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Bronchial

Asthma
DEFINITION

Reversible obstruction of
large & small airways due
to hyper-responsiveness to
various immunologic &
non immunologic stimuli.
Epidemiology

Common chronic lung disease.


Before puberty twice boys as
girls,
at puberty sex incidence is equal.
TRIGGERS
Resp; infections (viral, mycoplasma).

Irritants(air pollution, cold air, cigarette smoke),

Exercise.

Inhaled (dust mite).

Ingested allergens.

Changes in weather.

Emotional stress.

Medications (aspirin).

Gastro-esophageal reflux,

Sinusitis.
RISK FACTORS
RISK FACTORS
Extrinsic (allergic) asthma

Extrinsic (allergic)
asthma
INTRINSIC
ASTHMA

Clinically
similar, no Skin test –ve & Seen in 1st 2 yrs
evidence of lgE lgE low of life.
involvement.
PATHOPHYSIOLOGY

Bronchospam (bronchoconstriction or smooth muscle contraction).

Mucus production.

Edema & inflammation of airway mucosa.

Infiltration of inflammatory cells (eosoinophils, neutrophils, basophils,


macrophages).

Desquamation of epithelial & inflammatory cells.

Obstruction during expiration as airway approaches closing volume & distal airway gas trapping.
More sever asthma diminished airflow during inspiration.

↑ed intrathoracic pressure due to hyperinflation interfere with venous return & ↓ cardiac output
manifested as pulsus paradoxus.

Mismatching of ventilation with perfusion causes hypoxia which interferes with conversion of lactic
acid to CO₂ & H₂O causing metabolic acidosis. Hypercapnia ↑ carbonic acid which dissociates in to
H₂ ions & HCo₃ causing resp; acidosis.
PATHOPHSIOLOGY
Allergic inflammatory response occur in airway mucosa resulting in
bronchial hyper-reactivity.

Early immune response

• results in bronchoconstriction.
• Treatable with β2 receptor agonists &
• prevented by mast cell-stabilizing agents e.g; cromolyn.

Late phase reactions,


• 6-8 hrs later, continued airway hyper-responsiveness with eosinophilic &
neutrophilic infiltration,
• treated & prevented with steroids,
• prevented by mast cell stabilizing agents.
CLINICAL
FEATURS

Wheezing

With severe Cough, shortness of


obstruction, wheeze breath(dyspnea or
or rhonchi not heard chest congestion)
because of poor air tachypnoea &
movement. exercise intolerance.

If symptoms absent Persistent cough,


or mild, chest night cough,
auscultation during exercise- induced
forced expiration → cough, post tussive
prolonged expiratoy emesis, cough fol;
phase & wheezing. cold air exposure .
Airway patency ↓es
at night, many have
acute asthma at this
time.
CLINICAL
FEATURS

Flaring of nostrils, IC & suprasternal


retractions, use of accessory muscles of
respiration, hyper-inflated & hyper-resonant
chest →signs of severe obstruction.
Central cyanosis due to
. severe hypoxia.

Between attacks may be N. With


chronic asthma ↓ average for height
& weight . Chest barrel shaped with Tachycardia & pulsus
↑ AP diameter. Sternum prominent paradoxus
& Harrison’s sulci

Agitation, lethargy, inability to speak,


tripod sitting position or diaphoresis,
→ early signs of resp; failure.
DIAGNOSIS
Clinical

↑ TLC in
CBC acute severe eosinophilia ↑ lgE blood.
asthma

Sputm
eosinophilia

↑AP diameter of chest


Hyper-inflated & • (↑ed retro-sternal space on lateral
Chest X-ray
hyper lucent lungs. X-ray)

Flattening of
diaphragm.

More
horizontal ribs

Heart appears
narrow &
elongated.
• Reactive Airways Disease.
– (Top) Peribronchial thickening (white circles) seen en face shows small donut-like
rings in periphery of lungs, not normally seen.
• Contained in yellow circle are thickened bronchial walls seen in profile with a "tram-track
appearance.
– (Bottom) Close-up of left lower lung in same patient shows more donut shaped
thickened bronchial walls. (yellow arrows)
DIAGNOSIS

ABG’s: Hypoxemia from airway obstruction

In chronic asthma, skin test & radio-allergo


RAST test:
sorbent testing (RAST)

Pulmonary
PEFR VC FEV₁ RV FRC TLC
function
↓ ↓ ↓ ↑ ↑ ↑ed
tests:

Diurnal variation in PEFR i.e between morning & evening of > 15-
20% used as defining features of asthma.
Differential diagnosis

Croup,
Acute bronchiolitis,
Penumonia,
Pertussis.
Foreign body in airway.
Endobronchial TB or
Lymph node pressing bronchi.
Cystic fibrosis.
COMPLICATIONS
Pneumothorax,
pneumomediastinum

Delayed maturation &


slowing of pubertal
growth velocity.
MANAGEMENT

O₂ therapy: Nebulized salbutamol Adrenaline Side effects


• 2-3 L/min by mask or nasal • 1st line therapy • Is not used routinely • termors,
• 0.5 mg/kg/dose fol; by 0.1-0.5
prongs. • 0.01ml/kg(1.1000 sol;) • pallor,
mg/kg/dose at intervals of 20-30
min until adequate response subcutaneously. • anxiety,
• 5mg/ml, diluted with 1.5 ml N/S • Once or twice at intervals of • Palpitations
• Nebulization with O₂ at 6 L/min 20 min • Arrhythmias
prevent salbutamol-induced • infants & small children ,0.05
hypoxemia. ml
• ↓ dose for HR>180/min. • still in distress after 3 doses,
• Adverse effects do not give further doses.
• tachycardia,arrhythmias, • Not to be given if HR >
• CNS stimulation, hyperactivity & 180/min in infants ,
irritability. >160/min in older children.
• hypokalemia
• Irritability
Terbutaline Aminophylline Hydrocortisone Adequate Antibiotics: Ventilatory
• Selective β₂ Considered • To prevent late hydration • If bacterial infection support
agonists. • Receving phase reaction. suspected
• Dehydration
• alternate to maintenance • IV 5-10 mg/kg every
inadequate fluid
adrenaline. treatment with 4-6 hrs fol; by oral
intake ,↑ed
• 0.01 ml/kg/dose theophyline. (prednisolone 1
insensible water
(1:100 sol;) • Unable to tolerate mg/kg/d for 5 d) or
loss as a result of
• Duration of action: maximal treatment inhaled
tachypnea &
4 hrs. with inhaled β₂ (beclomethasone
diuretic effect of
agonist 500 μg or 2 puffs
theophylline.
• 5mg/kg in IV slow twice daily.
• 20ml/kg N.saline
diluted for 5-15 min over 1-2 hrs &
• Repeated at 6-8 hrs continue 1⅟₂ times
intervals total daily the maintenance
dose 20mg/kg rate for next 1-2 d.
• Rapid infusion • Circulatory
cardiac arrhythmias, overloaded &
• Hypotension & pulmonary edema
death. avoided β₂-agonists
produce
hypokalemia,
potassium added to
IV fluids after pt
voids.
SUBSEQUENT MANAGEMENT

Following a severe
episode of ac asthma,
small airway obstruction oral or inhaled salbutam
ol,
persist for ≥ 2 mons. steroid, theophyline
ns.
continued for wks or mo
MANAGEMENT OF
STATUS ASTHMATICUS

Continuous resp; distress


despite sympathomimetic drugs
with or without theophylline.

Defined as ↑ severe asthma


Mechanical ventilation resp;
not responsive to drugs that
failure inspite of measures.
are usually effective.

Others:
• salbutamol, nebulization,
• salbutamal+ ipratropium Admitt in ITC ,
nebulization, CBC, S.electrolytes, ABG’s &
• aminophyline infusion, cardiac status monitored.
• adequate hydration , or
• steroids .

To prevent hypoxia, O₂
If previously on steroid therapy,
(2-3L/min) to maintain 70-90
steriod given initially.
mmHg or O₂ saturation > 92% .
reactivityes& need c
for rescuealler o
bronchogen dialator
r
therapy. –
• Long term inclu
t
oral
use reserved
ded for i
bron
chronic asthma c
chos
only if other o
therapiespasfail; s
preferablem acwith t
an alternate
bronday e
• Improvement pt
schedule. chos
Side rcrom
skill in use of spacer
effects pas
with
devicesm. (MDIs). oolyn
• Use of peak
Usef flow i :
monitoring.
ul as d
• Use of self
prop s
management
hylac &
envirnomental
tic Pt
measure.
controlagen educ
• Assessment
ts & ation
monitoring
withof
asthmamildseverity.
• Avoidanceto of
controlmodof asthma
triggers.erate
• asth
Establishment
ma
comprehensive
LONG TERM MANAGEMENT OF CHRONIC ASTHMA.
plans ofno
kno
pharmacologic
therapy.wn
LONG TERM MANAGEMENT OF
CHRONIC ASTHMA.
β₂ adrenergic agonists:

Ac & chronic asthma

alone do not give LT control because not affect airway inflammation .

Relax airway smooth muscle enhance mucociliary clearance.

↓mediator release from mast cells & basophils.


Anti-cholinergic
Leukotriene antagonists:
agents,e.g;Ipratropium

LONG TERM MANAGEMENT OF CHRONIC


potent bronchodilator, Anti inflammatory agents
block reflex not bronchodilators.
bronchoconstriction
caused by inhaled
irritants.
Montelukast

ASTHMA.
less effective as
bronchodilators than β₂
agonists.
2-5yrs= 4mg/d

6-14 yrs =5 mg/d

>15yrs =10mg/d
Death always a
Aggressive therapy
result of under
is instituted early.
treatment.

Ultimate remission
5% severe disease .
50% free of
Recurrence may
symptoms within
occur in adulthood.
10-20yrs.
i
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PREVENTION
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Clinical features before Symptoms Night time symptoms Lung function
treatment
Step 4 Continual symptoms Frequent FEV₁ or PEFR < 60%
Severe persistent Limited physical activity predicated
PEFR variability > 30%
Step 3 Daily symptoms . >1 time a week FEV₁ or PEFR >60%-80%
Moderate persistent Daily use of inhaled predicated.
Short-acting β₂-agonist. PEFR variability > 30%
Exacerbations affect
activity.
Exacerbations > 2 times a
Week: may last days.

Step 2 Symptoms > 2 times a > 2 times a mon FEV₁ or PEFR >80%
Mild persistent week predicated.
But < 1 time a day PEFR variability 20-30%
Exacerbations may affect
activity.
Step 1 mild intermittent. Symptoms < 2 times a < 2times a mon FEV₁ or PEFR > 80%
week. predicated.
Asymptomatic & N. PEFR variability < 20%.
PEFR between
exacerbations brief (from
a few hrs to a few days)
Intensity may vary.
The presence of 1 of features of severity is sufficient to place a pt in that category.An individual should be assigned
to most severe grade in which any feature occur.characteristics noted in this figure are general & may overlap
because asthma is highly variable .furthermore, an individual classification may change over time
Stepwise approach for managing asthma in children 0 to 4 years of age. National
Institutes of Health. National Heart, Lung, and Blood Institute. National Asthma
Education and Prevention Program. Expert Panel Report 3: Guidelines for the diagnosis
and management of asthma. August 2007. NIH publication no. 07-4051. Available at:
http://www.nhlbi.nih.gov/guidelines/asthma/index.htm. 3 Accessed December 30,
2007. PRN, As necessary.
Use of nebulizer and face Use of spacer device and face
mask to give mask to give
bronchodilator treatment bronchodilator treatment
SEQ-1
SEQ-1
SEQ-2

3y old girl in emergency, has C/O cough & What is


breathlessness for last 6 hrs. she had 2 similar your
How will
complaints & was admitted in hospital over last 3- differential
you treat
mons. O/E; she is in obvious respiratory distress & has diagnosis in
her?
audible wheeze. Auscultation of chest reveals bilateral order of
rhonchi. priority?
SEQ-3

5 year old boy presented in ER with respiratory difficulty for 12 hours. He


was having low grade fever & mild cough for the last 3 days. There is H/O
recurrent similar episode since infancy. O/E; RR= 55/min with subcostal &
intercostal recessions. There are bilateral rhonchi & few crepitations.

Give steps of
What is the
emergency
diagnosis?
treatment?
SEQ-4
A/2014/UHS

A 9 years old boy presents


with cough,dyspnea,
restlessness & sweating. His
PR = 105/min,RR =45/min ,
chest is hyperinflated with ↓ What is the
movements & hyperresonent
percussion note. On diagnosis?
auscultation: air entry is
bilaterally ↓ed & there are
widespread expiratory
ronchi.

Write down 2
Give 2 common
important
complications of
investigations in
this condition?
this case?

Write down outline of management of this child?


SEQ-5
 A 10-year-old boy in respiratory distress arrives late in the evening to
ED; he has a 2-hour history of rapid breathing and a complaint that his
chest hurts. His mother gave him two nebulizer treatments without
improvement. She tells you that this is the fourth time in 3 months that
he has required ED visits for similar symptoms. O/E; an afebrile male
with RR = 60/min, HR = 120/min & BP = N. You note that his pulse varies
in amplitude with respiration but his capillary refill is somewhat
sluggish at 4 to 6 seconds. He is pale, appears drowsy, has mild perioral
cyanosis, and is using accessory chest muscles to breathe. You hear only
faint wheezing on chest auscultation.

A. What are the initial steps in evaluating this patient?


B. What is the most likely diagnosis?
C. What is the next step in evaluation?
KEY-5
• Initial steps:
– Treating this patient's respiratory distress is of immediate concern. The airway
is evaluated first, followed by an evaluation of breathing, and finally
assessment of the circulatory status (the "ABCs").
– Initial management includes administration of oxygen, an inhaled (β-agonist,
and a systemic dose of prednisone.
– Intravenous administration of fluids and medications is indicated for a patient
with this degree of distress.
– A stat blood gas determination and monitoring oxygen saturation levels will
aid further management.
• Most likely diagnosis:
– Asthma exacerbation.
• Next step in evaluation:
– After initial stabilization, past medical and family histories (medications,
triggers, frequency and severity of previous episodes, previous hospitalization
or intensive care unit admissions) and a review of systems are obtained.
– The physical examination, blood gas report, and response to initial treatments
will determine subsequent management.
SEQ-5
An 8 years old child presents with cough &
breathing difficulty.O/E; a thin afebrile child
with RR=60/min with intercostal & subcostal
retraction & bilateral reduced air entry with
few rhonchi.H/O 2 previous hospitalization
in last year with oral medication sparingly.
• What is the diagnosis?
• How would you manage?
MCQ-1
 A 12-year-old asthmatic girl presents to the ED with tachypnea,
intracostal retractions, perioral cyanosis, and minimal wheezing. You
administer oxygen, inhaled salbutamol, and intravenous prednisone.
Upon reassessment, wheezing increases in all fields, and the child's color
has improved. Which of the following is the appropriate explanation for
these findings?

A. The girl is not having an asthma attack.


B. The girl is not responding to the salbutamol, and her symptoms are
worsening.
C. The girl is responding to the salbutamol, and her symptoms are
improving.
D. The girl did not receive enough salbutamol.
E. The salbutamol was inadvertently left out of the inhalation treatment,
and the girl received only saline.
KEY-1

C.
 This child presented in severe respiratory distress. Her improved color
indicates reversible symptoms, confirming the diagnosis of asthma.
 Increased wheezing is auscultated after salbutamol treatment because
lung areas previously obstructed are now opening, allowing additional
airflow.
 Less-experienced examiners may misinterpret lack of air movement as
"clear" breath sounds, further delaying appropriate medical management.
MCQ-2
 A 15-year-old adolescent male uses his salbutamol inhaler shortly after
he mows the lawn because of a mild feeling of chest "tightness." He
later returns home early from dinner at a friend's house when he has the
sudden onset of wheezing, cough, and chest pain. Which of the
following is the most likely explanation for these circumstances?

A. He likely aspirated a piece of grass.


B. His salbutamol inhaler must be empty.
C. His salbutamol inhaler must be outdated.
D. He is having a late-phase reaction.
E. He has been exposed to a new allergen that is more irritating than grass.
KEY-2

D.
 A late-phase reaction typically occurs 2 to 4
hours after an initial wheezing episode. It is
caused by accumulation of inflammatory cells
in the airway.
MCQ-3
 A 5-year-old boy with a history of recurrent chest infections
has been admitted to hospital with increasing shortness of
breath, night-time cough and wheeze. Select the most likely
diagnosis.

A. Upper respiratory tract infection


B. Asthma
C. Inhaled foreign body
D. Bronchiolitis
E. Pertussis
KEY-3
B. Asthma

 Asthma is a condition of chronic airway inflammation, airway


hyperactivity and reversible airway obstruction.
 It affects 10-15% of the school-age population, and is the
cause of 10-20% of all acute hospital admissions.
 It can present subtly with a night-time cough, or with a full-
blown exacerbation.
 In the early stages it can often be misdiagnosed as recurrent
chest infections.
 There is usually a family history of atopic illnesses.
MCQ-4
 All of the following are triggers for asthma in a susceptible
child except:

A. Dust mite
B. Air pollution
C. Cigarette smoke
D. Gastro-oesophageal reflux
E. Exercise.
KEY-4

D
 Gastro-oesophageal reflux does not lead to
bronchospasm, although in babies it may
cause crying, posseting and rarely apnoea.
 The others in the list are all common triggers
for asthma in a susceptible child.
MCQ-5
 Which of the following is the accepted definition of
asthma?

A. Cough or wheeze in a child who has tested positive for


allergens on skin prick testing
B. Cough or wheeze in a child with a strong family history of
asthma
C. Recurrent cough or wheeze that responds to bronchodilator
therapy
D. Persistent cough or wheeze in a child exposed to passive
smoking in the home
E. All of the above.
KEY-5

C
 A family history of asthma is common in children with asthma
but
 the correct definition is recurrent cough or wheeze that
responds to bronchodilator therapy, (confirming that the
bronchospasm is reversible).
 Skin prick testing may be helpful in the identification of
allergens but is not a diagnostic feature.
 Passive smoking is a trigger for asthma but is also not a
defining feature.
MCQ-6
 It is important to use an appropriate device for
administering asthma treatment. An MDI (metered dose
inhaler) with a spacer device is appropriate for what age
child?

A. An infant
B. A preschool child
C. A school age child with severe asthma
D. All of the above.
E. None of the above.
KEY-6
D
 MDIs with a spacer device have been shown to be as
effective as nebulizers for administering
bronchodilators and inhaled steroids.
 A mask, rather than a mouth-piece, is attached to the
spacer device for babies.
 The use of a spacer device with an MDI can be
effective in older children who have difficulty
coordinating their breathing during a severe attack.
MCQ-7
 Which one of the following signs is not likely to
occur when asthma is life threatening?

A. Confusion
B. Hyperactivity
C. A silent chest
D. Hypotension
E. Being too breathless to talk.
KEY-7

B
 Confusion and drowsiness can occur as a result of hypoxia,
but hyperactivity is unlikely.
 Hypotension and severe breathlessness are common in very
severe asthma.
 The chest may appear to be silent as air entry is so poor, and
this may mislead an inexperienced doctor to believe that
there is no bronchospasm present.
MCQ-8
 A child with poor control of their asthma is likely to have any
of the following symptoms or signs except:

A. Clubbing
B. Poor growth
C. Chronic chest deformity
D. Frequent acute exacerbations
E. Persistent cough at night.
KEY-8

A
• Clubbing is not a sign of asthma and if present
suggests cystic fibrosis, bronchiectasis or
congenital heart disease.
MCQ-9
 A school girl is a known asthmatic for last five
years. She has been taking steroids and β₂
stimulant regularly. Which of the following is
indicator of her disease severity?

A. Platelet count
B. IgE level
C. IgM level
D. Absolute neutrophil count
E. CT scan chest.
KEY-9

•B
OSPE-1
Case Study: A wheezy child
An 18-month-old child presents with his
first episode of wheeze. He is pyrexial and
has shortness of breath with some
subcostal recession. Wheeze is heard all
over his chest.

(a) Which of the following diagnoses are


most likely?

• Asthma;
• Inhaled foreign body;
• Bronchiolitis
• Croup
 Asthma and bronchiolitis are both possible.
 A child of this age is at risk of inhaling a foreign body as they
are inquisitive & put small objects in their mouth. A foreign
body will either cause airway obstruction leading to choking,
stridor and cyanosis, or if inhaled into one main bronchus may
cause unilateral wheeze. Fever is less likely.
 Croup causes a characteristic cough & stridor but no wheeze.
 Whooping cough presents with coughing & sometimes
vomiting but not wheeze.
 Bronchiolitis due to RSV infection is very common in the first
2 years of life. There may be a fever.
 Asthma does not cause fever, but may be triggered by a viral
upper respiratory tract infection.

(b) If you were considering asthma as a likely


diagnosis, what family history may be relevant?
You should establish

• if there is a family history of atopy—asthma, hay fever or eczema in siblings or


parents suggest this.
• Does anybody smoke in the house?
• Are there any pets in the home?

(c) If you were considering bronchiolitis as a likely


diagnosis, what diagnostic test would you perform?
A nasopharyngeal aspirate or swab for The child is admitted to the ward.
RSV immunofluorescence, which can
identify the presence of RSV or other
respiratory viruses.

Over the next few hours the shortness


of breath settles with treatment.

A chest radiograph may be helpful if


there is diagnostic uncertainty or if the
child is very ill. The wheeze remains intermittently
present; worse prior to each treatment.

(d) What treatment is likely


to have been given?
 The response to treatment followed by recurrence suggests
reactive airways disease (asthma) which is responding to
bronchodilators such as short-acting beta-agonists (e.g.
salbutamol). These may be administered by inhaler (using a
spacer device) or by nebulizer.
 The next day the child is better and is discharged home.
 He is reviewed in the outpatient department 6 weeks later,
during which time he has had two further episodes of
shortness of breath. He coughs most nights.
 You decide to prescribe treatment.

(e) What would you prescribe and what would you tell
his parents about administering it?
• The child probably needs an inhaled beta-agonist such as salbutamol. It is
important that this is given via a spacer device as this child is too young to
use a metered dose inhaler directly. As he is coughing most nights the
bronchodilator should be given regularly at bedtime.
• On further review 3 months later he is well, but still coughing at night
several nights a week. He has been unable to attend nursery on a few
occasions.
• (f) What further treatment would you consider?
• He responds to the short-acting
bronchodilators but is having regular
symptoms despite these. Low-dose inhaled
corticosteroids should be given regularly for a
trial period to reduce airway inflammation and
gain symptom control.
Normal respiratory rate
Age Breaths/min
Preterm 40-60

Term 30-40

5 yrs 25

10 yrs 20

15 yrs 16

adult 12
Breathing pattern
Pattern Features
Obstructive
Mild ↓ rate
↑ TV
Slightly prolonged exp phase
moderate ↑ rate
↑ use of accessory muscles
Prolonged expiratory phase
Restrictive Rapid rate
↓tidal volume(TV)
Pattern features
Kussmaul respiration ↑ rate
↑tidal volume(TV)
Regular deep resp
Metabolic acidosis OR
DKA
Cheyne-stokes respiration Cyclic pattern of waxing & waning of breathing
interposed by central apneas/hypopneas
CNS injury
Depressant drugs
Heart failure
Uremia
Biot respiration Ataxic OR periodic breathing with a resp effort
fol by apnea
Brain stem injury
Posterior fossa mass
Gasping Slow rate
Variable TV
 Hypoxia
 Shock
 Sepsis
 Asphyxia
Tidal volume (TV)

• Amount of air expired with each relaxed breath.

Functional residual capacity (FRC)


• Volume of gas retained in the lung at the end of a relaxed exhalation.
• This gas volume maintains exchange of O₂ during exhalation.

Total lung capacity (TLC).

• Volume of gas in the lungs at the end of maximal inhalation

Residual volume (RV)

• Volume of gas left in the lungs at the end of a maximal exahalation.

Vital capacity (VC)


• Maximal amount of air that can be expelled from the lungs
• TLC-RV.

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