BRONCHITIS ,

BRONCHECTASIS,BRONCHIAL
ASTHMA.
DEEPIKA.R
M.SC (NURSING ) II YEAR
COLLEGE OF NURSING
MADRAS MEDICAL COLLEGE
CHENNAI-03
 BRONCHITIS
INTRODUCTION

It is a condition where the lining of bronchial tubes become infl amed or

infected. It have reduce ability to breath in air & oxygen into the lungs,
they have also heavy mucus forming in the airways .

INCIDENCE

The recent 'Indian Study of Asthma, Respiratory Symptoms and Chronic

Bronchitis' study of 85,105 men and 84,470 women from 12 urban and
11 rural sites repor ted the incidence of chronic bronchitis to be 3.49%
(4.29% in males and 2.7% in females) in adults > 35 years
Definition

• It is an inflammation and swelling

of the bronchial tubes (bronchi),
the air passage between the lungs.
BRONCHITIS
Types
1. ACUTE – it is a shorter illness that commonly follow a cold or viral
infection such as flu. It consist of a cough with mucus, chest
discomfort, throat soreness, fever, shortness of breath. It is usually a
last a few days or weeks (1-3 week).

2. CHRONIC – it is a serious ongoing illness , it is a persistent, mucus

producing cough that last longer then three month. The person is having
severe breathing difficulties & it may get worsen. It occurs with
emphysema and it may become COPD
ACUTE BRONCHITIS
Etiology

1. Acute – It is caused by virus, the same virus that cause cold & flu.
It can be caused by bacterial infection & exposure to substance that
irritate the lungs such as tobacco smoke, dust, fumes, vapours & air
pollution.

2. Chronic – It is caused by repeated irritation & damage of the lungs &

airway tissue . Smoking is most common cause with other causes
including long term exposure to air pollution, dust & fumes from the
environment & repeated episodes of acute bronchitis.
 Etiology
• Etiologic agent – bacteria, virus

• Predisposing factor (contribute

to the problem)– smoking, long
term illness, immune deficiency
and immobilization.

• Precipitating factor (trigger the

problem)– hospitalization,
environment, smoking and
malnutrition.
PATHOPHYSIOLOGY
Micro-organism enter into the respiratory tract through nasal inhalation.

Inflammation affecting the large and mid-sized airways (bronchi)

The inflammatory process triggers increased blood flow and cellular activity within the
affected bronchi

The inflammation of the bronchial wall leads to mucosal thickening,

Epithelial cell desquamation, and denudation of the basement membrane.

This results in symptoms such as coughing, shortness of breath, and low fever
 Clinical manifestation
 Sign & symptoms for both acute and chronic bronchitis.

 Persistent cough

 Production of mucus which can be clear, white, yellowish

gray or green in color, rarely it may be streaked with
blood.

 Crackles and Wheezing sound

 Low fever, chills, Headache

 Chest tightening

 Sore throat, dyspnoea

 Blocked nose & sinuses

 Diagnostic evaluation
 History

 Physical examination

 Chest x-ray –thickening of bronchial walls

 Sputum– for gram stain, culture and

sensitivity test may be obtained to determine
presence of bacterial infection.

 Pulmonary function test by using spirometer –

to determine peak expiratory flow (person's
maximum speed of expiration)-400-700
litres/mts.

 ABG Level
Management
 People with bronchitis are instruct to rest, drink fluid, breath warm & moist
air, & take OTC cough suppressant & pain relieve in order to manage symptoms &
ease breathing.

 Many case of acute condition may go away without any specific treatment, but
there is a no cure for chronic condition .

 To keep bronchitis symptoms under control & relieve symptoms, doctor may
prescribe –

Antibiotics – Azithromycin, for 7-10 days

Antitussive – Codeine for suppressing the cough

Bronchodilators – To dilate the bronchi
 Beta2-adrenergic agonist agents – Salbutamol, Terbutaline

 Anticholinergic agents – Ipratropium bromide

 Methylxanthines – Theophylline

Mucolytics - e.g. Acetylcysteine to thin the secretions.

Corticosteroids – Dexamethasone, Methylprednisolone to relieve the inflammation

Antipyretics - for fever

Other - Oxygen therapy, Pulmonary rehabilitation program, chest physiotherapy,

nutritional therapy
 Additional behaviour remedies include –
 Removing the source of irritants from
the lungs

 Using a humidifier – loosen mucus

 Exercise

 Breathing exercise – pursed lip breathing

 Postural Drainage

 Manual Techniques-Percussion,
shaking and vibrations can be used to
mobilize secretions and aid
expectoration
Complication
 Pneumonia

 Asthma

 COPD
Bronchiectasis

• Bronchiectasis is defined as
abnormal and irreversible
dilatation of the bronchi and
bronchioles (greater than 2mm
in diameter) developing
secondary to inflammatory
weakening of bronchial walls.
BRONCHIECTASIS
Etiology:

• Bronchiectasis has both congenital and acquired causes

• ACQUIRED CAUSES

• Tuberculosis,

• Pneumonia,

• Inhaled foreign bodies,

• Allergic bronchopulmonary aspergillosis and bronchial tumours are the

major acquired causes of bronchiectasis.
Infective causes associated with Bronchiectasis include

• Infections caused by the staphylococcus, klebsiella, or bordetella

pertussis, the causative agent of whooping cough.

• Aspiration of ammonia and other toxic gases,

• Pulmonary aspiration,

• Alcoholism, heroin (drug use),

• Various allergies all appear to be linked to the development of

bronchiectasis.
CONT…

• Childhood Acquired Immune Defi ciency Syndrome (AIDS),

which predisposes patients to a variety of pulmonary ailments,

such as pneumonia and other opportunistic infections.

• Infl ammatory bowel disease, especially ulcerative colitis.

• A Hiatal hernia can cause Bronchiectasis when the stomach

acid that is aspirated into the lungs causes tissue damage.

CONGENITAL CAUSES

• Kartagener syndrome (bronchiectasis, sinusitis, situs inversus)

• Primary immunodeficiencies (Hypogammaglobulinemia)

• Williams-campbell syndrome( Bronchomalacia) and

• Marfan's syndrome.

• Patients with alpha 1-antitrypsin deficiency have been found to be

particularly susceptible to bronchiectasis,

• Cystic fibrosis
 Morphological types
• Cylindrical or tubular bronchiectasis
• Varicose
• saccular or cystic bronchiectasis
PATTERNS OF BRONCHIECTASIS:
Three different patterns of bronchiectasis have been
described

 cylindrical bronchiectasis : Involved bronchi appear

uniformly dilated

 varicose bronchiectasis : Resembling varicose veins the

affected bronchi have an irregular or beaded pattern of
dilatation

• Saccular (cystic) bronchiectasis: The bronchi have a

ballooned appearance at the periphery , ending in blind sacs
without recognizable bronchial structures distal to the sacs
 PATHOPHYSIOLOGY.
Due to etiology factors

Destruction and infl ammatory changes in the wall of the medium sized airways

At the level of segmental and subsegmental bronchi

Infl ammation primarily mediated by neutrophils

upregulation of enzymes, such as elastase and matrix metalloproteinases.

PATHOPHYSIOLOGY- cont….

• The normal structural component of the wall, including car tilage, muscle and
elastic tissue are destroyed and replaced by fi brous tissue.

• The dilated airway frequently contain pools of thick purulent material

• while more peripheral airways are of ten occluded by secretion or obliterated

and replaced by fi brous tissue

• Bronchiectasis may occur

MECHANISM
• Dilation and distor tion of the bronchi

• Damage of air way epithelium

• Dilation and hyperplasia of blood capillar y

Airway Injury + Secretion Stimuli

Secretion Stasis Infection

Airway Destruction + Airway Dilation

Other types

• Upper Lobe Bronchiectasis

• Dry Bronchiectasis (Bronchiectasis Sicca)

• Middle Lobe Bronchiectasis (Brock’s Syndrome)

• Pseudo (Reversible) Bronchiectasis.

 TYPES

• Upper Lobe Dry Bronchiectasis

Bronchiectasis (Bronchiectasis Sicca)

• This involves posterior and • Only hemoptysis is present;

apical segments of upper • There is no sputum
lobe. production; usually seen in

• It is common in tuberculosis, upper lobe involvement in

cystic fi brosis and ABPA. tuberculosis.

Types- cont ,,,

• Middle Lobe Bronchiectasis (Brock’s • Pseudo(Reversible) Bronchiectasis

Syndrome) • It is a tem p ora r y b r onchi a l di l a ta ti on
occur r i ng i n a n a r ea of l ung a ff ected b y
• Thi s is a ter m a p p l i ed to r ecur r ent
p neum o ni c co nsol i d a ti o n, tra cheob r onchi ti s
a tel ecta si s of the r i g ht m i d dl e l ob e (RM L ) i n
or l ung col l a p se
the a bsence of endob r o nchi a l ob str ucti on.

• A f ter severa l ep i sod es of a tel ecta si s,

br onchi ecta si s a nd chr o ni c fi b r osi s of the
RM L m ay d evel op.

• It i s usua l l y seq uel a e to p r i m a r y p ul m ona r y

tuber cul osi s r esul ti ng fr om ob str ucti o n o f
mi dd l e l o be b r onchus b y TB l y m p h nod es.
Clinical manifestation
 1.The production of large quantities of purulent and of ten foul-smelling sputum.

 The volume of sputum can be used for estimating the severity of the disease

 Mild < 10 mL

 Moderate 10~150 mL

 Severe >150 mL

 2.Chronic cough

 3.Hemoptysis:

 Frequent

 More commonly in dr y variety

Clinical manifestation
 Usually mild (blood streaking of purulent
sputum)

 Massive hemoptysis is usually from dilated

bronchial arteries or bronchial-pulmonary
anastomoses under systemic pressure

 4. Recurrent pneumonia:

 same segment

 5. Systemic manifestations:

 fever, weight loss

Diagnostic evaluation:
• Histor y and physical examination -
saccharine Test (Assessment of Ciliar y
Function)

• Chest x-ray-Shows ring shadows, tram track

sign, gloved fi nger appearance, evidence of
fi brosis or cor pulmonale.

• CT (computerised tomography) scan

• It is a non-invasive diagnostic test. Thick

sections—more specifi c Thin sections—more
sensitive.

• High resolution CT
Diagnostic evaluation:

• Blood tests

• Testing of the mucus to identify any bacteria present

• Checking oxygen levels in the blood

• Lung function tests (spirometry).

• Bronchography

• It provides excellent visualization of bronchiectasis

airways, which helps in confirming diagnosis and for
planning surgery.
Complications

 Progressive suppuration. Amyloidosis

 Haemoptysis, major pulmonary  Local complication

haemorrhage.
 Recurrent pneumonia
 COPD,
 Lung abscess
 Emphysema,
 Empyema
 Chronic respiratory insuffi ciency
 Hemoptysis
Cor pulmonale and right
 Pulmonary hypertension
ventricular failure.
 Treatment
• Treatment of bronchiectasis includes Therapy has several major goals:

• Controlling infections and bronchial (1)Treatment of infection, par ticularly

secretions, during acute exacerbations

• Relieving air way obstructions,

• Rem oval of aff ected por tions of lung by (2)Improved clearance of tracheobronchial
su rgical removal or ar ter y embolization secretions

• Preventing complications. (3) Reduction of infl ammation

(4)Treatment of an identifi able underlying

problem.
Medical management

1 . Improving the drainage of airway

1) Mucolytics-guaifenesin 600-1200 mg every 4-6 hrs

2) Bronchodilators-albuterol 2 puff s(90 mcg) every 4-6 hours.

3) Postural drainage

2. Antibiotic

• The choice of antibiotics should be accurately by the results of sputum

culture and drug sensitivity test. Azithro -commonly used 500 mg three
times a week,Amoxicillin-250-500mg every 8 hrs.

• Empirical therapy ---antipseudomonal antibiotics.

 Antibiotics are the cornerstone of bronchiectasis management

• Antibiotics are used only during acute episodes

• Choice of an antibiotic should be guided by gram's stain and culture of

sputum

• Bronchodilator

• Bronchodilators to improve obstruction and aid clearance of secretions are

useful in patients with airway hyperreactivity and reversible airfl ow
obstruction
Surgical management is indicated

1. Recurrent and refractory clinical symptoms are due to a focal area of

disease involvement.

2. Massive hemoptysis

SURGICAL RESECTION (when disease is localised)

• Bronchial ar terial embolization - (when disease is widespread)

• Lung transplantation- (when disease is widespread)

 BRONCHIAL ASTHMA-DEFINITION

• Asthma is characterized by chronic airway inflammation and increased

airway hyperresponsiveness leading to symptoms of wheeze, cough,
chest tightness, and dyspnea.

• Asthma is an inflammatory disease of the small airways, characterized

by episodic, reversible bronchial obstruction due to hyper-
responsiveness of tracheobronchial tree to a multiplicity of intrinsic
and extrinsic stimuli manifested clinically by paroxysms of polyphonic
wheeze, dyspnea, and cough which may be relieved spontaneously or as
a result of therapy -manual of practical medicine.
Bronchial Asthma
prevalence

. In 2019, an estimated 262 million people worldwide were affected by asthma

• In the United States, asthma aff ects more than 18.7 million adults
and accounts for approximately 3,500 deaths per year

• Twenty-one percent of patients with asthma smoke even though

cigarette smoke is known to trigger an attack, while nearly 17% of
people without asthma smoke

• Asthma accounts for 1.8 million ED visits per year and close to
440,000 hospital admissions
STIMULI THAT CAN INCITE ASTHMA

• ALLERGEN INHALATION • AIR POLLUTANTS

• Animal danders( e.g, cats, mice, guinea • Exhaust fumes

pigs)
• Oxidants
• House dust mite
• Cigarette smoke
• Cockroaches
• Perfumes
• Pollens
• Sulfur dioxides
• Molds
• Aerosol sprays
STIMULI THAT CAN INCITE ASTHMA

• Viral upper respiratory tract infection, • Industrial chemicals and plastics

sinusitis, exercise and cold, dry air and
• Wood and vegetable dusts pharmaceutical
stress.
agents
• DRUGS
• FOOD ADDITIVES
• Aspirin
• Sulphide ( bisulphites and metabisulfite
• Non steroidal and inflammatory drugs
• Monosodium glutamate beer, wine, dried
• Beta adrenergic blockers fruit, shrimp, processed potatoes,

• OCCUPATIONAL EXPOSURE • Tartrazine.

• Metal salt
ETIOLOGY

• Respirator y tract in fections

• Allergens

• Cigarette smoke

• Air pollutants

• Occupational factors- occu pation al asthma is th e most common job-related respirator y

disorder. These irritants cause a change in th e respon siven ess of the air ways (wood
dusts, laundr y detergents, metal salts, ch emicals, pain ts, solvents, and plastics)

• Exercise- asthma that is in duced or worse during physical exer tion is called exercise-
induced asthma (EIA) or exercise-induced bronch ospasm (EIB) air way obstru ction may
occur due to changes in the air way mucosa caused by hyper ventilation during exercise,
with either cooling or rewarmin g of air an d capillar y leakage in the air way wall.

• It occur af ter vigorous exercise .

ETIOLOGY
• Drugs and Food Additives-asthma triad: nasal polyps, asthma, and sensitivity to
aspirin and nonsteroidal anti infl ammator y drugs (NSAIDs)-ASPIRIN INDUCED
ASTHMA.

• β-Adrenergic blockers in oral form (e.g., metoprolol [Toprol-XL]) or topical eye drops
(e.g., timolol [Timoptic]) may trigger an asthma attack because they can cause
bronchospasm.

• Angiotensin-conver ting enzyme (ACE) inhibitors (e.g., lisinopril) may cause a dr y,

hacking cough in susceptible persons, making asthma symptoms worse.

• Gastroesophageal Refl ux Disease - refl ux may trigger bronchoconstriction and cause

aspiration

• Genetics
ETIOLOGY
• Immune Response

• Psychological Factors - Any triggering event

can produce panic, stress, and anxiety.
These emotions, and other psychological
factors, can cause bronchoconstriction
through stimulation of the cholinergic refl ex
pathways.

• Extreme behavioral expressions (e.g.,

crying, laughing, anger, fear) can lead to
hyperventilation and hypocapnia, which can
cause airway narrowing.
Asthma subtypes
• Traditionally, asthma patients were divided into,

• Extrinsic Asthma (Atopic Asthma, Early Onset Asthma)

• Intrinsic Asthma (Non-atopic Asthma, Late Onset Asthma)

• Nowadays, asthma has been recognized as an extremely heterogeneous

disease in which pathophysiology the T-helper lymphocytes play a crucial
role.

• Recently classified as’

• Th2-high asthma (or type-2 or eosinophilic asthma)

• Th2-low asthma (or non-type-2, non-eosinophilic or neutrophilic asthma)

Extrinsic Asthma (Atopic Asthma, Early Onset Asthma)

• Onset is in childhood.

• It occurs in atopic individuals who readily form IgE antibodies in response to

allergens.

• Atopic patients can be identifi ed by skin sensitivity tests.

• Asthmatic infl ammatory reaction is characterized by a cellular infi ltrate rich

in eosinophils.
Intrinsic Asthma (Non-atopic Asthma, Late Onset Asthma)

• It can begin at any

age, especially in
late adulthood.

• There is no role for

allergens in the
production of the
disease
 Sent by you: extrinsic asthma

Th2-high asthma (or type-2 or eosinophilic asthma)

Th2-high asthma (or type-2 or eosinophilic asthma)

 An allergen is presented to naive t-cells by dendritic cells, leading to

development and activation of th2 cells producing cytokines (interleukin
(IL)-3, IL-4, IL-5, IL-9, and IL-13) in the bronchial submucosa.

 These cytokines contribute to an allergic airway infl ammation that triggers

activation and recruitment of immunoglobulin (Ig)E antibody-producing B-
lymphocytes, mast cells, basophils, and eosinophils.

 Th2-high asthma is often severe

Th2-low asthma(or non-type-2, non-eosinophilic or
neutrophilic asthma).
• An increased count of th1-cells producing interferon (IFN)γ and tumor necrosis
factor (TNF)α and of th17-cells producing IL-17 and IL-8 is presented by
predominantly neutrophilic inflammation.

• Th2-low asthma includes two main subtypes:

• Neutrophilic asthma: Characterized by an abundance of neutrophils (another

type of white blood cell) in the airways.

• Paucigranulocytic asthma: In this subtype, there are no significant elevations

in eosinophils or neutrophils.
Pathophysiology of bronchial asthma.
1.Early phase of asthma.it occur within 30 to 60 mts after exposure

Due to predisposing factors ( allergens , irritants)

Initiates inflammatory response

Variety of inflammatory cells involved in asthma

Such as mast calls, macrophages , eosinophils , neutrophils, T and B Lymphocytes, and

epithelial cells of the airways
Pathophysiology of bronchial asthma.
Due to inflammatory process ,there will be a Production of IgE antibodies

These IgE antibodies attached to mast cells at IgE receptors sites and cross linking of allergen with
IgE Antibodies.

Mast cell degranulation

Release multiple inflammatory mediators ,are leukotrienes, histamine, cytokines( e.g. interleukin 4 and
5),prostaglandins and nitric oxide.
Pathophysiology of bronchial asthma.
• So m e i nfl a m m a tor y m ed i a tor s a ff ects b l oo d vessel s ca use va sod i l a ti on a nd

C a pi l l a r y per m ea b i l i ty

Eosi nop hi l s , l y m pho cy tes, a nd m onocy tes i nfi l tra ted i n the a i r way s

D ue to i nfl a m m a tor y r esp onse ca use

 Va scul a r cong esti o n

 Ed em a f or m a ti on

 Pr o ducti on of thi ck , tena ci ous m ucus,

 B r onchi a l m uscl e sp a sm

 Thi ckeni ng of a i r way wa l l s

 Inc b r onchi a l hy p er r esp onsi veness

Pathophysiology of bronchial asthma.
2.Late phase of asthma (delayed response ,symptoms can recur 4 to 10 hrs )

After initial attack

Further release of more inflammatory mediators ( eosinophils and lymphocytes activation )

The epithelial cells also produce cytokines and other inflammatory mediators

Only 30% to 50% patients experience delayed response.it can be severe than the initial phase
and persist for 24 hrs or more
Pathophysiology of bronchial asthma.
• It can be sustainable cycle of inflammation , airflow limitation

• With or without bronchoconstriction

• If untreated leads to long term damage that is irreversible

• Chronic or recurrent inflammation of airway results in structural changes in the bronchial

wall is known as remodeling

Bronchial smooth muscle hypertrophies ,Hyperplasia and collagen deposited in the airway
walls
ACTIVATION OF INFLAMMATORY RESPONSE.
Classification of asthma- based upon severity.
OTHER TYPES

 Nocturnal Asthma

 Gastric Asthma

 Exercise-induced Asthma

 Episodic Asthma

 Chronic Asthma

 Acute Severe Asthma (Status Asthmaticus)

Nocturnal Asthma

• Nocturnal asthma is defined as an overnight fall of more than 20% in the FEV1 or
PEFR. It may be the sole manifestation of asthma. This is presumed to be due to:

• a. Early morning fall in circulating adrenaline

• b. Overnight changes in vagal tone (increased vagal tone in early morning)

• c. Airway cooling at night.

• d. circadian changes in plasma cortisol concentration (midnight to early morning

fall in cortisol level)
 GASTRIC ASTHMA

• Gastric Asthma Worsening of asthma after meals or dyspnoea

occurring only after meals is due to gastro-oesophageal reflux
(reflux-reflex).

• This is treated by avoiding oral bronchodilators and

instituting anti-reflux therapy
Exercise-induced Asthma

• Asthma is induced by exercise and inhaled bronchodilators should be

given before exercise. Usual therapy with pre-exercise bronchodilators
or sodium cromoglycate are advised

• Episodic Asthma

• Patient has no respiratory symptoms between episodes of asthma

• Chronic Asthma

• Symptoms may be chronic unless controlled by appropriate therapy. It may

simulate chronic bronchitis.
Acute Severe Asthma (Status Asthmaticus)

• It is a medical emergency. Patient is hypoxic and cyanosed

due to severe bronchospasm.

• It is characterized by tachycardia (pulse rate > 120),

tachypnoea (respiratory rate > 30/min), sweating, pulsus
paradoxus (> 10 abnormal; > 20, profound obstruction),

• Altered level of consciousness, and an inspiration-expiration

ratio of 1 : 3 or 1 : 4.
CLINICAL MANIFESTATION.

Recurrent
episodes…
……

Cough
particularly at
night and in
the early
morning
CLINICAL MANIFESTATION

Assessment
Prolonged • Hypoxemia,
expiration
• Restlessness,
• Increased anxiety,
• Inappropriate behavior,
• Tachycardia , tachypnea, inspiratory or
Inspiration-
expiration expiratory wheezing,
ratio is 1; 2 • Hypertension,
• Pulsus paradoxus.
 History
• Sudden onset of symptoms, of ten at night or in the early morning hours, typically
shor tness of breath and cough (productive or unproductive), par ticularly

• Af ter allergen exposure

• During (or, more commonly, af ter) physical exer tion or spor ts (so called exercise-
induced asthma)

• In the setting of upper respirator y infection

• On exposure to thermal stimuli , (e.g., Cold air), On exposure to smoke or dust

• Seasonal variation of symptoms (seasonal elevation of pollen count)

• Positive family histor y (allergy, asthma)

• Precipitants of asthmatic symptoms in the patient ’s environment at home, at work,

and during leisure activities
 Findings on physical examination
• Rales, rhonchi, wheezes • Expiratory wheeze is heard with
mild bronchoconstriction.
• Prolonged expiratory phase
• Inspiratory and expiratory
• Tachypnoea
wheezes are heard in moderate
• Orthopnoea
bronchoconstriction.
• Chest constriction
• Inspiratory wheeze is heard in
• WHEEZE severe bronchoconstriction.

• Widespread, polyphonic, high • In near fatal asthma, the chest is

pitched wheezes are heard. silent
 Peak fl ow meter

• Measure the highest volume of airflow during

a forced expiration.
• The patient takes a deep breath and places
lips around the mouthpiece
• (a). And then exhales hard and fast
• (B). Volume may be measured in color-
coded zones:
• The green zone signifies 80% to 100% of
personal best; yellow, 60% to 80%; and red,
less than 60%.
• If peak flow falls below the red zone, the
patient should take the appropriate actions
prescribed by their primary provider.
DIAGNOSIS OF ASTHMA.

PEAK EXPIATORY FLOW RATE

 Measured by the peak flow meter(4.5-3.5L in males,3.25-2.5L in females)
FEV in 1 sec (FEV1)
To diagnose and to monitor asthma.
It should be compared with patients own previous best measurements.

SPIROMETRY.

Decreased forced vital capacity,FEV1, PEFR, and FEV1 to FVC ratio

(FEV1/FVC)

To stop taking any bronchodilator medications for 6 t0 12 hrs. before the test
DIAGNOSIS OF ASTHMA.

• During an exacerbation of asthma , lung function parameters fall from their

baseline levels.

• EOSINOPHIL AND IgE

• Elevated serum eosinophils count

• Elevated serum IgE levels are highly suggestive of atopy

• Allergic skin testing determine sensitivity to specific allergens

• CHEST X RAY- to rule out other causes of wheezing and also to rule out the
presence of pneumothorax in all cases of severe acute asthma
Complications
• Pneum oni a ,

• Tensi on p neum othora x,

• Sta tus a sthm a ti cus, a nd

• A cute r esp i ra to r y f a i l ur e

• Sta tus A s thma ticus - sta tus a sthm a ti cus i s the m o st extr em e f or m o f a n a cute a sthm a
a tta ck . It i s cha ra cter i zed by hy p oxi a , hy per ca p ni a , a nd a cute r espi ra to r y f a i l ur e.

• Unr espo nsi ve to tr ea tm ent wi th b r o nchod i l a tor s a nd cor ti coster o i d s.

• MA NI F E STAT ION : Sever e shor tness b r ea th of , hy p otensi on, b ra d yca r d i a ,

r esp i ra to r y /ca r d i a c a r r est

• Intuba ti on a nd seda ti on , ver y l o w FEV1

Management of asthma.

• GOALS OF ASTHMA MANAGEMENT.

 Achieve and maintain control of symptoms

 Prevent asthma exacerbation

 Maintain pulmonary function as close to normal as possible.

 Avoid adverse effects from asthma medications

 Prevent development of irreversible airflow limitation

 Prevent asthma mortality

OXYGEN

• High concentration of oxygen

• Should maintain >92% in adults

• Warning sign –

• HIGH Paco2

• Failure to achieve appropriate

oxygenation is an indication for
assisted ventilation.
Monitoring of treatment

• PEF Should be recorded every 15-

30 mts and then every 4 -6 hrs.

• SaO2 >92% ,

• Repeat ABG are necessary if the

initial PaCo2 measurements were
normal or raised ,the PaO2 was<60
mm Hg , or patient detoriatess.
The Stepwise Management
• Hour 1 :

• (i) oxygen administration,

• (ii) hydration (intravenous fluids),

• (iii) up to four doses of inhaled

salbutamol with ipratropium,

• (iv) intravenous hydrocortisone

(100mg) or oral prednisolone (40-
60mg).
DRUG THERAPY
Dosage of inhaled corticosteroids
Management of asthma in diff erent stages at various
levels
The Stepwise Management
• Hour 2 :

• (i) four more doses of inhaled

salbutamol with ipratropium,

• (ii) intravenous aminophylline,

• (iii) intravenous magnesium

sulphate 2gm,

• (iv) subcutaneous terbutaline

0.3-0.5mg (0.01mg/kg-child)
 High doses of inhaled
bronchodilators
• Short acting beta 2 agonists

• Administer via nebulizer such as

salbutamol – metered dose inhaler

• As a “gold standard” therapy, β2-

adrenergic agonists and inhaled
corticosteroids (ICS) have been used,
providing broncho dilating and anti-
inflammatory actions, respectively.
Systemic corticosteroids
• It r ed uces the i nfl a m m a tor y r esp onse

• A dm i ni ster ed to a l l p a ti ents wi th a n
a cute sever e a tta ck .

• A dm i ni ster ed ora l l y- ( p r ed ni sol o ne

3 0 -6 0 m g ) b ut i ntraveno us
hydr ocor ti so ne 2 0 0 m g .
Intravenous fluid
• H ydra ti on thera p y

• Pota ssi um sup p l ements- r ep ea ted

doses of sa l b uta m ol ca n l ower ser um
pota ssi um .

• Subseq uent m a na g em ent.

• Intravenous m a g nesi um p r ov i d e
a ddi ti o na l f or b r onchod i l a tor s i n
pa ti ents p r esenti ng p ea k exp i ra to r y
fl ow i s<3 0 % pr ed i cted .

• A mi no phy l l i ne

• Iv l euko tr i ene r ecep tor s a nta g oni sts.

DRUGS USED IN ASTHMA

ANTI-INFLAMMATORY AGENTS MAST CELL STABILIZERS

• CORTICOSTEROIDS • Cromolyn

• Hydrocortisone • Nedocromil

• Triamcinolone

• Prednisolone

• Mometasone
DRUGS USED IN ASTHMA

LEUKOTRIENE MODIFIERS
ANTICHOLINERGICS • Leukotriene receptors blocker

• Short – acting: Ipratropium • Zafirlukast

• IgE Antagonists: Omalizumab • Montelukast

• Long – acting: Tiotropium • LEUKOTRIENE INHIBITORS

• Montelukast t (10 mg QID)

• Zafirlukast (20 mg BD)


5-LIPOXYGENASE INHIBITOR
• Z ile uton 6 0 0 mg qid
• p r i m a r i l y r eser ved f or sever e
a sthm a .
• It ca uses el eva ti on of l i ver
enzy m es. M onthl y esti m a ti on of
A LT i s essenti a l .
IGE ANTAGONISTS: OMALIZUMAB-
• Oma liz uma b is a monoclona l
a ntibody a ga ins t IgE a nd ha s a
r ol e i n the m a na g em ent o f
m od era te a nd sever e per si stent
a sthm a .
• Om a l i zum a b 3 0 - 7 0 0 IU/ m L SC
b a sed upo n the p a ti ent ’s
b a sel i ne Ig E l evel .
DRUGS USED IN ASTHMA

BETA 2 ADRENERGIC AGONISTS
• INHALED : SHORT – ACTING
• Metaproterenol
• Terbutaline - Terbutaline 5 mg three
times daily orally or by MDI
• IMMEDIATE ACTING
• Epinephrine- , most effective by
parenteral or inhalational routes.
Epinephrine (0.3–0.5 ml of 1 : 1000
solution subcutaneously )
• METHYLXANTHINES:

• bitolterol, levalbuterol
• Aminophylline
• INHALED : LONG – ACTING
• Theophyllin e
• Salmeterol
METHYL XANTHINE
• Oral theophylline

• IV amin o ph y lline (In children 9–16

y ears an d adu lt smokers—a loading
d ose o f 6 mg/kg followed by an
infusio n o f 1 mg/kg/hr for 12 hours
and 0.8 mg /kg/hr thereafter. In
n on smo kers— same loading dose if
p atien t h as no t received the drug
p revio usly, fo llowed by 0.1–0.5
mg /k g /h r as an infusion).
Management of Nocturnal Asthma

• Treatment with anti-inflammatory drugs (corticosteroids)

• Sustained-release theophylline or a β2 agonist or both

• Long acting β2 agonists.

Management of Acute Severe Asthma
• a . High concentration oxygen therapy

• b. High dose β2 agonists by nebuliser

• c. Systemic cor ticosteroids

• d. If no response with above treatment, ipratropium bromide by nebuliser or IV

aminophylline (250 mg over 20 minutes) or IV β2 agonists

• e. Monitor treatment with pulse oximetr y

• f. Assisted ventilation when needed

• g. Treatment with 70-80% helium (balanced oxygen) may be benefi cial. This gas
mixture reduces air way resistance and improves the eff ect of aerosolised
bronchodilators .
 NEW THERAPEUTIC CONCEPTS

 Treatment of Th2-high or eosinophilic type of asthma.

 Anti-IgE based therapy
 Cytokines as a target
 Treatments of eosinophilic type of asthma
 Global Initiative for Asthma (GINA) guidelines
 Role of Azithromycin
Treatment of Th2-high or eosinophilic type of asthma.
• Th2-high or eosinophilic asthma is characterized by

• Increased eosinophil counts in blood and sputum,

• Higher plasma ige levels,

• Positive skin prick-test,

• Activation of basophils, th2 cells, natural killers, innate lymphoid cells (ILC2), as well
as elevated synthesis of cytokines IL-4, IL-5, and IL-13 (1, 7).

• Th2-high asthma responds well to cs, however, most available therapeutic strategies
are focused on this kind of infl ammation
Anti-IgE based therapy
• Anti-ige based therapy approximately 70% of patients have an allergic, eosinophilic
asthma phenotype, characterized by increased ige specifi c to aeroallergens.

• The fi rst drug approved as an anti-ige mono clonal antibody was omalizumab
(approved by the us food and drug administration (fda): xolair, 2003; approved by
european medicines agency.

• Omalizumab binds to c 3 domain of free ige heavy chain and thereby binds to
circulating ige and downregulates the high-affi nity ige receptors ( fcεri ) on basophils
and mastocytes, as well as circulating dendritic cells.

• Nowadays, according to actual gina, omalizumab is indicated for ige-mediated

moderate-to-severe asthma inadequately responding to conventional therapy.
Cytokines as a target
• Cytokines as a target targeting IL-5 or IL-5 receptor is used to infl uence this
key mediator for proliferation, activation, and recruitment of eosinophils

• Two monoclonal antibodies

• Mepolizumab and

• Reslizumab

• Have been approved as add-on therapy in refractory eosinophilic asthma.

• Other drugs ,

• benralizumab
Treatments of eosinophilic type of asthma
Macrolides

• Macrolide antibiotics appeared to be effective off-label

strategy in a very small and specific subset of asthmatics.

• Several studies have revealed improved quality of life and

reduced exacerbation.
therapies are recommended

• When asthma is not well-controlled

despite using CS, the following add-
on therapies are recommended:

• Leukotriene receptor modifi ers.

• Theophylline with sustained release

(SR).

• Long-acting muscarinic antagonists

(LAMA).

• Biologics.
 Global Initiative for Asthma
(GINA) guidelines
GI NA d es cr i b es a 5 - s t ep s al g o r i t h m o f as t h ma
man ag emen t .

S TEP1 S ABA

S TEP2 As - n eed ed l o w d o s e I CS - f o r mo t er o l

S TEP3 Dai l y l o w/ med i u m d o s e I CS & LABA

S TEP4 med i u m d o s e I CS - LABA

S TEP5 h i g h d o s e I CS - LABA

S TEP6 Hi g h d o s e I CS - LABA- OCS

Stepwise approach for adjusting asthma treatment.
• (ICS)-inhaled corticosteroids

• (LABA)-long - acting β2-adrenoceptor

agonists.
 LAMA
• Long-acting muscarinic
antagonists (LAMAs):

• Triple therapy combinations

containing ICS, LABA, and LAMA
were added to the
recommendations at step 5 for
adults over 18 years.

• The evidence shows that adding

LAMA to medium or high dose ICS-
LABA improves lung function and
reduces exacerbations.
ICS-LABA
• In patients with severe asthma,
the blood eosinophils should be
repeated for confi rmation if
found low.

• This update is based on the

evidence that nearly two-thirds
(65%) of patients on medium or
high dose ICS-LABA had a
change in their eosinophil levels
over one year ;
 Role of Azithromycin:
• Add-on a z i t h r o my c i n for patients aged
≥18 years with severe asthma.

• B e n e fi t s i n r e d u c i n g s t e r o i d u s e i n t h e
eosinophilic and reduced antibiotic use in
the non-eosinophilic p h e n o ty p e s . Since
t h e m o s t s i g n i fi c a n t e v i d e n c e i n a s t h m a
i s w i t h a z i t h r o my c i n , t h e t e r m m a c r o l i d e
is substituted.

• The d u ra t i o n of t h e ra py should be at
least six months and prescribed after
specialist opinion, e l e c t r o c a r d i o g ra m ,
sputum for a ty p i c a l my c o b a c t e r i a , and
adequate c o n s i d e ra t i o n for emergent
drug resistance
ASTHMA EXACERBATION

MEANING

• Asthma exacerbations are

progressive increases in
• MILD-PEF or FEV1>70%
asthma symptoms, including
coughing, shortness of breath, or • Moderate- PEF or FEV1 40%-60%

wheezing. These increases are

• Severe – PEF orFEV1 < 40%
significant enough that the
individual needs to change their • Life threatening or impending

treatment methods or current asthma respiratory arrest – PEF or

action plan. FEV1<25%.
NURSING MANAGEMENT.

• Patient Teaching Pursed-Lip Breathing (PLB)

AMBULATORY CARE
NURSING DIAGNOSIS
• Impaired airway clearance related to thick mucus discharge secondary to bronchitis as
evidence by presence of rhonchi, cough and tachypnoea.

• Ineffective breathing pattern related to increased physical exertion secondary to

bronchitis as evidence by increased respiratory rate.

• Impaired gas exchange related to altered breathing pattern secondary to bronchitis as

evidenced by tachypnoea.

• Insomnia related to persistent cough secondary to acute bronchitis as evidenced by

altered mood.
 Nursing intervention

• Monitoring heart rate and rhythm, respiratory rate and WOB, and BP;

• Monitoring pulse oximetry, PEFR, and ABGS; and auscultating lung sounds

• Teach the patient to identify and avoid known personal triggers for asthma (e .G.,
Cigarette smoke, pet dander) and irritants (e .G., Cold air, aspirin, foods, cats,
indoor air pollution)

• Avoiding furred animals is suggested, but pet allergens are impossible to avoid.

• Aspirin and nsaids should be avoided if they are known to trigger an attack .

• Encourage the patient to maintain a fluid intake of 2 to 3 l/day, adequate nutrition,

and plenty of rest.