An old presentation that I made when I was an Intern in Pediatric department.
The presentation contains 71 slides. It discusses bronchial asthma in pediatric age group starting from the definition of bronchial asthma and its pathophysiology and ending by the management of acute attacks of asthma and long-term management of bronchial asthma patients.
1. Bronchial Asthma In Pediatric
Abdullah Mutwakil Gamal - Pediatric Department
Sebha Medical Center
16 – 12 - 2013
2. Definition
Chronic airway inflammation leading to increase
airway responsiveness that leads to recurrent
episodes of wheezing, breathlessness, chest
tightness and coughing particularly at night or early
morning.
3. Epidemiology
- Worldwide about 235 million person have asthma
- Approximately 250,000 people die per year from
the disease
- Boys : Girls = 2:1
- Adult Women : Adult men = 2:1
5. Genetics :
The inheritance pattern of asthma demonstrates
that it is a complex genetic disorder with
environmental influences as with hypertension,
atherosclerosis, arthritis, and diabetes mellitus.
One of the greatest challenges faced by
investigators in this area is the marked
heterogeneity of the asthmatic phenotype.
Although wheezing, coughing, and shortness of
breath are common clinical endpoints for the
6. asthmatic disease process, any individual with
asthma will respond differently to triggering
factors (eg, allergens, viruses, cold air, tobacco
smoke, exercise). The variability in the patterns
and severity of the disease, its close clinical
association with various atopic diseases, and the
manner in which the symptoms change in
relationship to age or in response to therapeutic
intervention have made finding a single genetic
“markerâ€elusive. Because asthma is
frequently associated with atopy and is
characterized by marked increases in airway
responsiveness and inflammation, it should come
as no surprise that various gene candidates
7. related to smooth muscle contractile mechanisms
and to the immune system have been sought.
Thus, linkage to 11q13 (the high-affinity IgE
receptor), 5q (the cytokine gene cluster), 12q
(IFN- خ³),14 q (T-cell antigen receptor), as well as
others have been considered as possible
candidate loci. Polymorphisms in genes such as
the خ± subunit of the IL-4 receptor, the خ²2-
adrenergic receptor, and the major cell surface
receptor for endotoxin (CD14) may further
influence disease expression and the response to
therapy
8. ENVIRONMENTAL ALLERGENS AND IRRITANTS :
Respiratory allergies are a major factor in the
pathogenesis of asthma in children. Furthermore,
limiting exposure to relevant indoor allergens
may lead to reductions in asthma symptoms,
bronchial hyperresponsiveness, and use of
asthma medications. Relevant indoor allergens
include dust mite, cockroach, and cat and dog
dander. One seemingly easily avoided irritant is
environmental tobacco smoke. However, despite
increased public awareness of the detrimental
effect of smoking, it is often difficult to avoid
second-hand smoke.
10. BRONCHIAL SMOOTH MUSCLE SPASM :
Bronchial smooth muscle spasm contributes
significantly to airway obstruction. Evidence
suggests that either the quantity or the function
of bronchial smooth muscle in asthma is
abnormal. Autopsy specimens obtained from
asthmatic patients dying of their disease have
demonstrated hypertrophy of the smooth muscle
lining the airways. Some investigators have
demonstrated a greater maximal
11. response to contractile agonists and an impaired
relaxation to خ²- agonists and theophylline in vitro.
The airway contains a number of resident cells
(mast cells, alveolar macrophages, airway
epithelium, and endothelium) as well as
immigrating inflammatory cells (eosinophils,
lymphocytes, neutrophils, basophils, and
platelets) that are capable of generating a wide
variety of mediators and signaling molecules that
can induce bronchospasm. These include
histamine, platelet-activating factor, and
12. a number of derivatives of arachidonic acid including
prostaglandin D2 and the cysteinyl leukotrienes
(LTC4, LTD4, LTE4). Thus, it is likely that infiltration
of inflammatory cells into the airway walls
contributes to bronchial smooth muscle tone
through the local effects of these various
mediators.
13. EDEMA OF AIRWAY MUCOSA :
Edema of the airway mucosa results from increased
capillary permeability with leakage of serum
proteins into interstitial areas. A number of cell-
derived mediators are capable of inducing edema
formation, including histamine, prostaglandin E,
LTC4, LTD4, LTE4, platelet-activating factor, and
bradykinin. Resulting edema and cellular
inflammation cause increased airway wall
thickness in patients, which contributes to the
mechanics of airway narrowing.
14. MUCOUS IMPACTION OF BRONCHI :
Mucous impaction of bronchi is another
characteristic pathologic feature seen in
untreated or undertreated asthma. Mucus
production results from hyperplasia and
metaplasia of goblet cells lining the airway.
Impacted mucus leads to hyperinflation, focal
atelectasis, and a productive cough.
15. Airway inflammation in asthma is a result of mast
cell activation. An immediate immunoglobulin (Ig)
E response to environmental triggers occurs
within 15 to 30 minutes and includes
vasodilation, increased vascular permeability,
smooth-muscle constriction, and mucus
secretion. Common triggers include dust mites,
animal dander, cigarette smoke, pollution,
weather changes, upper respiratory infections,
certain drugs (ie, β-adrenergic antagonists, and
some nonsteroidal anti-inflammatory agents),
16. and exercise (particularly when performed in a cold
environment). Two to four hours after this acute
response, a late-phase reaction (LPR) begins. The
LPR is characterized by infiltration of
inflammatory cells into the airway parenchyma; it
is responsible for the chronic inflammation seen
in asthma. Airway hyperresponsiveness may
persist for weeks after the LPR.
17. History
• Determine whether there is a reversible airway obstruction by
history. Are the wheezing and breathlessness reversible?
• Tightness in the chest.
• Recurrent cough.
• Exacerbation of the cough or wheeze at night or after
exercise.
• Improvement of the cough or wheeze with bronchodilator
therapy.
• History of atopy (eczema, hay fever).
• History of rhinitis, nasal polyps.
19. Managment
• Management of Acute Attack
– Assessing & Classifying.
– Managing According to severity
• Management of Chronic Asthma
– Assessing & Classifying.
– Managing According to Severity
20. Management of Acute Attack
• Classifying the patient :
– Group A : 1st attack of wheeze with no
respiratory distress
– Group B :
• 1t attack of wheeze with respiratory distress
• Or recurrent wheeze
- Group C : Severe life-threatening asthma
- Drowzy of unconcious child, cyanosis,
decreases oxygen saturation, child unable to
speak or drink
21. Group A : 1st attack of wheeze with no
respiratory distress
Can usually be managed at home with supportive
care. A bronchodilator is not necessary.
22. Group B : 1t attack of wheeze with
respiratory distress Or recurrent
wheeze
• give salbutamol by metered-dose inhaler and
spacer device or, if not available, by nebulizer
(see below for details). If salbutamol is not
available, give subcutaneous adrenaline.
• Reassess the child after 15 min to determine
subsequent treatment:
– If respiratory distress has resolved, and the
child does not have fast breathing, advise the
mother on home care with inhaled salbutamol
from a metered dose inhaler and spacer
23. – device (which can be made locally from plastic
bottles).
– If respiratory distress persists, admit to
hospital and treat with oxygen, rapid-acting
bronchodilators and other drugs.
24. Group C : Severe life-threatening
asthma
• If the child has life-threatening acute asthma, is in
severe respiratory distress with central cyanosis
or reduced oxygen saturation ≤ 90%, has poor air
entry (silent chest), is unable to drink or speak or
is exhausted and confused, admit to hospital and
treat with oxygen, rapid-acting bronchodilators
and other drugs.
• In children admitted to hospital, promptly give
oxygen, a rapid-acting bronchodilator and a first
dose of steroids.
25. Oxygen :
Give oxygen to keep oxygen saturation > 95% in all
children with asthma who are cyanosed (oxygen
saturation ≤ 90%) or whose difficulty in breathing
interferes with talking, eating or breastfeeding.
26. Rapid-acting bronchodilators :
Give the child a rapid-acting bronchodilator, such as
nebulized salbutamol or salbutamol by metered-
dose inhaler with a spacer device. If salbutamol is
not available, give subcutaneous adrenaline, as
described below.
Nebulized salbutamol
The driving source for the nebulizer must deliver at
least 6–9 litres/min. Recommended methods are
an air compressor, ultrasonic nebulizer or oxygen
27. In severe or life-threatening asthma, when a child
cannot speak, is hypoxic or tiring with lowered
consciousness, give continuous back-to-back
nebulizers until the child improves, while setting
up an IV cannula. As asthma improves, a nebulizer
can be given every 4 h and then every 6–8 h.
28. cylinder, but in severe or life-threatening asthma
oxygen must be used. If these are not available,
use an inhaler and spacer. An easy-to-operate
foot pump may be used but is less effective.
29. Put the dose of the bronchodilator solution in the
nebulizer compartment, add 2–4 ml of sterile
saline and nebulize the child until the liquid is
almost all used up. The dose of salbutamol is 2.5
mg (i.e. 0.5 ml of the 5 mg/ml nebulizer solution).
If the response to treatment is poor, give
salbutamol more frequently.
30. Giving salbutamol by metered-dose inhaler with a
spacer device :
Spacer devices with a volume of 750 ml are
commercially available.
Introduce two puffs (200 μg) into the spacer
chamber. Then, place the child’s mouth over the
opening in the spacer and allow normal breathing
for three to five breaths. This can be repeated in
rapid succession until six puffs of the drug have
31. been given to a child < 5 years, 12 puffs for > 5 years
of age. After 6 or 12 puffs, depending on age,
assess the response and repeat regularly until the
child’s condition improves. In severe cases, 6 or
12 puffs can be given several times an hour for a
short period.
Some infants and young children cooperate better
when a face mask is attached to the spacer
instead of the mouthpiece.
32. If commercial devices are not available, a spacer
device can be made from a plastic cup or a 1- litre
plastic bottle. These deliver three to four puffs of
salbutamol, and the child should breathe from
the device for up to 30s.
• Subcutaneous adrenaline
33. • If the above two methods of delivering
salbutamol are not available, give a subcutaneous
injection of adrenaline at 0.01 ml/kg of 1:1000
solution (up to a maximum of 0.3 ml), measured
accurately with a 1-ml syringe. If there is no
improvement after 15 min, repeat the dose once.
34. Steroids :
• If a child has a severe or life-threatening acute
attack of wheezing (asthma), give oral
prednisolone, 1 mg/kg, for 3–5 days (maximum,
60 mg) or 20 mg for children aged 2–5 years. If
the child remains very sick, continue the
treatment until improvement is seen.
• Repeat the dose of prednisolone for children who
vomit, and consider IV steroids if the child is
unable to retain orally ingested medication.
Treatment for up to 3 days is usually sufficient,
but the duration should be tailored to bring about
35. recovery. Tapering of short courses (7–14 days) of
steroids is not necessary. IV hydrocortisone (4
mg/kg repeated every 4 h) provides no benefit
and should be considered only for children who
are unable to retain oral medication
36. Magnesium sulfate :
• Intravenous magnesium sulfate may provide
additional benefi t in children with severe asthma
treated with bronchodilators and corticosteroids.
Magnesium sulfate has a better safety profi le in
the management of acute severe asthma than
aminophylline. As it is more widely available, it
can be used in children who are not responsive to
the medications described above.
• Give 50% magnesium sulfate as a bolus of 0.1
ml/kg (50 mg/kg) IV over 20 min.
37. Aminophylline :
• Aminophylline is not recommended in children
with mild-to-moderate acute asthma. It is
reserved for children who do not improve after
several doses of a rapid-acting bronchodilator
given at short intervals plus oral prednisolone. If
indicated in these circumstances:
38. • Admit the child ideally to a high-care or
intensive-care unit, if available, for continuous
monitoring.
• Weigh the child carefully and then give IV
aminophylline at an initial loading dose of 5–6
mg/kg (up to a maximum of 300 mg) over at least
20 min but preferably over 1 h, followed by a
maintenance dose of 5 mg/kg every 6 h.
39. • IV aminophylline can be dangerous at an
overdose or when given too rapidly.
• Omit the initial dose if the child has already
received any form of aminophylline or caffeine in
the previous 24 h.
• Stop giving it immediately if the child starts to
vomit, has a pulse rate > 180/ min, develops a
headache or has a convulsion.
40. Oral bronchodilators :
• Use of oral salbutamol (in syrup or tablets) is not
recommended in the treatment of severe or
persistent wheeze. It should be used only when
inhaled salbutamol is not available for a child who
has improved sufficiently to be discharged home.
• Dosage:
– Age 1 month to 2 years: 100 μg/kg (maximum,
2 mg) up to four times daily
– Age 2–6 years: 1–2 mg up to four times daily
41. Antibiotics :
• Antibiotics should not be given routinely for
asthma or to a child with asthma who has fast
breathing without fever. Antimicrobial treatment
is indicated, however, when there is persistent
fever and other signs of pneumonia
42. Supportive care :
• Ensure that the child receives daily maintenance
fluids appropriate for his or her age. Encourage
breastfeeding and oral fl uids. Encourage
adequate complementary feeding for the young
child, as soon as food can be taken.
43. Monitoring :
• A hospitalized child should be assessed by a nurse
every 3 h or every 6 h as the child shows
improvement (i.e. slower breathing rate, less
lower chest wall indrawing and less respiratory
distress) and by a doctor at least once a day.
Record the respiratory rate, and watch especially
for signs of respiratory failure – increasing
hypoxia and respiratory distress leading to
exhaustion.
44. Complications :
If the child fails to respond to the above therapy, or
the child’s condition worsens suddenly, obtain a
chest X-ray to look for evidence of
pneumothorax.
Be very careful in making this diagnosis as the
hyperinflation in asthma can mimic a
pneumothorax on a chest X-ray.
45. Follow-up care :
Asthma is a chronic and recurrent condition.
˃ Once the child has improved sufficiently to be
discharged home, inhaled salbutamol through a
metered dose inhaler should be prescribed with a
suitable (not necessarily commercial) spacer and
the mother instructed on how to use it.
46. ˃ A long-term treatment plan should be made on
the basis of the frequency and severity of
symptoms. This may include intermittent or
regular treatment with bronchodilators, regular
treatment with inhaled steroids or intermittent
courses of oral steroids. Up-to-date international
or specialized national guidelines should be
consulted for more information
47. Management of Chronic Asthma
Peristent Asthma
Episodic Asthma
FrequentInfrequent
3 episodes/wk, with
cough at
night/morning.
Episodes every
2–4 weeks
<4 episodes per
year
Characteristics
Regular treatment is
needed
- Use prophylactic
inhaled steroids.
- Long-acting B2-
bronchodilator may
be helpful.
- Oral steroids may
be needed.
- Oral leukotriene
inhibitors may help
reduce steroids
Regular
treatment is
needed
- Use B2-
bronchodilator
as required.
- Use regular,
low-dose
inhaled steroid.
No regular
treatment
needed.
- Treat acute
episodes with B2-
Agonists
- Use nebulized
bronchodilators
and short-course
prednisolone in
more severe
episodes
Management
Strategy
48. • Escalating therapy :
Having reviewed the history and categorized your
patient in terms of clinical pattern and severity,
use a logical, stepwise approach to escalating
therapy
Before altering a treatment, ensure that
treatment is being taken in an effective manner
49. The stepwise approach to drugs
Short-acting B2-bronchodilator for relief of symptomsStep 1 : occasional use of
relief bronchodilators
Short-acting B2-bronchodilator as required + low-dose
inhaled steroid (200–400micrograms/day)
Step 2 : regular inhaled
preventer therapy
• Short-acting B2-bronchodilator as required + high-dose
inhaled steroid or
• Low-dose inhaled steroid +/– long-acting bronchodilator
Step 3 : add-on therapy
• Short-acting B2-bronchodilator as required + high-dose
inhaled steroid (up to 800micrograms/day) + long-acting
bronchodilator or
• Theophyllines or ipratropium +/– alternate day steroid
Step 4 : persistent poor
control
• Use daily steroid tablet in lowest dose
• Maintain high-dose inhaled steroid at 800micrograms/day
• Refer to respiratory specialist
Step 5 : continuous or
frequent use of oral
steroid
50. Doses : 0–2yrs
In this age group, a spacer device with an
appropriate face mask is used, e.g. a small
volume Aerochamber® or Ablespacer® which can
take any inhaler; or a large volume Volumatic® or
Nebuhaler®, which only fi t certain inhalers.
Prophylactic therapy with inhaled steroids is more
effective than cromoglicate.
51.
52.
53. Doses : 0–2yrs - cont
• Salbutamol via Volumatic®: <2400micrograms/day (in 6
doses).
• Terbutaline via Nebuhaler®: <6000micrograms/day (in 6
doses).
• Ipratropium via Volumatic®: <480micrograms/day (in 4
doses).
Acute treatment
• Budesonide via Nebuhaler®: 100–400micrograms/day.
• Beclometasone via Volumatic®: 100–400micrograms/day.
Prophylactic treatment
54. Doses : 3–5yrs
• Salbutamol via Volumatic®: <3600micrograms/day (in 6
doses).
• Terbutaline via Nebuhaler®: <6000micrograms/day (in 6
doses).
Acute treatment
• Budesonide via Nebuhaler®: 100–800micrograms/day.
• Beclomethasone via Volumatic®: 100–800micrograms/day.
• Fluticasone via Volumatic®: (>4yrs) 100–
200micrograms/day..
• Salmeterol via Volumatic®: (>4yrs) 50micrograms/day.
Must never be given alone and only when the child is also
taking an inhaled steroid.
• Combination inhaler: Seretide® (contains fi xed doses of fl
uticasone and salmeterol).
Prophylactic treatment
55. Doses : 5–12yrs
• Salbutamol Accuhaler®: <7200micrograms/day (in 6
doses).
• Salbutamol inhaler: (>12 years) <7200micrograms/day (in
6 doses).
• Terbutaline inhaler: (>12 years) <7200micrograms/day (in
6 doses).
Acute treatment
• Budesonide Turbohaler®: 100–800micrograms/day.
• Beclometasone via Accuhaler®: 100–800micrograms/day.
• Fluticasone via Volumatic®: 100–400micrograms/day.
• Combination inhaler – Seretide® (contains fi xed doses of
fluticasoneand salmeterol); or Symbicort turbohaler® (fi xed
doses of budesonide and formoterol).
Prophylactic treatment
56. General Advices
• Removal of feather or woollen bedding
• Wrapping of mattress in plastic
• Cleaning of carpets and furniture
• No pets in the house if the child is allergic to them
Allergen avoidance
• No smoking in the house or car.
• Parents/carers must be strongly encouraged to stop
smoking completely.
Passive smoking
57. Oxygen therapy
Indications :
• Oxygen therapy should be guided by pulse oximetry .
Give oxygen to children with an oxygen saturation <
90%. When a pulse oximeter is not available, the
necessity for oxygen therapy should be guided by
clinical signs, although they are less reliable. Oxygen
should be given to children with very severe
pneumonia, bronchiolitis or asthma who have:
■ central cyanosis
■ inability to drink (when this is due to respiratory
distress)
58. ■ severe lower chest wall indrawing
■ respiratory rate ≥ 70/min
■ grunting with every breath (in young infants)
■ depressed mental status.
59. Sources
• Oxygen should be available at all times. The two
main sources of oxygen are cylinders and oxygen
concentrators. It is important that all equipment
is checked for compatibility
60. Oxygen delivery :
Nasal prongs are the preferred method of delivery in
most circumstances, as they are safe, non-
invasive, reliable and do not obstruct the nasal
airway. Nasal or nasopharyngeal catheters may be
used as an alternative only when nasal prongs are
not available. The use of headboxes is not
recommended. Face masks with a reservoir
attached to deliver 100% oxygen may be used for
resuscitation.
61. Nasal prongs :
These are short tubes inserted into the nostrils.
Place them just inside the nostrils, and secure
with a piece of tape on the cheeks near the nose.
Care should be taken to keep the nostrils clear of
mucus, which could block the flow of oxygen.
62.
63. ˃ Set a flow rate of 1–2 litres/min (0.5 litre/min
for young infants) to deliver an inspired
oxygen concentration of up to 40%.
Humidification is not required with nasal
prongs
64. Nasal catheter :
a 6 or 8 French gauge catheter that is passed to the
back of he nasal cavity. Insert the catheter at a
distance equal to that from the side of the nostril
to the inner margin of the eyebrow.
65. ˃ Set a fl ow rate of 1–2 litres/min.
Humidification is not required
Nasopharyngeal catheter :
A 6 or 8 French gauge catheter is passed to the
pharynx just below the level of the uvula. Insert
the catheter at a distance equal to that from the
side of the nostril to the front of the ear (see
figure). If it is placed too far down, gagging and
vomiting and, rarely, gastric distension can occur
66.
67. ˃ Set a flow rate of 1–2 litres/min to avoid
gastric distension. Humidification is required.
68. Monitoring :
Train nurses to place and secure the nasal prongs
correctly. Check regularly that the equipment is
working properly, and remove and clean the
prongs at least twice a day.
Monitor the child at least every 3 h to identify
and correct any problems, including:
69. • oxygen saturation, by pulse oximeter
• position of nasal prongs
• leaks in the oxygen delivery system
• correct oxygen flow rate
• airway obstructed by mucus (clear the nose with
a moist wick or by gentle suction)