chest assumes
inspiratory position and expiratory--------- are
considerably diminished. X-ray shows features of
emphysema in advanced stages.
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 Emphysema:
 Defined as a pathological increase in
the size of airspaces distal to terminal
bronchioles, with destruction of alveolar walls.
There is exert ional dyspnoea. The chest is
distended. Physical examination reveals barrel
shaped chest. Hyper resonance on percussion.
Lungs are hypertranslucent on x-ray.

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 Left sided heart failure:
 It complicates valvular heart disease,
systemic HT or IHD. It causes paroxysmal
dyspnoea in the first half of the night. Like
bronchial asthma in cardiac failure basal
crepitation are prominent and gallop rhythm
may be evident.

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 Metabolic acidosis:
 This is due to accumulation of any acid
other than carbolic acid. Several disorders can lead to
metabolic acidosis. Acid administration, acid
generation, impaired acid excretion, or bicarbonate
losses of GIT or kidneys. Calculation of plasma anion
gap is useful for confirmation of diagnosis.
 Clinically there is sign of ‘air hunger' or
kusmaul respiration and hyperventilation. Severe
acidosis is often associated with confusion and
fatigue.
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 Air way obstruction
May due to severe laryngitis,or to
laryngial oedema. Foreign body impaction or bilateral
abducter paralysis can also lead to obstruction.
 Cystic fibrosis
There is alteration in the viscosity $
tenacity of mucous pdn.Includes broncho pulmonary
infection $ pancreatic insufficiency,highsweat na$ cl
concentration.Breathlessness $ Heamoptysis occur in
late stages.Infertility,malnutrition,steatorrhoea are
also seen.

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 Fibrosing alveolitis
Progressive Breathlessness
&cyanosis.leads to PHT&corpulmonale.finger
clubbing is common.X-ray initially shows
ground glass appearance then nodular shadows
with streaky fibrosis& finally honey comb
appearance.A/C form known as Hamman rich
syndrome.

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 Extrinsic allergic alveoliti s
There is inflamatory reaction of
airways & alveoli.Due to inhalation of
antigens commonly microbial spores
contaminating vegetable matter[straw, hay
etc.] C/F are fever, malaise
,breathlessness,cyanosis ,weight loss etc.Xray
shows fluffy nodular shadows mostly in upper
zones.LFT shows restrictive ventillatory
defect. www.similima.com 43
 Occupational lung D/S
Exposure to dusts ,fumes,
gases at work can lead to devt of dyspnoea, a/
c bronchitis,fibrosis,etc.[eg;silicosis,
byssinosis,berrylliosis etc.]

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 Lung carcinoma
C/F are cough heamoptysis, chest
pain, malaise, dyspnoea, weight
loss,hoarseness,etc.Enlarged supraclavicular
lymph nodes are also seen with SCC. Chest
Xray shows round shadows,edge of tumour
has a fluffy or spiked appearance.HPOA
occurs in 3% of br. Cas.[Jt
stiffness,gynecomastia, clubbing]
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 Pneumothorax
Usual cause is underlying
COPD.C/Fare sudden onset of unilateral chest
pain or progressing dyspnoea.vocal resonance
is reduced or absent.percussion note is hyper
resonant.

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Connective tissue disorders
Asthma can be associated with PAN,SLE
etc .in SLE There recurrent pleurisy with or with out
effusion. ANA is +ve in almost all cases of SLE.

 Conditions causing weakness of respiratory muscles

result in dyspnoea. eg; Poliomyelitis, myesthenia
gravis ,polyneuropathy, MND, muscular dystrophies
etc.
 Extreme obesity can also produce same effect by
increasing work of moving chest wall.[pick wickian
syndrome.]
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 Psychogenic dyspnoea
underlying psychological disturbance often
anxiety,it is the tense obsessional pt complain
of dyspnoea without any organic
basis.Depression also lead to dyspnoea.Most
significant finding is gross irregularity of
respiration.During The attack of dyspnoea
breathing is shallow & chest is held in
inspiration.
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 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.
Wheexing respiration. Suffocative catarrha.
 Aralia: Asthma on lying down at night. With spasmodic
cough < after first sleep with tickling in throat.
Constriction in throat.

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 Aspidosperma: Uraemic 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.
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 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 -----
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.
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 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.
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 Sulphur: Dyspnoea in middle of night >sitting
up. Much rattling of mucous. Wants windows
open. Oppression as of a load in chest.
 Medorrhinum: Dyspn;oea cannot exhale.
>lying of stomach. Dry, night cough.
 Viscum: Asthma connected with rheumatism
or gout. Suffocation while lying on left side.
Spasmodic cough.
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